Richard M. Kirkner

Updated World Health Organization estimates are showing a downward trend in the incidence of gout in North America among 65-year-olds, but men in that age group on the continent are far more likely to suffer from gout than are men in Africa.

That’s a sampling of the updated data on a host of musculoskeletal disorders worldwide, including rheumatoid arthritis, said Dr. Lyn March at the Annual European Congress of Rheumatology.

She presented a preliminary report from the Musculoskeletal Expert Group that’s part of the new Global Burden of Diseases, Injuries, and Risk Factors Study, which began in the spring of 2007. This is the first major effort since the original Global Burden of Disease in 1990 study to carry out a complete systematic assessment of the data on all diseases and injuries, and to produce comprehensive and comparable estimates of the burden of diseases, injuries, and risk factors for two time periods (1990 and 2005), according to the WHO. The project is due to produce final estimates in the spring, said Dr. March of the Royal North Shore Hospital in Sydney.

Dr. March said the specific aims for the Musculoskeletal Expert Group are to include more population-based self-report data; to develop health-state descriptions for different levels of severity of osteoarthritis, rheumatoid arthritis, back pain, neck pain, gout, and other musculoskeletal disorders; and to update systematic literature reviews of incidence, prevalence, and mortality risk for these conditions. The group will also evaluate bone mineral density (g/cm²) as a risk factor for disability-adjusted life-year (DALY) burden, "which will put the [degenerative] bone condition on the map for policy making," she said.

"The methodology employed in the systematic review, development of lay health state descriptions, and generation of data estimates for calculating [DALYs] will be revealed," Dr. March said.

In 2000, the beginning of what the WHO declared "the Bone and Joint Decade," results from the previous Global Burden of Disease (GBD) study reported that rheumatoid arthritis accounted for 0.3% of global DALYs (a time-based measure that combined years of life lost to premature mortality and years of life lost to time lived in health states of less-than-ideal health). "These data enable, in part, an evaluation of the impact of the Bone and Joint Decade and the setting of the research agenda for the next decade," Dr. March said.

The GBD study investigated the incidence of 109 diseases and injuries and 10 risk factors across eight World Bank regions. In 2000, the WHO reported that osteoarthritis accounted for 1.1% of global DALYs, ranking 19th among all diseases and disorders, and rheumatoid arthritis accounted for 0.3% of DALYs. All musculoskeletal disorders combined had a prevalence of 2.1% of the worldwide population and ranked 12th in DALYs among all disorders, according to Dr. March. Preliminary data from the 2005 study show trends toward increases in the prevalence of osteoarthritis of the knee and hip, rheumatoid arthritis, and other musculoskeletal disease, and slight decreases in low-back pain and gout, she said, noting that the findings will likely have policy implications.

A 2005 update reported that musculoskeletal disorders are more common in developed countries.

Dr. March had no disclosures to report. The study received funding from the Bill and Melinda Gates Foundation and the Australian Commonwealth Government’s Department of Health and Aging.

Updated World Health Organization estimates are showing a downward trend in the incidence of gout in North America among 65-year-olds, but men in that age group on the continent are far more likely to suffer from gout than are men in Africa.

That’s a sampling of the updated data on a host of musculoskeletal disorders worldwide, including rheumatoid arthritis, said Dr. Lyn March at the Annual European Congress of Rheumatology.

She presented a preliminary report from the Musculoskeletal Expert Group that’s part of the new Global Burden of Diseases, Injuries, and Risk Factors Study, which began in the spring of 2007. This is the first major effort since the original Global Burden of Disease in 1990 study to carry out a complete systematic assessment of the data on all diseases and injuries, and to produce comprehensive and comparable estimates of the burden of diseases, injuries, and risk factors for two time periods (1990 and 2005), according to the WHO. The project is due to produce final estimates in the spring, said Dr. March of the Royal North Shore Hospital in Sydney.

Dr. March said the specific aims for the Musculoskeletal Expert Group are to include more population-based self-report data; to develop health-state descriptions for different levels of severity of osteoarthritis, rheumatoid arthritis, back pain, neck pain, gout, and other musculoskeletal disorders; and to update systematic literature reviews of incidence, prevalence, and mortality risk for these conditions. The group will also evaluate bone mineral density (g/cm²) as a risk factor for disability-adjusted life-year (DALY) burden, "which will put the [degenerative] bone condition on the map for policy making," she said.

"The methodology employed in the systematic review, development of lay health state descriptions, and generation of data estimates for calculating [DALYs] will be revealed," Dr. March said.

In 2000, the beginning of what the WHO declared "the Bone and Joint Decade," results from the previous Global Burden of Disease (GBD) study reported that rheumatoid arthritis accounted for 0.3% of global DALYs (a time-based measure that combined years of life lost to premature mortality and years of life lost to time lived in health states of less-than-ideal health). "These data enable, in part, an evaluation of the impact of the Bone and Joint Decade and the setting of the research agenda for the next decade," Dr. March said.

The GBD study investigated the incidence of 109 diseases and injuries and 10 risk factors across eight World Bank regions. In 2000, the WHO reported that osteoarthritis accounted for 1.1% of global DALYs, ranking 19th among all diseases and disorders, and rheumatoid arthritis accounted for 0.3% of DALYs. All musculoskeletal disorders combined had a prevalence of 2.1% of the worldwide population and ranked 12th in DALYs among all disorders, according to Dr. March. Preliminary data from the 2005 study show trends toward increases in the prevalence of osteoarthritis of the knee and hip, rheumatoid arthritis, and other musculoskeletal disease, and slight decreases in low-back pain and gout, she said, noting that the findings will likely have policy implications.

A 2005 update reported that musculoskeletal disorders are more common in developed countries.

Dr. March had no disclosures to report. The study received funding from the Bill and Melinda Gates Foundation and the Australian Commonwealth Government’s Department of Health and Aging.

Updated World Health Organization estimates are showing a downward trend in the incidence of gout in North America among 65-year-olds, but men in that age group on the continent are far more likely to suffer from gout than are men in Africa.

That’s a sampling of the updated data on a host of musculoskeletal disorders worldwide, including rheumatoid arthritis, said Dr. Lyn March at the Annual European Congress of Rheumatology.

She presented a preliminary report from the Musculoskeletal Expert Group that’s part of the new Global Burden of Diseases, Injuries, and Risk Factors Study, which began in the spring of 2007. This is the first major effort since the original Global Burden of Disease in 1990 study to carry out a complete systematic assessment of the data on all diseases and injuries, and to produce comprehensive and comparable estimates of the burden of diseases, injuries, and risk factors for two time periods (1990 and 2005), according to the WHO. The project is due to produce final estimates in the spring, said Dr. March of the Royal North Shore Hospital in Sydney.

Dr. March said the specific aims for the Musculoskeletal Expert Group are to include more population-based self-report data; to develop health-state descriptions for different levels of severity of osteoarthritis, rheumatoid arthritis, back pain, neck pain, gout, and other musculoskeletal disorders; and to update systematic literature reviews of incidence, prevalence, and mortality risk for these conditions. The group will also evaluate bone mineral density (g/cm²) as a risk factor for disability-adjusted life-year (DALY) burden, "which will put the [degenerative] bone condition on the map for policy making," she said.

"The methodology employed in the systematic review, development of lay health state descriptions, and generation of data estimates for calculating [DALYs] will be revealed," Dr. March said.

In 2000, the beginning of what the WHO declared "the Bone and Joint Decade," results from the previous Global Burden of Disease (GBD) study reported that rheumatoid arthritis accounted for 0.3% of global DALYs (a time-based measure that combined years of life lost to premature mortality and years of life lost to time lived in health states of less-than-ideal health). "These data enable, in part, an evaluation of the impact of the Bone and Joint Decade and the setting of the research agenda for the next decade," Dr. March said.

The GBD study investigated the incidence of 109 diseases and injuries and 10 risk factors across eight World Bank regions. In 2000, the WHO reported that osteoarthritis accounted for 1.1% of global DALYs, ranking 19th among all diseases and disorders, and rheumatoid arthritis accounted for 0.3% of DALYs. All musculoskeletal disorders combined had a prevalence of 2.1% of the worldwide population and ranked 12th in DALYs among all disorders, according to Dr. March. Preliminary data from the 2005 study show trends toward increases in the prevalence of osteoarthritis of the knee and hip, rheumatoid arthritis, and other musculoskeletal disease, and slight decreases in low-back pain and gout, she said, noting that the findings will likely have policy implications.

A 2005 update reported that musculoskeletal disorders are more common in developed countries.

Dr. March had no disclosures to report. The study received funding from the Bill and Melinda Gates Foundation and the Australian Commonwealth Government’s Department of Health and Aging.

Recent laboratory findings from Australia have shown a strong correlation between gum disease and worsening signs and symptoms of rheumatoid arthritis, one of the lead investigators reported May 25.

During his presentation at the annual European Congress of Rheumatology, Mark Bartold, Ph.D., who is a periodontist and the director of the Colgate Dental Research Centre at the University of Adelaide (South Australia), discussed his group’s recently published study of laboratory mice with preexisting periodontitis and worsening RA. "Emerging evidence now suggests a strong relationship between the extent and severity of periodontal disease and rheumatoid arthritis," Dr. Bartold said in an interview.

The experiments showed that mice with coexisting periodontitis and RA exhibited more severe joint inflammation than did the mice with just RA, he said. Also, mice with both periodontitis and RA were more likely to demonstrate signs of arthritis in their rear paws, compared with mice with arthritis only. The progress of RA in mice with both conditions followed a more rapid course than it did in mice with just RA or just periodontitis, he reported.

Gum disease and RA could be related through common underlying dysfunction of fundamental inflammatory mechanisms. The nature of the dysfunction remains unknown, but recent scientific studies have suggested a link between the two, he said.

Although this relationship is unlikely to be causal, it is clear that individuals with advanced RA are more likely to have significant periodontal problems, compared with their nonrheumatoid counterparts. Likewise, people with severe gingivitis are more likely to have severe RA. Data from earlier studies have shown that individuals with RA had a 3.6-fold greater risk of moderate to severe periodontitis, and those with gum disease had a 2.2-fold greater risk of RA than did the general population.

Other studies have demonstrated that OPG (osteoprotegerin) and RANKL (receptor-activated nuclear factor–kappaB ligand) are highly expressed in both RA synovium and periodontitis lesions. Dr. Bartold noted pilot studies that have confirmed the potential to identify periodontal pathogen DNA in synovial tissues and inflamed human periodontal tissues. "It remains to be established whether treatment of periodontal disease and reduction of periodontal inflammation in patients with chronic rheumatoid arthritis will reduce the disease activity of rheumatoid arthritis," Dr. Bartold said.

Dr. Bartold’s research suggests that periodontitis and rheumatoid arthritis share a common development pathway within the RANK/RANKL/OPG axis, where a drop in OPG leads to reduced vascular protection. "Increases in RANKL levels within inflamed tissues may result in not only the development of vascular damage, but also activation of osteoclasts and subsequent bone resorption," he said.

The role of bacteria in arthritis has also garnered considerable attention, noted Dr. Bartold. Animal studies have demonstrated that arthritis can develop in response to different stimuli and through different effector pathways, including exogenous infections or microbial antigens. "If these observations are also applicable to human rheumatoid arthritis, we might expect that different types of infections – as well as other environmental exposures with the capacity to induce excessive proinflammatory cytokines in genetically susceptible individuals – may contribute to disease," he said.

Among the pathogens that have been implicated in rheumatoid arthritis patients are periodontopathic bacteria including Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, Bacteroides forsythus, and Aggregatibacter actinomycetemcomitans. Elevated antibodies to B. forsythus and P. intermedia have also been found in synovial fluid, he added.

The ultimate goal of emerging research is to determine whether the reduction of periodontal inflammation improves the disease activity of RA, he said. The clinical implications of these findings are that early intervention strategies to aid in the overall management of rheumatoid arthritis could include a periodontal assessment.

Dr. Bartold disclosed that he receives research support from the National Health and Medical Research Council of Australia, and acts as a consultant for Colgate and Nobel Biocare.

Recent laboratory findings from Australia have shown a strong correlation between gum disease and worsening signs and symptoms of rheumatoid arthritis, one of the lead investigators reported May 25.

During his presentation at the annual European Congress of Rheumatology, Mark Bartold, Ph.D., who is a periodontist and the director of the Colgate Dental Research Centre at the University of Adelaide (South Australia), discussed his group’s recently published study of laboratory mice with preexisting periodontitis and worsening RA. "Emerging evidence now suggests a strong relationship between the extent and severity of periodontal disease and rheumatoid arthritis," Dr. Bartold said in an interview.

The experiments showed that mice with coexisting periodontitis and RA exhibited more severe joint inflammation than did the mice with just RA, he said. Also, mice with both periodontitis and RA were more likely to demonstrate signs of arthritis in their rear paws, compared with mice with arthritis only. The progress of RA in mice with both conditions followed a more rapid course than it did in mice with just RA or just periodontitis, he reported.

Gum disease and RA could be related through common underlying dysfunction of fundamental inflammatory mechanisms. The nature of the dysfunction remains unknown, but recent scientific studies have suggested a link between the two, he said.

Although this relationship is unlikely to be causal, it is clear that individuals with advanced RA are more likely to have significant periodontal problems, compared with their nonrheumatoid counterparts. Likewise, people with severe gingivitis are more likely to have severe RA. Data from earlier studies have shown that individuals with RA had a 3.6-fold greater risk of moderate to severe periodontitis, and those with gum disease had a 2.2-fold greater risk of RA than did the general population.

Other studies have demonstrated that OPG (osteoprotegerin) and RANKL (receptor-activated nuclear factor–kappaB ligand) are highly expressed in both RA synovium and periodontitis lesions. Dr. Bartold noted pilot studies that have confirmed the potential to identify periodontal pathogen DNA in synovial tissues and inflamed human periodontal tissues. "It remains to be established whether treatment of periodontal disease and reduction of periodontal inflammation in patients with chronic rheumatoid arthritis will reduce the disease activity of rheumatoid arthritis," Dr. Bartold said.

Dr. Bartold’s research suggests that periodontitis and rheumatoid arthritis share a common development pathway within the RANK/RANKL/OPG axis, where a drop in OPG leads to reduced vascular protection. "Increases in RANKL levels within inflamed tissues may result in not only the development of vascular damage, but also activation of osteoclasts and subsequent bone resorption," he said.

The role of bacteria in arthritis has also garnered considerable attention, noted Dr. Bartold. Animal studies have demonstrated that arthritis can develop in response to different stimuli and through different effector pathways, including exogenous infections or microbial antigens. "If these observations are also applicable to human rheumatoid arthritis, we might expect that different types of infections – as well as other environmental exposures with the capacity to induce excessive proinflammatory cytokines in genetically susceptible individuals – may contribute to disease," he said.

Among the pathogens that have been implicated in rheumatoid arthritis patients are periodontopathic bacteria including Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, Bacteroides forsythus, and Aggregatibacter actinomycetemcomitans. Elevated antibodies to B. forsythus and P. intermedia have also been found in synovial fluid, he added.

The ultimate goal of emerging research is to determine whether the reduction of periodontal inflammation improves the disease activity of RA, he said. The clinical implications of these findings are that early intervention strategies to aid in the overall management of rheumatoid arthritis could include a periodontal assessment.

Dr. Bartold disclosed that he receives research support from the National Health and Medical Research Council of Australia, and acts as a consultant for Colgate and Nobel Biocare.

Recent laboratory findings from Australia have shown a strong correlation between gum disease and worsening signs and symptoms of rheumatoid arthritis, one of the lead investigators reported May 25.

During his presentation at the annual European Congress of Rheumatology, Mark Bartold, Ph.D., who is a periodontist and the director of the Colgate Dental Research Centre at the University of Adelaide (South Australia), discussed his group’s recently published study of laboratory mice with preexisting periodontitis and worsening RA. "Emerging evidence now suggests a strong relationship between the extent and severity of periodontal disease and rheumatoid arthritis," Dr. Bartold said in an interview.

The experiments showed that mice with coexisting periodontitis and RA exhibited more severe joint inflammation than did the mice with just RA, he said. Also, mice with both periodontitis and RA were more likely to demonstrate signs of arthritis in their rear paws, compared with mice with arthritis only. The progress of RA in mice with both conditions followed a more rapid course than it did in mice with just RA or just periodontitis, he reported.

Gum disease and RA could be related through common underlying dysfunction of fundamental inflammatory mechanisms. The nature of the dysfunction remains unknown, but recent scientific studies have suggested a link between the two, he said.

Although this relationship is unlikely to be causal, it is clear that individuals with advanced RA are more likely to have significant periodontal problems, compared with their nonrheumatoid counterparts. Likewise, people with severe gingivitis are more likely to have severe RA. Data from earlier studies have shown that individuals with RA had a 3.6-fold greater risk of moderate to severe periodontitis, and those with gum disease had a 2.2-fold greater risk of RA than did the general population.

Other studies have demonstrated that OPG (osteoprotegerin) and RANKL (receptor-activated nuclear factor–kappaB ligand) are highly expressed in both RA synovium and periodontitis lesions. Dr. Bartold noted pilot studies that have confirmed the potential to identify periodontal pathogen DNA in synovial tissues and inflamed human periodontal tissues. "It remains to be established whether treatment of periodontal disease and reduction of periodontal inflammation in patients with chronic rheumatoid arthritis will reduce the disease activity of rheumatoid arthritis," Dr. Bartold said.

Dr. Bartold’s research suggests that periodontitis and rheumatoid arthritis share a common development pathway within the RANK/RANKL/OPG axis, where a drop in OPG leads to reduced vascular protection. "Increases in RANKL levels within inflamed tissues may result in not only the development of vascular damage, but also activation of osteoclasts and subsequent bone resorption," he said.

The role of bacteria in arthritis has also garnered considerable attention, noted Dr. Bartold. Animal studies have demonstrated that arthritis can develop in response to different stimuli and through different effector pathways, including exogenous infections or microbial antigens. "If these observations are also applicable to human rheumatoid arthritis, we might expect that different types of infections – as well as other environmental exposures with the capacity to induce excessive proinflammatory cytokines in genetically susceptible individuals – may contribute to disease," he said.

Among the pathogens that have been implicated in rheumatoid arthritis patients are periodontopathic bacteria including Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, Bacteroides forsythus, and Aggregatibacter actinomycetemcomitans. Elevated antibodies to B. forsythus and P. intermedia have also been found in synovial fluid, he added.

The ultimate goal of emerging research is to determine whether the reduction of periodontal inflammation improves the disease activity of RA, he said. The clinical implications of these findings are that early intervention strategies to aid in the overall management of rheumatoid arthritis could include a periodontal assessment.

Dr. Bartold disclosed that he receives research support from the National Health and Medical Research Council of Australia, and acts as a consultant for Colgate and Nobel Biocare.

Recent laboratory findings from Australia have shown a strong correlation between gum disease and worsening signs and symptoms of rheumatoid arthritis, one of the lead investigators reported May 25.

During his presentation at the annual European Congress of Rheumatology, Mark Bartold, Ph.D., who is a periodontist and the director of the Colgate Dental Research Centre at the University of Adelaide (South Australia), discussed his group’s recently published study of laboratory mice with preexisting periodontitis and worsening RA. "Emerging evidence now suggests a strong relationship between the extent and severity of periodontal disease and rheumatoid arthritis," Dr. Bartold said in an interview.

The experiments showed that mice with coexisting periodontitis and RA exhibited more severe joint inflammation than did the mice with just RA, he said. Also, mice with both periodontitis and RA were more likely to demonstrate signs of arthritis in their rear paws, compared with mice with arthritis only. The progress of RA in mice with both conditions followed a more rapid course than it did in mice with just RA or just periodontitis, he reported.

Gum disease and RA could be related through common underlying dysfunction of fundamental inflammatory mechanisms. The nature of the dysfunction remains unknown, but recent scientific studies have suggested a link between the two, he said.

Although this relationship is unlikely to be causal, it is clear that individuals with advanced RA are more likely to have significant periodontal problems, compared with their nonrheumatoid counterparts. Likewise, people with severe gingivitis are more likely to have severe RA. Data from earlier studies have shown that individuals with RA had a 3.6-fold greater risk of moderate to severe periodontitis, and those with gum disease had a 2.2-fold greater risk of RA than did the general population.

Other studies have demonstrated that OPG (osteoprotegerin) and RANKL (receptor-activated nuclear factor–kappaB ligand) are highly expressed in both RA synovium and periodontitis lesions. Dr. Bartold noted pilot studies that have confirmed the potential to identify periodontal pathogen DNA in synovial tissues and inflamed human periodontal tissues. "It remains to be established whether treatment of periodontal disease and reduction of periodontal inflammation in patients with chronic rheumatoid arthritis will reduce the disease activity of rheumatoid arthritis," Dr. Bartold said.

Dr. Bartold’s research suggests that periodontitis and rheumatoid arthritis share a common development pathway within the RANK/RANKL/OPG axis, where a drop in OPG leads to reduced vascular protection. "Increases in RANKL levels within inflamed tissues may result in not only the development of vascular damage, but also activation of osteoclasts and subsequent bone resorption," he said.

The role of bacteria in arthritis has also garnered considerable attention, noted Dr. Bartold. Animal studies have demonstrated that arthritis can develop in response to different stimuli and through different effector pathways, including exogenous infections or microbial antigens. "If these observations are also applicable to human rheumatoid arthritis, we might expect that different types of infections – as well as other environmental exposures with the capacity to induce excessive proinflammatory cytokines in genetically susceptible individuals – may contribute to disease," he said.

Among the pathogens that have been implicated in rheumatoid arthritis patients are periodontopathic bacteria including Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, Bacteroides forsythus, and Aggregatibacter actinomycetemcomitans. Elevated antibodies to B. forsythus and P. intermedia have also been found in synovial fluid, he added.

The ultimate goal of emerging research is to determine whether the reduction of periodontal inflammation improves the disease activity of RA, he said. The clinical implications of these findings are that early intervention strategies to aid in the overall management of rheumatoid arthritis could include a periodontal assessment.

Dr. Bartold disclosed that he receives research support from the National Health and Medical Research Council of Australia, and acts as a consultant for Colgate and Nobel Biocare.

Recent laboratory findings from Australia have shown a strong correlation between gum disease and worsening signs and symptoms of rheumatoid arthritis, one of the lead investigators reported May 25.

During his presentation at the annual European Congress of Rheumatology, Mark Bartold, Ph.D., who is a periodontist and the director of the Colgate Dental Research Centre at the University of Adelaide (South Australia), discussed his group’s recently published study of laboratory mice with preexisting periodontitis and worsening RA. "Emerging evidence now suggests a strong relationship between the extent and severity of periodontal disease and rheumatoid arthritis," Dr. Bartold said in an interview.

The experiments showed that mice with coexisting periodontitis and RA exhibited more severe joint inflammation than did the mice with just RA, he said. Also, mice with both periodontitis and RA were more likely to demonstrate signs of arthritis in their rear paws, compared with mice with arthritis only. The progress of RA in mice with both conditions followed a more rapid course than it did in mice with just RA or just periodontitis, he reported.

Gum disease and RA could be related through common underlying dysfunction of fundamental inflammatory mechanisms. The nature of the dysfunction remains unknown, but recent scientific studies have suggested a link between the two, he said.

Although this relationship is unlikely to be causal, it is clear that individuals with advanced RA are more likely to have significant periodontal problems, compared with their nonrheumatoid counterparts. Likewise, people with severe gingivitis are more likely to have severe RA. Data from earlier studies have shown that individuals with RA had a 3.6-fold greater risk of moderate to severe periodontitis, and those with gum disease had a 2.2-fold greater risk of RA than did the general population.

Other studies have demonstrated that OPG (osteoprotegerin) and RANKL (receptor-activated nuclear factor–kappaB ligand) are highly expressed in both RA synovium and periodontitis lesions. Dr. Bartold noted pilot studies that have confirmed the potential to identify periodontal pathogen DNA in synovial tissues and inflamed human periodontal tissues. "It remains to be established whether treatment of periodontal disease and reduction of periodontal inflammation in patients with chronic rheumatoid arthritis will reduce the disease activity of rheumatoid arthritis," Dr. Bartold said.

Dr. Bartold’s research suggests that periodontitis and rheumatoid arthritis share a common development pathway within the RANK/RANKL/OPG axis, where a drop in OPG leads to reduced vascular protection. "Increases in RANKL levels within inflamed tissues may result in not only the development of vascular damage, but also activation of osteoclasts and subsequent bone resorption," he said.

The role of bacteria in arthritis has also garnered considerable attention, noted Dr. Bartold. Animal studies have demonstrated that arthritis can develop in response to different stimuli and through different effector pathways, including exogenous infections or microbial antigens. "If these observations are also applicable to human rheumatoid arthritis, we might expect that different types of infections – as well as other environmental exposures with the capacity to induce excessive proinflammatory cytokines in genetically susceptible individuals – may contribute to disease," he said.

Among the pathogens that have been implicated in rheumatoid arthritis patients are periodontopathic bacteria including Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, Bacteroides forsythus, and Aggregatibacter actinomycetemcomitans. Elevated antibodies to B. forsythus and P. intermedia have also been found in synovial fluid, he added.

The ultimate goal of emerging research is to determine whether the reduction of periodontal inflammation improves the disease activity of RA, he said. The clinical implications of these findings are that early intervention strategies to aid in the overall management of rheumatoid arthritis could include a periodontal assessment.

Dr. Bartold disclosed that he receives research support from the National Health and Medical Research Council of Australia, and acts as a consultant for Colgate and Nobel Biocare.

Recent laboratory findings from Australia have shown a strong correlation between gum disease and worsening signs and symptoms of rheumatoid arthritis, one of the lead investigators reported May 25.

During his presentation at the annual European Congress of Rheumatology, Mark Bartold, Ph.D., who is a periodontist and the director of the Colgate Dental Research Centre at the University of Adelaide (South Australia), discussed his group’s recently published study of laboratory mice with preexisting periodontitis and worsening RA. "Emerging evidence now suggests a strong relationship between the extent and severity of periodontal disease and rheumatoid arthritis," Dr. Bartold said in an interview.

The experiments showed that mice with coexisting periodontitis and RA exhibited more severe joint inflammation than did the mice with just RA, he said. Also, mice with both periodontitis and RA were more likely to demonstrate signs of arthritis in their rear paws, compared with mice with arthritis only. The progress of RA in mice with both conditions followed a more rapid course than it did in mice with just RA or just periodontitis, he reported.

Gum disease and RA could be related through common underlying dysfunction of fundamental inflammatory mechanisms. The nature of the dysfunction remains unknown, but recent scientific studies have suggested a link between the two, he said.

Although this relationship is unlikely to be causal, it is clear that individuals with advanced RA are more likely to have significant periodontal problems, compared with their nonrheumatoid counterparts. Likewise, people with severe gingivitis are more likely to have severe RA. Data from earlier studies have shown that individuals with RA had a 3.6-fold greater risk of moderate to severe periodontitis, and those with gum disease had a 2.2-fold greater risk of RA than did the general population.

Other studies have demonstrated that OPG (osteoprotegerin) and RANKL (receptor-activated nuclear factor–kappaB ligand) are highly expressed in both RA synovium and periodontitis lesions. Dr. Bartold noted pilot studies that have confirmed the potential to identify periodontal pathogen DNA in synovial tissues and inflamed human periodontal tissues. "It remains to be established whether treatment of periodontal disease and reduction of periodontal inflammation in patients with chronic rheumatoid arthritis will reduce the disease activity of rheumatoid arthritis," Dr. Bartold said.

Dr. Bartold’s research suggests that periodontitis and rheumatoid arthritis share a common development pathway within the RANK/RANKL/OPG axis, where a drop in OPG leads to reduced vascular protection. "Increases in RANKL levels within inflamed tissues may result in not only the development of vascular damage, but also activation of osteoclasts and subsequent bone resorption," he said.

The role of bacteria in arthritis has also garnered considerable attention, noted Dr. Bartold. Animal studies have demonstrated that arthritis can develop in response to different stimuli and through different effector pathways, including exogenous infections or microbial antigens. "If these observations are also applicable to human rheumatoid arthritis, we might expect that different types of infections – as well as other environmental exposures with the capacity to induce excessive proinflammatory cytokines in genetically susceptible individuals – may contribute to disease," he said.

Among the pathogens that have been implicated in rheumatoid arthritis patients are periodontopathic bacteria including Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, Bacteroides forsythus, and Aggregatibacter actinomycetemcomitans. Elevated antibodies to B. forsythus and P. intermedia have also been found in synovial fluid, he added.

The ultimate goal of emerging research is to determine whether the reduction of periodontal inflammation improves the disease activity of RA, he said. The clinical implications of these findings are that early intervention strategies to aid in the overall management of rheumatoid arthritis could include a periodontal assessment.

Dr. Bartold disclosed that he receives research support from the National Health and Medical Research Council of Australia, and acts as a consultant for Colgate and Nobel Biocare.

NEW YORK – Clinical trials using biomarkers to guide therapy in systolic heart failure have shown that, while the approach is still considered investigative, it may help identify patients at risk of hospitalization, heart attack or death, according to Dr. Hans Peter Brunner-La Rocca of Maastricht (Netherlands) University.

Dr. Brunner-La Rocca presented an update on the use of intensified therapy guided by B-type natriuretic peptide (BNP) at the annual New York Cardiovascular Symposium. "The predictive value of BNP is quite high," he said. "If you see a patient for the first time who is untreated with low BNP, heart failure is rather unlikely." Dr. Brunner-La Rocca is a coinvestigator of TIME-CHF (Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure) (JAMA 2009;301:383-92).

[PROTECT Trial Opens Door to Biomarker-Guided Heart Failure Therapy]

While BNP-guided biomarker therapy has not been tested sufficiently to merit widespread use, it can be helpful in identifying at-risk patients, Dr. Brunner-La Rocca said. It can treat underlying coronary artery disease, heart valve disease or myocarditis, or complications from mitral valve regurgitation and anemia. He listed three prognostic factors that can help guide therapy: spiro-ergometry in transplantation, left ventricular ejection fraction in patients with implantable cardioverter devices, and hemodynamics.

Dr. Brunner-La Rocca discussed seven clinical trials that treated almost 14,000 patients with N-terminal BNP (NT-BNP) and almost 800 with BNP guidance. The TIME-CHF trial of NT-BNP showed that patients under age 75 years who had intensified BNP-guided therapy had fewer hospitalizations, improved survival, and fewer symptoms of heart failure than did those who received standard treatment. However, patients over age 75 showed almost identical outcomes for the BNP and standard therapy groups after 18 months.

"An end point we looked at was hospitalization-free survival because we thought when we intensify therapy maybe we do something good for the heart, but we’re not so certain when we provoke more side effects," he said. Compared with the symptom-guided group, the NT-BNP–guided group had fewer hospitalizations – 28% vs. 38% in the standard treatment group.

Meanwhile, Dr. Brunner-La Rocca pointed out the Systolic Heart Failure Treatment Supported by BNP (STARS-BNP) trial "showed a positive effect on survival and extensive reduction in cardiac events" (N. Engl. J. Med. 2008;358:2148-59).

However, Dr. Brunner-La Rocca also noted that the variance among the studies analyzed may cause confusion about the effectiveness of BNP-guided therapy. "The other studies were not all that positive," he said. "The largest study so far actually showed a negative result – basically no effect at all – and reported a substantial amount of events."

Two more recent meta-analyses have shown improved survival with BNP guidance (Arch. Intern. Med. 2010;170:507-14 and Am. Heart J. 2009;158:422-30). "When I looked at the results, I’m not quite sure where these numbers are coming from," Dr. Brunner-La Rocca said. "I think this part of the analysis is to some extent flawed."

An ongoing analysis of all the BNP trials may provide some answers when its results are published, he said.

Still, he uses BNP-guided therapy in some of his patients. "I happen to think it is still of value, particularly if I have doubts about the patient’s diagnostics," Dr. Brunner-La Rocca said. "Many of these patients have other disease, and to really know the BNP can help differentiate if the heart or some other disease mechanism is to blame. In addition, it may help to identify patients at risk, particularly younger ones."

Dr. Brunner-La Rocca had no disclosures.

NEW YORK – Clinical trials using biomarkers to guide therapy in systolic heart failure have shown that, while the approach is still considered investigative, it may help identify patients at risk of hospitalization, heart attack or death, according to Dr. Hans Peter Brunner-La Rocca of Maastricht (Netherlands) University.

Dr. Brunner-La Rocca presented an update on the use of intensified therapy guided by B-type natriuretic peptide (BNP) at the annual New York Cardiovascular Symposium. "The predictive value of BNP is quite high," he said. "If you see a patient for the first time who is untreated with low BNP, heart failure is rather unlikely." Dr. Brunner-La Rocca is a coinvestigator of TIME-CHF (Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure) (JAMA 2009;301:383-92).

[PROTECT Trial Opens Door to Biomarker-Guided Heart Failure Therapy]

While BNP-guided biomarker therapy has not been tested sufficiently to merit widespread use, it can be helpful in identifying at-risk patients, Dr. Brunner-La Rocca said. It can treat underlying coronary artery disease, heart valve disease or myocarditis, or complications from mitral valve regurgitation and anemia. He listed three prognostic factors that can help guide therapy: spiro-ergometry in transplantation, left ventricular ejection fraction in patients with implantable cardioverter devices, and hemodynamics.

Dr. Brunner-La Rocca discussed seven clinical trials that treated almost 14,000 patients with N-terminal BNP (NT-BNP) and almost 800 with BNP guidance. The TIME-CHF trial of NT-BNP showed that patients under age 75 years who had intensified BNP-guided therapy had fewer hospitalizations, improved survival, and fewer symptoms of heart failure than did those who received standard treatment. However, patients over age 75 showed almost identical outcomes for the BNP and standard therapy groups after 18 months.

"An end point we looked at was hospitalization-free survival because we thought when we intensify therapy maybe we do something good for the heart, but we’re not so certain when we provoke more side effects," he said. Compared with the symptom-guided group, the NT-BNP–guided group had fewer hospitalizations – 28% vs. 38% in the standard treatment group.

Meanwhile, Dr. Brunner-La Rocca pointed out the Systolic Heart Failure Treatment Supported by BNP (STARS-BNP) trial "showed a positive effect on survival and extensive reduction in cardiac events" (N. Engl. J. Med. 2008;358:2148-59).

However, Dr. Brunner-La Rocca also noted that the variance among the studies analyzed may cause confusion about the effectiveness of BNP-guided therapy. "The other studies were not all that positive," he said. "The largest study so far actually showed a negative result – basically no effect at all – and reported a substantial amount of events."

Two more recent meta-analyses have shown improved survival with BNP guidance (Arch. Intern. Med. 2010;170:507-14 and Am. Heart J. 2009;158:422-30). "When I looked at the results, I’m not quite sure where these numbers are coming from," Dr. Brunner-La Rocca said. "I think this part of the analysis is to some extent flawed."

An ongoing analysis of all the BNP trials may provide some answers when its results are published, he said.

Still, he uses BNP-guided therapy in some of his patients. "I happen to think it is still of value, particularly if I have doubts about the patient’s diagnostics," Dr. Brunner-La Rocca said. "Many of these patients have other disease, and to really know the BNP can help differentiate if the heart or some other disease mechanism is to blame. In addition, it may help to identify patients at risk, particularly younger ones."

Dr. Brunner-La Rocca had no disclosures.

NEW YORK – Clinical trials using biomarkers to guide therapy in systolic heart failure have shown that, while the approach is still considered investigative, it may help identify patients at risk of hospitalization, heart attack or death, according to Dr. Hans Peter Brunner-La Rocca of Maastricht (Netherlands) University.

Dr. Brunner-La Rocca presented an update on the use of intensified therapy guided by B-type natriuretic peptide (BNP) at the annual New York Cardiovascular Symposium. "The predictive value of BNP is quite high," he said. "If you see a patient for the first time who is untreated with low BNP, heart failure is rather unlikely." Dr. Brunner-La Rocca is a coinvestigator of TIME-CHF (Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure) (JAMA 2009;301:383-92).

[PROTECT Trial Opens Door to Biomarker-Guided Heart Failure Therapy]

While BNP-guided biomarker therapy has not been tested sufficiently to merit widespread use, it can be helpful in identifying at-risk patients, Dr. Brunner-La Rocca said. It can treat underlying coronary artery disease, heart valve disease or myocarditis, or complications from mitral valve regurgitation and anemia. He listed three prognostic factors that can help guide therapy: spiro-ergometry in transplantation, left ventricular ejection fraction in patients with implantable cardioverter devices, and hemodynamics.

Dr. Brunner-La Rocca discussed seven clinical trials that treated almost 14,000 patients with N-terminal BNP (NT-BNP) and almost 800 with BNP guidance. The TIME-CHF trial of NT-BNP showed that patients under age 75 years who had intensified BNP-guided therapy had fewer hospitalizations, improved survival, and fewer symptoms of heart failure than did those who received standard treatment. However, patients over age 75 showed almost identical outcomes for the BNP and standard therapy groups after 18 months.

"An end point we looked at was hospitalization-free survival because we thought when we intensify therapy maybe we do something good for the heart, but we’re not so certain when we provoke more side effects," he said. Compared with the symptom-guided group, the NT-BNP–guided group had fewer hospitalizations – 28% vs. 38% in the standard treatment group.

Meanwhile, Dr. Brunner-La Rocca pointed out the Systolic Heart Failure Treatment Supported by BNP (STARS-BNP) trial "showed a positive effect on survival and extensive reduction in cardiac events" (N. Engl. J. Med. 2008;358:2148-59).

However, Dr. Brunner-La Rocca also noted that the variance among the studies analyzed may cause confusion about the effectiveness of BNP-guided therapy. "The other studies were not all that positive," he said. "The largest study so far actually showed a negative result – basically no effect at all – and reported a substantial amount of events."

Two more recent meta-analyses have shown improved survival with BNP guidance (Arch. Intern. Med. 2010;170:507-14 and Am. Heart J. 2009;158:422-30). "When I looked at the results, I’m not quite sure where these numbers are coming from," Dr. Brunner-La Rocca said. "I think this part of the analysis is to some extent flawed."

An ongoing analysis of all the BNP trials may provide some answers when its results are published, he said.

Still, he uses BNP-guided therapy in some of his patients. "I happen to think it is still of value, particularly if I have doubts about the patient’s diagnostics," Dr. Brunner-La Rocca said. "Many of these patients have other disease, and to really know the BNP can help differentiate if the heart or some other disease mechanism is to blame. In addition, it may help to identify patients at risk, particularly younger ones."

Dr. Brunner-La Rocca had no disclosures.

NEW YORK – Clinical trials using biomarkers to guide therapy in systolic heart failure have shown that, while the approach is still considered investigative, it may help identify patients at risk of hospitalization, heart attack or death, according to Dr. Hans Peter Brunner-La Rocca of Maastricht (Netherlands) University.

Dr. Brunner-La Rocca presented an update on the use of intensified therapy guided by B-type natriuretic peptide (BNP) at the annual New York Cardiovascular Symposium. "The predictive value of BNP is quite high," he said. "If you see a patient for the first time who is untreated with low BNP, heart failure is rather unlikely." Dr. Brunner-La Rocca is a coinvestigator of TIME-CHF (Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure) (JAMA 2009;301:383-92).

[PROTECT Trial Opens Door to Biomarker-Guided Heart Failure Therapy]

While BNP-guided biomarker therapy has not been tested sufficiently to merit widespread use, it can be helpful in identifying at-risk patients, Dr. Brunner-La Rocca said. It can treat underlying coronary artery disease, heart valve disease or myocarditis, or complications from mitral valve regurgitation and anemia. He listed three prognostic factors that can help guide therapy: spiro-ergometry in transplantation, left ventricular ejection fraction in patients with implantable cardioverter devices, and hemodynamics.

Dr. Brunner-La Rocca discussed seven clinical trials that treated almost 14,000 patients with N-terminal BNP (NT-BNP) and almost 800 with BNP guidance. The TIME-CHF trial of NT-BNP showed that patients under age 75 years who had intensified BNP-guided therapy had fewer hospitalizations, improved survival, and fewer symptoms of heart failure than did those who received standard treatment. However, patients over age 75 showed almost identical outcomes for the BNP and standard therapy groups after 18 months.

"An end point we looked at was hospitalization-free survival because we thought when we intensify therapy maybe we do something good for the heart, but we’re not so certain when we provoke more side effects," he said. Compared with the symptom-guided group, the NT-BNP–guided group had fewer hospitalizations – 28% vs. 38% in the standard treatment group.

Meanwhile, Dr. Brunner-La Rocca pointed out the Systolic Heart Failure Treatment Supported by BNP (STARS-BNP) trial "showed a positive effect on survival and extensive reduction in cardiac events" (N. Engl. J. Med. 2008;358:2148-59).

However, Dr. Brunner-La Rocca also noted that the variance among the studies analyzed may cause confusion about the effectiveness of BNP-guided therapy. "The other studies were not all that positive," he said. "The largest study so far actually showed a negative result – basically no effect at all – and reported a substantial amount of events."

Two more recent meta-analyses have shown improved survival with BNP guidance (Arch. Intern. Med. 2010;170:507-14 and Am. Heart J. 2009;158:422-30). "When I looked at the results, I’m not quite sure where these numbers are coming from," Dr. Brunner-La Rocca said. "I think this part of the analysis is to some extent flawed."

An ongoing analysis of all the BNP trials may provide some answers when its results are published, he said.

Still, he uses BNP-guided therapy in some of his patients. "I happen to think it is still of value, particularly if I have doubts about the patient’s diagnostics," Dr. Brunner-La Rocca said. "Many of these patients have other disease, and to really know the BNP can help differentiate if the heart or some other disease mechanism is to blame. In addition, it may help to identify patients at risk, particularly younger ones."

Dr. Brunner-La Rocca had no disclosures.

NEW YORK – Clinical trials using biomarkers to guide therapy in systolic heart failure have shown that, while the approach is still considered investigative, it may help identify patients at risk of hospitalization, heart attack or death, according to Dr. Hans Peter Brunner-La Rocca of Maastricht (Netherlands) University.

Dr. Brunner-La Rocca presented an update on the use of intensified therapy guided by B-type natriuretic peptide (BNP) at the annual New York Cardiovascular Symposium. "The predictive value of BNP is quite high," he said. "If you see a patient for the first time who is untreated with low BNP, heart failure is rather unlikely." Dr. Brunner-La Rocca is a coinvestigator of TIME-CHF (Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure) (JAMA 2009;301:383-92).

[PROTECT Trial Opens Door to Biomarker-Guided Heart Failure Therapy]

While BNP-guided biomarker therapy has not been tested sufficiently to merit widespread use, it can be helpful in identifying at-risk patients, Dr. Brunner-La Rocca said. It can treat underlying coronary artery disease, heart valve disease or myocarditis, or complications from mitral valve regurgitation and anemia. He listed three prognostic factors that can help guide therapy: spiro-ergometry in transplantation, left ventricular ejection fraction in patients with implantable cardioverter devices, and hemodynamics.

Dr. Brunner-La Rocca discussed seven clinical trials that treated almost 14,000 patients with N-terminal BNP (NT-BNP) and almost 800 with BNP guidance. The TIME-CHF trial of NT-BNP showed that patients under age 75 years who had intensified BNP-guided therapy had fewer hospitalizations, improved survival, and fewer symptoms of heart failure than did those who received standard treatment. However, patients over age 75 showed almost identical outcomes for the BNP and standard therapy groups after 18 months.

"An end point we looked at was hospitalization-free survival because we thought when we intensify therapy maybe we do something good for the heart, but we’re not so certain when we provoke more side effects," he said. Compared with the symptom-guided group, the NT-BNP–guided group had fewer hospitalizations – 28% vs. 38% in the standard treatment group.

Meanwhile, Dr. Brunner-La Rocca pointed out the Systolic Heart Failure Treatment Supported by BNP (STARS-BNP) trial "showed a positive effect on survival and extensive reduction in cardiac events" (N. Engl. J. Med. 2008;358:2148-59).

However, Dr. Brunner-La Rocca also noted that the variance among the studies analyzed may cause confusion about the effectiveness of BNP-guided therapy. "The other studies were not all that positive," he said. "The largest study so far actually showed a negative result – basically no effect at all – and reported a substantial amount of events."

Two more recent meta-analyses have shown improved survival with BNP guidance (Arch. Intern. Med. 2010;170:507-14 and Am. Heart J. 2009;158:422-30). "When I looked at the results, I’m not quite sure where these numbers are coming from," Dr. Brunner-La Rocca said. "I think this part of the analysis is to some extent flawed."

An ongoing analysis of all the BNP trials may provide some answers when its results are published, he said.

Still, he uses BNP-guided therapy in some of his patients. "I happen to think it is still of value, particularly if I have doubts about the patient’s diagnostics," Dr. Brunner-La Rocca said. "Many of these patients have other disease, and to really know the BNP can help differentiate if the heart or some other disease mechanism is to blame. In addition, it may help to identify patients at risk, particularly younger ones."

Dr. Brunner-La Rocca had no disclosures.

NEW YORK – Clinical trials using biomarkers to guide therapy in systolic heart failure have shown that, while the approach is still considered investigative, it may help identify patients at risk of hospitalization, heart attack or death, according to Dr. Hans Peter Brunner-La Rocca of Maastricht (Netherlands) University.

Dr. Brunner-La Rocca presented an update on the use of intensified therapy guided by B-type natriuretic peptide (BNP) at the annual New York Cardiovascular Symposium. "The predictive value of BNP is quite high," he said. "If you see a patient for the first time who is untreated with low BNP, heart failure is rather unlikely." Dr. Brunner-La Rocca is a coinvestigator of TIME-CHF (Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure) (JAMA 2009;301:383-92).

[PROTECT Trial Opens Door to Biomarker-Guided Heart Failure Therapy]

While BNP-guided biomarker therapy has not been tested sufficiently to merit widespread use, it can be helpful in identifying at-risk patients, Dr. Brunner-La Rocca said. It can treat underlying coronary artery disease, heart valve disease or myocarditis, or complications from mitral valve regurgitation and anemia. He listed three prognostic factors that can help guide therapy: spiro-ergometry in transplantation, left ventricular ejection fraction in patients with implantable cardioverter devices, and hemodynamics.

Dr. Brunner-La Rocca discussed seven clinical trials that treated almost 14,000 patients with N-terminal BNP (NT-BNP) and almost 800 with BNP guidance. The TIME-CHF trial of NT-BNP showed that patients under age 75 years who had intensified BNP-guided therapy had fewer hospitalizations, improved survival, and fewer symptoms of heart failure than did those who received standard treatment. However, patients over age 75 showed almost identical outcomes for the BNP and standard therapy groups after 18 months.

"An end point we looked at was hospitalization-free survival because we thought when we intensify therapy maybe we do something good for the heart, but we’re not so certain when we provoke more side effects," he said. Compared with the symptom-guided group, the NT-BNP–guided group had fewer hospitalizations – 28% vs. 38% in the standard treatment group.

Meanwhile, Dr. Brunner-La Rocca pointed out the Systolic Heart Failure Treatment Supported by BNP (STARS-BNP) trial "showed a positive effect on survival and extensive reduction in cardiac events" (N. Engl. J. Med. 2008;358:2148-59).

However, Dr. Brunner-La Rocca also noted that the variance among the studies analyzed may cause confusion about the effectiveness of BNP-guided therapy. "The other studies were not all that positive," he said. "The largest study so far actually showed a negative result – basically no effect at all – and reported a substantial amount of events."

Two more recent meta-analyses have shown improved survival with BNP guidance (Arch. Intern. Med. 2010;170:507-14 and Am. Heart J. 2009;158:422-30). "When I looked at the results, I’m not quite sure where these numbers are coming from," Dr. Brunner-La Rocca said. "I think this part of the analysis is to some extent flawed."

An ongoing analysis of all the BNP trials may provide some answers when its results are published, he said.

Still, he uses BNP-guided therapy in some of his patients. "I happen to think it is still of value, particularly if I have doubts about the patient’s diagnostics," Dr. Brunner-La Rocca said. "Many of these patients have other disease, and to really know the BNP can help differentiate if the heart or some other disease mechanism is to blame. In addition, it may help to identify patients at risk, particularly younger ones."

Dr. Brunner-La Rocca had no disclosures.

NEW YORK – Preliminary data from the Mayo Clinic may provide insight into differentiating patients with hypertrophic obstructive cardiomyopathy who would benefit most from either surgical septal myectomy or percutaneous septal ablation, according to an investigator’s report at the annual New York Cardiology Symposium.

Dr. Steve Ommen presented data showing that the percutaneous procedure had higher mortality and complication rates than did surgical myectomy, but noted that emerging data have identified patient characteristics that can guide a clinician’s choice of procedure. Either procedure can be indicated for a symptomatic patient with HOCM in whom drug treatment has failed. "If medications don’t work, if the patient’s quality of life is not satisfactory, that’s where we get into the controversy over whether or percutaneous alcohol ablation ought to be considered," he said.

Surgical myectomy has been considered the standard for HOCM treatment, but alcohol septal ablation has gained attention in recent years as a less-invasive approach. The determining factor for intervention is the left ventricular outflow tract (LVOT) pressure gradient, Dr. Ommen said: An LVOT gradient measure of 50 mm Hg or higher portends significant symptoms, but a measure of 30 mm Hg at rest in an otherwise symptomatic patient with a negative echocardiogram may require further testing. "You owe it to that patient to see if he or she can be easily provoked to a higher gradient on testing," he said.

Surgical myectomy has been shown to reduce the mortality rate in HOCM patients by half (from 2% to 1%), Dr. Ommen said. However, he noted that no randomized data have been published on outcomes of myectomy in HOCM. "These observational data show that overall survival in myectomy is similar to that of the general population," he said. "Survival is better than the historic population reports of HOCM, and arrhythmogenic death rates appear to be dramatically lower than other reports of patients with similar risk profiles."

On the other hand, published mortality rates in HOCM patients who had septal alcohol ablation have averaged 1.9% (range, 0%-4%), according to an analysis of 19 series that Dr. Ommen reported. The same analysis showed an overall complication rate of 20%. "The complication rates are largely driven by the need for a permanent pacemaker because of the complete cardioblock the ablation induced," he said.

The analysis also showed a technical success rate of 75% with septal alcohol ablation, he said. A separate study in which Dr. Ommen participated showed that HOCM patients younger than age 65 were more likely than myectomy patient to regress to New York Heart Association class III or IV symptoms within 4 years (JACC Cardiovasc. Interv. 2008;1:552-60) "On this basis, we generally prefer surgery for our younger patients," he said.

The Mayo analysis has provided clarity on who may succeed with septal alcohol ablation, according to Dr. Ommen. The patients who have the best success with ablation are over age 65 [and] have mild to moderate hypertrophy and a gradient that’s not severe," he said. HOCM patients with all three of those factors have a success rate of 90%; if they have just one of those factors, the success rate drops below 60%, he said.

"We can start to get our hands around patient selection for those who would succeed with the percutaneous procedure rather than the surgical procedure," he said.

He also cited two large 2008 studies that showed a long-term, annualized death rate of 1.5%-3% with percutaneous septal ablation. "These data would suggest that there may not be an increase in the death rate with ablation, but perhaps not the decrease that we saw with the surgical data," Dr. Ommen added.

He acknowledged the concern among some clinicians that septal ablation may raise the risk for arrhythmia in this patient population. "HOCM patients who have no risk for sudden cardiac death can still have a sudden cardiac death rate of 0.8% a year, but in patients who had ablation, about 2.8% had inappropriate implantable cardioverter defibrillator discharge," he said. "If they had one or more risk factors for sudden cardiac death, that then went to 13.4%, which is comparable to secondary prevention ICD discharge rates in the acute myocardial infarction CT from the National Registry of Myocardial Infarction."

Dr. Ommen had no relationships to disclose.

NEW YORK – Preliminary data from the Mayo Clinic may provide insight into differentiating patients with hypertrophic obstructive cardiomyopathy who would benefit most from either surgical septal myectomy or percutaneous septal ablation, according to an investigator’s report at the annual New York Cardiology Symposium.

Dr. Steve Ommen presented data showing that the percutaneous procedure had higher mortality and complication rates than did surgical myectomy, but noted that emerging data have identified patient characteristics that can guide a clinician’s choice of procedure. Either procedure can be indicated for a symptomatic patient with HOCM in whom drug treatment has failed. "If medications don’t work, if the patient’s quality of life is not satisfactory, that’s where we get into the controversy over whether or percutaneous alcohol ablation ought to be considered," he said.

Surgical myectomy has been considered the standard for HOCM treatment, but alcohol septal ablation has gained attention in recent years as a less-invasive approach. The determining factor for intervention is the left ventricular outflow tract (LVOT) pressure gradient, Dr. Ommen said: An LVOT gradient measure of 50 mm Hg or higher portends significant symptoms, but a measure of 30 mm Hg at rest in an otherwise symptomatic patient with a negative echocardiogram may require further testing. "You owe it to that patient to see if he or she can be easily provoked to a higher gradient on testing," he said.

Surgical myectomy has been shown to reduce the mortality rate in HOCM patients by half (from 2% to 1%), Dr. Ommen said. However, he noted that no randomized data have been published on outcomes of myectomy in HOCM. "These observational data show that overall survival in myectomy is similar to that of the general population," he said. "Survival is better than the historic population reports of HOCM, and arrhythmogenic death rates appear to be dramatically lower than other reports of patients with similar risk profiles."

On the other hand, published mortality rates in HOCM patients who had septal alcohol ablation have averaged 1.9% (range, 0%-4%), according to an analysis of 19 series that Dr. Ommen reported. The same analysis showed an overall complication rate of 20%. "The complication rates are largely driven by the need for a permanent pacemaker because of the complete cardioblock the ablation induced," he said.

The analysis also showed a technical success rate of 75% with septal alcohol ablation, he said. A separate study in which Dr. Ommen participated showed that HOCM patients younger than age 65 were more likely than myectomy patient to regress to New York Heart Association class III or IV symptoms within 4 years (JACC Cardiovasc. Interv. 2008;1:552-60) "On this basis, we generally prefer surgery for our younger patients," he said.

The Mayo analysis has provided clarity on who may succeed with septal alcohol ablation, according to Dr. Ommen. The patients who have the best success with ablation are over age 65 [and] have mild to moderate hypertrophy and a gradient that’s not severe," he said. HOCM patients with all three of those factors have a success rate of 90%; if they have just one of those factors, the success rate drops below 60%, he said.

"We can start to get our hands around patient selection for those who would succeed with the percutaneous procedure rather than the surgical procedure," he said.

He also cited two large 2008 studies that showed a long-term, annualized death rate of 1.5%-3% with percutaneous septal ablation. "These data would suggest that there may not be an increase in the death rate with ablation, but perhaps not the decrease that we saw with the surgical data," Dr. Ommen added.

He acknowledged the concern among some clinicians that septal ablation may raise the risk for arrhythmia in this patient population. "HOCM patients who have no risk for sudden cardiac death can still have a sudden cardiac death rate of 0.8% a year, but in patients who had ablation, about 2.8% had inappropriate implantable cardioverter defibrillator discharge," he said. "If they had one or more risk factors for sudden cardiac death, that then went to 13.4%, which is comparable to secondary prevention ICD discharge rates in the acute myocardial infarction CT from the National Registry of Myocardial Infarction."

Dr. Ommen had no relationships to disclose.

NEW YORK – Preliminary data from the Mayo Clinic may provide insight into differentiating patients with hypertrophic obstructive cardiomyopathy who would benefit most from either surgical septal myectomy or percutaneous septal ablation, according to an investigator’s report at the annual New York Cardiology Symposium.

Dr. Steve Ommen presented data showing that the percutaneous procedure had higher mortality and complication rates than did surgical myectomy, but noted that emerging data have identified patient characteristics that can guide a clinician’s choice of procedure. Either procedure can be indicated for a symptomatic patient with HOCM in whom drug treatment has failed. "If medications don’t work, if the patient’s quality of life is not satisfactory, that’s where we get into the controversy over whether or percutaneous alcohol ablation ought to be considered," he said.

Surgical myectomy has been considered the standard for HOCM treatment, but alcohol septal ablation has gained attention in recent years as a less-invasive approach. The determining factor for intervention is the left ventricular outflow tract (LVOT) pressure gradient, Dr. Ommen said: An LVOT gradient measure of 50 mm Hg or higher portends significant symptoms, but a measure of 30 mm Hg at rest in an otherwise symptomatic patient with a negative echocardiogram may require further testing. "You owe it to that patient to see if he or she can be easily provoked to a higher gradient on testing," he said.

Surgical myectomy has been shown to reduce the mortality rate in HOCM patients by half (from 2% to 1%), Dr. Ommen said. However, he noted that no randomized data have been published on outcomes of myectomy in HOCM. "These observational data show that overall survival in myectomy is similar to that of the general population," he said. "Survival is better than the historic population reports of HOCM, and arrhythmogenic death rates appear to be dramatically lower than other reports of patients with similar risk profiles."

On the other hand, published mortality rates in HOCM patients who had septal alcohol ablation have averaged 1.9% (range, 0%-4%), according to an analysis of 19 series that Dr. Ommen reported. The same analysis showed an overall complication rate of 20%. "The complication rates are largely driven by the need for a permanent pacemaker because of the complete cardioblock the ablation induced," he said.

The analysis also showed a technical success rate of 75% with septal alcohol ablation, he said. A separate study in which Dr. Ommen participated showed that HOCM patients younger than age 65 were more likely than myectomy patient to regress to New York Heart Association class III or IV symptoms within 4 years (JACC Cardiovasc. Interv. 2008;1:552-60) "On this basis, we generally prefer surgery for our younger patients," he said.

The Mayo analysis has provided clarity on who may succeed with septal alcohol ablation, according to Dr. Ommen. The patients who have the best success with ablation are over age 65 [and] have mild to moderate hypertrophy and a gradient that’s not severe," he said. HOCM patients with all three of those factors have a success rate of 90%; if they have just one of those factors, the success rate drops below 60%, he said.

"We can start to get our hands around patient selection for those who would succeed with the percutaneous procedure rather than the surgical procedure," he said.

He also cited two large 2008 studies that showed a long-term, annualized death rate of 1.5%-3% with percutaneous septal ablation. "These data would suggest that there may not be an increase in the death rate with ablation, but perhaps not the decrease that we saw with the surgical data," Dr. Ommen added.

He acknowledged the concern among some clinicians that septal ablation may raise the risk for arrhythmia in this patient population. "HOCM patients who have no risk for sudden cardiac death can still have a sudden cardiac death rate of 0.8% a year, but in patients who had ablation, about 2.8% had inappropriate implantable cardioverter defibrillator discharge," he said. "If they had one or more risk factors for sudden cardiac death, that then went to 13.4%, which is comparable to secondary prevention ICD discharge rates in the acute myocardial infarction CT from the National Registry of Myocardial Infarction."

Dr. Ommen had no relationships to disclose.

NEW YORK – Preliminary data from the Mayo Clinic may provide insight into differentiating patients with hypertrophic obstructive cardiomyopathy who would benefit most from either surgical septal myectomy or percutaneous septal ablation, according to an investigator’s report at the annual New York Cardiology Symposium.

Dr. Steve Ommen presented data showing that the percutaneous procedure had higher mortality and complication rates than did surgical myectomy, but noted that emerging data have identified patient characteristics that can guide a clinician’s choice of procedure. Either procedure can be indicated for a symptomatic patient with HOCM in whom drug treatment has failed. "If medications don’t work, if the patient’s quality of life is not satisfactory, that’s where we get into the controversy over whether or percutaneous alcohol ablation ought to be considered," he said.

Surgical myectomy has been considered the standard for HOCM treatment, but alcohol septal ablation has gained attention in recent years as a less-invasive approach. The determining factor for intervention is the left ventricular outflow tract (LVOT) pressure gradient, Dr. Ommen said: An LVOT gradient measure of 50 mm Hg or higher portends significant symptoms, but a measure of 30 mm Hg at rest in an otherwise symptomatic patient with a negative echocardiogram may require further testing. "You owe it to that patient to see if he or she can be easily provoked to a higher gradient on testing," he said.

Surgical myectomy has been shown to reduce the mortality rate in HOCM patients by half (from 2% to 1%), Dr. Ommen said. However, he noted that no randomized data have been published on outcomes of myectomy in HOCM. "These observational data show that overall survival in myectomy is similar to that of the general population," he said. "Survival is better than the historic population reports of HOCM, and arrhythmogenic death rates appear to be dramatically lower than other reports of patients with similar risk profiles."

On the other hand, published mortality rates in HOCM patients who had septal alcohol ablation have averaged 1.9% (range, 0%-4%), according to an analysis of 19 series that Dr. Ommen reported. The same analysis showed an overall complication rate of 20%. "The complication rates are largely driven by the need for a permanent pacemaker because of the complete cardioblock the ablation induced," he said.

The analysis also showed a technical success rate of 75% with septal alcohol ablation, he said. A separate study in which Dr. Ommen participated showed that HOCM patients younger than age 65 were more likely than myectomy patient to regress to New York Heart Association class III or IV symptoms within 4 years (JACC Cardiovasc. Interv. 2008;1:552-60) "On this basis, we generally prefer surgery for our younger patients," he said.

The Mayo analysis has provided clarity on who may succeed with septal alcohol ablation, according to Dr. Ommen. The patients who have the best success with ablation are over age 65 [and] have mild to moderate hypertrophy and a gradient that’s not severe," he said. HOCM patients with all three of those factors have a success rate of 90%; if they have just one of those factors, the success rate drops below 60%, he said.

"We can start to get our hands around patient selection for those who would succeed with the percutaneous procedure rather than the surgical procedure," he said.

He also cited two large 2008 studies that showed a long-term, annualized death rate of 1.5%-3% with percutaneous septal ablation. "These data would suggest that there may not be an increase in the death rate with ablation, but perhaps not the decrease that we saw with the surgical data," Dr. Ommen added.

He acknowledged the concern among some clinicians that septal ablation may raise the risk for arrhythmia in this patient population. "HOCM patients who have no risk for sudden cardiac death can still have a sudden cardiac death rate of 0.8% a year, but in patients who had ablation, about 2.8% had inappropriate implantable cardioverter defibrillator discharge," he said. "If they had one or more risk factors for sudden cardiac death, that then went to 13.4%, which is comparable to secondary prevention ICD discharge rates in the acute myocardial infarction CT from the National Registry of Myocardial Infarction."

Dr. Ommen had no relationships to disclose.

NEW YORK – Preliminary data from the Mayo Clinic may provide insight into differentiating patients with hypertrophic obstructive cardiomyopathy who would benefit most from either surgical septal myectomy or percutaneous septal ablation, according to an investigator’s report at the annual New York Cardiology Symposium.

Dr. Steve Ommen presented data showing that the percutaneous procedure had higher mortality and complication rates than did surgical myectomy, but noted that emerging data have identified patient characteristics that can guide a clinician’s choice of procedure. Either procedure can be indicated for a symptomatic patient with HOCM in whom drug treatment has failed. "If medications don’t work, if the patient’s quality of life is not satisfactory, that’s where we get into the controversy over whether or percutaneous alcohol ablation ought to be considered," he said.

Surgical myectomy has been considered the standard for HOCM treatment, but alcohol septal ablation has gained attention in recent years as a less-invasive approach. The determining factor for intervention is the left ventricular outflow tract (LVOT) pressure gradient, Dr. Ommen said: An LVOT gradient measure of 50 mm Hg or higher portends significant symptoms, but a measure of 30 mm Hg at rest in an otherwise symptomatic patient with a negative echocardiogram may require further testing. "You owe it to that patient to see if he or she can be easily provoked to a higher gradient on testing," he said.

Surgical myectomy has been shown to reduce the mortality rate in HOCM patients by half (from 2% to 1%), Dr. Ommen said. However, he noted that no randomized data have been published on outcomes of myectomy in HOCM. "These observational data show that overall survival in myectomy is similar to that of the general population," he said. "Survival is better than the historic population reports of HOCM, and arrhythmogenic death rates appear to be dramatically lower than other reports of patients with similar risk profiles."

On the other hand, published mortality rates in HOCM patients who had septal alcohol ablation have averaged 1.9% (range, 0%-4%), according to an analysis of 19 series that Dr. Ommen reported. The same analysis showed an overall complication rate of 20%. "The complication rates are largely driven by the need for a permanent pacemaker because of the complete cardioblock the ablation induced," he said.

The analysis also showed a technical success rate of 75% with septal alcohol ablation, he said. A separate study in which Dr. Ommen participated showed that HOCM patients younger than age 65 were more likely than myectomy patient to regress to New York Heart Association class III or IV symptoms within 4 years (JACC Cardiovasc. Interv. 2008;1:552-60) "On this basis, we generally prefer surgery for our younger patients," he said.

The Mayo analysis has provided clarity on who may succeed with septal alcohol ablation, according to Dr. Ommen. The patients who have the best success with ablation are over age 65 [and] have mild to moderate hypertrophy and a gradient that’s not severe," he said. HOCM patients with all three of those factors have a success rate of 90%; if they have just one of those factors, the success rate drops below 60%, he said.

"We can start to get our hands around patient selection for those who would succeed with the percutaneous procedure rather than the surgical procedure," he said.

He also cited two large 2008 studies that showed a long-term, annualized death rate of 1.5%-3% with percutaneous septal ablation. "These data would suggest that there may not be an increase in the death rate with ablation, but perhaps not the decrease that we saw with the surgical data," Dr. Ommen added.

He acknowledged the concern among some clinicians that septal ablation may raise the risk for arrhythmia in this patient population. "HOCM patients who have no risk for sudden cardiac death can still have a sudden cardiac death rate of 0.8% a year, but in patients who had ablation, about 2.8% had inappropriate implantable cardioverter defibrillator discharge," he said. "If they had one or more risk factors for sudden cardiac death, that then went to 13.4%, which is comparable to secondary prevention ICD discharge rates in the acute myocardial infarction CT from the National Registry of Myocardial Infarction."

Dr. Ommen had no relationships to disclose.

NEW YORK – Preliminary data from the Mayo Clinic may provide insight into differentiating patients with hypertrophic obstructive cardiomyopathy who would benefit most from either surgical septal myectomy or percutaneous septal ablation, according to an investigator’s report at the annual New York Cardiology Symposium.

Dr. Steve Ommen presented data showing that the percutaneous procedure had higher mortality and complication rates than did surgical myectomy, but noted that emerging data have identified patient characteristics that can guide a clinician’s choice of procedure. Either procedure can be indicated for a symptomatic patient with HOCM in whom drug treatment has failed. "If medications don’t work, if the patient’s quality of life is not satisfactory, that’s where we get into the controversy over whether or percutaneous alcohol ablation ought to be considered," he said.

Surgical myectomy has been considered the standard for HOCM treatment, but alcohol septal ablation has gained attention in recent years as a less-invasive approach. The determining factor for intervention is the left ventricular outflow tract (LVOT) pressure gradient, Dr. Ommen said: An LVOT gradient measure of 50 mm Hg or higher portends significant symptoms, but a measure of 30 mm Hg at rest in an otherwise symptomatic patient with a negative echocardiogram may require further testing. "You owe it to that patient to see if he or she can be easily provoked to a higher gradient on testing," he said.

Surgical myectomy has been shown to reduce the mortality rate in HOCM patients by half (from 2% to 1%), Dr. Ommen said. However, he noted that no randomized data have been published on outcomes of myectomy in HOCM. "These observational data show that overall survival in myectomy is similar to that of the general population," he said. "Survival is better than the historic population reports of HOCM, and arrhythmogenic death rates appear to be dramatically lower than other reports of patients with similar risk profiles."

On the other hand, published mortality rates in HOCM patients who had septal alcohol ablation have averaged 1.9% (range, 0%-4%), according to an analysis of 19 series that Dr. Ommen reported. The same analysis showed an overall complication rate of 20%. "The complication rates are largely driven by the need for a permanent pacemaker because of the complete cardioblock the ablation induced," he said.

The analysis also showed a technical success rate of 75% with septal alcohol ablation, he said. A separate study in which Dr. Ommen participated showed that HOCM patients younger than age 65 were more likely than myectomy patient to regress to New York Heart Association class III or IV symptoms within 4 years (JACC Cardiovasc. Interv. 2008;1:552-60) "On this basis, we generally prefer surgery for our younger patients," he said.

The Mayo analysis has provided clarity on who may succeed with septal alcohol ablation, according to Dr. Ommen. The patients who have the best success with ablation are over age 65 [and] have mild to moderate hypertrophy and a gradient that’s not severe," he said. HOCM patients with all three of those factors have a success rate of 90%; if they have just one of those factors, the success rate drops below 60%, he said.

"We can start to get our hands around patient selection for those who would succeed with the percutaneous procedure rather than the surgical procedure," he said.

He also cited two large 2008 studies that showed a long-term, annualized death rate of 1.5%-3% with percutaneous septal ablation. "These data would suggest that there may not be an increase in the death rate with ablation, but perhaps not the decrease that we saw with the surgical data," Dr. Ommen added.

He acknowledged the concern among some clinicians that septal ablation may raise the risk for arrhythmia in this patient population. "HOCM patients who have no risk for sudden cardiac death can still have a sudden cardiac death rate of 0.8% a year, but in patients who had ablation, about 2.8% had inappropriate implantable cardioverter defibrillator discharge," he said. "If they had one or more risk factors for sudden cardiac death, that then went to 13.4%, which is comparable to secondary prevention ICD discharge rates in the acute myocardial infarction CT from the National Registry of Myocardial Infarction."

Dr. Ommen had no relationships to disclose.

PHILADELPHIA — With hospitals buying up physician practices, many physicians are tempted to take the bait, but Alice G. Gosfield, an attorney who specializes in physician practice ownership strategies, called this the “employment delusion” and the “acquisition fantasy” during the meeting.

Many physicians don't recognize that “the common law term for the employer-employee relationship is 'master-servant,'” she said. “It's a one-on-one relationship [in which the] master gets to tell you who, what, where, when, and why and how, and if you think that a contract can prevent that from happening, you would be wrong.”

Regarding the myth about how selling out to a hospital group can guarantee financial security, she said “The hospital is getting paid under the same stupid reimbursement formula that you are. The only way that revenue stream ends up being more than what you're getting in your practice is if they are paying you for doing other things besides clinical work.”

Another delusion is that the contract is a safeguard, according to Ms. Gosfield. “A contract is only as good as the will of the parties to abide by it,” she said.

She singled out two strategies for selling a practice to a hospital: the sale of physical assets, including diagnostic “toys and weapons,” in her words, but not the practice per se; and noncompete covenants. “It has to be fair-market value under the Stark regulations,” she said of the latter, “and somebody – not a lawyer – has to do a valuation.”

For self-preservation, she implored physicians to adopt the quality improvement measures that will provide the basis for Medicare reimbursement in 2012. “Now is the time to change your clinical and administrative processes,” she said. “We all know what the conditions are.” That information is already available from the National Quality Forum, she pointed out.

Cardiologists are in a particularly strong position to deal with hospitals, she said. “Hospitals cannot function without cardiologists,” she said, citing the “20/80 rule” in which “20% of the doctors generate 80% of the medical staff's billings.” She added, “They know that they make money on it, and they pay attention to you because you are cardiologists.”

Among the alternatives to selling the practice offered by Ms. Gosfield were leasing the practice to the hospital, entering into comanagement contracts, having the hospital place a new physician in the practice, gainsharing, giving the hospital the right of first refusal if another entity offers to buy the practice, having the hospital provide continuing education for practice physicians and ancillary staff, leasing practice staff to the hospital, and having the practice provide contract services (such as billing and claims processing) to the hospital.

Ms. Gosfield described how a hospital would lease a practice: “Your group stays as your group,” she said. “In essence what you do is, you reassign your right to get paid to the hospital. They pay you a salary. They will require some kind of productivity measures, but they can pay you irrespective of whether they get paid.”

A comanagement contract involves the physician providing on-call services or advising the hospital on its care delivery systems. This could include performance bonuses when the hospital achieves specified results, she said, but she advised against getting paid an hourly fee. “Swapping an hour in your office for an hour of their time – you can't make it up,” she said.

Having the hospital place a physician in the practice should be carefully structured, Ms. Gosfield said. Her preferred arrangement would have the hospital subsidize the up-front costs with a loan, then forgive the loan for each month the doctor stays in the community after the subsidy ends. One problem with this approach, she pointed out, is that “you can't then have a restricted covenant which prohibits this young doctor that you brought in and introduced to your patients from opening up next door,” Ms. Gosfield said.

She reported no disclosures.

PHILADELPHIA — With hospitals buying up physician practices, many physicians are tempted to take the bait, but Alice G. Gosfield, an attorney who specializes in physician practice ownership strategies, called this the “employment delusion” and the “acquisition fantasy” during the meeting.

Many physicians don't recognize that “the common law term for the employer-employee relationship is 'master-servant,'” she said. “It's a one-on-one relationship [in which the] master gets to tell you who, what, where, when, and why and how, and if you think that a contract can prevent that from happening, you would be wrong.”

Regarding the myth about how selling out to a hospital group can guarantee financial security, she said “The hospital is getting paid under the same stupid reimbursement formula that you are. The only way that revenue stream ends up being more than what you're getting in your practice is if they are paying you for doing other things besides clinical work.”

Another delusion is that the contract is a safeguard, according to Ms. Gosfield. “A contract is only as good as the will of the parties to abide by it,” she said.

She singled out two strategies for selling a practice to a hospital: the sale of physical assets, including diagnostic “toys and weapons,” in her words, but not the practice per se; and noncompete covenants. “It has to be fair-market value under the Stark regulations,” she said of the latter, “and somebody – not a lawyer – has to do a valuation.”

For self-preservation, she implored physicians to adopt the quality improvement measures that will provide the basis for Medicare reimbursement in 2012. “Now is the time to change your clinical and administrative processes,” she said. “We all know what the conditions are.” That information is already available from the National Quality Forum, she pointed out.

Cardiologists are in a particularly strong position to deal with hospitals, she said. “Hospitals cannot function without cardiologists,” she said, citing the “20/80 rule” in which “20% of the doctors generate 80% of the medical staff's billings.” She added, “They know that they make money on it, and they pay attention to you because you are cardiologists.”

Among the alternatives to selling the practice offered by Ms. Gosfield were leasing the practice to the hospital, entering into comanagement contracts, having the hospital place a new physician in the practice, gainsharing, giving the hospital the right of first refusal if another entity offers to buy the practice, having the hospital provide continuing education for practice physicians and ancillary staff, leasing practice staff to the hospital, and having the practice provide contract services (such as billing and claims processing) to the hospital.

Ms. Gosfield described how a hospital would lease a practice: “Your group stays as your group,” she said. “In essence what you do is, you reassign your right to get paid to the hospital. They pay you a salary. They will require some kind of productivity measures, but they can pay you irrespective of whether they get paid.”

A comanagement contract involves the physician providing on-call services or advising the hospital on its care delivery systems. This could include performance bonuses when the hospital achieves specified results, she said, but she advised against getting paid an hourly fee. “Swapping an hour in your office for an hour of their time – you can't make it up,” she said.

Having the hospital place a physician in the practice should be carefully structured, Ms. Gosfield said. Her preferred arrangement would have the hospital subsidize the up-front costs with a loan, then forgive the loan for each month the doctor stays in the community after the subsidy ends. One problem with this approach, she pointed out, is that “you can't then have a restricted covenant which prohibits this young doctor that you brought in and introduced to your patients from opening up next door,” Ms. Gosfield said.

She reported no disclosures.

PHILADELPHIA — With hospitals buying up physician practices, many physicians are tempted to take the bait, but Alice G. Gosfield, an attorney who specializes in physician practice ownership strategies, called this the “employment delusion” and the “acquisition fantasy” during the meeting.

Many physicians don't recognize that “the common law term for the employer-employee relationship is 'master-servant,'” she said. “It's a one-on-one relationship [in which the] master gets to tell you who, what, where, when, and why and how, and if you think that a contract can prevent that from happening, you would be wrong.”

Regarding the myth about how selling out to a hospital group can guarantee financial security, she said “The hospital is getting paid under the same stupid reimbursement formula that you are. The only way that revenue stream ends up being more than what you're getting in your practice is if they are paying you for doing other things besides clinical work.”

Another delusion is that the contract is a safeguard, according to Ms. Gosfield. “A contract is only as good as the will of the parties to abide by it,” she said.

She singled out two strategies for selling a practice to a hospital: the sale of physical assets, including diagnostic “toys and weapons,” in her words, but not the practice per se; and noncompete covenants. “It has to be fair-market value under the Stark regulations,” she said of the latter, “and somebody – not a lawyer – has to do a valuation.”

For self-preservation, she implored physicians to adopt the quality improvement measures that will provide the basis for Medicare reimbursement in 2012. “Now is the time to change your clinical and administrative processes,” she said. “We all know what the conditions are.” That information is already available from the National Quality Forum, she pointed out.

Cardiologists are in a particularly strong position to deal with hospitals, she said. “Hospitals cannot function without cardiologists,” she said, citing the “20/80 rule” in which “20% of the doctors generate 80% of the medical staff's billings.” She added, “They know that they make money on it, and they pay attention to you because you are cardiologists.”

Among the alternatives to selling the practice offered by Ms. Gosfield were leasing the practice to the hospital, entering into comanagement contracts, having the hospital place a new physician in the practice, gainsharing, giving the hospital the right of first refusal if another entity offers to buy the practice, having the hospital provide continuing education for practice physicians and ancillary staff, leasing practice staff to the hospital, and having the practice provide contract services (such as billing and claims processing) to the hospital.

Ms. Gosfield described how a hospital would lease a practice: “Your group stays as your group,” she said. “In essence what you do is, you reassign your right to get paid to the hospital. They pay you a salary. They will require some kind of productivity measures, but they can pay you irrespective of whether they get paid.”

A comanagement contract involves the physician providing on-call services or advising the hospital on its care delivery systems. This could include performance bonuses when the hospital achieves specified results, she said, but she advised against getting paid an hourly fee. “Swapping an hour in your office for an hour of their time – you can't make it up,” she said.

Having the hospital place a physician in the practice should be carefully structured, Ms. Gosfield said. Her preferred arrangement would have the hospital subsidize the up-front costs with a loan, then forgive the loan for each month the doctor stays in the community after the subsidy ends. One problem with this approach, she pointed out, is that “you can't then have a restricted covenant which prohibits this young doctor that you brought in and introduced to your patients from opening up next door,” Ms. Gosfield said.

She reported no disclosures.

NEW YORK – About one in four patients with abdominal aortic aneurysm may be at risk for thoracic aortic aneurysm, judging by results of a single-center retrospective study of more than 1,000 patients.

Dr. Rabih Chaer, a vascular surgeon at the University of Pittsburgh, and his colleagues found that, among 1,082 patients diagnosed with abdominal aortic aneurysms (AAA) who had chest CT at follow-up, 23.4% had some sort of thoracic aneurysm afterward.

“Despite the clinical associations that have been observed between AAAs and peripheral aneurysms and thoracic aneurysms, screening for other common aneurysms continues to be controversial,” Dr. Chaer said at the meeting.

Therefore, they conducted the study to quantify the risk for thoracic aorticaneurysm in these patients and to identify risk factors that could provide screening parameters, he said. The researchers defined an aneurysm as a greater than 50% increase in the adjacent aorta diameter or a 3 cm or larger increase in the setting of AAA, Dr. Chaer said. Thoracic aneurysms were categorized by two subgroups: synchronous (occurring within 2 years of initial AAA diagnosis) and metachronous (occurring 2 years or more after diagnosis). About 11% of patients had the former, and 12.6% the latter, Dr. Chaer said. The average time to diagnosis was 2.3 years, he said.

In all, the researchers considered 2,196 patients diagnosed with AAA between 2000 and 2008, but only 49% (1,082) had chest CT that qualified them for further analysis, Dr. Chaer noted. The chest studies were conducted for suspected pulmonary disease in 74% of patients, for chest screening in 15%, and for miscellaneous reasons in 11%.

One predisposing factor for thoracic aneurysm was the type of AAA, Dr. Chaer explained. “Those patients who had a thoracic aneurysm component were more likely to have a suprarenal or juxtarenal aortic aneurysm, and those patients who did not have any thoracic aneurysm were more likely to have had an infrarenal aneurysm,” he said.

The median age of patients who had a thoracic aneurysm vs. those who did not was 76 years vs. 74 years, he said.

Other predictors for thoracic aortic aneurysm included African American race, family history of thoracic aneurysm, personal history of obesity hypertension, and an AAA diameter more than 5 cm on presentation, he said. Factors that conferred a protective effect were a diagnosis of diabetes mellitus, infrarenal AAA location, and – “counterintuitively” – a history of smoking.

“We propose that routine or targeted screening with chest CT at the time of aortic aneurysm diagnosis may be indicated, not only to really define the natural history of disease, but more importantly to try to prevent late aortic events,” Dr. Chaer said.

But Dr. James Black, of Johns Hopkins University in Baltimore, questioned the cost-effectiveness of routine screening. At his institution, chest CT would add about $3,000 per patient, he said.

“If you took a chest CT at diagnosis of AAA for 100 patients, 90% of the scans would be negative for thoracic aneurysm, at a rough cost in our institution of about $300,000 a year,” he said.

Cost of routine chest CT is an issue, Dr. Chaer acknowledged, although the chest CT could be done in the same scan as the abdominal CT.

“It would be nice to have a surrogate marker for thoracic aneurysm,” Dr. Chaer said. “Although we found that a thoracic aneurysm was more common in patients who had a juxtarenal aneurysm, those numbers were not hard enough to confidently say that the juxtarenal component is always predictive of a surrogate marker of thoracic aneurysm development. It is something that could be the subject of future studies.”

Dr. Chaer noted that the heterogeneous population and the retrospective nature were limitations of the study. He reported no disclosures relevant to the presentation.

NEW YORK – About one in four patients with abdominal aortic aneurysm may be at risk for thoracic aortic aneurysm, judging by results of a single-center retrospective study of more than 1,000 patients.

Dr. Rabih Chaer, a vascular surgeon at the University of Pittsburgh, and his colleagues found that, among 1,082 patients diagnosed with abdominal aortic aneurysms (AAA) who had chest CT at follow-up, 23.4% had some sort of thoracic aneurysm afterward.

“Despite the clinical associations that have been observed between AAAs and peripheral aneurysms and thoracic aneurysms, screening for other common aneurysms continues to be controversial,” Dr. Chaer said at the meeting.

Therefore, they conducted the study to quantify the risk for thoracic aorticaneurysm in these patients and to identify risk factors that could provide screening parameters, he said. The researchers defined an aneurysm as a greater than 50% increase in the adjacent aorta diameter or a 3 cm or larger increase in the setting of AAA, Dr. Chaer said. Thoracic aneurysms were categorized by two subgroups: synchronous (occurring within 2 years of initial AAA diagnosis) and metachronous (occurring 2 years or more after diagnosis). About 11% of patients had the former, and 12.6% the latter, Dr. Chaer said. The average time to diagnosis was 2.3 years, he said.

In all, the researchers considered 2,196 patients diagnosed with AAA between 2000 and 2008, but only 49% (1,082) had chest CT that qualified them for further analysis, Dr. Chaer noted. The chest studies were conducted for suspected pulmonary disease in 74% of patients, for chest screening in 15%, and for miscellaneous reasons in 11%.

One predisposing factor for thoracic aneurysm was the type of AAA, Dr. Chaer explained. “Those patients who had a thoracic aneurysm component were more likely to have a suprarenal or juxtarenal aortic aneurysm, and those patients who did not have any thoracic aneurysm were more likely to have had an infrarenal aneurysm,” he said.

The median age of patients who had a thoracic aneurysm vs. those who did not was 76 years vs. 74 years, he said.

Other predictors for thoracic aortic aneurysm included African American race, family history of thoracic aneurysm, personal history of obesity hypertension, and an AAA diameter more than 5 cm on presentation, he said. Factors that conferred a protective effect were a diagnosis of diabetes mellitus, infrarenal AAA location, and – “counterintuitively” – a history of smoking.

“We propose that routine or targeted screening with chest CT at the time of aortic aneurysm diagnosis may be indicated, not only to really define the natural history of disease, but more importantly to try to prevent late aortic events,” Dr. Chaer said.

But Dr. James Black, of Johns Hopkins University in Baltimore, questioned the cost-effectiveness of routine screening. At his institution, chest CT would add about $3,000 per patient, he said.

“If you took a chest CT at diagnosis of AAA for 100 patients, 90% of the scans would be negative for thoracic aneurysm, at a rough cost in our institution of about $300,000 a year,” he said.

Cost of routine chest CT is an issue, Dr. Chaer acknowledged, although the chest CT could be done in the same scan as the abdominal CT.

“It would be nice to have a surrogate marker for thoracic aneurysm,” Dr. Chaer said. “Although we found that a thoracic aneurysm was more common in patients who had a juxtarenal aneurysm, those numbers were not hard enough to confidently say that the juxtarenal component is always predictive of a surrogate marker of thoracic aneurysm development. It is something that could be the subject of future studies.”

Dr. Chaer noted that the heterogeneous population and the retrospective nature were limitations of the study. He reported no disclosures relevant to the presentation.

NEW YORK – About one in four patients with abdominal aortic aneurysm may be at risk for thoracic aortic aneurysm, judging by results of a single-center retrospective study of more than 1,000 patients.

Dr. Rabih Chaer, a vascular surgeon at the University of Pittsburgh, and his colleagues found that, among 1,082 patients diagnosed with abdominal aortic aneurysms (AAA) who had chest CT at follow-up, 23.4% had some sort of thoracic aneurysm afterward.

“Despite the clinical associations that have been observed between AAAs and peripheral aneurysms and thoracic aneurysms, screening for other common aneurysms continues to be controversial,” Dr. Chaer said at the meeting.

Therefore, they conducted the study to quantify the risk for thoracic aorticaneurysm in these patients and to identify risk factors that could provide screening parameters, he said. The researchers defined an aneurysm as a greater than 50% increase in the adjacent aorta diameter or a 3 cm or larger increase in the setting of AAA, Dr. Chaer said. Thoracic aneurysms were categorized by two subgroups: synchronous (occurring within 2 years of initial AAA diagnosis) and metachronous (occurring 2 years or more after diagnosis). About 11% of patients had the former, and 12.6% the latter, Dr. Chaer said. The average time to diagnosis was 2.3 years, he said.

In all, the researchers considered 2,196 patients diagnosed with AAA between 2000 and 2008, but only 49% (1,082) had chest CT that qualified them for further analysis, Dr. Chaer noted. The chest studies were conducted for suspected pulmonary disease in 74% of patients, for chest screening in 15%, and for miscellaneous reasons in 11%.

One predisposing factor for thoracic aneurysm was the type of AAA, Dr. Chaer explained. “Those patients who had a thoracic aneurysm component were more likely to have a suprarenal or juxtarenal aortic aneurysm, and those patients who did not have any thoracic aneurysm were more likely to have had an infrarenal aneurysm,” he said.

The median age of patients who had a thoracic aneurysm vs. those who did not was 76 years vs. 74 years, he said.

Other predictors for thoracic aortic aneurysm included African American race, family history of thoracic aneurysm, personal history of obesity hypertension, and an AAA diameter more than 5 cm on presentation, he said. Factors that conferred a protective effect were a diagnosis of diabetes mellitus, infrarenal AAA location, and – “counterintuitively” – a history of smoking.

“We propose that routine or targeted screening with chest CT at the time of aortic aneurysm diagnosis may be indicated, not only to really define the natural history of disease, but more importantly to try to prevent late aortic events,” Dr. Chaer said.

But Dr. James Black, of Johns Hopkins University in Baltimore, questioned the cost-effectiveness of routine screening. At his institution, chest CT would add about $3,000 per patient, he said.

“If you took a chest CT at diagnosis of AAA for 100 patients, 90% of the scans would be negative for thoracic aneurysm, at a rough cost in our institution of about $300,000 a year,” he said.

Cost of routine chest CT is an issue, Dr. Chaer acknowledged, although the chest CT could be done in the same scan as the abdominal CT.

“It would be nice to have a surrogate marker for thoracic aneurysm,” Dr. Chaer said. “Although we found that a thoracic aneurysm was more common in patients who had a juxtarenal aneurysm, those numbers were not hard enough to confidently say that the juxtarenal component is always predictive of a surrogate marker of thoracic aneurysm development. It is something that could be the subject of future studies.”

Dr. Chaer noted that the heterogeneous population and the retrospective nature were limitations of the study. He reported no disclosures relevant to the presentation.

PHILADELPHIA – The American College of Cardiology Foundation and the American Heart Association have endorsed stepwise guidelines for using nuclear imaging to manage and diagnose heart failure, but they do not obviate the need for the hands-on patient examination, said Dr. Alfred Bove of Temple University, Philadelphia.

“The beginning of management of a patient with heart failure is clinical,” Dr. Bove said. “We have to understand the patient's status. I always think it's important to put a stethoscope there first.” That provides a basis for interpreting data generated by subsequent imaging, as called for in the ACCF/AHA guidelines (J. Am. Coll. Cardiol. 2009;53:1343-832), he said.

“The first thing we're trying to understand is both the etiology of ventricular dysfunction and actual function when a patient shows up with symptoms of congestive heart failure to determine whether it is ischemic, dilated, valvular, or congenital,” he said. “We need imaging to sort out these etiologies.”

Ejection fraction is a key measure to determine left ventricle function, as are left ventricle dimensions, he said. “We are always looking at diastolic dimensions in particular; the degree of hypertrophy; whether there's any evidence of coronary disease or coronary stenosis or valvular stenosis or insufficiency; and finally, with congenital heart disease, the presence of shunts.”

The guidelines first recommend obtaining a two-dimensional echocardiogram. “It will tell us what the ejection fraction is, and tell us about valve size and function,” he said

The guidelines then “jump” to radionuclide ventriculography to assess ejection fraction and volume. In a patient with ischemic cardiomyopathy, coronary arteriography can help evaluate indications for revascularization, he said.

In the patient with no history of coronary disease, myocardial perfusion imaging (MPI) can determine the presence of perfusion defects. “We can use that as a basis to go forward to do some further studies,” he said. But in the patient with nonischemic cardiomyopathy and no history of coronary disease, MPI can also have a high number of false-positive readings. “We're more interested here in getting ejection fraction and some measure of heart size from the imaging as well as perfusion,” Dr. Bove said.

The guidelines also call for appropriate follow-up with gated SPECT (single-photon emission CT) or MUGA (multiple gated acquisition) because echocardiography is inconclusive in about 20% of patients, particularly those who are obese or have large chests, Dr. Bove said. “In many cases [when] we see someone with borderline ejection fraction, we send that person for a gated scan and it comes back normal,” he said.

A gated SPECT or MUGA scan provides an “important second backup in left ventricle measures,” particularly in patients whose echocardiograms are of poor quality, he said.

In cases of suspected ischemic cardiomyopathy, the ACCF/AHA guidelines call for coronary CT angiography. “This has a very good negative predictive value,” Dr. Bove said. “If we get a negative CT angiogram, we can be pretty comfortable in saying this is not an ischemic cardiomyopathy.”

When the case mandates further study, MRI can help evaluate structural anomalies in the myocardium. “When there's a question of etiology in the absence of coronary disease, the MRI becomes very important in assessing the etiology of the myocardial dysfunction,” he said.

Dr. Bove disclosed that he is a consultant to Insight Telehealth Systems.

In cases of suspected ischemic cardiomyopathy, the guidelines call for coronary CT angiography.

Source DR. BOVE

PHILADELPHIA – The American College of Cardiology Foundation and the American Heart Association have endorsed stepwise guidelines for using nuclear imaging to manage and diagnose heart failure, but they do not obviate the need for the hands-on patient examination, said Dr. Alfred Bove of Temple University, Philadelphia.

“The beginning of management of a patient with heart failure is clinical,” Dr. Bove said. “We have to understand the patient's status. I always think it's important to put a stethoscope there first.” That provides a basis for interpreting data generated by subsequent imaging, as called for in the ACCF/AHA guidelines (J. Am. Coll. Cardiol. 2009;53:1343-832), he said.

“The first thing we're trying to understand is both the etiology of ventricular dysfunction and actual function when a patient shows up with symptoms of congestive heart failure to determine whether it is ischemic, dilated, valvular, or congenital,” he said. “We need imaging to sort out these etiologies.”

Ejection fraction is a key measure to determine left ventricle function, as are left ventricle dimensions, he said. “We are always looking at diastolic dimensions in particular; the degree of hypertrophy; whether there's any evidence of coronary disease or coronary stenosis or valvular stenosis or insufficiency; and finally, with congenital heart disease, the presence of shunts.”

The guidelines first recommend obtaining a two-dimensional echocardiogram. “It will tell us what the ejection fraction is, and tell us about valve size and function,” he said

The guidelines then “jump” to radionuclide ventriculography to assess ejection fraction and volume. In a patient with ischemic cardiomyopathy, coronary arteriography can help evaluate indications for revascularization, he said.

In the patient with no history of coronary disease, myocardial perfusion imaging (MPI) can determine the presence of perfusion defects. “We can use that as a basis to go forward to do some further studies,” he said. But in the patient with nonischemic cardiomyopathy and no history of coronary disease, MPI can also have a high number of false-positive readings. “We're more interested here in getting ejection fraction and some measure of heart size from the imaging as well as perfusion,” Dr. Bove said.

The guidelines also call for appropriate follow-up with gated SPECT (single-photon emission CT) or MUGA (multiple gated acquisition) because echocardiography is inconclusive in about 20% of patients, particularly those who are obese or have large chests, Dr. Bove said. “In many cases [when] we see someone with borderline ejection fraction, we send that person for a gated scan and it comes back normal,” he said.

A gated SPECT or MUGA scan provides an “important second backup in left ventricle measures,” particularly in patients whose echocardiograms are of poor quality, he said.

In cases of suspected ischemic cardiomyopathy, the ACCF/AHA guidelines call for coronary CT angiography. “This has a very good negative predictive value,” Dr. Bove said. “If we get a negative CT angiogram, we can be pretty comfortable in saying this is not an ischemic cardiomyopathy.”

When the case mandates further study, MRI can help evaluate structural anomalies in the myocardium. “When there's a question of etiology in the absence of coronary disease, the MRI becomes very important in assessing the etiology of the myocardial dysfunction,” he said.

Dr. Bove disclosed that he is a consultant to Insight Telehealth Systems.

In cases of suspected ischemic cardiomyopathy, the guidelines call for coronary CT angiography.

Source DR. BOVE

PHILADELPHIA – The American College of Cardiology Foundation and the American Heart Association have endorsed stepwise guidelines for using nuclear imaging to manage and diagnose heart failure, but they do not obviate the need for the hands-on patient examination, said Dr. Alfred Bove of Temple University, Philadelphia.

“The beginning of management of a patient with heart failure is clinical,” Dr. Bove said. “We have to understand the patient's status. I always think it's important to put a stethoscope there first.” That provides a basis for interpreting data generated by subsequent imaging, as called for in the ACCF/AHA guidelines (J. Am. Coll. Cardiol. 2009;53:1343-832), he said.

“The first thing we're trying to understand is both the etiology of ventricular dysfunction and actual function when a patient shows up with symptoms of congestive heart failure to determine whether it is ischemic, dilated, valvular, or congenital,” he said. “We need imaging to sort out these etiologies.”

Ejection fraction is a key measure to determine left ventricle function, as are left ventricle dimensions, he said. “We are always looking at diastolic dimensions in particular; the degree of hypertrophy; whether there's any evidence of coronary disease or coronary stenosis or valvular stenosis or insufficiency; and finally, with congenital heart disease, the presence of shunts.”

The guidelines first recommend obtaining a two-dimensional echocardiogram. “It will tell us what the ejection fraction is, and tell us about valve size and function,” he said

The guidelines then “jump” to radionuclide ventriculography to assess ejection fraction and volume. In a patient with ischemic cardiomyopathy, coronary arteriography can help evaluate indications for revascularization, he said.

In the patient with no history of coronary disease, myocardial perfusion imaging (MPI) can determine the presence of perfusion defects. “We can use that as a basis to go forward to do some further studies,” he said. But in the patient with nonischemic cardiomyopathy and no history of coronary disease, MPI can also have a high number of false-positive readings. “We're more interested here in getting ejection fraction and some measure of heart size from the imaging as well as perfusion,” Dr. Bove said.

The guidelines also call for appropriate follow-up with gated SPECT (single-photon emission CT) or MUGA (multiple gated acquisition) because echocardiography is inconclusive in about 20% of patients, particularly those who are obese or have large chests, Dr. Bove said. “In many cases [when] we see someone with borderline ejection fraction, we send that person for a gated scan and it comes back normal,” he said.

A gated SPECT or MUGA scan provides an “important second backup in left ventricle measures,” particularly in patients whose echocardiograms are of poor quality, he said.

In cases of suspected ischemic cardiomyopathy, the ACCF/AHA guidelines call for coronary CT angiography. “This has a very good negative predictive value,” Dr. Bove said. “If we get a negative CT angiogram, we can be pretty comfortable in saying this is not an ischemic cardiomyopathy.”

When the case mandates further study, MRI can help evaluate structural anomalies in the myocardium. “When there's a question of etiology in the absence of coronary disease, the MRI becomes very important in assessing the etiology of the myocardial dysfunction,” he said.

Dr. Bove disclosed that he is a consultant to Insight Telehealth Systems.

In cases of suspected ischemic cardiomyopathy, the guidelines call for coronary CT angiography.

Source DR. BOVE