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European Society of Cardiology (ESC): Annual Congress
ESC: Too much TV boosts PE risk
LONDON – Middle-aged adults who watch TV for an average of 5 or more hours per night face an adjusted 6.5-fold increased risk of fatal pulmonary embolism, compared with those who watch less than 2.5 hours per night, Toru Shirakawa reported at the annual congress of the European Society of Cardiology.
This was the key lesson gleaned from an analysis from the Japan Collaborative Cohort Study, the first large-scale prospective investigation of the relationship between prolonged television watching and pulmonary embolism (PE). The study included 86,024 Japanese participants aged 40-79 years prospectively followed for a median of 18.4 years, explained Mr. Shirakawa, a medical student at Osaka (Japan) University.
And while many busy medical professionals might presume 5 hours–plus of TV watching per night constitutes extreme behavior, that’s hardly the case. Indeed, according to the Nielsen survey, American adults watch an average of 4.85 hours of TV nightly.
During the study period there were 59 confirmed deaths from PE. In a multivariate analysis adjusted for sex and baseline age, cardiovascular risk factors, and physical activity level, a strong dose-response relationship was evident between hours of TV viewing and fatal PE.
This association was most pronounced in the 40- to 59-year-olds. Using as a reference group subjects who watched less than 2.5 hours per day, those who watched 2.5-4.9 hours had an adjusted 3.14-fold increased risk of fatal PE. Individuals who watched 5 hours or more – less than the average length of two American football games – were at 6.49-fold increased risk.
The same dose-response association was evident in the full study population spanning ages 40 through 79 years at entry. However, the magnitude of risk attributable to prolonged television watching in the overall group wasn’t as great, since 60- to 79-year-olds face multiple age-related competing mortality risks. Still, 40- to 79-year-olds who watched at least 5 hours of TV daily had an adjusted 2.36-fold greater risk of fatal PE, compared with those who watched for less than 2.5 hours.
Mr. Shirakawa observed that the mechanism of injury is presumably the same as previously reported in studies of “shelter death” during the bombing of London during World War II, as well as “economy-class syndrome,” first described in conjunction with long-distance airplane flights in 1954. Basically, prolonged leg immobility leads to inadequate circulation and resultant venous clot formation. But prolonged TV watching is a much more common risk factor than is economy-class syndrome, he noted.
“The take-home message is this: Public awareness of the risk of pulmonary embolism from lengthy leg immobility is essential. To prevent the occurrence of pulmonary embolism, we recommend the same preventive behavior used against economy-class syndrome. That is, take a break, stand up, and walk around during the television viewing. And drink water to prevent dehydration; that is also important,” Mr. Shirakawa said.
Session cochair Dr. José Ramón González Juanatey observed that the true burden of PE triggered by prolonged TV watching is far greater than documented in the Japanese study because the analysis focused exclusively on fatal cases.
“Only about 10% of cases of pulmonary embolism are immediately fatal events,” commented Dr. González Juanatey of the University of Santiago de Compostela and president of the Spanish Society of Cardiology.
“The absolute risk may be fairly small, but it’s a devastating thing to have happen to you,” added cochair Dr. Ian Graham, professor of cardiovascular medicine at Trinity College, Dublin.
The Japan Collaborative Cohort Study has been funded by scientific grants from various Japanese health and education ministries. Mr. Shirakawa reported having no financial conflicts.
LONDON – Middle-aged adults who watch TV for an average of 5 or more hours per night face an adjusted 6.5-fold increased risk of fatal pulmonary embolism, compared with those who watch less than 2.5 hours per night, Toru Shirakawa reported at the annual congress of the European Society of Cardiology.
This was the key lesson gleaned from an analysis from the Japan Collaborative Cohort Study, the first large-scale prospective investigation of the relationship between prolonged television watching and pulmonary embolism (PE). The study included 86,024 Japanese participants aged 40-79 years prospectively followed for a median of 18.4 years, explained Mr. Shirakawa, a medical student at Osaka (Japan) University.
And while many busy medical professionals might presume 5 hours–plus of TV watching per night constitutes extreme behavior, that’s hardly the case. Indeed, according to the Nielsen survey, American adults watch an average of 4.85 hours of TV nightly.
During the study period there were 59 confirmed deaths from PE. In a multivariate analysis adjusted for sex and baseline age, cardiovascular risk factors, and physical activity level, a strong dose-response relationship was evident between hours of TV viewing and fatal PE.
This association was most pronounced in the 40- to 59-year-olds. Using as a reference group subjects who watched less than 2.5 hours per day, those who watched 2.5-4.9 hours had an adjusted 3.14-fold increased risk of fatal PE. Individuals who watched 5 hours or more – less than the average length of two American football games – were at 6.49-fold increased risk.
The same dose-response association was evident in the full study population spanning ages 40 through 79 years at entry. However, the magnitude of risk attributable to prolonged television watching in the overall group wasn’t as great, since 60- to 79-year-olds face multiple age-related competing mortality risks. Still, 40- to 79-year-olds who watched at least 5 hours of TV daily had an adjusted 2.36-fold greater risk of fatal PE, compared with those who watched for less than 2.5 hours.
Mr. Shirakawa observed that the mechanism of injury is presumably the same as previously reported in studies of “shelter death” during the bombing of London during World War II, as well as “economy-class syndrome,” first described in conjunction with long-distance airplane flights in 1954. Basically, prolonged leg immobility leads to inadequate circulation and resultant venous clot formation. But prolonged TV watching is a much more common risk factor than is economy-class syndrome, he noted.
“The take-home message is this: Public awareness of the risk of pulmonary embolism from lengthy leg immobility is essential. To prevent the occurrence of pulmonary embolism, we recommend the same preventive behavior used against economy-class syndrome. That is, take a break, stand up, and walk around during the television viewing. And drink water to prevent dehydration; that is also important,” Mr. Shirakawa said.
Session cochair Dr. José Ramón González Juanatey observed that the true burden of PE triggered by prolonged TV watching is far greater than documented in the Japanese study because the analysis focused exclusively on fatal cases.
“Only about 10% of cases of pulmonary embolism are immediately fatal events,” commented Dr. González Juanatey of the University of Santiago de Compostela and president of the Spanish Society of Cardiology.
“The absolute risk may be fairly small, but it’s a devastating thing to have happen to you,” added cochair Dr. Ian Graham, professor of cardiovascular medicine at Trinity College, Dublin.
The Japan Collaborative Cohort Study has been funded by scientific grants from various Japanese health and education ministries. Mr. Shirakawa reported having no financial conflicts.
LONDON – Middle-aged adults who watch TV for an average of 5 or more hours per night face an adjusted 6.5-fold increased risk of fatal pulmonary embolism, compared with those who watch less than 2.5 hours per night, Toru Shirakawa reported at the annual congress of the European Society of Cardiology.
This was the key lesson gleaned from an analysis from the Japan Collaborative Cohort Study, the first large-scale prospective investigation of the relationship between prolonged television watching and pulmonary embolism (PE). The study included 86,024 Japanese participants aged 40-79 years prospectively followed for a median of 18.4 years, explained Mr. Shirakawa, a medical student at Osaka (Japan) University.
And while many busy medical professionals might presume 5 hours–plus of TV watching per night constitutes extreme behavior, that’s hardly the case. Indeed, according to the Nielsen survey, American adults watch an average of 4.85 hours of TV nightly.
During the study period there were 59 confirmed deaths from PE. In a multivariate analysis adjusted for sex and baseline age, cardiovascular risk factors, and physical activity level, a strong dose-response relationship was evident between hours of TV viewing and fatal PE.
This association was most pronounced in the 40- to 59-year-olds. Using as a reference group subjects who watched less than 2.5 hours per day, those who watched 2.5-4.9 hours had an adjusted 3.14-fold increased risk of fatal PE. Individuals who watched 5 hours or more – less than the average length of two American football games – were at 6.49-fold increased risk.
The same dose-response association was evident in the full study population spanning ages 40 through 79 years at entry. However, the magnitude of risk attributable to prolonged television watching in the overall group wasn’t as great, since 60- to 79-year-olds face multiple age-related competing mortality risks. Still, 40- to 79-year-olds who watched at least 5 hours of TV daily had an adjusted 2.36-fold greater risk of fatal PE, compared with those who watched for less than 2.5 hours.
Mr. Shirakawa observed that the mechanism of injury is presumably the same as previously reported in studies of “shelter death” during the bombing of London during World War II, as well as “economy-class syndrome,” first described in conjunction with long-distance airplane flights in 1954. Basically, prolonged leg immobility leads to inadequate circulation and resultant venous clot formation. But prolonged TV watching is a much more common risk factor than is economy-class syndrome, he noted.
“The take-home message is this: Public awareness of the risk of pulmonary embolism from lengthy leg immobility is essential. To prevent the occurrence of pulmonary embolism, we recommend the same preventive behavior used against economy-class syndrome. That is, take a break, stand up, and walk around during the television viewing. And drink water to prevent dehydration; that is also important,” Mr. Shirakawa said.
Session cochair Dr. José Ramón González Juanatey observed that the true burden of PE triggered by prolonged TV watching is far greater than documented in the Japanese study because the analysis focused exclusively on fatal cases.
“Only about 10% of cases of pulmonary embolism are immediately fatal events,” commented Dr. González Juanatey of the University of Santiago de Compostela and president of the Spanish Society of Cardiology.
“The absolute risk may be fairly small, but it’s a devastating thing to have happen to you,” added cochair Dr. Ian Graham, professor of cardiovascular medicine at Trinity College, Dublin.
The Japan Collaborative Cohort Study has been funded by scientific grants from various Japanese health and education ministries. Mr. Shirakawa reported having no financial conflicts.
AT THE ESC CONGRESS 2015
Key clinical point: Tuning in to the television for an average of 5 hours or more per day is independently associated with a sharply increased pulmonary embolism risk.
Major finding: Middle-aged Japanese adults who spent 5 or more hours per day watching television were at an adjusted 6.5-fold greater risk of fatal pulmonary embolism than were those who averaged less than 2.5 hours of viewing.
Data source: This prospective Japanese national study included 86,024 participants aged 40-79 years who were followed for a median of 18.4 years.
Disclosures: The Japan Collaborative Cohort Study has been funded by scientific grants from various Japanese health and education ministries. The presenter reported having no financial conflicts.
ESC: Rivaroxaban safety highlighted in real-world setting
LONDON – The factor Xa inhibitor rivaroxaban was associated with low rates of bleeding and stroke in two observational studies that included more than 45,000 people with nonvalvular atrial fibrillation.
The XANTUS (Xarelto for Prevention of Stroke in Patients With Atrial Fibrillation) study involved 6,784 individuals treated at centers in Europe, Canada, and Israel. The incidence of major bleeding was 2.1% per year and the risk of stroke was 0.7% per year. Rates of fatal, critical organ, and intracranial bleeding were also low at 0.2%, 0.7%, and 0.4% per year, respectively.
“The rates of stroke and systemic embolism, all strokes and gastrointestinal bleeding were markedly lower in XANTUS in comparison to ROCKET-AF,” noted Dr. John Camm who presented the XANTUS study findings at the annual congress of the European Society of Cardiology. “Major bleeding was also largely reduced in XANTUS, however the death rate and intracranial hemorrhage rate was similar,” he added.
Dr. Camm, who is professor of clinical cardiology at St George’s Hospital in London, noted that the patient populations and the design of the XANTUS study and phase III ROCKET-AF trial (N Engl J Med. 2011;365:883-91) were slightly different. Patients in the single-arm, prospective, observational XANTUS study were recruited from routine primary care practices and had an overall lower risk of stroke than those enrolled in the randomized, double-blind, controlled clinical trial who were at more moderate to high risk respective CHADS2 scores of 2.0 and 3.5. The incidence of major bleeding was also slightly higher in the ROCKET-AF, at 3.6% per year, which was similar to that seen with warfarin (3.4%; P = .58), the active comparator used.
Nevertheless, the findings of the XANTUS study, which were published online simultaneously with their presentation at the conference (Eur Heart J. Sep 1. doi: 10.1093/eurheartj/ehv466), highlight the “real-world” safety of rivaroxaban, Dr. Camm said.
Results from the separate PMSS (Post-Marketing Safety Surveillance) study reported in a poster at the meeting were similar. The PMSS study is being conducted in the United States and is an ongoing, retrospective, 5-year, observational study of more than 39,000 patients with nonvalvular atrial fibrillation. At 2 years follow-up, the incidence of major bleeding was 2.89% per year and the incidence of fatal bleeding was 0.1% per year (Eur Heart J. 2015;36:687.P4066).
“Real-world research is an essential complement to clinical trials and helps inform treatment decisions,” PMSS study investigator Dr. Frank Peacock said in a press release issued by Janssen. Dr. Peacock, who is professor of emergency medicine at Baylor College of Medicine in Houston, added, “These studies confirm the safety profile of rivaroxaban in real-world settings around the globe.”
The XANTUS and PMSS studies are part of a large postlicensing program and were respectively designed to meet European Medicines Agency and U.S. Food and Drug Administration requirements on the long-term monitoring of medicines. There are also similar programs running in other world regions, such as XANTUS-EL and XANAP.
Other real-world data gleaned from electronic medical records (EMRs) comparing the potential bleeding risks of the factor Xa inhibitor apixaban (Eliquis) versus other available non–vitamin K antagonists (NOACs) including rivaroxaban and the direct thrombin inhibitor dabigatran (Pradaxa) were reported in several posters supported by Bristol-Myers Squibb and Pfizer and in an oral presentation given by Dr. Gregory Lip of the University of Birmingham, England.
Two of the posters reported data from retrospective analyses of different United States EMRs of 29,338 and 35, 757 patients, respectively, with nonvalvular atrial fibrillation newly started on a NOAC or warfarin in 2013 or 2014. Most were started on warfarin (43.3%/69.6%), followed by rivaroxaban (34.3%/17.9%), dabigatran (14.2%/6.8%), and apixaban (8.2%/5.7%).
Results of the first study (Eur Heart J. 2015;36:1085.P6217) showed that patients newly starting treatment with a NOAC had significantly lower rates of major bleeding than those starting treatment with warfarin, which was 4.6% per year versus 2.35% per year for apixiban, 3.38% per year for dabigatran, and 4.57% per year for rivaroxaban in the first study.
In the second study (Eur Heart J. 2015;36:1085.P6215) the respective adjusted hazard ratios for bleeding risk were 1.094, 0.747 and 0.679, comparing rivaroxaban, apixaban, and dabigatran against warfarin.
Other data gleaned from separate U.S. EMRs suggested that apixaban was associated with fewer bleeding-related hospital readmissions than either rivaroxaban or dabigatran in hospitalized patients with nonvalvular atrial fibrillation (Eur Heart J. 2015;36: 1085.P6211).
Dr. Lip presented 6-month follow-up data on more than 60,000 patients with nonvalvular atrial fibrillation who were treated with one of the three NOACs that was recorded in a U.S. medical claims database (Eur Heart J. 2015;36:339.1975). Most of the patients were treated with rivaroxaban (50.6%), with 34.8% treated with dabigatran and 14.6% with apixaban. Unadjusted data showed that the rates of major bleeding were 20.2% per year, 13.2% per year, and 14.5% per year, respectively.
Dr. Lip observed that, after adjusting the data, patients taking dabigatran had higher rates of clinically relevant nonmajor gastrointestinal bleeding (HR =1.24), and that those taking rivaroxaban were more likely to have major (HR = 3.6), clinically relevant nonmajor (HR = 1.43), or any bleeding (HR = 1.41) when compared with apixaban users.
“Larger cohort studies and longer follow-up data of general nonvalvular atrial fibrillation populations will be needed to confirm these early observations,” Dr. Lip concluded.
While real-world research of course has its limitations and cannot replace clinical trial findings as a means to accurately compare the clinical efficacy or safety profiles of different medicines, such studies do provide information that can help inform clinical practice.
“With 10 million people in Europe alone affected by atrial fibrillation, a number that is only expected to increase, real-world insights on routine anticoagulation management in everyday clinical practice is increasingly important for physicians and patients,” Dr. Camm noted in a media release on the XANTUS trial issued by the European Society of Cardiology.
Dr. Camm added: “These real-world insights from XANTAS complement and expand on what we already know from clinical trials, and provide physicians with reassurance to prescribe rivaroxaban as an effective and well-tolerated treatment option for the broad range of patients with atrial fibrillation seen in their everyday practice.”
The XANTUS and PMSS studies were supported by Bayer HealthCare and Janssen. The other studies mentioned were supported by Bristol-Myers Squibb and Pfizer. Dr. Camm disclosed acting as a consultant for Bayer Healthcare and other health care companies. Dr. Lip disclosed acting as a consultant for Bayer Healthcare, Bristol-Myers Squibb, and Pfizer as well as other health care companies.
LONDON – The factor Xa inhibitor rivaroxaban was associated with low rates of bleeding and stroke in two observational studies that included more than 45,000 people with nonvalvular atrial fibrillation.
The XANTUS (Xarelto for Prevention of Stroke in Patients With Atrial Fibrillation) study involved 6,784 individuals treated at centers in Europe, Canada, and Israel. The incidence of major bleeding was 2.1% per year and the risk of stroke was 0.7% per year. Rates of fatal, critical organ, and intracranial bleeding were also low at 0.2%, 0.7%, and 0.4% per year, respectively.
“The rates of stroke and systemic embolism, all strokes and gastrointestinal bleeding were markedly lower in XANTUS in comparison to ROCKET-AF,” noted Dr. John Camm who presented the XANTUS study findings at the annual congress of the European Society of Cardiology. “Major bleeding was also largely reduced in XANTUS, however the death rate and intracranial hemorrhage rate was similar,” he added.
Dr. Camm, who is professor of clinical cardiology at St George’s Hospital in London, noted that the patient populations and the design of the XANTUS study and phase III ROCKET-AF trial (N Engl J Med. 2011;365:883-91) were slightly different. Patients in the single-arm, prospective, observational XANTUS study were recruited from routine primary care practices and had an overall lower risk of stroke than those enrolled in the randomized, double-blind, controlled clinical trial who were at more moderate to high risk respective CHADS2 scores of 2.0 and 3.5. The incidence of major bleeding was also slightly higher in the ROCKET-AF, at 3.6% per year, which was similar to that seen with warfarin (3.4%; P = .58), the active comparator used.
Nevertheless, the findings of the XANTUS study, which were published online simultaneously with their presentation at the conference (Eur Heart J. Sep 1. doi: 10.1093/eurheartj/ehv466), highlight the “real-world” safety of rivaroxaban, Dr. Camm said.
Results from the separate PMSS (Post-Marketing Safety Surveillance) study reported in a poster at the meeting were similar. The PMSS study is being conducted in the United States and is an ongoing, retrospective, 5-year, observational study of more than 39,000 patients with nonvalvular atrial fibrillation. At 2 years follow-up, the incidence of major bleeding was 2.89% per year and the incidence of fatal bleeding was 0.1% per year (Eur Heart J. 2015;36:687.P4066).
“Real-world research is an essential complement to clinical trials and helps inform treatment decisions,” PMSS study investigator Dr. Frank Peacock said in a press release issued by Janssen. Dr. Peacock, who is professor of emergency medicine at Baylor College of Medicine in Houston, added, “These studies confirm the safety profile of rivaroxaban in real-world settings around the globe.”
The XANTUS and PMSS studies are part of a large postlicensing program and were respectively designed to meet European Medicines Agency and U.S. Food and Drug Administration requirements on the long-term monitoring of medicines. There are also similar programs running in other world regions, such as XANTUS-EL and XANAP.
Other real-world data gleaned from electronic medical records (EMRs) comparing the potential bleeding risks of the factor Xa inhibitor apixaban (Eliquis) versus other available non–vitamin K antagonists (NOACs) including rivaroxaban and the direct thrombin inhibitor dabigatran (Pradaxa) were reported in several posters supported by Bristol-Myers Squibb and Pfizer and in an oral presentation given by Dr. Gregory Lip of the University of Birmingham, England.
Two of the posters reported data from retrospective analyses of different United States EMRs of 29,338 and 35, 757 patients, respectively, with nonvalvular atrial fibrillation newly started on a NOAC or warfarin in 2013 or 2014. Most were started on warfarin (43.3%/69.6%), followed by rivaroxaban (34.3%/17.9%), dabigatran (14.2%/6.8%), and apixaban (8.2%/5.7%).
Results of the first study (Eur Heart J. 2015;36:1085.P6217) showed that patients newly starting treatment with a NOAC had significantly lower rates of major bleeding than those starting treatment with warfarin, which was 4.6% per year versus 2.35% per year for apixiban, 3.38% per year for dabigatran, and 4.57% per year for rivaroxaban in the first study.
In the second study (Eur Heart J. 2015;36:1085.P6215) the respective adjusted hazard ratios for bleeding risk were 1.094, 0.747 and 0.679, comparing rivaroxaban, apixaban, and dabigatran against warfarin.
Other data gleaned from separate U.S. EMRs suggested that apixaban was associated with fewer bleeding-related hospital readmissions than either rivaroxaban or dabigatran in hospitalized patients with nonvalvular atrial fibrillation (Eur Heart J. 2015;36: 1085.P6211).
Dr. Lip presented 6-month follow-up data on more than 60,000 patients with nonvalvular atrial fibrillation who were treated with one of the three NOACs that was recorded in a U.S. medical claims database (Eur Heart J. 2015;36:339.1975). Most of the patients were treated with rivaroxaban (50.6%), with 34.8% treated with dabigatran and 14.6% with apixaban. Unadjusted data showed that the rates of major bleeding were 20.2% per year, 13.2% per year, and 14.5% per year, respectively.
Dr. Lip observed that, after adjusting the data, patients taking dabigatran had higher rates of clinically relevant nonmajor gastrointestinal bleeding (HR =1.24), and that those taking rivaroxaban were more likely to have major (HR = 3.6), clinically relevant nonmajor (HR = 1.43), or any bleeding (HR = 1.41) when compared with apixaban users.
“Larger cohort studies and longer follow-up data of general nonvalvular atrial fibrillation populations will be needed to confirm these early observations,” Dr. Lip concluded.
While real-world research of course has its limitations and cannot replace clinical trial findings as a means to accurately compare the clinical efficacy or safety profiles of different medicines, such studies do provide information that can help inform clinical practice.
“With 10 million people in Europe alone affected by atrial fibrillation, a number that is only expected to increase, real-world insights on routine anticoagulation management in everyday clinical practice is increasingly important for physicians and patients,” Dr. Camm noted in a media release on the XANTUS trial issued by the European Society of Cardiology.
Dr. Camm added: “These real-world insights from XANTAS complement and expand on what we already know from clinical trials, and provide physicians with reassurance to prescribe rivaroxaban as an effective and well-tolerated treatment option for the broad range of patients with atrial fibrillation seen in their everyday practice.”
The XANTUS and PMSS studies were supported by Bayer HealthCare and Janssen. The other studies mentioned were supported by Bristol-Myers Squibb and Pfizer. Dr. Camm disclosed acting as a consultant for Bayer Healthcare and other health care companies. Dr. Lip disclosed acting as a consultant for Bayer Healthcare, Bristol-Myers Squibb, and Pfizer as well as other health care companies.
LONDON – The factor Xa inhibitor rivaroxaban was associated with low rates of bleeding and stroke in two observational studies that included more than 45,000 people with nonvalvular atrial fibrillation.
The XANTUS (Xarelto for Prevention of Stroke in Patients With Atrial Fibrillation) study involved 6,784 individuals treated at centers in Europe, Canada, and Israel. The incidence of major bleeding was 2.1% per year and the risk of stroke was 0.7% per year. Rates of fatal, critical organ, and intracranial bleeding were also low at 0.2%, 0.7%, and 0.4% per year, respectively.
“The rates of stroke and systemic embolism, all strokes and gastrointestinal bleeding were markedly lower in XANTUS in comparison to ROCKET-AF,” noted Dr. John Camm who presented the XANTUS study findings at the annual congress of the European Society of Cardiology. “Major bleeding was also largely reduced in XANTUS, however the death rate and intracranial hemorrhage rate was similar,” he added.
Dr. Camm, who is professor of clinical cardiology at St George’s Hospital in London, noted that the patient populations and the design of the XANTUS study and phase III ROCKET-AF trial (N Engl J Med. 2011;365:883-91) were slightly different. Patients in the single-arm, prospective, observational XANTUS study were recruited from routine primary care practices and had an overall lower risk of stroke than those enrolled in the randomized, double-blind, controlled clinical trial who were at more moderate to high risk respective CHADS2 scores of 2.0 and 3.5. The incidence of major bleeding was also slightly higher in the ROCKET-AF, at 3.6% per year, which was similar to that seen with warfarin (3.4%; P = .58), the active comparator used.
Nevertheless, the findings of the XANTUS study, which were published online simultaneously with their presentation at the conference (Eur Heart J. Sep 1. doi: 10.1093/eurheartj/ehv466), highlight the “real-world” safety of rivaroxaban, Dr. Camm said.
Results from the separate PMSS (Post-Marketing Safety Surveillance) study reported in a poster at the meeting were similar. The PMSS study is being conducted in the United States and is an ongoing, retrospective, 5-year, observational study of more than 39,000 patients with nonvalvular atrial fibrillation. At 2 years follow-up, the incidence of major bleeding was 2.89% per year and the incidence of fatal bleeding was 0.1% per year (Eur Heart J. 2015;36:687.P4066).
“Real-world research is an essential complement to clinical trials and helps inform treatment decisions,” PMSS study investigator Dr. Frank Peacock said in a press release issued by Janssen. Dr. Peacock, who is professor of emergency medicine at Baylor College of Medicine in Houston, added, “These studies confirm the safety profile of rivaroxaban in real-world settings around the globe.”
The XANTUS and PMSS studies are part of a large postlicensing program and were respectively designed to meet European Medicines Agency and U.S. Food and Drug Administration requirements on the long-term monitoring of medicines. There are also similar programs running in other world regions, such as XANTUS-EL and XANAP.
Other real-world data gleaned from electronic medical records (EMRs) comparing the potential bleeding risks of the factor Xa inhibitor apixaban (Eliquis) versus other available non–vitamin K antagonists (NOACs) including rivaroxaban and the direct thrombin inhibitor dabigatran (Pradaxa) were reported in several posters supported by Bristol-Myers Squibb and Pfizer and in an oral presentation given by Dr. Gregory Lip of the University of Birmingham, England.
Two of the posters reported data from retrospective analyses of different United States EMRs of 29,338 and 35, 757 patients, respectively, with nonvalvular atrial fibrillation newly started on a NOAC or warfarin in 2013 or 2014. Most were started on warfarin (43.3%/69.6%), followed by rivaroxaban (34.3%/17.9%), dabigatran (14.2%/6.8%), and apixaban (8.2%/5.7%).
Results of the first study (Eur Heart J. 2015;36:1085.P6217) showed that patients newly starting treatment with a NOAC had significantly lower rates of major bleeding than those starting treatment with warfarin, which was 4.6% per year versus 2.35% per year for apixiban, 3.38% per year for dabigatran, and 4.57% per year for rivaroxaban in the first study.
In the second study (Eur Heart J. 2015;36:1085.P6215) the respective adjusted hazard ratios for bleeding risk were 1.094, 0.747 and 0.679, comparing rivaroxaban, apixaban, and dabigatran against warfarin.
Other data gleaned from separate U.S. EMRs suggested that apixaban was associated with fewer bleeding-related hospital readmissions than either rivaroxaban or dabigatran in hospitalized patients with nonvalvular atrial fibrillation (Eur Heart J. 2015;36: 1085.P6211).
Dr. Lip presented 6-month follow-up data on more than 60,000 patients with nonvalvular atrial fibrillation who were treated with one of the three NOACs that was recorded in a U.S. medical claims database (Eur Heart J. 2015;36:339.1975). Most of the patients were treated with rivaroxaban (50.6%), with 34.8% treated with dabigatran and 14.6% with apixaban. Unadjusted data showed that the rates of major bleeding were 20.2% per year, 13.2% per year, and 14.5% per year, respectively.
Dr. Lip observed that, after adjusting the data, patients taking dabigatran had higher rates of clinically relevant nonmajor gastrointestinal bleeding (HR =1.24), and that those taking rivaroxaban were more likely to have major (HR = 3.6), clinically relevant nonmajor (HR = 1.43), or any bleeding (HR = 1.41) when compared with apixaban users.
“Larger cohort studies and longer follow-up data of general nonvalvular atrial fibrillation populations will be needed to confirm these early observations,” Dr. Lip concluded.
While real-world research of course has its limitations and cannot replace clinical trial findings as a means to accurately compare the clinical efficacy or safety profiles of different medicines, such studies do provide information that can help inform clinical practice.
“With 10 million people in Europe alone affected by atrial fibrillation, a number that is only expected to increase, real-world insights on routine anticoagulation management in everyday clinical practice is increasingly important for physicians and patients,” Dr. Camm noted in a media release on the XANTUS trial issued by the European Society of Cardiology.
Dr. Camm added: “These real-world insights from XANTAS complement and expand on what we already know from clinical trials, and provide physicians with reassurance to prescribe rivaroxaban as an effective and well-tolerated treatment option for the broad range of patients with atrial fibrillation seen in their everyday practice.”
The XANTUS and PMSS studies were supported by Bayer HealthCare and Janssen. The other studies mentioned were supported by Bristol-Myers Squibb and Pfizer. Dr. Camm disclosed acting as a consultant for Bayer Healthcare and other health care companies. Dr. Lip disclosed acting as a consultant for Bayer Healthcare, Bristol-Myers Squibb, and Pfizer as well as other health care companies.
AT THE ESC CONGRESS 2015
Key clinical point: Data from routine clinical practice studies suggest a low risk of bleeding and stroke with rivaroxaban and other non–vitamin K antagonists.
Major finding: The incidence of major bleeding with rivaroxaban was 2.1% per year and the risk of stroke was 0.7% per year in the XANTUS study.
Data source: More than 45,000 patients with nonvalvular atrial fibrillation treated with rivaroxaban for stroke prevention in two, real-world observational studies and separate electronic medical record analyses of patients treated with apixaban, rivaroxaban, and dabigatran.
Disclosures: The XANTUS and PMSS studies were supported by Bayer HealthCare and Janssen. The other studies mentioned were supported by Bristol-Myers Squibb and Pfizer. Dr. Camm disclosed acting as a consultant for Bayer Healthcare and other health care companies. Dr. Lip disclosed acting as a consultant for Bayer Healthcare, Bristol-Myers Squibb, and Pfizer as well as other health care companies.
ESC: CERTITUDE casts doubt on defibrillator benefit in CRT
LONDON – Heart failure patients who are candidates for cardiac resynchronization therapy in a routine clinical practice setting will likely not benefit from the addition of a defibrillator to a pacemaker, according to results of the CERTITUDE cohort study.
In CERTITUDE, most of the deaths in patients fitted with a cardiac resynchronization therapy–pacemaker (CRT-P) device were predominantly from causes other than sudden cardiac death (SCD), which is the main rationale for using a CRT-defibrillator (CRT-D) device, said lead investigator Jean-Yves Le Heuzey at the annual congress of the European Society of Cardiology.
“Our results should not be interpreted as a general lack of benefit from CRT-D vs. CRT-P or vice versa. Rather we demonstrate that given currently selected CRT-P patients in the French population, addition of a defibrillator may not significantly add to survival.” Therefore, patients who may be eligible for CRT should not “automatically” be considered as requiring a CRT-D, suggested Dr. Le Heuzey and his coinvestigators in an article that was published online at the time of the study’s presentation (Eur Heart J. 2015 Sep 1. doi: 10.1093/eurheartj/ehv455).
Current ESC guidelines on cardiac pacing and cardiac resynchronization therapy “leave flexibility for the physician” on the use of CRT-P and CRT-D” because there was no evidence of a superior effect of the latter over CRT alone, said Dr. Le Heuzey of René Descartes University in Paris at the meeting. A randomized, controlled trial would be the only way to determine this, but such a trial is unlikely to ever be conducted, he noted.
Despite the lack of evidence, however, CRT-D is widely used, more so in the United States than in Europe, Dr. Le Heuzey observed, where more than 90% of patients needing CRT would likely have a CRT-D rather than a CRT-P device implanted.
The aims of the CERTITUDE cohort study were to look at the extent to which CRT-P patients differ from CRT-D patients in a real-life setting, and to also see if there were patients in the CRT-P group that might have benefited from CRT-D.
The prospective, observational study involved 1,705 patients who were recruited at 41 centers throughout France over a 2-year period starting in January 2008. Of these, 31% were fitted with a CRT-P device and 69% with a CRT-D.
Results showed that patients who had a CRT-P versus a CRT-D implanted were significantly older, more often female, and more symptomatic. They were also significantly less likely to have coronary artery disease, more likely to have wider QRS intervals and to have atrial fibrillation, and more often had at least two comorbidities.
Analysis of the causes of death was performed at 2 years’ follow-up, which Dr. Le Heuzey conceded was a short period of time. At this point, 267 of 1,611 patients with complete follow-up data had died, giving an overall mortality rate of 8.4% per 100 patient-years for the entire cohort.
The crude mortality rate was found to be higher among CRT-P than CRT-D patients, at 13.1% versus 6.5% per 100 patient-years (relative risk, 2.01; 95% confidence interval, 1.56-2.58; P less than .0001). But when the cause of death was examined more closely, there was no significant difference in the number of SCDs between the groups (RR, 1.57; 95% CI, 0.71-3.46; P = .42) and no significant difference when a specific cause of death analysis was performed.
The main reasons for the almost doubled risk of death in the CRT-P group was an increase in non-SCD cardiovascular mortality, mainly progressive heart failure (RR, 0.27; 95% CI, 1.62-3.18) and other cardiovascular causes (RR, 4.4; 95% CI, 1.29-15.03), Dr. Le Heuzey and associates noted in the article.
“Overall, 95% of the excess mortality among CRT-P recipients was not related to SCD,” they wrote, noting that this “suggests that the presence of a back-up defibrillator would probably not have been beneficial in terms of improving survival for these patients.”
So where does this leave clinicians? Dr. Le Heuzey referred to Table 17 in the European guidelines (Eur Heart J. 2013;34:2281-2329) with guidance on factors favoring CRT-P or CRT-D. For instance, CRT-P might be favorable in a patient with advanced heart failure or one with severe renal insufficiency or on dialysis. Other major comorbidities or frailty or cachexia might veer a decision towards CRT without a defibrillator. On the other hand, factors favoring CRT-D include a life expectancy of more than 1 year; stable, moderate (New York Heart Association class II) disease; or low to moderate–risk ischemic heart disease, with a lack of comorbidities.
CERTITUDE was funded by grants from the French Institute of Health and Medical Research (INSERM) and from the French Cardiology Society. The latter received specific grants from Biotronik, Boston Scientific, Medtronic, Saint Jude Medical, and Sorin in order to perform the study. Dr. Le Heuzey disclosed receiving fees for participation in advisory boards and conferences from AstraZeneca, Bayer, Boehringer-Ingelheim, Bristol Myers Squibb/Pfizer, Correvio, Daiichi-Sankyo, Meda, Sanofi, and Servier.
LONDON – Heart failure patients who are candidates for cardiac resynchronization therapy in a routine clinical practice setting will likely not benefit from the addition of a defibrillator to a pacemaker, according to results of the CERTITUDE cohort study.
In CERTITUDE, most of the deaths in patients fitted with a cardiac resynchronization therapy–pacemaker (CRT-P) device were predominantly from causes other than sudden cardiac death (SCD), which is the main rationale for using a CRT-defibrillator (CRT-D) device, said lead investigator Jean-Yves Le Heuzey at the annual congress of the European Society of Cardiology.
“Our results should not be interpreted as a general lack of benefit from CRT-D vs. CRT-P or vice versa. Rather we demonstrate that given currently selected CRT-P patients in the French population, addition of a defibrillator may not significantly add to survival.” Therefore, patients who may be eligible for CRT should not “automatically” be considered as requiring a CRT-D, suggested Dr. Le Heuzey and his coinvestigators in an article that was published online at the time of the study’s presentation (Eur Heart J. 2015 Sep 1. doi: 10.1093/eurheartj/ehv455).
Current ESC guidelines on cardiac pacing and cardiac resynchronization therapy “leave flexibility for the physician” on the use of CRT-P and CRT-D” because there was no evidence of a superior effect of the latter over CRT alone, said Dr. Le Heuzey of René Descartes University in Paris at the meeting. A randomized, controlled trial would be the only way to determine this, but such a trial is unlikely to ever be conducted, he noted.
Despite the lack of evidence, however, CRT-D is widely used, more so in the United States than in Europe, Dr. Le Heuzey observed, where more than 90% of patients needing CRT would likely have a CRT-D rather than a CRT-P device implanted.
The aims of the CERTITUDE cohort study were to look at the extent to which CRT-P patients differ from CRT-D patients in a real-life setting, and to also see if there were patients in the CRT-P group that might have benefited from CRT-D.
The prospective, observational study involved 1,705 patients who were recruited at 41 centers throughout France over a 2-year period starting in January 2008. Of these, 31% were fitted with a CRT-P device and 69% with a CRT-D.
Results showed that patients who had a CRT-P versus a CRT-D implanted were significantly older, more often female, and more symptomatic. They were also significantly less likely to have coronary artery disease, more likely to have wider QRS intervals and to have atrial fibrillation, and more often had at least two comorbidities.
Analysis of the causes of death was performed at 2 years’ follow-up, which Dr. Le Heuzey conceded was a short period of time. At this point, 267 of 1,611 patients with complete follow-up data had died, giving an overall mortality rate of 8.4% per 100 patient-years for the entire cohort.
The crude mortality rate was found to be higher among CRT-P than CRT-D patients, at 13.1% versus 6.5% per 100 patient-years (relative risk, 2.01; 95% confidence interval, 1.56-2.58; P less than .0001). But when the cause of death was examined more closely, there was no significant difference in the number of SCDs between the groups (RR, 1.57; 95% CI, 0.71-3.46; P = .42) and no significant difference when a specific cause of death analysis was performed.
The main reasons for the almost doubled risk of death in the CRT-P group was an increase in non-SCD cardiovascular mortality, mainly progressive heart failure (RR, 0.27; 95% CI, 1.62-3.18) and other cardiovascular causes (RR, 4.4; 95% CI, 1.29-15.03), Dr. Le Heuzey and associates noted in the article.
“Overall, 95% of the excess mortality among CRT-P recipients was not related to SCD,” they wrote, noting that this “suggests that the presence of a back-up defibrillator would probably not have been beneficial in terms of improving survival for these patients.”
So where does this leave clinicians? Dr. Le Heuzey referred to Table 17 in the European guidelines (Eur Heart J. 2013;34:2281-2329) with guidance on factors favoring CRT-P or CRT-D. For instance, CRT-P might be favorable in a patient with advanced heart failure or one with severe renal insufficiency or on dialysis. Other major comorbidities or frailty or cachexia might veer a decision towards CRT without a defibrillator. On the other hand, factors favoring CRT-D include a life expectancy of more than 1 year; stable, moderate (New York Heart Association class II) disease; or low to moderate–risk ischemic heart disease, with a lack of comorbidities.
CERTITUDE was funded by grants from the French Institute of Health and Medical Research (INSERM) and from the French Cardiology Society. The latter received specific grants from Biotronik, Boston Scientific, Medtronic, Saint Jude Medical, and Sorin in order to perform the study. Dr. Le Heuzey disclosed receiving fees for participation in advisory boards and conferences from AstraZeneca, Bayer, Boehringer-Ingelheim, Bristol Myers Squibb/Pfizer, Correvio, Daiichi-Sankyo, Meda, Sanofi, and Servier.
LONDON – Heart failure patients who are candidates for cardiac resynchronization therapy in a routine clinical practice setting will likely not benefit from the addition of a defibrillator to a pacemaker, according to results of the CERTITUDE cohort study.
In CERTITUDE, most of the deaths in patients fitted with a cardiac resynchronization therapy–pacemaker (CRT-P) device were predominantly from causes other than sudden cardiac death (SCD), which is the main rationale for using a CRT-defibrillator (CRT-D) device, said lead investigator Jean-Yves Le Heuzey at the annual congress of the European Society of Cardiology.
“Our results should not be interpreted as a general lack of benefit from CRT-D vs. CRT-P or vice versa. Rather we demonstrate that given currently selected CRT-P patients in the French population, addition of a defibrillator may not significantly add to survival.” Therefore, patients who may be eligible for CRT should not “automatically” be considered as requiring a CRT-D, suggested Dr. Le Heuzey and his coinvestigators in an article that was published online at the time of the study’s presentation (Eur Heart J. 2015 Sep 1. doi: 10.1093/eurheartj/ehv455).
Current ESC guidelines on cardiac pacing and cardiac resynchronization therapy “leave flexibility for the physician” on the use of CRT-P and CRT-D” because there was no evidence of a superior effect of the latter over CRT alone, said Dr. Le Heuzey of René Descartes University in Paris at the meeting. A randomized, controlled trial would be the only way to determine this, but such a trial is unlikely to ever be conducted, he noted.
Despite the lack of evidence, however, CRT-D is widely used, more so in the United States than in Europe, Dr. Le Heuzey observed, where more than 90% of patients needing CRT would likely have a CRT-D rather than a CRT-P device implanted.
The aims of the CERTITUDE cohort study were to look at the extent to which CRT-P patients differ from CRT-D patients in a real-life setting, and to also see if there were patients in the CRT-P group that might have benefited from CRT-D.
The prospective, observational study involved 1,705 patients who were recruited at 41 centers throughout France over a 2-year period starting in January 2008. Of these, 31% were fitted with a CRT-P device and 69% with a CRT-D.
Results showed that patients who had a CRT-P versus a CRT-D implanted were significantly older, more often female, and more symptomatic. They were also significantly less likely to have coronary artery disease, more likely to have wider QRS intervals and to have atrial fibrillation, and more often had at least two comorbidities.
Analysis of the causes of death was performed at 2 years’ follow-up, which Dr. Le Heuzey conceded was a short period of time. At this point, 267 of 1,611 patients with complete follow-up data had died, giving an overall mortality rate of 8.4% per 100 patient-years for the entire cohort.
The crude mortality rate was found to be higher among CRT-P than CRT-D patients, at 13.1% versus 6.5% per 100 patient-years (relative risk, 2.01; 95% confidence interval, 1.56-2.58; P less than .0001). But when the cause of death was examined more closely, there was no significant difference in the number of SCDs between the groups (RR, 1.57; 95% CI, 0.71-3.46; P = .42) and no significant difference when a specific cause of death analysis was performed.
The main reasons for the almost doubled risk of death in the CRT-P group was an increase in non-SCD cardiovascular mortality, mainly progressive heart failure (RR, 0.27; 95% CI, 1.62-3.18) and other cardiovascular causes (RR, 4.4; 95% CI, 1.29-15.03), Dr. Le Heuzey and associates noted in the article.
“Overall, 95% of the excess mortality among CRT-P recipients was not related to SCD,” they wrote, noting that this “suggests that the presence of a back-up defibrillator would probably not have been beneficial in terms of improving survival for these patients.”
So where does this leave clinicians? Dr. Le Heuzey referred to Table 17 in the European guidelines (Eur Heart J. 2013;34:2281-2329) with guidance on factors favoring CRT-P or CRT-D. For instance, CRT-P might be favorable in a patient with advanced heart failure or one with severe renal insufficiency or on dialysis. Other major comorbidities or frailty or cachexia might veer a decision towards CRT without a defibrillator. On the other hand, factors favoring CRT-D include a life expectancy of more than 1 year; stable, moderate (New York Heart Association class II) disease; or low to moderate–risk ischemic heart disease, with a lack of comorbidities.
CERTITUDE was funded by grants from the French Institute of Health and Medical Research (INSERM) and from the French Cardiology Society. The latter received specific grants from Biotronik, Boston Scientific, Medtronic, Saint Jude Medical, and Sorin in order to perform the study. Dr. Le Heuzey disclosed receiving fees for participation in advisory boards and conferences from AstraZeneca, Bayer, Boehringer-Ingelheim, Bristol Myers Squibb/Pfizer, Correvio, Daiichi-Sankyo, Meda, Sanofi, and Servier.
AT THE ESC CONGRESS 2015
Key clinical point:There appears to be no survival benefit of cardiac resynchronization therapy with a defibrillator CRT-D over a pacemaker (CRT-P).
Major finding: Although there was a higher death rate among CRT-P recipients, 95% of the excess mortality, compared with CRT-D recipients, was not related to sudden cardiac death.
Data source: The prospective, observational CERTITUDE cohort study in 1,705 French patients fitted with a CRT-P or CRT-D.
Disclosures: CERTITUDE was funded by grants from the French Institute of Health and Medical Research (INSERM) and from the French Cardiology Society. The latter received specific grants from Biotronik, Boston Scientific, Medtronic, St. Jude Medical, and Sorin in order to perform the study. Dr. Le Heuzey disclosed receiving fees for participation in advisory boards and conferences from AstraZeneca, Bayer, Boehringer-Ingelheim, Bristol Myers Squibb/Pfizer, Correvio, Daiichi-Sankyo, Meda, Sanofi, and Servier.
VIDEO: Adverse ventilation effect means rethinking Cheyne-Stokes respiration
LONDON – The management of Cheyne-Stokes respiration in patients with heart failure with reduced ejection fraction needs to be reconsidered following the troubling outcome of a major trial that tested adaptive servo-ventilation as treatment for this symptom, Dr. Lars Køber commented during an interview at the annual congress of the European Society of Cardiology.
Cheyne-Stokes respiration, a form of central sleep apnea, differs from obstructive sleep apnea in that heart failure patients do not seem to derive symptomatic benefit from adaptive servo-ventilation treatment, but “physicians have thought they could treat this sleep apnea [with ventilation] and it would change prognosis,” said Dr. Køber. “Treatment of sleep apnea is possible, so physicians had started doing it.” But instead of helping patients, the trial results strongly suggested that patients were harmed by treatment, which was significantly linked with increased rates of both all-cause and cardiovascular mortality (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459).
In our video interview, Dr. Køber, professor of cardiology at Rigshospitalet and the University of Copenhagen, discusses the results and what the findings imply for future treatment.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @mitchelzoler
LONDON – The management of Cheyne-Stokes respiration in patients with heart failure with reduced ejection fraction needs to be reconsidered following the troubling outcome of a major trial that tested adaptive servo-ventilation as treatment for this symptom, Dr. Lars Køber commented during an interview at the annual congress of the European Society of Cardiology.
Cheyne-Stokes respiration, a form of central sleep apnea, differs from obstructive sleep apnea in that heart failure patients do not seem to derive symptomatic benefit from adaptive servo-ventilation treatment, but “physicians have thought they could treat this sleep apnea [with ventilation] and it would change prognosis,” said Dr. Køber. “Treatment of sleep apnea is possible, so physicians had started doing it.” But instead of helping patients, the trial results strongly suggested that patients were harmed by treatment, which was significantly linked with increased rates of both all-cause and cardiovascular mortality (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459).
In our video interview, Dr. Køber, professor of cardiology at Rigshospitalet and the University of Copenhagen, discusses the results and what the findings imply for future treatment.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @mitchelzoler
LONDON – The management of Cheyne-Stokes respiration in patients with heart failure with reduced ejection fraction needs to be reconsidered following the troubling outcome of a major trial that tested adaptive servo-ventilation as treatment for this symptom, Dr. Lars Køber commented during an interview at the annual congress of the European Society of Cardiology.
Cheyne-Stokes respiration, a form of central sleep apnea, differs from obstructive sleep apnea in that heart failure patients do not seem to derive symptomatic benefit from adaptive servo-ventilation treatment, but “physicians have thought they could treat this sleep apnea [with ventilation] and it would change prognosis,” said Dr. Køber. “Treatment of sleep apnea is possible, so physicians had started doing it.” But instead of helping patients, the trial results strongly suggested that patients were harmed by treatment, which was significantly linked with increased rates of both all-cause and cardiovascular mortality (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459).
In our video interview, Dr. Køber, professor of cardiology at Rigshospitalet and the University of Copenhagen, discusses the results and what the findings imply for future treatment.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @mitchelzoler
AT THE ESC CONGRESS 2015
ESC: Statins reduce postoperative noncardiac surgery event rates
LONDON – Statin therapy, given the week before a host of noncardiac surgical procedures, reduced the postoperative risk for death and cardiac complications at 30 days by 17% when compared with no statin use in a large, international observational study.
Results of the prospective VISION (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) study showed that the primary composite endpoint of all-cause mortality, myocardial injury after noncardiac surgery (MINS), or stroke at 30 days was 11.8% in a propensity-matched cohort of patients, 2,845 of whom were treated with a statin and 4,492 who were not. The relative risk (RR) for this composite endpoint was 0.83 favoring the use of preoperative statins, with a 95% confidence interval (CI) of 0.73-0.95 and a P value of .007.
Perioperative statin vs. no statin use also cut all-cause mortality by 42% (RR, 0.58; 95% CI, 0.40-0.83; P = .003), cardiovascular mortality by 58% (RR, 0.42; 95% CI, 0.23-0.76; P = .004), and MINS by 14% (RR, 0.86; 95% CI, 0.73-0.98; P = .002).
“These study results are hypothesis generating at most,” emphasized Dr. Otavio Berwanger, who presented the findings at the annual congress of the European Society of Cardiology while they were simultaneously published online (Eur Heart J. 2015 Sept. 1. doi: 10.1093/eurheartj/ehv456).
“It is true that, in this large representative cohort of contemporary patients, statins were associated with lower event rates,” added Dr. Berwanger of Hospital do Coração in São Paulo, Brazil, and “together with the previous body of evidence, statins appear to be an interesting and attractive intervention to reduce postoperative events.” A large-scale, randomized trial is needed, however, to answer the question of whether statins should be used preoperatively to prevent postoperative events in noncardiac surgery patients.
Over a 4-year period that started in August 2007, more than 15,000 individuals aged 45 years or older who were undergoing a variety of noncardiac surgical procedures that required regional or a general anesthetic and at least an overnight stay in the hospital were recruited at 12 centers in eight countries in North and South America, Africa, Asia, Australia, and Europe.
One of the objectives of the study was to examine the use of perioperative statins on cardiovascular events at 30 days, and to do this, the VISION investigators identified the patients who had received a statin in the 7 days prior to surgery and then used propensity matching to form a control group of patients that had not received a statin in the week before surgery.
Just under half of the propensity-matched population was male, with an average age of nearly 69 years. Around 70% of the population had hypertension, 9%-10% had a prior stroke, and 13% had active cancer. Surgeries were urgent in about 2% and emergent in 8%. Around a quarter had undergone orthopedic procedures, and 4% were vascular surgeries. Overall, 36% of surgeries were classified as low risk and 39% as other.
One of the limitations of the study, however, is that, despite the propensity matching, there were some variables that remained different between the two groups, with higher rates of coronary artery disease (20% vs. 14%), peripheral vascular disease (8% vs. 5%), diabetes (30% vs. 25%), and preoperative use of aspirin (25% vs. 19%) and angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (53% vs. 48%) in the statin- versus nonstatin-treated patients.
Other limitations are that these data are observational and the use of statins could be just a surrogate for unmeasured confounders that relate to prognosis. Information on the type and dosing of statins also was not obtained, and there was no information collected on potential liver or muscle function side effects.
Nevertheless, the VISION investigators noted in the published paper that the results are consistent with those from other observational studies and prior small-scale, randomized trials and so do add important information. They noted that these data were collected prospectively in a broader range of patients and types of surgeries than has been reported previously. In addition, patients were recruited from several countries and were actively monitored for outcomes and events were centrally adjudicated. VISION is also the only study to report on the effects of statins on MINS.
“Another message from our results is that the use of long-term statins is sub-optimal in high cardiovascular risk patients, who should be on long-term lipid-lowering therapy independently of surgery,” the VISION investigators wrote in their report.
The study was funded by Hamilton Health Sciences Corp. at McMaster University. Dr. Berwanger disclosed receiving research contracts from AstraZeneca, Bayer Healthcare, Amgen, Boehringer-Ingelheim, Pfizer, and Roche Diagnostics.
LONDON – Statin therapy, given the week before a host of noncardiac surgical procedures, reduced the postoperative risk for death and cardiac complications at 30 days by 17% when compared with no statin use in a large, international observational study.
Results of the prospective VISION (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) study showed that the primary composite endpoint of all-cause mortality, myocardial injury after noncardiac surgery (MINS), or stroke at 30 days was 11.8% in a propensity-matched cohort of patients, 2,845 of whom were treated with a statin and 4,492 who were not. The relative risk (RR) for this composite endpoint was 0.83 favoring the use of preoperative statins, with a 95% confidence interval (CI) of 0.73-0.95 and a P value of .007.
Perioperative statin vs. no statin use also cut all-cause mortality by 42% (RR, 0.58; 95% CI, 0.40-0.83; P = .003), cardiovascular mortality by 58% (RR, 0.42; 95% CI, 0.23-0.76; P = .004), and MINS by 14% (RR, 0.86; 95% CI, 0.73-0.98; P = .002).
“These study results are hypothesis generating at most,” emphasized Dr. Otavio Berwanger, who presented the findings at the annual congress of the European Society of Cardiology while they were simultaneously published online (Eur Heart J. 2015 Sept. 1. doi: 10.1093/eurheartj/ehv456).
“It is true that, in this large representative cohort of contemporary patients, statins were associated with lower event rates,” added Dr. Berwanger of Hospital do Coração in São Paulo, Brazil, and “together with the previous body of evidence, statins appear to be an interesting and attractive intervention to reduce postoperative events.” A large-scale, randomized trial is needed, however, to answer the question of whether statins should be used preoperatively to prevent postoperative events in noncardiac surgery patients.
Over a 4-year period that started in August 2007, more than 15,000 individuals aged 45 years or older who were undergoing a variety of noncardiac surgical procedures that required regional or a general anesthetic and at least an overnight stay in the hospital were recruited at 12 centers in eight countries in North and South America, Africa, Asia, Australia, and Europe.
One of the objectives of the study was to examine the use of perioperative statins on cardiovascular events at 30 days, and to do this, the VISION investigators identified the patients who had received a statin in the 7 days prior to surgery and then used propensity matching to form a control group of patients that had not received a statin in the week before surgery.
Just under half of the propensity-matched population was male, with an average age of nearly 69 years. Around 70% of the population had hypertension, 9%-10% had a prior stroke, and 13% had active cancer. Surgeries were urgent in about 2% and emergent in 8%. Around a quarter had undergone orthopedic procedures, and 4% were vascular surgeries. Overall, 36% of surgeries were classified as low risk and 39% as other.
One of the limitations of the study, however, is that, despite the propensity matching, there were some variables that remained different between the two groups, with higher rates of coronary artery disease (20% vs. 14%), peripheral vascular disease (8% vs. 5%), diabetes (30% vs. 25%), and preoperative use of aspirin (25% vs. 19%) and angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (53% vs. 48%) in the statin- versus nonstatin-treated patients.
Other limitations are that these data are observational and the use of statins could be just a surrogate for unmeasured confounders that relate to prognosis. Information on the type and dosing of statins also was not obtained, and there was no information collected on potential liver or muscle function side effects.
Nevertheless, the VISION investigators noted in the published paper that the results are consistent with those from other observational studies and prior small-scale, randomized trials and so do add important information. They noted that these data were collected prospectively in a broader range of patients and types of surgeries than has been reported previously. In addition, patients were recruited from several countries and were actively monitored for outcomes and events were centrally adjudicated. VISION is also the only study to report on the effects of statins on MINS.
“Another message from our results is that the use of long-term statins is sub-optimal in high cardiovascular risk patients, who should be on long-term lipid-lowering therapy independently of surgery,” the VISION investigators wrote in their report.
The study was funded by Hamilton Health Sciences Corp. at McMaster University. Dr. Berwanger disclosed receiving research contracts from AstraZeneca, Bayer Healthcare, Amgen, Boehringer-Ingelheim, Pfizer, and Roche Diagnostics.
LONDON – Statin therapy, given the week before a host of noncardiac surgical procedures, reduced the postoperative risk for death and cardiac complications at 30 days by 17% when compared with no statin use in a large, international observational study.
Results of the prospective VISION (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) study showed that the primary composite endpoint of all-cause mortality, myocardial injury after noncardiac surgery (MINS), or stroke at 30 days was 11.8% in a propensity-matched cohort of patients, 2,845 of whom were treated with a statin and 4,492 who were not. The relative risk (RR) for this composite endpoint was 0.83 favoring the use of preoperative statins, with a 95% confidence interval (CI) of 0.73-0.95 and a P value of .007.
Perioperative statin vs. no statin use also cut all-cause mortality by 42% (RR, 0.58; 95% CI, 0.40-0.83; P = .003), cardiovascular mortality by 58% (RR, 0.42; 95% CI, 0.23-0.76; P = .004), and MINS by 14% (RR, 0.86; 95% CI, 0.73-0.98; P = .002).
“These study results are hypothesis generating at most,” emphasized Dr. Otavio Berwanger, who presented the findings at the annual congress of the European Society of Cardiology while they were simultaneously published online (Eur Heart J. 2015 Sept. 1. doi: 10.1093/eurheartj/ehv456).
“It is true that, in this large representative cohort of contemporary patients, statins were associated with lower event rates,” added Dr. Berwanger of Hospital do Coração in São Paulo, Brazil, and “together with the previous body of evidence, statins appear to be an interesting and attractive intervention to reduce postoperative events.” A large-scale, randomized trial is needed, however, to answer the question of whether statins should be used preoperatively to prevent postoperative events in noncardiac surgery patients.
Over a 4-year period that started in August 2007, more than 15,000 individuals aged 45 years or older who were undergoing a variety of noncardiac surgical procedures that required regional or a general anesthetic and at least an overnight stay in the hospital were recruited at 12 centers in eight countries in North and South America, Africa, Asia, Australia, and Europe.
One of the objectives of the study was to examine the use of perioperative statins on cardiovascular events at 30 days, and to do this, the VISION investigators identified the patients who had received a statin in the 7 days prior to surgery and then used propensity matching to form a control group of patients that had not received a statin in the week before surgery.
Just under half of the propensity-matched population was male, with an average age of nearly 69 years. Around 70% of the population had hypertension, 9%-10% had a prior stroke, and 13% had active cancer. Surgeries were urgent in about 2% and emergent in 8%. Around a quarter had undergone orthopedic procedures, and 4% were vascular surgeries. Overall, 36% of surgeries were classified as low risk and 39% as other.
One of the limitations of the study, however, is that, despite the propensity matching, there were some variables that remained different between the two groups, with higher rates of coronary artery disease (20% vs. 14%), peripheral vascular disease (8% vs. 5%), diabetes (30% vs. 25%), and preoperative use of aspirin (25% vs. 19%) and angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (53% vs. 48%) in the statin- versus nonstatin-treated patients.
Other limitations are that these data are observational and the use of statins could be just a surrogate for unmeasured confounders that relate to prognosis. Information on the type and dosing of statins also was not obtained, and there was no information collected on potential liver or muscle function side effects.
Nevertheless, the VISION investigators noted in the published paper that the results are consistent with those from other observational studies and prior small-scale, randomized trials and so do add important information. They noted that these data were collected prospectively in a broader range of patients and types of surgeries than has been reported previously. In addition, patients were recruited from several countries and were actively monitored for outcomes and events were centrally adjudicated. VISION is also the only study to report on the effects of statins on MINS.
“Another message from our results is that the use of long-term statins is sub-optimal in high cardiovascular risk patients, who should be on long-term lipid-lowering therapy independently of surgery,” the VISION investigators wrote in their report.
The study was funded by Hamilton Health Sciences Corp. at McMaster University. Dr. Berwanger disclosed receiving research contracts from AstraZeneca, Bayer Healthcare, Amgen, Boehringer-Ingelheim, Pfizer, and Roche Diagnostics.
AT THE ESC CONGRESS 2015
Key clinical point: Statin therapy, given the week before a host of noncardiac surgical procedures, reduced the postoperative risk for death and cardiac complications at 30 days, but the findings are hypothesis generating and need validation in a randomized controlled clinical trial.
Major finding: The primary composite outcome (all-cause mortality, myocardial injury after noncardiac surgery, or stroke at 30 days) was 11.8% overall in the propensity-matched cohort, with a 17% relative risk reduction favoring the use of statin versus no statin (P = .007).
Data source: The VISION study is an international, prospective, observational study of more than 15,000 patients who underwent noncardiac surgery between 2007 and 2011.
Disclosures: The study was funded by Hamilton Health Sciences Corp. at McMaster University. Dr. Berwanger disclosed receiving research contracts from AstraZeneca, Bayer Healthcare, Amgen, Boehringer-Ingelheim, Pfizer, and Roche Diagnostics.
VIDEO: FFR-CT could redefine interventional cardiology
LONDON – A potential revolution may be underway in how patients with stable, new-onset chest pain are selected for invasive cardiac catheterization.
Fractional flow reserve–computed tomography (FFR-CT) utilized sophisticated computer software to noninvasively assess both coronary anatomy and function in symptomatic, intermediate-risk patients in the randomized PLATFORM trial. It proved a safe alternative to conventional invasive diagnostic cardiac catheterization in the 584-patient, 11-center study, Dr. Pamela S. Douglas said in an interview during the annual congress of the European Society of Cardiology.
Using FFR-CT safely resulted in cancellation of 61% of planned diagnostic catheterizations on the basis of finding no obstructive CAD lesions, explained Dr. Douglas of Duke University, Durham, N.C.
The big remaining question now concerns the cost-effectiveness of the HeartFlow FFR-CT method, now commercially available in both the United States and Europe. Those embargoed data will be presented by Dr. Mark A. Hlatky of Stanford (Calif.) University at the Transcatheter Cardiovascular Therapeutics (TCT) conference in San Francisco in October.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
LONDON – A potential revolution may be underway in how patients with stable, new-onset chest pain are selected for invasive cardiac catheterization.
Fractional flow reserve–computed tomography (FFR-CT) utilized sophisticated computer software to noninvasively assess both coronary anatomy and function in symptomatic, intermediate-risk patients in the randomized PLATFORM trial. It proved a safe alternative to conventional invasive diagnostic cardiac catheterization in the 584-patient, 11-center study, Dr. Pamela S. Douglas said in an interview during the annual congress of the European Society of Cardiology.
Using FFR-CT safely resulted in cancellation of 61% of planned diagnostic catheterizations on the basis of finding no obstructive CAD lesions, explained Dr. Douglas of Duke University, Durham, N.C.
The big remaining question now concerns the cost-effectiveness of the HeartFlow FFR-CT method, now commercially available in both the United States and Europe. Those embargoed data will be presented by Dr. Mark A. Hlatky of Stanford (Calif.) University at the Transcatheter Cardiovascular Therapeutics (TCT) conference in San Francisco in October.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
LONDON – A potential revolution may be underway in how patients with stable, new-onset chest pain are selected for invasive cardiac catheterization.
Fractional flow reserve–computed tomography (FFR-CT) utilized sophisticated computer software to noninvasively assess both coronary anatomy and function in symptomatic, intermediate-risk patients in the randomized PLATFORM trial. It proved a safe alternative to conventional invasive diagnostic cardiac catheterization in the 584-patient, 11-center study, Dr. Pamela S. Douglas said in an interview during the annual congress of the European Society of Cardiology.
Using FFR-CT safely resulted in cancellation of 61% of planned diagnostic catheterizations on the basis of finding no obstructive CAD lesions, explained Dr. Douglas of Duke University, Durham, N.C.
The big remaining question now concerns the cost-effectiveness of the HeartFlow FFR-CT method, now commercially available in both the United States and Europe. Those embargoed data will be presented by Dr. Mark A. Hlatky of Stanford (Calif.) University at the Transcatheter Cardiovascular Therapeutics (TCT) conference in San Francisco in October.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
AT THE ESC CONGRESS 2015
Heart Failure’s Surprises Keep Coming
Heart failure has historically been one of the most poorly understood and hard to treat cardiovascular diseases, and many reports at the annual congress of the European Society of Cardiology in London hammered home how many mysteries remain about heart failure and how many tricks it still keeps up its sleeves.
Probably the most high-profile example was the stunning result of the SERVE-HF trial, reported as a hot-line talk and published concurrently (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459). The trial randomized more than 1,300 patients with heart failure with reduced ejection fraction and central sleep apnea presenting as Cheyne-Stokes respiration to nocturnal treatment with adaptive servo-ventilation. The idea was simple: These heart failure patients have trouble breathing while asleep, so help them with a ventilator.
“We had a technology that could alleviate central sleep apnea, and we just wanted to prove how large the benefit was,” said Dr. Martin R. Cowie, the trial’s lead investigator. But in results that “surprised us completely,” said Dr. Cowie, ventilation not only failed to produce a significant benefit for the trial’s primary, combined endpoint, it also showed a significant deleterious effect for the secondary endpoints of death by any cause and for cardiovascular death. In short, treating these patients with a ventilator was killing them. “We don’t understand what’s going on here,” Dr. Cowie said. He characterized the outcome as a “game changer” because many physicians had already begun using this form of ventilation on patients as it made such perfect sense.
“It’s unbelievable. We thought it was a slam dunk,” commented Dr. Frank Rushitka when he summed up the congress’ heart failure program at the end of the meeting.
Dr. Athena Poppas, who delivered the invited commentary on SERVE-HF, highlighted the “complexity” of heart failure and how “poorly understood” it is. “We’ve seen so many times where we saw something that we thought was bad [and treated] without fully understanding the mechanisms,” she said in an interview.
A great example was the misbegotten flirtation a couple of decades ago with inotropic therapy. It was another no-brainer: drugs that stimulate the heart’s pumping function will help patients with impaired cardiac output. But then trial results showed that chronic inotropic treatment actually hastened patients’ demise. “Patients felt better but they died faster,” Dr. Poppas noted.
Heart failure’s surprises keep coming. During the congress, heart failure expert Dr. Marriel L. Jessup said, “We used to think the reason why patients with acute heart failure were diuretic resistant was because of poor cardiac output. Now we know that they have a lot of venous congestion that impacts the kidneys and liver.”
Another researcher, Dr. John C. Burnett Jr. added, “It’s not just plumbing” that harms the kidneys and liver, but also “deleterious molecules” released because of venous congestion that causes organ damage. The identify of those molecules is only now being explored. And recognition that liver damage is an important part of the heart failure syndrome occurred only recently.
Heart failure continues to reveal its mysteries slowly and reluctantly. Clinicians who believe they know all they need about how to safely and effectively treat it are fooling themselves and run the risk of hurting their patients.
Heart failure has historically been one of the most poorly understood and hard to treat cardiovascular diseases, and many reports at the annual congress of the European Society of Cardiology in London hammered home how many mysteries remain about heart failure and how many tricks it still keeps up its sleeves.
Probably the most high-profile example was the stunning result of the SERVE-HF trial, reported as a hot-line talk and published concurrently (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459). The trial randomized more than 1,300 patients with heart failure with reduced ejection fraction and central sleep apnea presenting as Cheyne-Stokes respiration to nocturnal treatment with adaptive servo-ventilation. The idea was simple: These heart failure patients have trouble breathing while asleep, so help them with a ventilator.
“We had a technology that could alleviate central sleep apnea, and we just wanted to prove how large the benefit was,” said Dr. Martin R. Cowie, the trial’s lead investigator. But in results that “surprised us completely,” said Dr. Cowie, ventilation not only failed to produce a significant benefit for the trial’s primary, combined endpoint, it also showed a significant deleterious effect for the secondary endpoints of death by any cause and for cardiovascular death. In short, treating these patients with a ventilator was killing them. “We don’t understand what’s going on here,” Dr. Cowie said. He characterized the outcome as a “game changer” because many physicians had already begun using this form of ventilation on patients as it made such perfect sense.
“It’s unbelievable. We thought it was a slam dunk,” commented Dr. Frank Rushitka when he summed up the congress’ heart failure program at the end of the meeting.
Dr. Athena Poppas, who delivered the invited commentary on SERVE-HF, highlighted the “complexity” of heart failure and how “poorly understood” it is. “We’ve seen so many times where we saw something that we thought was bad [and treated] without fully understanding the mechanisms,” she said in an interview.
A great example was the misbegotten flirtation a couple of decades ago with inotropic therapy. It was another no-brainer: drugs that stimulate the heart’s pumping function will help patients with impaired cardiac output. But then trial results showed that chronic inotropic treatment actually hastened patients’ demise. “Patients felt better but they died faster,” Dr. Poppas noted.
Heart failure’s surprises keep coming. During the congress, heart failure expert Dr. Marriel L. Jessup said, “We used to think the reason why patients with acute heart failure were diuretic resistant was because of poor cardiac output. Now we know that they have a lot of venous congestion that impacts the kidneys and liver.”
Another researcher, Dr. John C. Burnett Jr. added, “It’s not just plumbing” that harms the kidneys and liver, but also “deleterious molecules” released because of venous congestion that causes organ damage. The identify of those molecules is only now being explored. And recognition that liver damage is an important part of the heart failure syndrome occurred only recently.
Heart failure continues to reveal its mysteries slowly and reluctantly. Clinicians who believe they know all they need about how to safely and effectively treat it are fooling themselves and run the risk of hurting their patients.
Heart failure has historically been one of the most poorly understood and hard to treat cardiovascular diseases, and many reports at the annual congress of the European Society of Cardiology in London hammered home how many mysteries remain about heart failure and how many tricks it still keeps up its sleeves.
Probably the most high-profile example was the stunning result of the SERVE-HF trial, reported as a hot-line talk and published concurrently (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459). The trial randomized more than 1,300 patients with heart failure with reduced ejection fraction and central sleep apnea presenting as Cheyne-Stokes respiration to nocturnal treatment with adaptive servo-ventilation. The idea was simple: These heart failure patients have trouble breathing while asleep, so help them with a ventilator.
“We had a technology that could alleviate central sleep apnea, and we just wanted to prove how large the benefit was,” said Dr. Martin R. Cowie, the trial’s lead investigator. But in results that “surprised us completely,” said Dr. Cowie, ventilation not only failed to produce a significant benefit for the trial’s primary, combined endpoint, it also showed a significant deleterious effect for the secondary endpoints of death by any cause and for cardiovascular death. In short, treating these patients with a ventilator was killing them. “We don’t understand what’s going on here,” Dr. Cowie said. He characterized the outcome as a “game changer” because many physicians had already begun using this form of ventilation on patients as it made such perfect sense.
“It’s unbelievable. We thought it was a slam dunk,” commented Dr. Frank Rushitka when he summed up the congress’ heart failure program at the end of the meeting.
Dr. Athena Poppas, who delivered the invited commentary on SERVE-HF, highlighted the “complexity” of heart failure and how “poorly understood” it is. “We’ve seen so many times where we saw something that we thought was bad [and treated] without fully understanding the mechanisms,” she said in an interview.
A great example was the misbegotten flirtation a couple of decades ago with inotropic therapy. It was another no-brainer: drugs that stimulate the heart’s pumping function will help patients with impaired cardiac output. But then trial results showed that chronic inotropic treatment actually hastened patients’ demise. “Patients felt better but they died faster,” Dr. Poppas noted.
Heart failure’s surprises keep coming. During the congress, heart failure expert Dr. Marriel L. Jessup said, “We used to think the reason why patients with acute heart failure were diuretic resistant was because of poor cardiac output. Now we know that they have a lot of venous congestion that impacts the kidneys and liver.”
Another researcher, Dr. John C. Burnett Jr. added, “It’s not just plumbing” that harms the kidneys and liver, but also “deleterious molecules” released because of venous congestion that causes organ damage. The identify of those molecules is only now being explored. And recognition that liver damage is an important part of the heart failure syndrome occurred only recently.
Heart failure continues to reveal its mysteries slowly and reluctantly. Clinicians who believe they know all they need about how to safely and effectively treat it are fooling themselves and run the risk of hurting their patients.
Heart failure’s surprises keep coming
Heart failure has historically been one of the most poorly understood and hard to treat cardiovascular diseases, and many reports at the annual congress of the European Society of Cardiology in London hammered home how many mysteries remain about heart failure and how many tricks it still keeps up its sleeves.
Probably the most high-profile example was the stunning result of the SERVE-HF trial, reported as a hot-line talk and published concurrently (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459). The trial randomized more than 1,300 patients with heart failure with reduced ejection fraction and central sleep apnea presenting as Cheyne-Stokes respiration to nocturnal treatment with adaptive servo-ventilation. The idea was simple: These heart failure patients have trouble breathing while asleep, so help them with a ventilator.
“We had a technology that could alleviate central sleep apnea, and we just wanted to prove how large the benefit was,” said Dr. Martin R. Cowie, the trial’s lead investigator. But in results that “surprised us completely,” said Dr. Cowie, ventilation not only failed to produce a significant benefit for the trial’s primary, combined endpoint, it also showed a significant deleterious effect for the secondary endpoints of death by any cause and for cardiovascular death. In short, treating these patients with a ventilator was killing them. “We don’t understand what’s going on here,” Dr. Cowie said. He characterized the outcome as a “game changer” because many physicians had already begun using this form of ventilation on patients as it made such perfect sense.
“It’s unbelievable. We thought it was a slam dunk,” commented Dr. Frank Rushitka when he summed up the congress’ heart failure program at the end of the meeting.
Dr. Athena Poppas, who delivered the invited commentary on SERVE-HF, highlighted the “complexity” of heart failure and how “poorly understood” it is. “We’ve seen so many times where we saw something that we thought was bad [and treated] without fully understanding the mechanisms,” she said in an interview.
A great example was the misbegotten flirtation a couple of decades ago with inotropic therapy. It was another no-brainer: drugs that stimulate the heart’s pumping function will help patients with impaired cardiac output. But then trial results showed that chronic inotropic treatment actually hastened patients’ demise. “Patients felt better but they died faster,” Dr. Poppas noted.
Heart failure’s surprises keep coming. During the congress, heart failure expert Dr. Marriel L. Jessup said, “We used to think the reason why patients with acute heart failure were diuretic resistant was because of poor cardiac output. Now we know that they have a lot of venous congestion that impacts the kidneys and liver.”
Another researcher, Dr. John C. Burnett Jr. added, “It’s not just plumbing” that harms the kidneys and liver, but also “deleterious molecules” released because of venous congestion that causes organ damage. The identity of those molecules is only now being explored. And recognition that liver damage is an important part of the heart failure syndrome occurred only recently.
Heart failure continues to reveal its mysteries slowly and reluctantly. Clinicians who believe they know all they need about how to safely and effectively treat it are fooling themselves and run the risk of hurting their patients.
On Twitter @mitchelzoler
Heart failure has historically been one of the most poorly understood and hard to treat cardiovascular diseases, and many reports at the annual congress of the European Society of Cardiology in London hammered home how many mysteries remain about heart failure and how many tricks it still keeps up its sleeves.
Probably the most high-profile example was the stunning result of the SERVE-HF trial, reported as a hot-line talk and published concurrently (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459). The trial randomized more than 1,300 patients with heart failure with reduced ejection fraction and central sleep apnea presenting as Cheyne-Stokes respiration to nocturnal treatment with adaptive servo-ventilation. The idea was simple: These heart failure patients have trouble breathing while asleep, so help them with a ventilator.
“We had a technology that could alleviate central sleep apnea, and we just wanted to prove how large the benefit was,” said Dr. Martin R. Cowie, the trial’s lead investigator. But in results that “surprised us completely,” said Dr. Cowie, ventilation not only failed to produce a significant benefit for the trial’s primary, combined endpoint, it also showed a significant deleterious effect for the secondary endpoints of death by any cause and for cardiovascular death. In short, treating these patients with a ventilator was killing them. “We don’t understand what’s going on here,” Dr. Cowie said. He characterized the outcome as a “game changer” because many physicians had already begun using this form of ventilation on patients as it made such perfect sense.
“It’s unbelievable. We thought it was a slam dunk,” commented Dr. Frank Rushitka when he summed up the congress’ heart failure program at the end of the meeting.
Dr. Athena Poppas, who delivered the invited commentary on SERVE-HF, highlighted the “complexity” of heart failure and how “poorly understood” it is. “We’ve seen so many times where we saw something that we thought was bad [and treated] without fully understanding the mechanisms,” she said in an interview.
A great example was the misbegotten flirtation a couple of decades ago with inotropic therapy. It was another no-brainer: drugs that stimulate the heart’s pumping function will help patients with impaired cardiac output. But then trial results showed that chronic inotropic treatment actually hastened patients’ demise. “Patients felt better but they died faster,” Dr. Poppas noted.
Heart failure’s surprises keep coming. During the congress, heart failure expert Dr. Marriel L. Jessup said, “We used to think the reason why patients with acute heart failure were diuretic resistant was because of poor cardiac output. Now we know that they have a lot of venous congestion that impacts the kidneys and liver.”
Another researcher, Dr. John C. Burnett Jr. added, “It’s not just plumbing” that harms the kidneys and liver, but also “deleterious molecules” released because of venous congestion that causes organ damage. The identity of those molecules is only now being explored. And recognition that liver damage is an important part of the heart failure syndrome occurred only recently.
Heart failure continues to reveal its mysteries slowly and reluctantly. Clinicians who believe they know all they need about how to safely and effectively treat it are fooling themselves and run the risk of hurting their patients.
On Twitter @mitchelzoler
Heart failure has historically been one of the most poorly understood and hard to treat cardiovascular diseases, and many reports at the annual congress of the European Society of Cardiology in London hammered home how many mysteries remain about heart failure and how many tricks it still keeps up its sleeves.
Probably the most high-profile example was the stunning result of the SERVE-HF trial, reported as a hot-line talk and published concurrently (N Engl J Med. 2015 Sep 1. doi: 10.1056/NEJMoa1506459). The trial randomized more than 1,300 patients with heart failure with reduced ejection fraction and central sleep apnea presenting as Cheyne-Stokes respiration to nocturnal treatment with adaptive servo-ventilation. The idea was simple: These heart failure patients have trouble breathing while asleep, so help them with a ventilator.
“We had a technology that could alleviate central sleep apnea, and we just wanted to prove how large the benefit was,” said Dr. Martin R. Cowie, the trial’s lead investigator. But in results that “surprised us completely,” said Dr. Cowie, ventilation not only failed to produce a significant benefit for the trial’s primary, combined endpoint, it also showed a significant deleterious effect for the secondary endpoints of death by any cause and for cardiovascular death. In short, treating these patients with a ventilator was killing them. “We don’t understand what’s going on here,” Dr. Cowie said. He characterized the outcome as a “game changer” because many physicians had already begun using this form of ventilation on patients as it made such perfect sense.
“It’s unbelievable. We thought it was a slam dunk,” commented Dr. Frank Rushitka when he summed up the congress’ heart failure program at the end of the meeting.
Dr. Athena Poppas, who delivered the invited commentary on SERVE-HF, highlighted the “complexity” of heart failure and how “poorly understood” it is. “We’ve seen so many times where we saw something that we thought was bad [and treated] without fully understanding the mechanisms,” she said in an interview.
A great example was the misbegotten flirtation a couple of decades ago with inotropic therapy. It was another no-brainer: drugs that stimulate the heart’s pumping function will help patients with impaired cardiac output. But then trial results showed that chronic inotropic treatment actually hastened patients’ demise. “Patients felt better but they died faster,” Dr. Poppas noted.
Heart failure’s surprises keep coming. During the congress, heart failure expert Dr. Marriel L. Jessup said, “We used to think the reason why patients with acute heart failure were diuretic resistant was because of poor cardiac output. Now we know that they have a lot of venous congestion that impacts the kidneys and liver.”
Another researcher, Dr. John C. Burnett Jr. added, “It’s not just plumbing” that harms the kidneys and liver, but also “deleterious molecules” released because of venous congestion that causes organ damage. The identity of those molecules is only now being explored. And recognition that liver damage is an important part of the heart failure syndrome occurred only recently.
Heart failure continues to reveal its mysteries slowly and reluctantly. Clinicians who believe they know all they need about how to safely and effectively treat it are fooling themselves and run the risk of hurting their patients.
On Twitter @mitchelzoler
MATRIX trial update: No clear winner
LONDON—The latest results* of the MATRIX trial haven’t provided any cut-and-dried answers when it comes to anticoagulation in the context of percutaneous coronary intervention (PCI), according to articles published in NEJM and data presented at the ESC Congress 2015.
The trial suggested that, overall, bivalirudin and heparin produce comparable results in patients undergoing PCI.
The drugs produced similar rates of major adverse cardiovascular events (MACE) and net adverse clinical events (NACE).
In addition, among patients in the bivalirudin arm, there was no significant difference in a composite primary outcome between patients who received an additional infusion of bivalirudin after PCI and those who did not.
Results from this trial were published in NEJM alongside a related editorial. At the ESC Congress 2015, the bivalirudin dosing comparison was reported in abstract 6004.
MATRIX was sponsored by the Societa Italiana di Cardiologia Invasiva (GISE), with funding from The Medicines Company and Terumo.
The trial enrolled 7213 patients with acute coronary syndrome who were set to undergo PCI. Patients were randomized to receive bivalirudin (n=3610) or unfractionated heparin (n=3603). Patients in the bivalirudin arm were then randomized to either receive a post-PCI infusion of bivalirudin (n=1799) or not (n=1811).
Primary outcomes for the comparison between bivalirudin and heparin were the occurrence of MACE (a composite of death, myocardial infarction, or stroke) and NACE (a composite of major bleeding or a major adverse cardiovascular event).
The primary outcome for the comparison of post-PCI bivalirudin infusion with no infusion was a composite of urgent target-vessel revascularization, definite stent thrombosis, or NACE.
Heparin vs bivalirudin
There was no significant difference between the bivalirudin and heparin groups with regard to MACE—10.3% and 10.9%, respectively (P=0.44). And the same was true for NACE—11.2% and 12.4%, respectively (P=0.12).
Likewise, there was no significant difference between the bivalirudin arm and the heparin arm with regard to myocardial infarction—8.6% and 8.5%, respectively (P=0.93)—or stroke—0.4% and 0.5%, respectively (P=0.57).
However, bivalirudin was associated with a significantly lower rate of all-cause mortality than heparin—1.7% and 2.3%, respectively (P=0.04)—and a significantly lower rate of cardiac-related death—1.5% and 2.2%, respectively (P=0.03).
The rate of definite stent thrombosis was significantly higher in the bivalirudin group than the heparin group—1.0% and 0.6%, respectively (P=0.048). But there was no significant difference in the rate of definite or probable stent thrombosis—1.3% and 1.0% (P=0.27).
The rate of any bleeding was significantly lower with bivalirudin than with heparin—11.0% and 13.6%, respectively (P=0.001). And the same was true for major bleeding (BARC 3 or 5)—1.4% and 2.5%, respectively (P<0.001).
Bivalirudin duration
“Post-PCI bivalirudin did not reduce the composite outcome of ischemic and bleeding outcomes, including stent thrombosis risk, as compared to no post-PCI bivalirudin infusion,” said study investigator Marco Valgimigli, MD, PhD, of the Swiss Cardiovascular Center in Bern, Switzerland.
The proportion of patients who met the primary endpoint was 11.0% in the post-PCI infusion group and 11.9% in the no-infusion group (P=0.34).
Similarly, there was no significant difference between the infusion and no-infusion groups in the risk of definite stent thrombosis—1.3% and 0.7%, respectively (P=0.09)—or definite/probable stent thrombosis—1.5% and 1.1%, respectively (P=0.29).
And there was no significant difference in the rate of any bleeding—11.3% and 10.7%, respectively (P=0.62)—but the rate of BARC 3 or 5 bleeding was lower in the group that received the post-PCI infusion—1.0% vs 1.8% (P=0.03).
“Both treatment options are allowed per current European label and observational studies,” Dr Valgimigli said.
“Hence, I believe the option to prolong or stop bivalirudin infusion after PCI remains open for clinicians, who will have to decide based on the ischemic and bleeding risk of individual patients, as well as perhaps based on type of acute coronary syndrome, timing of loading dose, and type of oral P2Y12 inhibitors. This is in keeping with the current labeling of the drug in EU and USA.”
Cost concerns
In the NEJM editorial, Peter Berger, MD, of North Shore–Long Island Jewish Health System in Great Neck, New York, noted that bivalirudin costs more than 400 times the price of heparin.
“Many studies have shown that bivalirudin is safer than heparin—that it causes fewer bleeding complications,” Dr Berger said. “But other studies have shown that heparin is every bit as safe, especially when used in lower doses. And one recent, large study actually suggested that heparin is more effective than bivalirudin.”
Despite these conflicting results, Dr Berger said “nearly everyone” agrees that if the more expensive drug is not superior in some way, the less expensive one should be used.
“Many studies raise more questions than they answer,” he added. “It will be interesting to see whether doctors accept the results of the MATRIX trial or wait for more studies before deciding which blood thinner they prefer.” 
*MATRIX investigators previously compared vascular access sites and found that radial access outperformed femoral access. These results were published earlier this year in The Lancet.
LONDON—The latest results* of the MATRIX trial haven’t provided any cut-and-dried answers when it comes to anticoagulation in the context of percutaneous coronary intervention (PCI), according to articles published in NEJM and data presented at the ESC Congress 2015.
The trial suggested that, overall, bivalirudin and heparin produce comparable results in patients undergoing PCI.
The drugs produced similar rates of major adverse cardiovascular events (MACE) and net adverse clinical events (NACE).
In addition, among patients in the bivalirudin arm, there was no significant difference in a composite primary outcome between patients who received an additional infusion of bivalirudin after PCI and those who did not.
Results from this trial were published in NEJM alongside a related editorial. At the ESC Congress 2015, the bivalirudin dosing comparison was reported in abstract 6004.
MATRIX was sponsored by the Societa Italiana di Cardiologia Invasiva (GISE), with funding from The Medicines Company and Terumo.
The trial enrolled 7213 patients with acute coronary syndrome who were set to undergo PCI. Patients were randomized to receive bivalirudin (n=3610) or unfractionated heparin (n=3603). Patients in the bivalirudin arm were then randomized to either receive a post-PCI infusion of bivalirudin (n=1799) or not (n=1811).
Primary outcomes for the comparison between bivalirudin and heparin were the occurrence of MACE (a composite of death, myocardial infarction, or stroke) and NACE (a composite of major bleeding or a major adverse cardiovascular event).
The primary outcome for the comparison of post-PCI bivalirudin infusion with no infusion was a composite of urgent target-vessel revascularization, definite stent thrombosis, or NACE.
Heparin vs bivalirudin
There was no significant difference between the bivalirudin and heparin groups with regard to MACE—10.3% and 10.9%, respectively (P=0.44). And the same was true for NACE—11.2% and 12.4%, respectively (P=0.12).
Likewise, there was no significant difference between the bivalirudin arm and the heparin arm with regard to myocardial infarction—8.6% and 8.5%, respectively (P=0.93)—or stroke—0.4% and 0.5%, respectively (P=0.57).
However, bivalirudin was associated with a significantly lower rate of all-cause mortality than heparin—1.7% and 2.3%, respectively (P=0.04)—and a significantly lower rate of cardiac-related death—1.5% and 2.2%, respectively (P=0.03).
The rate of definite stent thrombosis was significantly higher in the bivalirudin group than the heparin group—1.0% and 0.6%, respectively (P=0.048). But there was no significant difference in the rate of definite or probable stent thrombosis—1.3% and 1.0% (P=0.27).
The rate of any bleeding was significantly lower with bivalirudin than with heparin—11.0% and 13.6%, respectively (P=0.001). And the same was true for major bleeding (BARC 3 or 5)—1.4% and 2.5%, respectively (P<0.001).
Bivalirudin duration
“Post-PCI bivalirudin did not reduce the composite outcome of ischemic and bleeding outcomes, including stent thrombosis risk, as compared to no post-PCI bivalirudin infusion,” said study investigator Marco Valgimigli, MD, PhD, of the Swiss Cardiovascular Center in Bern, Switzerland.
The proportion of patients who met the primary endpoint was 11.0% in the post-PCI infusion group and 11.9% in the no-infusion group (P=0.34).
Similarly, there was no significant difference between the infusion and no-infusion groups in the risk of definite stent thrombosis—1.3% and 0.7%, respectively (P=0.09)—or definite/probable stent thrombosis—1.5% and 1.1%, respectively (P=0.29).
And there was no significant difference in the rate of any bleeding—11.3% and 10.7%, respectively (P=0.62)—but the rate of BARC 3 or 5 bleeding was lower in the group that received the post-PCI infusion—1.0% vs 1.8% (P=0.03).
“Both treatment options are allowed per current European label and observational studies,” Dr Valgimigli said.
“Hence, I believe the option to prolong or stop bivalirudin infusion after PCI remains open for clinicians, who will have to decide based on the ischemic and bleeding risk of individual patients, as well as perhaps based on type of acute coronary syndrome, timing of loading dose, and type of oral P2Y12 inhibitors. This is in keeping with the current labeling of the drug in EU and USA.”
Cost concerns
In the NEJM editorial, Peter Berger, MD, of North Shore–Long Island Jewish Health System in Great Neck, New York, noted that bivalirudin costs more than 400 times the price of heparin.
“Many studies have shown that bivalirudin is safer than heparin—that it causes fewer bleeding complications,” Dr Berger said. “But other studies have shown that heparin is every bit as safe, especially when used in lower doses. And one recent, large study actually suggested that heparin is more effective than bivalirudin.”
Despite these conflicting results, Dr Berger said “nearly everyone” agrees that if the more expensive drug is not superior in some way, the less expensive one should be used.
“Many studies raise more questions than they answer,” he added. “It will be interesting to see whether doctors accept the results of the MATRIX trial or wait for more studies before deciding which blood thinner they prefer.”
*MATRIX investigators previously compared vascular access sites and found that radial access outperformed femoral access. These results were published earlier this year in The Lancet.
LONDON—The latest results* of the MATRIX trial haven’t provided any cut-and-dried answers when it comes to anticoagulation in the context of percutaneous coronary intervention (PCI), according to articles published in NEJM and data presented at the ESC Congress 2015.
The trial suggested that, overall, bivalirudin and heparin produce comparable results in patients undergoing PCI.
The drugs produced similar rates of major adverse cardiovascular events (MACE) and net adverse clinical events (NACE).
In addition, among patients in the bivalirudin arm, there was no significant difference in a composite primary outcome between patients who received an additional infusion of bivalirudin after PCI and those who did not.
Results from this trial were published in NEJM alongside a related editorial. At the ESC Congress 2015, the bivalirudin dosing comparison was reported in abstract 6004.
MATRIX was sponsored by the Societa Italiana di Cardiologia Invasiva (GISE), with funding from The Medicines Company and Terumo.
The trial enrolled 7213 patients with acute coronary syndrome who were set to undergo PCI. Patients were randomized to receive bivalirudin (n=3610) or unfractionated heparin (n=3603). Patients in the bivalirudin arm were then randomized to either receive a post-PCI infusion of bivalirudin (n=1799) or not (n=1811).
Primary outcomes for the comparison between bivalirudin and heparin were the occurrence of MACE (a composite of death, myocardial infarction, or stroke) and NACE (a composite of major bleeding or a major adverse cardiovascular event).
The primary outcome for the comparison of post-PCI bivalirudin infusion with no infusion was a composite of urgent target-vessel revascularization, definite stent thrombosis, or NACE.
Heparin vs bivalirudin
There was no significant difference between the bivalirudin and heparin groups with regard to MACE—10.3% and 10.9%, respectively (P=0.44). And the same was true for NACE—11.2% and 12.4%, respectively (P=0.12).
Likewise, there was no significant difference between the bivalirudin arm and the heparin arm with regard to myocardial infarction—8.6% and 8.5%, respectively (P=0.93)—or stroke—0.4% and 0.5%, respectively (P=0.57).
However, bivalirudin was associated with a significantly lower rate of all-cause mortality than heparin—1.7% and 2.3%, respectively (P=0.04)—and a significantly lower rate of cardiac-related death—1.5% and 2.2%, respectively (P=0.03).
The rate of definite stent thrombosis was significantly higher in the bivalirudin group than the heparin group—1.0% and 0.6%, respectively (P=0.048). But there was no significant difference in the rate of definite or probable stent thrombosis—1.3% and 1.0% (P=0.27).
The rate of any bleeding was significantly lower with bivalirudin than with heparin—11.0% and 13.6%, respectively (P=0.001). And the same was true for major bleeding (BARC 3 or 5)—1.4% and 2.5%, respectively (P<0.001).
Bivalirudin duration
“Post-PCI bivalirudin did not reduce the composite outcome of ischemic and bleeding outcomes, including stent thrombosis risk, as compared to no post-PCI bivalirudin infusion,” said study investigator Marco Valgimigli, MD, PhD, of the Swiss Cardiovascular Center in Bern, Switzerland.
The proportion of patients who met the primary endpoint was 11.0% in the post-PCI infusion group and 11.9% in the no-infusion group (P=0.34).
Similarly, there was no significant difference between the infusion and no-infusion groups in the risk of definite stent thrombosis—1.3% and 0.7%, respectively (P=0.09)—or definite/probable stent thrombosis—1.5% and 1.1%, respectively (P=0.29).
And there was no significant difference in the rate of any bleeding—11.3% and 10.7%, respectively (P=0.62)—but the rate of BARC 3 or 5 bleeding was lower in the group that received the post-PCI infusion—1.0% vs 1.8% (P=0.03).
“Both treatment options are allowed per current European label and observational studies,” Dr Valgimigli said.
“Hence, I believe the option to prolong or stop bivalirudin infusion after PCI remains open for clinicians, who will have to decide based on the ischemic and bleeding risk of individual patients, as well as perhaps based on type of acute coronary syndrome, timing of loading dose, and type of oral P2Y12 inhibitors. This is in keeping with the current labeling of the drug in EU and USA.”
Cost concerns
In the NEJM editorial, Peter Berger, MD, of North Shore–Long Island Jewish Health System in Great Neck, New York, noted that bivalirudin costs more than 400 times the price of heparin.
“Many studies have shown that bivalirudin is safer than heparin—that it causes fewer bleeding complications,” Dr Berger said. “But other studies have shown that heparin is every bit as safe, especially when used in lower doses. And one recent, large study actually suggested that heparin is more effective than bivalirudin.”
Despite these conflicting results, Dr Berger said “nearly everyone” agrees that if the more expensive drug is not superior in some way, the less expensive one should be used.
“Many studies raise more questions than they answer,” he added. “It will be interesting to see whether doctors accept the results of the MATRIX trial or wait for more studies before deciding which blood thinner they prefer.”
*MATRIX investigators previously compared vascular access sites and found that radial access outperformed femoral access. These results were published earlier this year in The Lancet.
Most cardiologists flunk auscultation skills test
LONDON – Cardiologists’ auscultation skills in the detection of valvular murmurs are “alarmingly low,” Dr. Michael J. Barrett reported at the annual congress of the European Society of Cardiology.
He formally tested the auscultation abilities of 1,098 cardiologists attending meetings of the American College of Cardiology. The results proved disheartening: The cardiologists, all voluntary participants in the project, were able to identify on average only 48% of the basic murmurs, which included aortic stenosis, aortic regurgitation, and mitral stenosis or regurgitation.
They did somewhat better in identifying the advanced murmurs, including mitral valve prolapse, bicuspid aortic valve, combined aortic stenosis and regurgitation, or combined mitral stenosis and regurgitation. But they still got only 66% of those murmurs right, according to Dr. Barrett, a cardiologist at Lehigh Valley Health Network, Allentown, Pa.
Their low success rates were quite similar to the scores achieved by primary care physicians in other studies, even though cardiologists are the ones who are supposed to be the experts in matters of the heart.
All is not lost, however. The participating cardiologists then underwent an intensive 90-minute auscultation training program in which they listened carefully to 400 repetitions of each murmur while viewing visual memory aids, including murmur phonocardiograms. Psychoacoustic research has shown that it takes this sort of dedicated repetition to master new sounds, he explained.
Upon retesting in which the murmurs were presented in random order so as to avoid test/retest score inflation, the cardiologists’ performance improved dramatically. Identification rates of the basic murmurs jumped from 48% to 88%, while scores for advanced murmurs zipped up to 93% from the pretest average of 66%.
Other studies carried out by Dr. Barrett have shown that the improvement in auscultation skills achieved through the learning program is durable.
Accurate auscultation is key to the cost-effective and timely detection of valve disorders, which is more important than ever now that dramatically effective transcatheter therapies are available for diseased aortic and mitral valves, the cardiologist observed.
Dr. Barrett is editor-in-chief of Heart Songs, the downloadable American College of Cardiology auscultation skills improvement program used in the study.
LONDON – Cardiologists’ auscultation skills in the detection of valvular murmurs are “alarmingly low,” Dr. Michael J. Barrett reported at the annual congress of the European Society of Cardiology.
He formally tested the auscultation abilities of 1,098 cardiologists attending meetings of the American College of Cardiology. The results proved disheartening: The cardiologists, all voluntary participants in the project, were able to identify on average only 48% of the basic murmurs, which included aortic stenosis, aortic regurgitation, and mitral stenosis or regurgitation.
They did somewhat better in identifying the advanced murmurs, including mitral valve prolapse, bicuspid aortic valve, combined aortic stenosis and regurgitation, or combined mitral stenosis and regurgitation. But they still got only 66% of those murmurs right, according to Dr. Barrett, a cardiologist at Lehigh Valley Health Network, Allentown, Pa.
Their low success rates were quite similar to the scores achieved by primary care physicians in other studies, even though cardiologists are the ones who are supposed to be the experts in matters of the heart.
All is not lost, however. The participating cardiologists then underwent an intensive 90-minute auscultation training program in which they listened carefully to 400 repetitions of each murmur while viewing visual memory aids, including murmur phonocardiograms. Psychoacoustic research has shown that it takes this sort of dedicated repetition to master new sounds, he explained.
Upon retesting in which the murmurs were presented in random order so as to avoid test/retest score inflation, the cardiologists’ performance improved dramatically. Identification rates of the basic murmurs jumped from 48% to 88%, while scores for advanced murmurs zipped up to 93% from the pretest average of 66%.
Other studies carried out by Dr. Barrett have shown that the improvement in auscultation skills achieved through the learning program is durable.
Accurate auscultation is key to the cost-effective and timely detection of valve disorders, which is more important than ever now that dramatically effective transcatheter therapies are available for diseased aortic and mitral valves, the cardiologist observed.
Dr. Barrett is editor-in-chief of Heart Songs, the downloadable American College of Cardiology auscultation skills improvement program used in the study.
LONDON – Cardiologists’ auscultation skills in the detection of valvular murmurs are “alarmingly low,” Dr. Michael J. Barrett reported at the annual congress of the European Society of Cardiology.
He formally tested the auscultation abilities of 1,098 cardiologists attending meetings of the American College of Cardiology. The results proved disheartening: The cardiologists, all voluntary participants in the project, were able to identify on average only 48% of the basic murmurs, which included aortic stenosis, aortic regurgitation, and mitral stenosis or regurgitation.
They did somewhat better in identifying the advanced murmurs, including mitral valve prolapse, bicuspid aortic valve, combined aortic stenosis and regurgitation, or combined mitral stenosis and regurgitation. But they still got only 66% of those murmurs right, according to Dr. Barrett, a cardiologist at Lehigh Valley Health Network, Allentown, Pa.
Their low success rates were quite similar to the scores achieved by primary care physicians in other studies, even though cardiologists are the ones who are supposed to be the experts in matters of the heart.
All is not lost, however. The participating cardiologists then underwent an intensive 90-minute auscultation training program in which they listened carefully to 400 repetitions of each murmur while viewing visual memory aids, including murmur phonocardiograms. Psychoacoustic research has shown that it takes this sort of dedicated repetition to master new sounds, he explained.
Upon retesting in which the murmurs were presented in random order so as to avoid test/retest score inflation, the cardiologists’ performance improved dramatically. Identification rates of the basic murmurs jumped from 48% to 88%, while scores for advanced murmurs zipped up to 93% from the pretest average of 66%.
Other studies carried out by Dr. Barrett have shown that the improvement in auscultation skills achieved through the learning program is durable.
Accurate auscultation is key to the cost-effective and timely detection of valve disorders, which is more important than ever now that dramatically effective transcatheter therapies are available for diseased aortic and mitral valves, the cardiologist observed.
Dr. Barrett is editor-in-chief of Heart Songs, the downloadable American College of Cardiology auscultation skills improvement program used in the study.
AT THE ESC CONGRESS 2015
Key clinical point: Most cardiologists get an F on auscultation skills, but they can improve dramatically through systematic repetition and training.
Major finding: Cardiologists’ accuracy in identifying basic aortic and mitral murmurs improved from a dismal 48% at baseline to 88% after a 90-minute skills training program.
Data source: This 1,098-cardiologist study involved a test of auscultation skills followed by a 90-minute training program and repeat testing.
Disclosures: The study was funded by the American College of Cardiology. The presenter serves as editor-in-chief of the college’s Heart Songs auscultation skills improvement program.
