BOSTON — Patients with spondyloarthropathy (SpA) who undergo therapy with the tumor necrosis factor-α inhibitor etanercept are at low risk of developing antibodies associated with systemic lupus erythematosus, according to a poster presentation at the annual meeting of the Federation of Clinical Immunology Societies.

Although these potentially harmful antibodies seem to be increased in patients receiving infliximab, neither of the biologics induced lupus-like symptoms, one of the feared side effects of anti-TNF-α therapy.

Recent studies have shown promising results of anti-TNF-α therapy in patients with SpA. Many more have documented their efficacy in rheumatoid arthritis (RA). But enthusiasm for the new drugs has been muted by widespread concern over side effects that range from headache to infection and lymphoma.

In addition, numerous reports in the RA literature now show that infliximab induces antibodies associated with SLE. But the actual induction of clinically relevant lupus appears to be rare, and tracing its origin to drug-induced TNF-α blockade has been difficult to do.

In a previous study, Leen De Rycke, M.D., and colleagues from Ghent University Hospital, Belgium, reported for the first time that RA and SpA patients taking infliximab tended to produce high levels of the SLE antibodies, antinuclear antibodies (ANAs) and anti-double-stranded DNA (anti-dsDNA) antibodies (Arthritis Rheum. 2003;48:1015–23).

In their new study, they set out to see what happened to these patients over the long term, and whether etanercept therapy induces high antibody responses similar to those of infliximab.

Dr. De Rycke and associates followed 20 SpA patients for 1 year of treatment with etanercept. They compared the number of patients who developed newly induced autoantibodies in this cohort with those of 34 SpA patients who underwent infliximab therapy for 2 years.

On average, patients in the etanercept group were a decade younger (37 years of age) than those in the infliximab group (47 years). Autoimmunity at baseline was low. None of the patients was taking concomitant methotrexate. After 1 year, 10% of the SpA patients on etanercept had evidence of newly induced ANAs compared with 62% of the patients taking infliximab.

Similarly, newly induced anti-dsDNA antibodies were present in the sera of 10% of patients receiving etanercept, and in 71% of those receiving infliximab. Neither drug induced anti-ENA or antihistone antibodies.

Nor did any patients in either group develop lupus-like symptoms. Titers of IgM, but not IgG, anticardiolipin were selectively increased after infliximab but not etanercept therapy. The anti-dsDNA antibodies were predominantly of the immunoglobulin M (IgM) and immunoglobulin G (IgG) isotype. Lupus-associated anti-dsDNA antibodies are classically of the IgG isotope.

“This study indicates that the prominent ANA and anti-dsDNA autoantibody response is not a pure class effect of TNF-α blockers,” Dr. De Rycke and colleagues concluded. Moreover, it “is not associated with clinically relevant lupus symptoms,” they said.

BOSTON — Patients with spondyloarthropathy (SpA) who undergo therapy with the tumor necrosis factor-α inhibitor etanercept are at low risk of developing antibodies associated with systemic lupus erythematosus, according to a poster presentation at the annual meeting of the Federation of Clinical Immunology Societies.

Although these potentially harmful antibodies seem to be increased in patients receiving infliximab, neither of the biologics induced lupus-like symptoms, one of the feared side effects of anti-TNF-α therapy.

Recent studies have shown promising results of anti-TNF-α therapy in patients with SpA. Many more have documented their efficacy in rheumatoid arthritis (RA). But enthusiasm for the new drugs has been muted by widespread concern over side effects that range from headache to infection and lymphoma.

In addition, numerous reports in the RA literature now show that infliximab induces antibodies associated with SLE. But the actual induction of clinically relevant lupus appears to be rare, and tracing its origin to drug-induced TNF-α blockade has been difficult to do.

In a previous study, Leen De Rycke, M.D., and colleagues from Ghent University Hospital, Belgium, reported for the first time that RA and SpA patients taking infliximab tended to produce high levels of the SLE antibodies, antinuclear antibodies (ANAs) and anti-double-stranded DNA (anti-dsDNA) antibodies (Arthritis Rheum. 2003;48:1015–23).

In their new study, they set out to see what happened to these patients over the long term, and whether etanercept therapy induces high antibody responses similar to those of infliximab.

Dr. De Rycke and associates followed 20 SpA patients for 1 year of treatment with etanercept. They compared the number of patients who developed newly induced autoantibodies in this cohort with those of 34 SpA patients who underwent infliximab therapy for 2 years.

On average, patients in the etanercept group were a decade younger (37 years of age) than those in the infliximab group (47 years). Autoimmunity at baseline was low. None of the patients was taking concomitant methotrexate. After 1 year, 10% of the SpA patients on etanercept had evidence of newly induced ANAs compared with 62% of the patients taking infliximab.

Similarly, newly induced anti-dsDNA antibodies were present in the sera of 10% of patients receiving etanercept, and in 71% of those receiving infliximab. Neither drug induced anti-ENA or antihistone antibodies.

Nor did any patients in either group develop lupus-like symptoms. Titers of IgM, but not IgG, anticardiolipin were selectively increased after infliximab but not etanercept therapy. The anti-dsDNA antibodies were predominantly of the immunoglobulin M (IgM) and immunoglobulin G (IgG) isotype. Lupus-associated anti-dsDNA antibodies are classically of the IgG isotope.

“This study indicates that the prominent ANA and anti-dsDNA autoantibody response is not a pure class effect of TNF-α blockers,” Dr. De Rycke and colleagues concluded. Moreover, it “is not associated with clinically relevant lupus symptoms,” they said.

BOSTON — Patients with spondyloarthropathy (SpA) who undergo therapy with the tumor necrosis factor-α inhibitor etanercept are at low risk of developing antibodies associated with systemic lupus erythematosus, according to a poster presentation at the annual meeting of the Federation of Clinical Immunology Societies.

Although these potentially harmful antibodies seem to be increased in patients receiving infliximab, neither of the biologics induced lupus-like symptoms, one of the feared side effects of anti-TNF-α therapy.

Recent studies have shown promising results of anti-TNF-α therapy in patients with SpA. Many more have documented their efficacy in rheumatoid arthritis (RA). But enthusiasm for the new drugs has been muted by widespread concern over side effects that range from headache to infection and lymphoma.

In addition, numerous reports in the RA literature now show that infliximab induces antibodies associated with SLE. But the actual induction of clinically relevant lupus appears to be rare, and tracing its origin to drug-induced TNF-α blockade has been difficult to do.

In a previous study, Leen De Rycke, M.D., and colleagues from Ghent University Hospital, Belgium, reported for the first time that RA and SpA patients taking infliximab tended to produce high levels of the SLE antibodies, antinuclear antibodies (ANAs) and anti-double-stranded DNA (anti-dsDNA) antibodies (Arthritis Rheum. 2003;48:1015–23).

In their new study, they set out to see what happened to these patients over the long term, and whether etanercept therapy induces high antibody responses similar to those of infliximab.

Dr. De Rycke and associates followed 20 SpA patients for 1 year of treatment with etanercept. They compared the number of patients who developed newly induced autoantibodies in this cohort with those of 34 SpA patients who underwent infliximab therapy for 2 years.

On average, patients in the etanercept group were a decade younger (37 years of age) than those in the infliximab group (47 years). Autoimmunity at baseline was low. None of the patients was taking concomitant methotrexate. After 1 year, 10% of the SpA patients on etanercept had evidence of newly induced ANAs compared with 62% of the patients taking infliximab.

Similarly, newly induced anti-dsDNA antibodies were present in the sera of 10% of patients receiving etanercept, and in 71% of those receiving infliximab. Neither drug induced anti-ENA or antihistone antibodies.

Nor did any patients in either group develop lupus-like symptoms. Titers of IgM, but not IgG, anticardiolipin were selectively increased after infliximab but not etanercept therapy. The anti-dsDNA antibodies were predominantly of the immunoglobulin M (IgM) and immunoglobulin G (IgG) isotype. Lupus-associated anti-dsDNA antibodies are classically of the IgG isotope.

“This study indicates that the prominent ANA and anti-dsDNA autoantibody response is not a pure class effect of TNF-α blockers,” Dr. De Rycke and colleagues concluded. Moreover, it “is not associated with clinically relevant lupus symptoms,” they said.

NEW YORK — Treatment of Wegener's granulomatosis continues to challenge and evolve, as researchers investigate the complex molecular cross-talk underlying immune dysfunction, looking for new ways to target therapy, and clinicians seek new ways to balance necessarily aggressive cytotoxic treatment against the potential for serious adverse events.

Standard induction treatment for severe vasculitis associated with the presence of antineutrophil cytoplasmic antibodies (ANCA) remains cyclophosphamide plus glucocorticoids—a regimen that is lifesaving, Gary S. Hoffman, M.D., said at a rheumatology meeting sponsored by New York University.

But because of the high incidence of bladder cancer and other serious toxicities associated with long-term use of cyclophosphamide, once remission is achieved, maintenance therapy with methotrexate or azathioprine is now preferred, he said.

Relapse remains problematic, however, and a subset of patients do not respond to the most cytotoxic cyclophosphamide-based regimen.

For these patients, a potential new approach has emerged: B-cell depletion with rituximab, said Dr. Hoffman, chair of the department of rheumatic and immunologic diseases at the Cleveland Clinic Foundation.

A group of 11 patients who had active, ANCA-positive vasculitis and either did not respond to cyclophosphamide or who had contraindications to its use were given infusions of rituximab (Rituxan) plus glucocorticoids on a compassionate use basis. Ten of the patients had Wegener's granulomatosis, and one had a related ANCA-associated vasculitis, microscopic polyangiitis.

Not only did all 11 achieve remission, but they also were able to discontinue steroids, which has not been possible before, said Dr. Hoffman, who was not involved in the study.

All patients had significant decreases in ANCA, which are thought to mediate the glomerulonephritis and small vessel vasculitis, and 8 of the 11 became ANCA negative.

B-cell depletion typically persists for months following rituximab treatment; all patients remained in remission while B cells were undetectable.

Reappearance of B cells occurred in nine patients, 4–12 months after infusion. Two patients experienced disease relapse following discontinuation of glucocorticoids but recovered after resuming the rituximab/glucocorticoid regimen. Three others whose ANCA titers began to rise were retreated preemptively with rituximab alone and have remained in remission (Arthritis Rheum. 2005;52:262–8). The remaining four patients whose B cells repopulated did not revert to ANCA positivity.

Rituximab targets the CD20 receptor on the surface of B cells, and one rationale for using the drug in Wegener's granulomatosis is that it is able to deplete CD20-expressing precursors of ANCA-producing plasma cells (Arthritis Rheum. 2005;52:1–5).

A randomized, double-blind trial, Rituximab in ANCA-Associated Vasculitis (RAVE) is underway, with the goal of addressing the issue of whether targeted therapy, rather than broad-based immunosuppression, can provide enduring remission.

Many mediators other than B cells are involved in the inflammatory process of vasculitis, including dendritic cells, macrophages, and various different cytokines that interact with one another.

A previous trial evaluated the tumor necrosis factor (TNF)-α blocking agent etanercept (Enbrel), because the evidence suggested that this cytokine plays a role.

But a randomized, placebo-controlled trial that included 174 patients from eight centers found no benefit in the addition of etanercept to standard therapy. Furthermore, six patients who were taking etanercept plus cyclophosphamide developed solid tumors (N. Engl. J. Med. 2005;352:351–61).

“We didn't see this with people who were on methotrexate plus etanercept, and it's a major concern,” said Dr. Hoffman, who was coprincipal investigator for the trial.

“The new opportunities for selective targets certainly are seductive, and we hope they will work, but we cannot dismiss what we've learned from the history of this disease, which is that it carries a very high risk of morbidity and mortality, and that although our conventional therapy has risks, it is lifesaving,” he said.

Before glucocorticoids began being used for Wegener's granulomatosis, survival was only 50% at 5 months, and most patients died within 2 years of diagnosis. Even with glucocorticoids, survival increased only slightly, to 50% at 1 year.

The addition of cyclophosphamide to the regimen, first reported by the National Institutes of Health in the early 1970s, increased survival to 80% at 8 years.

“But I think we still have a long road ahead of us. I hope the future looks great, but I view it with guarded optimism,” Dr. Hoffman said.

NEW YORK — Treatment of Wegener's granulomatosis continues to challenge and evolve, as researchers investigate the complex molecular cross-talk underlying immune dysfunction, looking for new ways to target therapy, and clinicians seek new ways to balance necessarily aggressive cytotoxic treatment against the potential for serious adverse events.

Standard induction treatment for severe vasculitis associated with the presence of antineutrophil cytoplasmic antibodies (ANCA) remains cyclophosphamide plus glucocorticoids—a regimen that is lifesaving, Gary S. Hoffman, M.D., said at a rheumatology meeting sponsored by New York University.

But because of the high incidence of bladder cancer and other serious toxicities associated with long-term use of cyclophosphamide, once remission is achieved, maintenance therapy with methotrexate or azathioprine is now preferred, he said.

Relapse remains problematic, however, and a subset of patients do not respond to the most cytotoxic cyclophosphamide-based regimen.

For these patients, a potential new approach has emerged: B-cell depletion with rituximab, said Dr. Hoffman, chair of the department of rheumatic and immunologic diseases at the Cleveland Clinic Foundation.

A group of 11 patients who had active, ANCA-positive vasculitis and either did not respond to cyclophosphamide or who had contraindications to its use were given infusions of rituximab (Rituxan) plus glucocorticoids on a compassionate use basis. Ten of the patients had Wegener's granulomatosis, and one had a related ANCA-associated vasculitis, microscopic polyangiitis.

Not only did all 11 achieve remission, but they also were able to discontinue steroids, which has not been possible before, said Dr. Hoffman, who was not involved in the study.

All patients had significant decreases in ANCA, which are thought to mediate the glomerulonephritis and small vessel vasculitis, and 8 of the 11 became ANCA negative.

B-cell depletion typically persists for months following rituximab treatment; all patients remained in remission while B cells were undetectable.

Reappearance of B cells occurred in nine patients, 4–12 months after infusion. Two patients experienced disease relapse following discontinuation of glucocorticoids but recovered after resuming the rituximab/glucocorticoid regimen. Three others whose ANCA titers began to rise were retreated preemptively with rituximab alone and have remained in remission (Arthritis Rheum. 2005;52:262–8). The remaining four patients whose B cells repopulated did not revert to ANCA positivity.

Rituximab targets the CD20 receptor on the surface of B cells, and one rationale for using the drug in Wegener's granulomatosis is that it is able to deplete CD20-expressing precursors of ANCA-producing plasma cells (Arthritis Rheum. 2005;52:1–5).

A randomized, double-blind trial, Rituximab in ANCA-Associated Vasculitis (RAVE) is underway, with the goal of addressing the issue of whether targeted therapy, rather than broad-based immunosuppression, can provide enduring remission.

Many mediators other than B cells are involved in the inflammatory process of vasculitis, including dendritic cells, macrophages, and various different cytokines that interact with one another.

A previous trial evaluated the tumor necrosis factor (TNF)-α blocking agent etanercept (Enbrel), because the evidence suggested that this cytokine plays a role.

But a randomized, placebo-controlled trial that included 174 patients from eight centers found no benefit in the addition of etanercept to standard therapy. Furthermore, six patients who were taking etanercept plus cyclophosphamide developed solid tumors (N. Engl. J. Med. 2005;352:351–61).

“We didn't see this with people who were on methotrexate plus etanercept, and it's a major concern,” said Dr. Hoffman, who was coprincipal investigator for the trial.

“The new opportunities for selective targets certainly are seductive, and we hope they will work, but we cannot dismiss what we've learned from the history of this disease, which is that it carries a very high risk of morbidity and mortality, and that although our conventional therapy has risks, it is lifesaving,” he said.

Before glucocorticoids began being used for Wegener's granulomatosis, survival was only 50% at 5 months, and most patients died within 2 years of diagnosis. Even with glucocorticoids, survival increased only slightly, to 50% at 1 year.

The addition of cyclophosphamide to the regimen, first reported by the National Institutes of Health in the early 1970s, increased survival to 80% at 8 years.

“But I think we still have a long road ahead of us. I hope the future looks great, but I view it with guarded optimism,” Dr. Hoffman said.

NEW YORK — Treatment of Wegener's granulomatosis continues to challenge and evolve, as researchers investigate the complex molecular cross-talk underlying immune dysfunction, looking for new ways to target therapy, and clinicians seek new ways to balance necessarily aggressive cytotoxic treatment against the potential for serious adverse events.

Standard induction treatment for severe vasculitis associated with the presence of antineutrophil cytoplasmic antibodies (ANCA) remains cyclophosphamide plus glucocorticoids—a regimen that is lifesaving, Gary S. Hoffman, M.D., said at a rheumatology meeting sponsored by New York University.

But because of the high incidence of bladder cancer and other serious toxicities associated with long-term use of cyclophosphamide, once remission is achieved, maintenance therapy with methotrexate or azathioprine is now preferred, he said.

Relapse remains problematic, however, and a subset of patients do not respond to the most cytotoxic cyclophosphamide-based regimen.

For these patients, a potential new approach has emerged: B-cell depletion with rituximab, said Dr. Hoffman, chair of the department of rheumatic and immunologic diseases at the Cleveland Clinic Foundation.

A group of 11 patients who had active, ANCA-positive vasculitis and either did not respond to cyclophosphamide or who had contraindications to its use were given infusions of rituximab (Rituxan) plus glucocorticoids on a compassionate use basis. Ten of the patients had Wegener's granulomatosis, and one had a related ANCA-associated vasculitis, microscopic polyangiitis.

Not only did all 11 achieve remission, but they also were able to discontinue steroids, which has not been possible before, said Dr. Hoffman, who was not involved in the study.

All patients had significant decreases in ANCA, which are thought to mediate the glomerulonephritis and small vessel vasculitis, and 8 of the 11 became ANCA negative.

B-cell depletion typically persists for months following rituximab treatment; all patients remained in remission while B cells were undetectable.

Reappearance of B cells occurred in nine patients, 4–12 months after infusion. Two patients experienced disease relapse following discontinuation of glucocorticoids but recovered after resuming the rituximab/glucocorticoid regimen. Three others whose ANCA titers began to rise were retreated preemptively with rituximab alone and have remained in remission (Arthritis Rheum. 2005;52:262–8). The remaining four patients whose B cells repopulated did not revert to ANCA positivity.

Rituximab targets the CD20 receptor on the surface of B cells, and one rationale for using the drug in Wegener's granulomatosis is that it is able to deplete CD20-expressing precursors of ANCA-producing plasma cells (Arthritis Rheum. 2005;52:1–5).

A randomized, double-blind trial, Rituximab in ANCA-Associated Vasculitis (RAVE) is underway, with the goal of addressing the issue of whether targeted therapy, rather than broad-based immunosuppression, can provide enduring remission.

Many mediators other than B cells are involved in the inflammatory process of vasculitis, including dendritic cells, macrophages, and various different cytokines that interact with one another.

A previous trial evaluated the tumor necrosis factor (TNF)-α blocking agent etanercept (Enbrel), because the evidence suggested that this cytokine plays a role.

But a randomized, placebo-controlled trial that included 174 patients from eight centers found no benefit in the addition of etanercept to standard therapy. Furthermore, six patients who were taking etanercept plus cyclophosphamide developed solid tumors (N. Engl. J. Med. 2005;352:351–61).

“We didn't see this with people who were on methotrexate plus etanercept, and it's a major concern,” said Dr. Hoffman, who was coprincipal investigator for the trial.

“The new opportunities for selective targets certainly are seductive, and we hope they will work, but we cannot dismiss what we've learned from the history of this disease, which is that it carries a very high risk of morbidity and mortality, and that although our conventional therapy has risks, it is lifesaving,” he said.

Before glucocorticoids began being used for Wegener's granulomatosis, survival was only 50% at 5 months, and most patients died within 2 years of diagnosis. Even with glucocorticoids, survival increased only slightly, to 50% at 1 year.

The addition of cyclophosphamide to the regimen, first reported by the National Institutes of Health in the early 1970s, increased survival to 80% at 8 years.

“But I think we still have a long road ahead of us. I hope the future looks great, but I view it with guarded optimism,” Dr. Hoffman said.

PONTE VEDRA BEACH, FLA. — When a coronary artery is too tight to accommodate a stent, it may be necessary to apply a little grease.

A lubricant suited to the job was an olive oil and egg yolk phospholipid-based emulsion sold commercially as Rotaglide, Mark Awar, M.D., and associates reported in a poster at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

The 20 patients in the series they reported on were those who failed initial stent placement out of 813 consecutive patients who underwent a percutaneous coronary intervention at Jefferson Medical College in Philadelphia.

In these 20 cases stent delivery was unsuccessful despite predilation and several other steps: substitution of a moderate-to-stiff guidewire, reattempts with a new guiding catheter or a new stent, use of a buddy wire, and in one case use of rotational atherectomy. After failed delivery, the stents were removed from their guiding catheters, saturated with Rotaglide using a 20-cc syringe, and a second delivery was immediately attempted.

Application of Rotaglide led to successful delivery for 17 of the 20 stents, reported Dr. Awar, a cardiologist at Jefferson. Angiography showed excellent anatomic results in all 17 patients. There were no major adverse coronary events or subacute stent thromboses.

All 20 patients had arteries with complex anatomy and unfavorable morphologic features: 17 (85%) had tortuous vessels, 13 (65%) had calcification, and 10 (50%) had diffuse disease (several patients had more than one feature). The target vessels included 10 left circumflex arteries, 8 right coronary arteries, and 2 left anterior descending arteries. Average patient age was 69 years, and 75% were men.

Use of Rotaglide to smooth the way for a stubborn stent had previously been reported in isolated case studies, but not in such a large series. Prior reports also have documented up to a 4% rate of failure in delivering stents to their target lesions (in this series the rate was 2.5%: 20 out of 813).

Rotaglide is sold by Boston Scientific to reduce catheter friction during rotational atherectomy.

The study was not sponsored by Boston Scientific.

PONTE VEDRA BEACH, FLA. — When a coronary artery is too tight to accommodate a stent, it may be necessary to apply a little grease.

A lubricant suited to the job was an olive oil and egg yolk phospholipid-based emulsion sold commercially as Rotaglide, Mark Awar, M.D., and associates reported in a poster at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

The 20 patients in the series they reported on were those who failed initial stent placement out of 813 consecutive patients who underwent a percutaneous coronary intervention at Jefferson Medical College in Philadelphia.

In these 20 cases stent delivery was unsuccessful despite predilation and several other steps: substitution of a moderate-to-stiff guidewire, reattempts with a new guiding catheter or a new stent, use of a buddy wire, and in one case use of rotational atherectomy. After failed delivery, the stents were removed from their guiding catheters, saturated with Rotaglide using a 20-cc syringe, and a second delivery was immediately attempted.

Application of Rotaglide led to successful delivery for 17 of the 20 stents, reported Dr. Awar, a cardiologist at Jefferson. Angiography showed excellent anatomic results in all 17 patients. There were no major adverse coronary events or subacute stent thromboses.

All 20 patients had arteries with complex anatomy and unfavorable morphologic features: 17 (85%) had tortuous vessels, 13 (65%) had calcification, and 10 (50%) had diffuse disease (several patients had more than one feature). The target vessels included 10 left circumflex arteries, 8 right coronary arteries, and 2 left anterior descending arteries. Average patient age was 69 years, and 75% were men.

Use of Rotaglide to smooth the way for a stubborn stent had previously been reported in isolated case studies, but not in such a large series. Prior reports also have documented up to a 4% rate of failure in delivering stents to their target lesions (in this series the rate was 2.5%: 20 out of 813).

Rotaglide is sold by Boston Scientific to reduce catheter friction during rotational atherectomy.

The study was not sponsored by Boston Scientific.

PONTE VEDRA BEACH, FLA. — When a coronary artery is too tight to accommodate a stent, it may be necessary to apply a little grease.

A lubricant suited to the job was an olive oil and egg yolk phospholipid-based emulsion sold commercially as Rotaglide, Mark Awar, M.D., and associates reported in a poster at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

The 20 patients in the series they reported on were those who failed initial stent placement out of 813 consecutive patients who underwent a percutaneous coronary intervention at Jefferson Medical College in Philadelphia.

In these 20 cases stent delivery was unsuccessful despite predilation and several other steps: substitution of a moderate-to-stiff guidewire, reattempts with a new guiding catheter or a new stent, use of a buddy wire, and in one case use of rotational atherectomy. After failed delivery, the stents were removed from their guiding catheters, saturated with Rotaglide using a 20-cc syringe, and a second delivery was immediately attempted.

Application of Rotaglide led to successful delivery for 17 of the 20 stents, reported Dr. Awar, a cardiologist at Jefferson. Angiography showed excellent anatomic results in all 17 patients. There were no major adverse coronary events or subacute stent thromboses.

All 20 patients had arteries with complex anatomy and unfavorable morphologic features: 17 (85%) had tortuous vessels, 13 (65%) had calcification, and 10 (50%) had diffuse disease (several patients had more than one feature). The target vessels included 10 left circumflex arteries, 8 right coronary arteries, and 2 left anterior descending arteries. Average patient age was 69 years, and 75% were men.

Use of Rotaglide to smooth the way for a stubborn stent had previously been reported in isolated case studies, but not in such a large series. Prior reports also have documented up to a 4% rate of failure in delivering stents to their target lesions (in this series the rate was 2.5%: 20 out of 813).

Rotaglide is sold by Boston Scientific to reduce catheter friction during rotational atherectomy.

The study was not sponsored by Boston Scientific.

PONTE VEDRA BEACH, FLA. — Now that the first thoracic-aorta endograft is on the U.S. market, a revolution has begun in managing thoracic aorta aneurysms and dissections.

“This is a big deal. Dramatic changes are taking place in managing thoracic-aorta diseases,” Alan B. Lumsden, M.D., said at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

On March 23, the Food and Drug Administration approved the Gore TAG endoprosthesis for repair of aneurysms in the descending thoracic aorta. Several additional endoprostheses are in development, and the types of patients who are candidates for receiving these devices are expanding.

Thoracic-aorta aneurysms appear to be less prevalent than abdominal-aorta aneurysms, but thoracic defects also are underdiagnosed. Current prevalence numbers are 10.4/100,000 people. The risk factors for both abdominal and thoracic aneurysms largely overlap. The incidence of thoracic aneurysms increases markedly as people age, and the incidence also seems to be increasing overall in the United States, said Dr. Lumsden, chief of the division of vascular surgery and endovascular therapy at Baylor College of Medicine in Houston.

Most patients with thoracic-aorta aneurysms are asymptomatic; the defects are picked up incidentally in chest x-rays and CT scans. The most common symptom is pain in the shoulders or back.

Like abdominal-aortic aneurysms, the risk of rupture in thoracic aneurysms rises with the size of the aneurysm. Surgical repairs usually have not been done until the aneurysm reached about 6 cm in diameter because of the high rate of surgical complications. In patients without Marfan's syndrome, an ascending thoracic aneurysm usually has been repaired when it reached 5.5 cm in diameter, and a descending thoracic aneurysm has been repaired when it reached 6.5 cm. In patients with Marfan's syndrome, the thresholds for repair have usually been scaled back by 0.5 cm.

Endovascular repair is already the treatment of choice for symptomatic patients and those with a risk of an impending rupture. But increasingly, more complicated aneurysm patients, as well as patients with uncomplicated aortic dissections, will be treated endovascularly.

Several recent reports have documented new types of surgical procedures that have “increased the landing zone” for endovascular stenting. “In the past, we were limited by the location of the celiac, subclavian, and carotid arteries, but now there are good ways to move those around,” he said.

A descending thoracic-aorta aneurysm is repaired with an endovascular stent. Courtesy Dr. Alan B. Lumsden

PONTE VEDRA BEACH, FLA. — Now that the first thoracic-aorta endograft is on the U.S. market, a revolution has begun in managing thoracic aorta aneurysms and dissections.

“This is a big deal. Dramatic changes are taking place in managing thoracic-aorta diseases,” Alan B. Lumsden, M.D., said at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

On March 23, the Food and Drug Administration approved the Gore TAG endoprosthesis for repair of aneurysms in the descending thoracic aorta. Several additional endoprostheses are in development, and the types of patients who are candidates for receiving these devices are expanding.

Thoracic-aorta aneurysms appear to be less prevalent than abdominal-aorta aneurysms, but thoracic defects also are underdiagnosed. Current prevalence numbers are 10.4/100,000 people. The risk factors for both abdominal and thoracic aneurysms largely overlap. The incidence of thoracic aneurysms increases markedly as people age, and the incidence also seems to be increasing overall in the United States, said Dr. Lumsden, chief of the division of vascular surgery and endovascular therapy at Baylor College of Medicine in Houston.

Most patients with thoracic-aorta aneurysms are asymptomatic; the defects are picked up incidentally in chest x-rays and CT scans. The most common symptom is pain in the shoulders or back.

Like abdominal-aortic aneurysms, the risk of rupture in thoracic aneurysms rises with the size of the aneurysm. Surgical repairs usually have not been done until the aneurysm reached about 6 cm in diameter because of the high rate of surgical complications. In patients without Marfan's syndrome, an ascending thoracic aneurysm usually has been repaired when it reached 5.5 cm in diameter, and a descending thoracic aneurysm has been repaired when it reached 6.5 cm. In patients with Marfan's syndrome, the thresholds for repair have usually been scaled back by 0.5 cm.

Endovascular repair is already the treatment of choice for symptomatic patients and those with a risk of an impending rupture. But increasingly, more complicated aneurysm patients, as well as patients with uncomplicated aortic dissections, will be treated endovascularly.

Several recent reports have documented new types of surgical procedures that have “increased the landing zone” for endovascular stenting. “In the past, we were limited by the location of the celiac, subclavian, and carotid arteries, but now there are good ways to move those around,” he said.

A descending thoracic-aorta aneurysm is repaired with an endovascular stent. Courtesy Dr. Alan B. Lumsden

PONTE VEDRA BEACH, FLA. — Now that the first thoracic-aorta endograft is on the U.S. market, a revolution has begun in managing thoracic aorta aneurysms and dissections.

“This is a big deal. Dramatic changes are taking place in managing thoracic-aorta diseases,” Alan B. Lumsden, M.D., said at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

On March 23, the Food and Drug Administration approved the Gore TAG endoprosthesis for repair of aneurysms in the descending thoracic aorta. Several additional endoprostheses are in development, and the types of patients who are candidates for receiving these devices are expanding.

Thoracic-aorta aneurysms appear to be less prevalent than abdominal-aorta aneurysms, but thoracic defects also are underdiagnosed. Current prevalence numbers are 10.4/100,000 people. The risk factors for both abdominal and thoracic aneurysms largely overlap. The incidence of thoracic aneurysms increases markedly as people age, and the incidence also seems to be increasing overall in the United States, said Dr. Lumsden, chief of the division of vascular surgery and endovascular therapy at Baylor College of Medicine in Houston.

Most patients with thoracic-aorta aneurysms are asymptomatic; the defects are picked up incidentally in chest x-rays and CT scans. The most common symptom is pain in the shoulders or back.

Like abdominal-aortic aneurysms, the risk of rupture in thoracic aneurysms rises with the size of the aneurysm. Surgical repairs usually have not been done until the aneurysm reached about 6 cm in diameter because of the high rate of surgical complications. In patients without Marfan's syndrome, an ascending thoracic aneurysm usually has been repaired when it reached 5.5 cm in diameter, and a descending thoracic aneurysm has been repaired when it reached 6.5 cm. In patients with Marfan's syndrome, the thresholds for repair have usually been scaled back by 0.5 cm.

Endovascular repair is already the treatment of choice for symptomatic patients and those with a risk of an impending rupture. But increasingly, more complicated aneurysm patients, as well as patients with uncomplicated aortic dissections, will be treated endovascularly.

Several recent reports have documented new types of surgical procedures that have “increased the landing zone” for endovascular stenting. “In the past, we were limited by the location of the celiac, subclavian, and carotid arteries, but now there are good ways to move those around,” he said.

A descending thoracic-aorta aneurysm is repaired with an endovascular stent. Courtesy Dr. Alan B. Lumsden

PONTE VEDRA BEACH, FLA. — Patients with critical carotid stenosis were more likely to have a stroke following carotid artery stenting than were those without critical stenosis in a study with 350 patients.

But this doesn't mean that stenting is not a good option for these patients. Although endarterectomy is also a “viable option” for patients with critical carotid stenosis, “these patients would be challenging for endarterectomy as well” because they are at high risk for stroke after any carotid intervention, David S. Lee, M.D., said at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

In the study, critical carotid stenosis was defined as a stenosis of at least 90% that also required balloon predilation before it was possible to pass an embolic-protection device through the affected coronary artery. The need for predilation “was a marker for complex lesions and complex vessel morphology,” said Dr. Lee, a cardiologist at the Cleveland Clinic Foundation.

The study involved the 350 patients in a registry of those who underwent carotid stenting with an embolic protection device during August 1999-October 2003 at the Cleveland Clinic, of whom 21 required balloon predilation of their affected coronary artery to allow passage of an embolic protection device. All 350 patients began treatment with both aspirin and a thienopyridine (either clopidogrel or ticlopidine) at least 24 hours before their carotid procedure, and with unfractionated heparin during procedure. After the procedure, aspirin and thienopyridine treatment was continued for at least 4 weeks.

The study's primary end point was the incidence of stroke within 30 days of stenting. Two strokes occurred among the 21 patients with critical carotid stenosis (9.5%), and seven occurred among the other 329 patients (2.1%), a significant difference. The two strokes in the patients with critical carotid stenosis were not secondary to the balloon predilation procedures, Dr. Lee said.

PONTE VEDRA BEACH, FLA. — Patients with critical carotid stenosis were more likely to have a stroke following carotid artery stenting than were those without critical stenosis in a study with 350 patients.

But this doesn't mean that stenting is not a good option for these patients. Although endarterectomy is also a “viable option” for patients with critical carotid stenosis, “these patients would be challenging for endarterectomy as well” because they are at high risk for stroke after any carotid intervention, David S. Lee, M.D., said at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

In the study, critical carotid stenosis was defined as a stenosis of at least 90% that also required balloon predilation before it was possible to pass an embolic-protection device through the affected coronary artery. The need for predilation “was a marker for complex lesions and complex vessel morphology,” said Dr. Lee, a cardiologist at the Cleveland Clinic Foundation.

The study involved the 350 patients in a registry of those who underwent carotid stenting with an embolic protection device during August 1999-October 2003 at the Cleveland Clinic, of whom 21 required balloon predilation of their affected coronary artery to allow passage of an embolic protection device. All 350 patients began treatment with both aspirin and a thienopyridine (either clopidogrel or ticlopidine) at least 24 hours before their carotid procedure, and with unfractionated heparin during procedure. After the procedure, aspirin and thienopyridine treatment was continued for at least 4 weeks.

The study's primary end point was the incidence of stroke within 30 days of stenting. Two strokes occurred among the 21 patients with critical carotid stenosis (9.5%), and seven occurred among the other 329 patients (2.1%), a significant difference. The two strokes in the patients with critical carotid stenosis were not secondary to the balloon predilation procedures, Dr. Lee said.

PONTE VEDRA BEACH, FLA. — Patients with critical carotid stenosis were more likely to have a stroke following carotid artery stenting than were those without critical stenosis in a study with 350 patients.

But this doesn't mean that stenting is not a good option for these patients. Although endarterectomy is also a “viable option” for patients with critical carotid stenosis, “these patients would be challenging for endarterectomy as well” because they are at high risk for stroke after any carotid intervention, David S. Lee, M.D., said at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

In the study, critical carotid stenosis was defined as a stenosis of at least 90% that also required balloon predilation before it was possible to pass an embolic-protection device through the affected coronary artery. The need for predilation “was a marker for complex lesions and complex vessel morphology,” said Dr. Lee, a cardiologist at the Cleveland Clinic Foundation.

The study involved the 350 patients in a registry of those who underwent carotid stenting with an embolic protection device during August 1999-October 2003 at the Cleveland Clinic, of whom 21 required balloon predilation of their affected coronary artery to allow passage of an embolic protection device. All 350 patients began treatment with both aspirin and a thienopyridine (either clopidogrel or ticlopidine) at least 24 hours before their carotid procedure, and with unfractionated heparin during procedure. After the procedure, aspirin and thienopyridine treatment was continued for at least 4 weeks.

The study's primary end point was the incidence of stroke within 30 days of stenting. Two strokes occurred among the 21 patients with critical carotid stenosis (9.5%), and seven occurred among the other 329 patients (2.1%), a significant difference. The two strokes in the patients with critical carotid stenosis were not secondary to the balloon predilation procedures, Dr. Lee said.

PONTE VEDRA BEACH, FLA. — Administration of an antiplatelet IIb/IIIa drug to patients undergoing percutaneous coronary intervention for bypass-graft stenosis significantly boosted the incidence of myocardial infarctions in a registry with more than 34,000 patients.

The study used data from the American College of Cardiology National Cardiovascular Data Registry, which included more than 448,000 percutaneous coronary interventions (PCIs) done during 2001–2003, reported Satish K. Surabhi, M.D., at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

The registry included 34,720 patients who had PCI of a coronary artery bypass graft; 24,279 (70%) were treated with a glycoprotein IIb/IIIa inhibitor and 10,441 (30%) were not.

Following PCI, the in-hospital mortality rate was almost identical in the two subgroups: a 1.4% death rate in patients who received a IIb/IIIa inhibitor and a 1.3% rate in those who didn't get the drug.

In the first weeks following PCI, the incidence of MIs was significantly higher in patients treated with a IIb/IIIa inhibitor, 2.4% than in those who did not, 1.4%. The MIs included all new ST-segment elevations, Q-wave events, left bundle branch blocks, and elevations in serum levels of creatine kinase that exceeded three times the upper limit of normal.

In a multivariate analysis that controlled for various baseline differences in demographic and clinical variables, use of a IIb/IIIa inhibitor was linked with a significant 63% increased rate in MIs following PCI, said Dr. Surabhi, a cardiologist in private practice in Greer, S.C.

Most patients in this registry were not treated with a distal protection device, which may have been the most important element of their management, he said. “Only 5% of these patients were treated with a distal protection device. The major factor [causing bad outcomes] seems to be distal embolization, not formation of a thrombus.”

If a distal protection device or distal balloon occlusion is not used during a PCI of an aortocoronary bypass graft, then the patient should not receive a IIb/IIIa inhibitor, on the basis of the new findings, said Dr. Surabhi.

The study did not address whether it's useful to use a IIb/IIIa inhibitor to treat a patient who's undergoing a bypass graft PCI with distal protection, but Dr. Surabhi suggested that adding the drug may not help.

PONTE VEDRA BEACH, FLA. — Administration of an antiplatelet IIb/IIIa drug to patients undergoing percutaneous coronary intervention for bypass-graft stenosis significantly boosted the incidence of myocardial infarctions in a registry with more than 34,000 patients.

The study used data from the American College of Cardiology National Cardiovascular Data Registry, which included more than 448,000 percutaneous coronary interventions (PCIs) done during 2001–2003, reported Satish K. Surabhi, M.D., at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

The registry included 34,720 patients who had PCI of a coronary artery bypass graft; 24,279 (70%) were treated with a glycoprotein IIb/IIIa inhibitor and 10,441 (30%) were not.

Following PCI, the in-hospital mortality rate was almost identical in the two subgroups: a 1.4% death rate in patients who received a IIb/IIIa inhibitor and a 1.3% rate in those who didn't get the drug.

In the first weeks following PCI, the incidence of MIs was significantly higher in patients treated with a IIb/IIIa inhibitor, 2.4% than in those who did not, 1.4%. The MIs included all new ST-segment elevations, Q-wave events, left bundle branch blocks, and elevations in serum levels of creatine kinase that exceeded three times the upper limit of normal.

In a multivariate analysis that controlled for various baseline differences in demographic and clinical variables, use of a IIb/IIIa inhibitor was linked with a significant 63% increased rate in MIs following PCI, said Dr. Surabhi, a cardiologist in private practice in Greer, S.C.

Most patients in this registry were not treated with a distal protection device, which may have been the most important element of their management, he said. “Only 5% of these patients were treated with a distal protection device. The major factor [causing bad outcomes] seems to be distal embolization, not formation of a thrombus.”

If a distal protection device or distal balloon occlusion is not used during a PCI of an aortocoronary bypass graft, then the patient should not receive a IIb/IIIa inhibitor, on the basis of the new findings, said Dr. Surabhi.

The study did not address whether it's useful to use a IIb/IIIa inhibitor to treat a patient who's undergoing a bypass graft PCI with distal protection, but Dr. Surabhi suggested that adding the drug may not help.

PONTE VEDRA BEACH, FLA. — Administration of an antiplatelet IIb/IIIa drug to patients undergoing percutaneous coronary intervention for bypass-graft stenosis significantly boosted the incidence of myocardial infarctions in a registry with more than 34,000 patients.

The study used data from the American College of Cardiology National Cardiovascular Data Registry, which included more than 448,000 percutaneous coronary interventions (PCIs) done during 2001–2003, reported Satish K. Surabhi, M.D., at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

The registry included 34,720 patients who had PCI of a coronary artery bypass graft; 24,279 (70%) were treated with a glycoprotein IIb/IIIa inhibitor and 10,441 (30%) were not.

Following PCI, the in-hospital mortality rate was almost identical in the two subgroups: a 1.4% death rate in patients who received a IIb/IIIa inhibitor and a 1.3% rate in those who didn't get the drug.

In the first weeks following PCI, the incidence of MIs was significantly higher in patients treated with a IIb/IIIa inhibitor, 2.4% than in those who did not, 1.4%. The MIs included all new ST-segment elevations, Q-wave events, left bundle branch blocks, and elevations in serum levels of creatine kinase that exceeded three times the upper limit of normal.

In a multivariate analysis that controlled for various baseline differences in demographic and clinical variables, use of a IIb/IIIa inhibitor was linked with a significant 63% increased rate in MIs following PCI, said Dr. Surabhi, a cardiologist in private practice in Greer, S.C.

Most patients in this registry were not treated with a distal protection device, which may have been the most important element of their management, he said. “Only 5% of these patients were treated with a distal protection device. The major factor [causing bad outcomes] seems to be distal embolization, not formation of a thrombus.”

If a distal protection device or distal balloon occlusion is not used during a PCI of an aortocoronary bypass graft, then the patient should not receive a IIb/IIIa inhibitor, on the basis of the new findings, said Dr. Surabhi.

The study did not address whether it's useful to use a IIb/IIIa inhibitor to treat a patient who's undergoing a bypass graft PCI with distal protection, but Dr. Surabhi suggested that adding the drug may not help.

PHILADELPHIA — Left ventricular dysfunction is a powerful predictor of poor outcome in patients who have received a heart transplant.

During 13 years of follow-up of almost 19,000 patients with transplanted hearts, the cumulative rate of left ventricular (LV) dysfunction (ejection fraction of 40% or less) was 23%, Katherine Lietz, M.D., reported at the annual meeting of the International Society for Heart and Lung Transplantation.

In heart transplant patients with LV dysfunction, the relative risk of cardiac death was 2.65-fold higher than the risk in those without LV dysfunction. The risk of noncardiac death in patients with impaired LV function was almost twice that of controls, due mostly to renal dysfunction that was secondary to heart failure, said Dr. Lietz, a cardiologist at the University of Minnesota in Minneapolis.

The study used data from the U.S. Scientific Registry of Transplant Recipients for heart transplants done during 1990–2003 on 25,719 patients. Exclusion of patients who were lost to follow-up or did not survive for at least 1 year left a study group of 18,854 patients, who were followed until they died, until their transplanted hearts failed, or through May 2004.

Aside from the patients who developed heart failure, LV function stayed fairly constant through follow-up, which lasted up to 13 years. The average LV ejection fraction (EF) for the entire group was about 59% after 1 year of follow-up and 57% after 13 years. Development of heart failure occurred at a fairly constant rate, occurring in about 2% of patients a year.

The two most powerful risk factors for LV dysfunction were coronary vasculopathy and renal dysfunction; each more than doubled the risk. Other significant risk factors were African American race, which raised the risk by 89%; need for retransplantation (67%); and acute rejection (65%).

The prevalence of vasculopathy was 34% in patients with an EF of more than 40%. Among those with lower EFs, the prevalence was 57%.

The increased risk of death associated with LV dysfunction was proportional to the severity of the dysfunction. Patients with EFs of 45%–55% had a 25% higher risk of death than did patients with EFs of more than 65%. The mortality risk was 57% higher in patients with EFs of 35%–45%, and was 2.6-fold higher in those with EFs of less than 35%.

PHILADELPHIA — Left ventricular dysfunction is a powerful predictor of poor outcome in patients who have received a heart transplant.

During 13 years of follow-up of almost 19,000 patients with transplanted hearts, the cumulative rate of left ventricular (LV) dysfunction (ejection fraction of 40% or less) was 23%, Katherine Lietz, M.D., reported at the annual meeting of the International Society for Heart and Lung Transplantation.

In heart transplant patients with LV dysfunction, the relative risk of cardiac death was 2.65-fold higher than the risk in those without LV dysfunction. The risk of noncardiac death in patients with impaired LV function was almost twice that of controls, due mostly to renal dysfunction that was secondary to heart failure, said Dr. Lietz, a cardiologist at the University of Minnesota in Minneapolis.

The study used data from the U.S. Scientific Registry of Transplant Recipients for heart transplants done during 1990–2003 on 25,719 patients. Exclusion of patients who were lost to follow-up or did not survive for at least 1 year left a study group of 18,854 patients, who were followed until they died, until their transplanted hearts failed, or through May 2004.

Aside from the patients who developed heart failure, LV function stayed fairly constant through follow-up, which lasted up to 13 years. The average LV ejection fraction (EF) for the entire group was about 59% after 1 year of follow-up and 57% after 13 years. Development of heart failure occurred at a fairly constant rate, occurring in about 2% of patients a year.

The two most powerful risk factors for LV dysfunction were coronary vasculopathy and renal dysfunction; each more than doubled the risk. Other significant risk factors were African American race, which raised the risk by 89%; need for retransplantation (67%); and acute rejection (65%).

The prevalence of vasculopathy was 34% in patients with an EF of more than 40%. Among those with lower EFs, the prevalence was 57%.

The increased risk of death associated with LV dysfunction was proportional to the severity of the dysfunction. Patients with EFs of 45%–55% had a 25% higher risk of death than did patients with EFs of more than 65%. The mortality risk was 57% higher in patients with EFs of 35%–45%, and was 2.6-fold higher in those with EFs of less than 35%.

PHILADELPHIA — Left ventricular dysfunction is a powerful predictor of poor outcome in patients who have received a heart transplant.

During 13 years of follow-up of almost 19,000 patients with transplanted hearts, the cumulative rate of left ventricular (LV) dysfunction (ejection fraction of 40% or less) was 23%, Katherine Lietz, M.D., reported at the annual meeting of the International Society for Heart and Lung Transplantation.

In heart transplant patients with LV dysfunction, the relative risk of cardiac death was 2.65-fold higher than the risk in those without LV dysfunction. The risk of noncardiac death in patients with impaired LV function was almost twice that of controls, due mostly to renal dysfunction that was secondary to heart failure, said Dr. Lietz, a cardiologist at the University of Minnesota in Minneapolis.

The study used data from the U.S. Scientific Registry of Transplant Recipients for heart transplants done during 1990–2003 on 25,719 patients. Exclusion of patients who were lost to follow-up or did not survive for at least 1 year left a study group of 18,854 patients, who were followed until they died, until their transplanted hearts failed, or through May 2004.

Aside from the patients who developed heart failure, LV function stayed fairly constant through follow-up, which lasted up to 13 years. The average LV ejection fraction (EF) for the entire group was about 59% after 1 year of follow-up and 57% after 13 years. Development of heart failure occurred at a fairly constant rate, occurring in about 2% of patients a year.

The two most powerful risk factors for LV dysfunction were coronary vasculopathy and renal dysfunction; each more than doubled the risk. Other significant risk factors were African American race, which raised the risk by 89%; need for retransplantation (67%); and acute rejection (65%).

The prevalence of vasculopathy was 34% in patients with an EF of more than 40%. Among those with lower EFs, the prevalence was 57%.

The increased risk of death associated with LV dysfunction was proportional to the severity of the dysfunction. Patients with EFs of 45%–55% had a 25% higher risk of death than did patients with EFs of more than 65%. The mortality risk was 57% higher in patients with EFs of 35%–45%, and was 2.6-fold higher in those with EFs of less than 35%.

PHILADELPHIA — Patients with mild or moderate coronary artery disease can safely undergo lung transplantation, according to a review of more than 200 patients at Washington University in St. Louis.

In this series, the incidence of perioperative death, long-term death, and long-term cardiac morbidity was similar between patients with mild or moderate CAD and those with no detectable disease, Cliff K.C. Choong, M.B., said at the annual meeting of the International Society for Heart and Lung Transplantation.

Most U.S. transplant centers do lung transplantation in patients with mild or moderate CAD, but this is the first report to document that this approach is okay, said Dr. Choong, who is now a cardiothoracic surgeon at Papworth Hospital, Cambridge, England.

Patients with severe CAD—at least one coronary artery stenosis of 50% or greater—would require revascularization before undergoing lung transplantation, Dr. Choong told this newspaper. This should only be an option if the CAD is discrete, if left ventricular function is normal, and if the coronary anatomy is suitable for revascularization. If feasible, it should be done during the lung transplant surgery, preferably with stents, because coronary artery bypass surgery during lung transplantation requires more complex surgery that takes substantially more time, he said.

The study reviewed all 268 adults who had lung transplantation surgery at Washington University during June 1998-June 2003. Patients were excluded if they had sever CAD (3) or if they didn't undergo coronary angiography before transplant (55).

At the university, lung transplant candidates undergo routine coronary angiography if they are at least 45 years old, regardless any history or symptoms of CAD. Younger patients have angiography only if they also have risk factors for CAD.

Of the 210 patients, 177 had no evidence of CAD, 16 patients had mild CAD (coronary stenosis of less than 30%), and 17 had moderate CAD (stenosis of 30%–50%).

Thirteen of the 177 patients with no CAD died while they were hospitalized for their transplantation, compared with none of the 33 patients with CAD, he said. During an average follow-up of about 2 years, mortality was 23% in the patients without CAD and 27% in those with CAD.

PHILADELPHIA — Patients with mild or moderate coronary artery disease can safely undergo lung transplantation, according to a review of more than 200 patients at Washington University in St. Louis.

In this series, the incidence of perioperative death, long-term death, and long-term cardiac morbidity was similar between patients with mild or moderate CAD and those with no detectable disease, Cliff K.C. Choong, M.B., said at the annual meeting of the International Society for Heart and Lung Transplantation.

Most U.S. transplant centers do lung transplantation in patients with mild or moderate CAD, but this is the first report to document that this approach is okay, said Dr. Choong, who is now a cardiothoracic surgeon at Papworth Hospital, Cambridge, England.

Patients with severe CAD—at least one coronary artery stenosis of 50% or greater—would require revascularization before undergoing lung transplantation, Dr. Choong told this newspaper. This should only be an option if the CAD is discrete, if left ventricular function is normal, and if the coronary anatomy is suitable for revascularization. If feasible, it should be done during the lung transplant surgery, preferably with stents, because coronary artery bypass surgery during lung transplantation requires more complex surgery that takes substantially more time, he said.

The study reviewed all 268 adults who had lung transplantation surgery at Washington University during June 1998-June 2003. Patients were excluded if they had sever CAD (3) or if they didn't undergo coronary angiography before transplant (55).

At the university, lung transplant candidates undergo routine coronary angiography if they are at least 45 years old, regardless any history or symptoms of CAD. Younger patients have angiography only if they also have risk factors for CAD.

Of the 210 patients, 177 had no evidence of CAD, 16 patients had mild CAD (coronary stenosis of less than 30%), and 17 had moderate CAD (stenosis of 30%–50%).

Thirteen of the 177 patients with no CAD died while they were hospitalized for their transplantation, compared with none of the 33 patients with CAD, he said. During an average follow-up of about 2 years, mortality was 23% in the patients without CAD and 27% in those with CAD.

PHILADELPHIA — Patients with mild or moderate coronary artery disease can safely undergo lung transplantation, according to a review of more than 200 patients at Washington University in St. Louis.

In this series, the incidence of perioperative death, long-term death, and long-term cardiac morbidity was similar between patients with mild or moderate CAD and those with no detectable disease, Cliff K.C. Choong, M.B., said at the annual meeting of the International Society for Heart and Lung Transplantation.

Most U.S. transplant centers do lung transplantation in patients with mild or moderate CAD, but this is the first report to document that this approach is okay, said Dr. Choong, who is now a cardiothoracic surgeon at Papworth Hospital, Cambridge, England.

Patients with severe CAD—at least one coronary artery stenosis of 50% or greater—would require revascularization before undergoing lung transplantation, Dr. Choong told this newspaper. This should only be an option if the CAD is discrete, if left ventricular function is normal, and if the coronary anatomy is suitable for revascularization. If feasible, it should be done during the lung transplant surgery, preferably with stents, because coronary artery bypass surgery during lung transplantation requires more complex surgery that takes substantially more time, he said.

The study reviewed all 268 adults who had lung transplantation surgery at Washington University during June 1998-June 2003. Patients were excluded if they had sever CAD (3) or if they didn't undergo coronary angiography before transplant (55).

At the university, lung transplant candidates undergo routine coronary angiography if they are at least 45 years old, regardless any history or symptoms of CAD. Younger patients have angiography only if they also have risk factors for CAD.

Of the 210 patients, 177 had no evidence of CAD, 16 patients had mild CAD (coronary stenosis of less than 30%), and 17 had moderate CAD (stenosis of 30%–50%).

Thirteen of the 177 patients with no CAD died while they were hospitalized for their transplantation, compared with none of the 33 patients with CAD, he said. During an average follow-up of about 2 years, mortality was 23% in the patients without CAD and 27% in those with CAD.

PHILADELPHIA — Heart and lung transplants are increasingly for older patients, on the basis of data collected in the International Heart and Lung Transplant Registry.

During 1999–2003, the most recent period with available registry data, patients aged at least 60 years made up about 25% of all patients who underwent heart transplants, up from about 15% a decade earlier, Marshall I. Hertz, M.D., reported at the annual meeting of the International Society for Heart and Lung Transplantation.

The rise in transplants in elderly patients was matched by an almost identical drop in patients aged 40–49 years, from about 23% of the total in 1989–1993 to about 15% in 1999–2003. The percentage of transplants done in patients aged 50–59, held steady at about 33% of the total, reported Dr. Hertz, professor of medicine at the University of Minnesota, Minneapolis, and medical director of the transplant registry.

A similar trend existed for lung transplantations. During 1997–2004, about 15% of all lung transplants were in patients aged 60–64, up from about 8% of the total in 1985–1996. Another clear increase was in patients aged 65 and older, rising from about 2% of all lung transplants in 1985–1996 to about 4% in the most recent period. In contrast, the percentage of transplants fell in all adult patients younger than 55. The biggest drop was in patients aged 45–49, where the figure sank from about 15% of all transplants in the earlier years to about 10% of all lung transplants in 1997–2003.

These trends reflect the “greater comfort” physicians have in transplanting older patients, Dr. Hertz told this newspaper. The rise in heart transplants in older patients has also been triggered by an increased prevalence of heart failure. But the registry data also confirm that survival following transplantation of either a heart or a lung is worse in older patients, Dr. Hertz said.

PHILADELPHIA — Heart and lung transplants are increasingly for older patients, on the basis of data collected in the International Heart and Lung Transplant Registry.

During 1999–2003, the most recent period with available registry data, patients aged at least 60 years made up about 25% of all patients who underwent heart transplants, up from about 15% a decade earlier, Marshall I. Hertz, M.D., reported at the annual meeting of the International Society for Heart and Lung Transplantation.

The rise in transplants in elderly patients was matched by an almost identical drop in patients aged 40–49 years, from about 23% of the total in 1989–1993 to about 15% in 1999–2003. The percentage of transplants done in patients aged 50–59, held steady at about 33% of the total, reported Dr. Hertz, professor of medicine at the University of Minnesota, Minneapolis, and medical director of the transplant registry.

A similar trend existed for lung transplantations. During 1997–2004, about 15% of all lung transplants were in patients aged 60–64, up from about 8% of the total in 1985–1996. Another clear increase was in patients aged 65 and older, rising from about 2% of all lung transplants in 1985–1996 to about 4% in the most recent period. In contrast, the percentage of transplants fell in all adult patients younger than 55. The biggest drop was in patients aged 45–49, where the figure sank from about 15% of all transplants in the earlier years to about 10% of all lung transplants in 1997–2003.

These trends reflect the “greater comfort” physicians have in transplanting older patients, Dr. Hertz told this newspaper. The rise in heart transplants in older patients has also been triggered by an increased prevalence of heart failure. But the registry data also confirm that survival following transplantation of either a heart or a lung is worse in older patients, Dr. Hertz said.

PHILADELPHIA — Heart and lung transplants are increasingly for older patients, on the basis of data collected in the International Heart and Lung Transplant Registry.

During 1999–2003, the most recent period with available registry data, patients aged at least 60 years made up about 25% of all patients who underwent heart transplants, up from about 15% a decade earlier, Marshall I. Hertz, M.D., reported at the annual meeting of the International Society for Heart and Lung Transplantation.

The rise in transplants in elderly patients was matched by an almost identical drop in patients aged 40–49 years, from about 23% of the total in 1989–1993 to about 15% in 1999–2003. The percentage of transplants done in patients aged 50–59, held steady at about 33% of the total, reported Dr. Hertz, professor of medicine at the University of Minnesota, Minneapolis, and medical director of the transplant registry.

A similar trend existed for lung transplantations. During 1997–2004, about 15% of all lung transplants were in patients aged 60–64, up from about 8% of the total in 1985–1996. Another clear increase was in patients aged 65 and older, rising from about 2% of all lung transplants in 1985–1996 to about 4% in the most recent period. In contrast, the percentage of transplants fell in all adult patients younger than 55. The biggest drop was in patients aged 45–49, where the figure sank from about 15% of all transplants in the earlier years to about 10% of all lung transplants in 1997–2003.

These trends reflect the “greater comfort” physicians have in transplanting older patients, Dr. Hertz told this newspaper. The rise in heart transplants in older patients has also been triggered by an increased prevalence of heart failure. But the registry data also confirm that survival following transplantation of either a heart or a lung is worse in older patients, Dr. Hertz said.

GAITHERSBURG — By a vote of 9-4, the Food and Drug Administration's Circulatory Systems Devices Panel decided not to recommend the CorCap cardiac support device for approval, citing concerns about missing end point data and uncertainty about the device's effectiveness.

The cardiac support device (CSD), made by Acorn Cardiovascular Inc., is a polyester mesh wrap that is implanted around both ventricles of the heart to stop cardiac enlargement caused by heart failure. It is intended to improve the heart's function by providing beneficial changes in cardiac structure and a decrease in the need for major cardiac procedures. Acorn also claimed that patient quality of life would be improved significantly.

Acorn presented data from a prospective, randomized, controlled trial of 300 heart failure patients. The 193 patients in whom mitral valve repair or replacement was indicated were randomized to undergo surgery with (91) or without (102) CSD placement. The remaining 107 patients were randomized to undergo a thoracotomy for placement of the Acorn device and continued medical therapy (57) medical therapy alone (50).

The primary end point was a composite of survival, the need for additional major cardiac procedures, and change in New York Heart Association (NYHA) classification. Of patients treated with CorCap, 38% improved, compared with 27% of control patients. Additionally, 25% of CorCap recipients remained the same, compared with 28% of patients in the control group. A total of 37% of CorCap recipients were reported to have worsened, compared with 45% of control group patients.

The FDA questioned both the company's statistical analysis and CorCap's clinical efficacy. FDA statistician Laura Thompson, Ph.D., raised concerns that more than a third of patients were missing primary end point measurements, and more than half were missing appropriate baseline NYHA class data. FDA consultant Ileana L. Piña, M.D., professor of medicine at Case Western Reserve University, Cleveland, also highlighted the missing data and pointed out that the only component of the primary end point that was significant was that of major cardiac procedures; there were no significant differences between the CorCap group and the controls in mortality or rehospitalization.

Citing these concerns, the committee voted against approving the device. The FDA usually follows the recommendations of its advisory panels, but is under no statutory obligation to do so.

GAITHERSBURG — By a vote of 9-4, the Food and Drug Administration's Circulatory Systems Devices Panel decided not to recommend the CorCap cardiac support device for approval, citing concerns about missing end point data and uncertainty about the device's effectiveness.

The cardiac support device (CSD), made by Acorn Cardiovascular Inc., is a polyester mesh wrap that is implanted around both ventricles of the heart to stop cardiac enlargement caused by heart failure. It is intended to improve the heart's function by providing beneficial changes in cardiac structure and a decrease in the need for major cardiac procedures. Acorn also claimed that patient quality of life would be improved significantly.

Acorn presented data from a prospective, randomized, controlled trial of 300 heart failure patients. The 193 patients in whom mitral valve repair or replacement was indicated were randomized to undergo surgery with (91) or without (102) CSD placement. The remaining 107 patients were randomized to undergo a thoracotomy for placement of the Acorn device and continued medical therapy (57) medical therapy alone (50).

The primary end point was a composite of survival, the need for additional major cardiac procedures, and change in New York Heart Association (NYHA) classification. Of patients treated with CorCap, 38% improved, compared with 27% of control patients. Additionally, 25% of CorCap recipients remained the same, compared with 28% of patients in the control group. A total of 37% of CorCap recipients were reported to have worsened, compared with 45% of control group patients.

The FDA questioned both the company's statistical analysis and CorCap's clinical efficacy. FDA statistician Laura Thompson, Ph.D., raised concerns that more than a third of patients were missing primary end point measurements, and more than half were missing appropriate baseline NYHA class data. FDA consultant Ileana L. Piña, M.D., professor of medicine at Case Western Reserve University, Cleveland, also highlighted the missing data and pointed out that the only component of the primary end point that was significant was that of major cardiac procedures; there were no significant differences between the CorCap group and the controls in mortality or rehospitalization.

Citing these concerns, the committee voted against approving the device. The FDA usually follows the recommendations of its advisory panels, but is under no statutory obligation to do so.

GAITHERSBURG — By a vote of 9-4, the Food and Drug Administration's Circulatory Systems Devices Panel decided not to recommend the CorCap cardiac support device for approval, citing concerns about missing end point data and uncertainty about the device's effectiveness.

The cardiac support device (CSD), made by Acorn Cardiovascular Inc., is a polyester mesh wrap that is implanted around both ventricles of the heart to stop cardiac enlargement caused by heart failure. It is intended to improve the heart's function by providing beneficial changes in cardiac structure and a decrease in the need for major cardiac procedures. Acorn also claimed that patient quality of life would be improved significantly.

Acorn presented data from a prospective, randomized, controlled trial of 300 heart failure patients. The 193 patients in whom mitral valve repair or replacement was indicated were randomized to undergo surgery with (91) or without (102) CSD placement. The remaining 107 patients were randomized to undergo a thoracotomy for placement of the Acorn device and continued medical therapy (57) medical therapy alone (50).

The primary end point was a composite of survival, the need for additional major cardiac procedures, and change in New York Heart Association (NYHA) classification. Of patients treated with CorCap, 38% improved, compared with 27% of control patients. Additionally, 25% of CorCap recipients remained the same, compared with 28% of patients in the control group. A total of 37% of CorCap recipients were reported to have worsened, compared with 45% of control group patients.

The FDA questioned both the company's statistical analysis and CorCap's clinical efficacy. FDA statistician Laura Thompson, Ph.D., raised concerns that more than a third of patients were missing primary end point measurements, and more than half were missing appropriate baseline NYHA class data. FDA consultant Ileana L. Piña, M.D., professor of medicine at Case Western Reserve University, Cleveland, also highlighted the missing data and pointed out that the only component of the primary end point that was significant was that of major cardiac procedures; there were no significant differences between the CorCap group and the controls in mortality or rehospitalization.

Citing these concerns, the committee voted against approving the device. The FDA usually follows the recommendations of its advisory panels, but is under no statutory obligation to do so.