(Circulation. 1996;94:1-5.)
© 1996 American Heart Association, Inc.
Articles |
Meeting Highlights
American College of Cardiology 45th Annual Scientific Session, Orlando, Florida, March 24 to 27, 1996
St Luke's Episcopal Hospital, Texas Heart Institute, Baylor College of Medicine, University of Texas Health Science Center at Houston.
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GUSTO IIb |
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 Top GUSTO IIb HEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Frans Van de Werf, from the University Hospital Gasthuisberg in Leuven, Belgium, Drs Robert Califf and Christopher Granger from Duke University, Durham, NC, and Dr Eric Topol, from the Cleveland (Ohio) Clinic, presented the results of the GUSTO IIb study, a large, international, multicenter trial of heparin versus hirudin in patients with acute MI and unstable angina. A total of 12 142 qualifying patients (onset of symptoms within 12 hours and ischemic ECG changes) were stratified into two groups on the basis of whether or not ST-segment elevation was present and randomized to receive heparin or hirudin. The primary end point of the study was the 30-day incidence of death and MI. Because of prior experience with a high level of bleeding complications in GUSTO IIa, the doses of study drug (both heparin and hirudin) used in GUSTO IIb were significantly reduced from GUSTO IIa. Patients treated with hirudin were noted to require fewer adjustments to maintain therapeutic levels (a mean of two adjustments versus four with heparin), and there were more hirudin patients who did not require any dose adjustments (28.5% versus 5.4% with heparin). In the ST-segment elevation group (n=4131), there was marked benefit of hirudin at 24 hours in the incidence of death and MI but no significant differences between the hirudin and heparin groups in terms of severe bleeding events (1.1% with hirudin, 1.5% with heparin), stroke (1.3% with hirudin, 0.8% with heparin), death at 30 days (5.9% versus 6.3%), and reinfarction at 30 days (5.0% versus 6.0%). In the overall population, there was significant benefit with hirudin in death or MI at 24 hours (1.3% with hirudin and 2.1% with heparin, a 37% relative decrease; P<.001). However, with time, the relative benefits of hirudin declined. By 48 hours, the incidence of death or MI was 2.3% in the hirudin group and 3.1% in the heparin group (a 25% relative decrease; P=.006). By 30 days, in all patients, the incidence of death or MI was 8.9% in the hirudin group and 9.8% in the heparin group (a 10.2% relative decrease; P=.058); in patients with ST-segment elevation, the incidence was 9.9% in the hirudin group and 11.3% in the heparin group (a 12.8% relative decrease; P=.13); and in patients without ST-segment elevation, the incidence was 8.3% in the hirudin group and 9.1% in the heparin group (an 8.5% relative decrease; P=.22). At 30 days, there were significantly fewer reinfarctions with hirudin. There appeared to be a slight excess of bleeding events with hirudin (28% versus 25% with heparin). The total incidence of stroke was low in both groups (0.9% with hirudin, 0.8% with heparin).
The presenters concluded that hirudin shows considerable benefit at 24 hours, is modestly effective in preventing reinfarction at 30 days, and provides a more reliable activated partial thromboplastin time response than heparin. However, the survival benefits are minimal at 30 days and come at the expense of an increase in bleeding events and a 1/1000 risk of intracranial hemorrhage.
Dr Stephen Ellis, from the Cleveland (Ohio) Clinic, and Dr Amadeo Betriu, from Barcelona, Spain, presented the results of a substudy of GUSTO IIb that further randomized a total of 1137 patients eligible for thrombolytic therapy from the ST-segment elevation group to receive either direct angioplasty or thrombolytic therapy with an accelerated regimen of TPA. At 30 days, there was a trend in the PTCA group toward a lower incidence of death (6% versus 7% with TPA), reinfarction (4% versus 6% with TPA), disabling stroke (0.2% versus 0.8% with TPA), or the combined end point (10% versus 13% with TPA; P=.06). The difference favoring PTCA in the combined end point was present in both high-risk patients (13.2% versus 16.4% with TPA) and low-risk patients (5.6% versus 8.1% with TPA). Drs Ellis and Betriu concluded that the results of the study show a strong trend in favor of angioplasty, with 
30 additional events prevented per 1000 patients when direct angioplasty was used. These differences, however, do not appear as dramatic as might have been predicted from prior studies.
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HERO |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Harvey White, from Auckland, New Zealand, presented the results of the HERO trial, an international multicenter study that compared two doses of the direct-acting thrombin inhibitor Hirulog with heparin in patients with acute MI treated with streptokinase. The primary end point of the study was the presence of TIMI grade 3 flow in the infarct-related artery at 90 minutes after drug administration. To qualify for the study, patients had to have onset of symptoms within 12 hours before randomization and documented ST-segment elevation. Patients with cardiogenic shock were excluded. A total of 412 patients were randomized to heparin (n=140), low-dose Hirulog (n=136), or high-dose Hirulog (n=136). From the perspective of the primary study end point, TIMI grade 3 flow at 90 minutes was documented in 35% of the heparin patients, 45% of the low-dose Hirulog patients, and 50% of the high-dose Hirulog patients (P=.016). Of patients who presented within 6 hours of symptom onset, 40% achieved TIMI grade 3 flow at 90 minutes with heparin, 49% with low-dose Hirulog, and 56% with high-dose Hirulog. In patients treated early (<3 hours after symptom onset) with high-dose Hirulog, the incidence of TIMI grade 3 flow at 90 minutes was 73%. Subsequent repeat catheterization (2 to 4 days after treatment) demonstrated similar rates of TIMI 3 flow in the three treatment groups. There did appear to be less bleeding in the low-dose Hirulog group. Dr White concluded that Hirulog appears to be more effective than heparin in promoting early patency in MI patients treated with streptokinase, without any concomitant increase in the risk of bleeding.
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EPILOG |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Michael Lincoff, from the Cleveland Clinic in Ohio, presented the interim results of EPILOG, a randomized, placebo-controlled trial of the platelet glycoprotein IIb/IIIa antibody c7E3 Fab (ReoPro) in patients undergoing coronary intervention. A total of 69 US sites participated in the study, which randomized both low- and high-risk patients to receive either: (1) standard-dose heparin (100 U/kg bolus, titrated to ACTs >300 s) plus placebo; (2) standard-dose heparin plus ReoPro (0.25 mg/kg bolus, 0.125 µg·kg-1·min-1 up to 10 µg·kg-1·min-1, 0.125 µg·kg-1·min-1 infusion for 12 hours); or (3) low-dose heparin (70 U/kg, ACTs >200 s) plus ReoPro. The primary end point of the study was the 30-day combined incidence of death, MI, and urgent revascularization. The trial originally was designed to include 4800 patients but was terminated prematurely because an interim analysis of the first 1500 patients demonstrated positive effects of ReoPro that exceeded prespecified criteria for discontinuing the trial. Dr Lincoff presented the results of these first 1500 patients; complete data will be available at a later date on the 2792 patients who had been enrolled at the time the trial was halted. At 30 days, the combined incidence of death and MI (creatine kinase elevation at least 3x baseline) was 8.1% in the standard heparin plus placebo group, 3.8% in the standard heparin plus ReoPro group, and 2.6% in the low heparin plus ReoPro group. This relative decrease of 68% in adverse events was almost twice the benefit shown in the prior EPIC study, which included only high-risk patients. Moreover, the relatively high incidence of bleeding in the EPIC study (7% with placebo, 14% with bolus/infusion ReoPro) was markedly reduced in EPILOG (3.1% with standard heparin plus placebo versus 1.4% with low heparin plus ReoPro). The clinical benefits of ReoPro were noted in both high- and low-risk strata. Dr Lincoff concluded that there is significant clinical benefit associated with potent IIb/IIIa blockade, regardless of risk stratum. The previously noted high incidence of bleeding can be reduced with more judicious heparin administration, resulting in enhanced overall clinical efficacy of this form of therapy compared with prior studies.
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CAPTURE |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Maarten Simoons, from the Thorax Center, Erasmus University, Rotterdam, Netherlands, presented the interim results of the CAPTURE study. In CAPTURE, patients with refractory unstable angina (receiving heparin, aspirin, and nitrates) with recurrent pain were randomized to receive 18 to 24 hours of pretreatment with either placebo or c7E3 Fab (ReoPro, 0.25 mg/kg bolus, 10 µg·kg-1·min-1 infusion) before undergoing PTCA. The primary end point of the study was the 30-day combined incidence of death, MI, and urgent intervention. The trial originally was designed to include 1400 patients but was stopped prematurely after an interim analysis of 1050 patients showed significant clinical benefit. The primary combined end point was reduced from 16.4% in the placebo group to 10.8% in the ReoPro group; death and MI similarly were reduced from 10.3% to 5.1%. All of the individual events that composed the primary end point were also reduced (death, from 1.5% to 1.0%; MI, from 9.4% to 4.4%; and urgent intervention, from 10.2% to 6.9%). ReoPro was associated with an increase in bleeding complications (any bleeding, from 5.4% to 9.7%; major bleeding, from 1.7% to 2.9%), but bleeding complications were much lower than in the prior EPIC study.
The final results for all 1266 patients who were enrolled in the study will be presented at the Congress of the European Society of Cardiology in Birmingham, United Kingdom, in August 1996.
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RESTORE |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Spencer King from Emory University in Atlanta, Ga, presented the results of RESTORE, a trial of the arginine-glycine-aspartic acid (RGD)-mimetic platelet glycoprotein IIb/IIIa blocking drug Tirofiban in patients with acute coronary syndromes (unstable angina or acute MI) undergoing PTCA or directional coronary atherectomy (DCA) within 72 hours of presentation. As originally designed, 2100 patients were to be randomized to a bolus and 36-hour infusion of placebo or Tirofiban after guidewire passage past the target lesion. Subsequent clinical follow-up was to be obtained at 30 days and at 6 months; a subset of 500 patients was also to undergo 6-month follow-up angiography. The primary end point of the study was the composite occurrence of death, nonfatal MI, repeat revascularization, repeat angiography, or stent placement at 30 days.
Recruitment took place between January 1995 and November 1995. Approximately 64% of patients had unstable angina (ECG changes or visible thrombus on angiogram); 29% were enrolled after acute MI, and 7% were undergoing primary PTCA of an acute MI. At 48 hours, Tirofiban therapy was associated with a significant (P<.005) decrease in the incidence of the composite end point (from 8.7% to 5.4%, a 38% relative decrease). By 7 days, there was still significant (P=.027) improvement in the primary end point with Tirofiban (from 10.1% to 7.4%, a 27% relative decrease). However, by 30 days, there was only a nonsignificant trend (P=.16) in the incidence of the primary end point favoring Tirofiban (from 12.2% to 10.3%, a 16% relative decrease). The benefit at 30 days was more prominent in the primary PTCA for acute MI group (from 11.6% to 7.7%) than in the unstable angina group (from 12.6% to 10.8%) or the acute MI group (from 11.3% to 9.7%). Tirofiban was associated with no significant increase in major bleeding events, including transfusions of >2 U (from 4.2% to 5.4%; P=.225). Dr King concluded that Tirofiban therapy acutely reduces procedural complications but that the protective effects diminish over time, so that by 30 days, there appears to be no significant benefit.
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Ibopamine in Heart Failure |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr John Hampton, from University Hospital in Nottingham, United Kingdom, presented the results of PRIME-2, a prospective, placebo-controlled, randomized study of Ibopamine (an oral drug stimulating dopaminergic type 1 and 2 receptors, with primary effects of peripheral and renal dilation and little inotropic or proarrhythmic effects) in patients with heart failure. The previous PRIME-1 study had demonstrated that Ibopamine was equivalent to captopril in reducing heart failure symptoms. PRIME-2 extended this to compare the effect of Ibopamine (100 mg TID) with placebo when added to optimal therapy, including ACE inhibitors. A total of 165 clinical centers in Europe participated in the study, which was originally designed to include
2200 patients with advanced heart failure. The trial was stopped prematurely (after 1906 patients had been enrolled) because of an adverse effect of the study drug.
Approximately 60% of patients had heart failure of ischemic origin, 30% had nonischemic dilated cardiomyopathy, and 10% had cardiomyopathy of other origins (eg, valvular). Eighty percent of enrolled patients were treated with ACE inhibitors. Interim analysis showed 232 deaths in the 953 Ibopamine patients compared with 193 deaths in the 953 placebo patients, an adverse effect that was significant at a level of P=.017. Dr Hampton concluded that the addition of Ibopamine to standard therapy in patients with congestive heart failure does not convey any clinical benefit; rather, it appears to be associated with excess mortality.
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Digitalis in Heart Failure |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Richard Gorlin, from Mount Sinai Medical Center in New York, NY, and Dr Rekha Garg, from the NHLBI at the NIH in Bethesda, Md, presented the results of a large, prospective, multicenter trial of digitalis in heart failure. A total of 7788 patients with symptoms of heart failure and an ejection fraction
45% were randomized to digitalis (0.125 to 0.5 mg/d) or placebo (an ancillary study looked at 1000 patients with ejection fractions of >45%). Patients with an ejection fraction 45% were recommended to be taking diuretic and ACE inhibitor therapy before entry; the mean follow-up of patients in the study was 37 months (range, 28 to 58 months). From the standpoint of all-cause mortality, digitalis therapy had no effect; event-free survival was identical between digitalis and placebo in both the low and normal ejection fraction subgroups. The digitalis group did appear to have fewer deaths due to worsening heart failure but more deaths due to other causes, including arrhythmias and MI. The digitalis group, particularly the normal ejection fraction subgroup, had fewer repeat hospitalizations with worsening heart failure and no significant increase in the incidence of nonfatal MI or unstable angina. The authors concluded that although digitalis does not convey any mortality benefit to heart failure patients treated with diuretics and ACE inhibitors, its use is associated with fewer hospital admissions associated with congestive heart failure. |
Antioxidant Therapy and Coronary Artery Disease |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Nigel Stephens, from Cambridge, United Kingdom, presented the results of the recently published1 CHAOS trial. In this study, 2002 patients with angiographically proven symptomatic coronary artery disease were randomized to receive either placebo (n=967) or one of two daily doses of vitamin E: 400 IU (n=489) or 800 IU (n=546). Patients were followed up for a mean of 510 days (range, 3 to 981 days). The primary end point of the study was the combined rate of cardiovascular death and nonfatal MI. Vitamin E therapy was associated with a significant decrease in the primary end point: 41 events in the vitamin E group and 64 events in the placebo group (OR=0.53; 95% CI, 0.34 to 0.83; P=.005). This difference was primarily due to a difference in the incidence of nonfatal MI: 14 events in the vitamin E group and 41 events in the placebo group (OR=0.23; 95% CI, 0.11 to 0.47; P<.001). The incidence of death was not significantly different between groups (27 events in the vitamin E group and 23 events in the placebo group; P=NS). The investigators concluded that vitamin E therapy significantly reduces the incidence of nonfatal MI in patients with angiographically proven symptomatic coronary artery disease. They recommended that patients with symptomatic coronary artery disease receive 800 IU of vitamin E per day.
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Cholesterol Reduction in Patients With a History of MI |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Drs Eugene Braunwald, Marc Pfeffer, and Frank Sacks, from Brigham and Women's Hospital and Harvard Medical School in Boston, Mass, presented the results of the CARE trial. The CARE trial, involving 80 clinical centers in the United States and Canada, enrolled 4159 patients with a history of MI in the past 2 years in a 5-year randomized, double-blind trial of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor pravastatin. In contrast to prior studies that focused on patients with significantly elevated cholesterol levels, the average total cholesterol level in the CARE trial was 209±17 mg/dL, the average LDL was 139±15 mg/dL, and the average HDL was 39±9 mg/dL. Preliminary analyses of the data showed that on average, the pravastatin group had a 20% reduction in total cholesterol, a 28% reduction in LDL, and an 8% increase in HDL, along with a 14% reduction in triglycerides. The pravastatin group had significant reductions in the combined incidence of fatal coronary heart disease and nonfatal MI (211 patients versus 273 with placebo, a 24% relative decrease; P=.003) and MI alone (156 patients versus 206 with placebo, a 25% relative decrease; P=.007), as well as a significantly lower likelihood of requiring CABG surgery or coronary angioplasty (293 patients versus 390 with placebo, a 26% relative decrease; P=.001). This benefit was present among diabetics and nondiabetics, smokers and nonsmokers, patients >60 years of age, and women. There appeared to be no additional benefit to reducing LDL levels to values <125 mg/dL. There was no significant increase in the incidence of noncardiac mortality, but there was a trend, which did not achieve statistical significance, toward lower all-cause mortality in the pravastatin group. Drs Braunwald, Pfeffer, and Sacks concluded that there are potential significant benefits to lipid-reduction therapy in patients without a markedly elevated serum cholesterol level.
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Long-term Anticoagulation After MI |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Valentin Fuster, from Mount Sinai Medical Center in New York, NY, presented the results of CARS, a multicenter study that compared the long-term safety and efficacy of aspirin alone (160 mg/d) versus aspirin (80 mg/d) plus a fixed low dose of Coumadin (1 or 3 mg/d) started within 3 weeks after acute MI and continued for 4 years. The primary end point of the study was the combined incidence of cardiovascular death, nonfatal MI, and stroke. The study involved 272 clinical sites in the United States and Canada. After 8803 patients had been enrolled, the study was terminated prematurely on February 15, 1996, because an interim analysis showed no significant benefit. There was no significant difference in mortality between groups (2.7% with aspirin alone, 3.0% with aspirin plus 1 mg Coumadin, and 3.1% with aspirin plus 3 mg Coumadin); the incidence of ischemic stroke was elevated with Coumadin (1.5% with aspirin plus 1 mg Coumadin, 1.1% with aspirin plus 3 mg Coumadin) compared with aspirin alone (0.5%). Dr Fuster speculated that the increase in the incidence of ischemic stroke in the combined therapy groups is perhaps related to the low dose of aspirin used in combination with Coumadin. The overall incidence of major hemorrhage was low (0.6%).
Some interesting trends were noted in the management strategy in the United States versus that in Canada. In the United States, 44% of MI patients were treated with thrombolytic therapy versus 48% in Canada; 57% of these in the United States underwent additional PTCA versus 2% in Canada. In the United States, 56% of CARS patients underwent PTCA versus 3% in Canada. Interestingly, 84% of the US CARS patients underwent cardiac catheterization versus 8% in Canada. Analyses of outcome as a function of treatment strategy are still pending. Dr Fuster concluded that a fixed dose of Coumadin (1 mg or 3 mg) plus low-dose aspirin (80 mg) is no more effective than aspirin alone (160 mg).
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Amiodarone in Post-MI Patients |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Stuart Connolly and Dr John Cairns, from McMaster University in Ontario, Canada, presented the results of CAMIAT. This study was a randomized trial that compared amiodarone (mean dose at 12 months of 200 mg/d) with placebo in 1202 patients enrolled within 6 to 45 days after MI. To qualify, patients had to have a Holter ECG that showed either >10 ventricular premature depolarizations per hour or nonsustained ventricular tachycardia. Patients were followed up for 1 to 2 years. Enrollment took place between June 1990 and November 1994; follow-up was completed in November 1995. The primary end point of the study was the combined end point of arrhythmic death or resuscitated VF. Secondary end points included arrhythmic death alone, cardiac death, and all-cause mortality. Holter monitoring was performed at 4 and 8 months and in selected patients was repeated at 12 and 16 months. Two-year outcome data were presented. Amiodarone treatment resulted in a significant reduction in the primary end point at 2 years, both from a treatment-only standpoint (6.0% with placebo and 3.3% with amiodarone, a 48.5% relative reduction; P=.016) and by intention to treat (6.9% with placebo and 4.5% with amiodarone, a 38.2% relative reduction). Amiodarone was 83% effective in suppressing ventricular premature contractions at 4 months and 86% effective at 8 months compared with 35% effectiveness at 4 months and 38% at 8 months with placebo. Outcomes were found to be significantly better in patients in whom ventricular premature contractions were suppressed. Amiodarone therapy was associated with a larger number of side effects. By 2 years, 42.3% of amiodarone patients had discontinued therapy compared with 28.5% of placebo patients. Adverse events leading to medication discontinuation were experienced by 28% of amiodarone patients and 12% of placebo patients, including hypothyroidism (3.5% amiodarone, 0.2% placebo) and pulmonary infiltrates (3.0% amiodarone, 1.2% placebo). The investigators concluded that amiodarone is effective in reducing arrhythmic death and resuscitated VF in post-MI patients.
Prof John Camm from St George's Hospital Medical School in London, United Kingdom, and Prof Peter Schwartz, from the Department of Cardiology at the University of Pavia, Italy, presented the results of the EMIAT Trial. This large study began in November 1990 and enrolled 1486 patients at 75 clinical centers in 15 European countries. Qualifying patients, who were between day 5 and day 21 after MI and who had a radionuclide ejection fraction <40%, were randomized to treatment with amiodarone (800 mg/d for 14 days followed by 400 mg/d for the remainder of the first 4 months and 200 mg/d for the remainder of the study; n=743) or placebo (n=743) and followed up for a mean of 20 months. The primary end point of the trial, total mortality, was not significantly reduced with amiodarone. However, secondary end points of arrhythmic death and the combination of arrhythmic death and resuscitated cardiac arrest were significantly lower (a relative decrease of 35%) in the amiodarone-treated group. Interestingly, 40% of all deaths occurred in patients without any evidence of arrhythmia on baseline Holter examination. A larger number of patients receiving amiodarone had to discontinue therapy because of changes in biochemical thyroid tests (168 versus 49 with placebo). However, 86% of the patients in the amiodarone group whose therapy was stopped for this reason had no accompanying clinical signs of thyroid dysfunction. There were 3 drug-related deaths due to pulmonary toxicity in the amiodarone group.
The investigators concluded that although amiodarone cannot be routinely recommended for all post-MI patients, it may be of significant benefit in patients who are at high risk for arrhythmic death and who have impaired left ventricular function.
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NHLBI Post-CABG Study |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Michael Domanski, from the NHLBI in Bethesda, Md, Dr Donald Hunninghake, from the University of Minnesota (Minneapolis), and Dr Lucien Campeau, from the Montreal Heart Institute, presented the results of the NHLBI-sponsored Post-CABG Trial. This study was designed to answer two major questions regarding the optimal care of patients after CABG: (1) Is an aggressive cholesterol-lowering regimen better than a moderate one for improving outcome? and (2) Can a low-dose anticoagulant regimen that uses Coumadin affect outcome? A total of 1351 patients who had undergone bypass surgery 1 to 11 years previously were enrolled between March 1989 and August 1991. To qualify, patients had to have an LDL level <200 mg/dL and a triglyceride level <300 mg/dL; qualifying patients were randomized in a factorial design to (1) aggressive cholesterol reduction versus moderate cholesterol reduction or (2) low-dose Coumadin (target INR of 1.8 to 2.0) versus placebo. Target anticoagulation was frequently not achieved in the study; the mean INR in the Coumadin group was 1.4. Quantitative angiography was performed at baseline and after 4 to 5 years of follow-up (achieved in 88% of enrolled patients). The primary end point of the study was the percent of patients in each group that showed substantial angiographic progression (decrease in MLD by 0.6 mm or more).
With regard to the primary end point, 27.9% of patients treated with aggressive cholesterol reduction showed substantial progression compared with 38.8% in the moderate cholesterol reduction group, a 29% relative decrease (P<.0001). In contrast, 34.2% of the warfarin-treated group and 32.5% of the placebo-treated group showed substantial progression (P=NS). There was no interaction found between the two treatment modalities. There was a trend toward fewer clinical events in the aggressive cholesterol reduction group (12.6% versus 15.3%; P=.09), although the study was not powered to detect a difference in clinical events. The investigators concluded that aggressive cholesterol reduction is more effective than moderate cholesterol reduction in preventing disease progression in CABGs. Low-dose anticoagulation with Coumadin did not affect outcome.
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Optimal Atherectomy |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr Jeffrey Popma, from Washington Hospital Center in Washington, DC, presented the results of the OARS on behalf of the study investigators. The purpose of this study was to prospectively assess the long-term results of a more aggressive atherectomy strategy directed at achieving a residual diameter stenosis of <20%. A total of 199 patients were treated; 194 of the procedures were successful. Follow-up angiography with complete quantitative analysis was available in 165 patients. Preprocedure MLD was 1.22 mm, postprocedure MLD was 3.18 mm, and at 6 months, the MLD was 2.01 mm. The average gain was 1.97 mm, and the average loss was 1.18 mm. The average percent diameter stenosis was 63% at baseline, 7% after the procedure, and 37% at 6-month follow-up. The binary restenosis rate (>50% diameter stenosis at follow-up) was 29%. By multivariable modeling, for every 1-mm increase in postprocedure MLD, there was on average a 9% absolute reduction in the degree of stenosis at 6-month follow-up. For every 1% decrease in postprocedure percent diameter stenosis, there was a 0.31% decrease in the percent diameter stenosis at 6-month follow-up. This aggressive atherectomy strategy (postprocedure 7% residual diameter stenosis) was accomplished without an excess of procedural complications. Smaller vessels also tended to have lower residual percent diameter stenosis. Dr Popma concluded that the results of this study support the procedural safety of a more aggressive atherectomy strategy and that such a strategy appears to have a relatively low (29%) incidence of 6-month angiographic restenosis. The success of this strategy will be assessed further in BOAT, a randomized trial comparing optimal atherectomy and balloon angioplasty in 1000 patients with new lesions in native coronary arteries. Full angiographic data from BOAT will be presented at the 28th Congress of the European Society of Cardiology in August 1996; 1-year follow-up data should be available at the Annual Scientific Sessions of the American Heart Association in November 1996.
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SPAF III |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
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Dr John McAnulty, from the Oregon Health Science Center in Portland, presented the results of the third SPAF study. The object of SPAF III was threefold: (1) to assess the efficacy of warfarin therapy (INR 2-3) in patients with atrial fibrillation at high risk for embolic stroke while on aspirin (women aged >75 years, blood pressure >160 mm Hg, poor left ventricular function, prior thromboembolic events); (2) to compare the efficacy of standard-dose warfarin to combination therapy with low-dose warfarin plus aspirin (325 mg qd) in this population; and (3) to confirm the efficacy of aspirin in atrial fibrillation patients without high risk factors. Qualifying patients with atrial fibrillation were stratified into low- and high-risk groups. The primary end point of this study was a combined end point of ischemic stroke or systemic embolism. The high-risk arm of the study was terminated prematurely because of a lack of demonstrated efficacy of low-dose Coumadin/aspirin combination therapy.
A total of 1044 patients in the high-risk group were randomized to standard-dose warfarin (INR 2 to 3, achieved in 60% of follow-up measurements) or combination therapy with low-dose warfarin (INR 1.2 to 1.5, achieved in 55% of follow-up measurements with aspirin). The participation of the high-risk group in the trial was stopped when an interim analysis showed a significant excess of strokes (7.8% with combination therapy versus 2.6% with standard-dose Coumadin; P<.001) as well as a trend toward more cardiovascular events of MI (1.8% versus 0.9%) and death (7.0% versus 5.8%). Patients with prior thromboembolism were particularly at risk; their primary event rate was 11.9% with combination therapy versus 3.4% with standard-dose Coumadin.
Dr McAnulty concluded that standard-dose warfarin is effective in reducing the risk of stroke in high-risk patients below that seen with aspirin therapy alone in prior studies. Low-dose Coumadin in combination with aspirin is not an effective form of therapy in this population. The low-risk arm of SPAF III is continuing enrollment.
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Selected Abbreviations and Acronyms |
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Footnotes |
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Reprint requests to James J. Ferguson, MD, Cardiology Research, MC 1-191, Texas Heart Institute, PO Box 20345, Houston, TX 77225-0345.
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References |
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TopGUSTO IIbHEROEPILOGCAPTURERESTOREIbopamine in Heart FailureDigitalis in Heart FailureAntioxidant Therapy and Coronary...Cholesterol Reduction in...Long-term Anticoagulation After...Amiodarone in Post-MI PatientsNHLBI Post-CABG StudyOptimal AtherectomySPAF IIIReferences |
|---|
1. Stephens NG, Parsons A, Schofield PM, Kelly F, Cheeseman K, Mitchinson MJ, Brown MJ. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet. 1996;347:781-786.[Medline] [Order article via Infotrieve]
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|
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|
|
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|
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|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
R. H. Dave, S. L. Hale, and R. A. Kloner The Effect of Melatonin on Hemodynamics, Blood Flow, and Myocardial Infarct Size in a Rabbit Model of Ischemia-Reperfusion Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 1998; 3(2): 153 - 159. [Abstract] [PDF]
|
|
|
|
|
|
W. E. Cohn, H. C. Suen, R. M. Weintraub, and R. G. Johnson The "H" graft: An alternative approach for performing minimally invasive direct coronary artery bypass J. Thorac. Cardiovasc. Surg., January 1, 1998; 115(1): 148 - 151. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
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|
|
|
|
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|
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|
|
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