Joel Kupersmith

ACC/AHA Guidelines for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction: Executive Summary and Recommendations A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina)

The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines was formed to make recommendations regarding the diagnosis and treatment of patients with known or suspected cardiovascular disease. Coronary artery disease (CAD) is the leading cause of death in the United States. Unstable angina (UA) and the closely related condition non–ST-segment elevation myocardial infarction (NSTEMI) are very common manifestations of this disease. These life-threatening disorders are a major cause of emergency medical care and hospitalizations in the United States. In 1996, the National Center for Health Statistics reported 1 433 000 hospitalizations for UA or NSTEMI. In recognition of the importance of the management of this common entity and of the rapid advances in the management of this condition, the need to revise guidelines published by the Agency for Health Care Policy and Research (AHCPR) and the National Heart, Lung and Blood Institute in 1994 was evident. This Task Force therefore formed the current committee to develop guidelines for the management of UA and NSTEMI. The present guidelines supersede the 1994 guidelines. The customary ACC/AHA classifications I, II, and III summarize both the evidence and expert opinion and provide final recommendations for both patient evaluation and therapy: Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective . Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy. Class IIb: Usefulness/efficacy is less well established by evidence/opinion. Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful. The weight of the evidence was ranked highest (A) if the data …

ACC/AHA Guideline Update for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction—2002: Summary Article

The American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for the management of unstable angina and non–ST-segment elevation myocardial infarction (UA/NSTEMI) were published in September 2000.1 Since then, a number of clinical trials and observational studies have been published or presented that, when taken together, alter significantly the recommendations made in that document. Therefore, the ACC/AHA Committee on the Management of Patients With Unstable Angina, with the concurrence of the ACC/AHA Task Force on Practice Guidelines, revised these guidelines. These revisions were prepared in December 2001, reviewed and approved, and then published on the ACC World Wide Web site (www.acc.org) and AHA World Wide Web site (www.americanheart.org) on March 15, 2002. The present article describes these revisions and provides further updates in this rapidly moving field. Minor clarifications in the wording of three recommendations that now appear differently from those that were previously published on the ACC and AHA Web sites are noted in footnotes. The ACC/AHA classifications I, II, and III are used to summarize indications as follows: Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective. Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. IIa: Weight of evidence/opinion is in favor of usefulness/efficacy. IIb: Usefulness/efficacy is less well established by evidence/opinion. Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful. The weight of the evidence was ranked highest (A) if the data were derived from multiple randomized clinical trials that involved large numbers of patients and intermediate (B) if the data were derived from a limited number of randomized trials that involved small numbers of …

ACC/AHA guidelines for the management of patients with unstable angina and non–st-segment elevation myocardial infarction: A report of the american college of cardiology/ american heart association task force on practice guidelines (committee on the management of patients with unstable angina)

Preamble......971 I. Introduction ......972 A. Organization of Committee and Evidence Review......972 B. Purpose of These Guidelines......973 C. Overview of the Acute Coronary Syndrome......973 1. Definition of Terms......973 2. Pathogenesis of UA/NSTEMI ......974 3. Presentations of

ACC/AHA Guidelines for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction: Executive Summary and Recommendations

The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines was formed to make recommendations regarding the diagnosis and treatment of patients with known or suspected cardiovascular disease. Coronary artery disease (CAD) is the leading cause of death in the United States. Unstable angina (UA) and the closely related condition non–ST-segment elevation myocardial infarction (NSTEMI) are very common manifestations of this disease. These life-threatening disorders are a major cause of emergency medical care and hospitalizations in the United States. In 1996, the National Center for Health Statistics reported 1 433 000 hospitalizations for UA or NSTEMI. In recognition of the importance of the management of this common entity and of the rapid advances in the management of this condition, the need to revise guidelines published by the Agency for Health Care Policy and Research (AHCPR) and the National Heart, Lung and Blood Institute in 1994 was evident. This Task Force therefore formed the current committee to develop guidelines for the management of UA and NSTEMI. The present guidelines supersede the 1994 guidelines. The customary ACC/AHA classifications I, II, and III summarize both the evidence and expert opinion and provide final recommendations for both patient evaluation and therapy: Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective . Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy. Class IIb: Usefulness/efficacy is less well established by evidence/opinion. Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful. The weight of the evidence was ranked highest (A) if the data …

ACC/AHA guidelines for the management of patients with unstable angina and non–st-segment elevation myocardial infarction

Preamble......971 I. Introduction ......972 A. Organization of Committee and Evidence Review......972 B. Purpose of These Guidelines......973 C. Overview of the Acute Coronary Syndrome......973 1. Definition of Terms......973 2. Pathogenesis of UA/NSTEMI ......974 3. Presentations of

In vivo electrophysiological effects of lidocaine in canine acute myocardial infarction.

Lidocaine was administered as a rapid intravenous bolus injection followed by a constant-rate intravenous infusion to nine dogs with 2-hour-old myocardial infarctions. Bipolar electrograms were recorded from and effective refractory periods were determined in the infarcted and normal zones of the heart. Intervals (Q-EG) were measured from the onset of the QRS complex in a standard electrocardiogram limb lead to the major deflection of the recorded electrograms from the normal and infarcted zones. QRS duration and serum lidocaine concentration were also determined. At serum concentrations considered to be therapeutic, lidocaine prolonged the Q-EG intervals in the infarcted zones of the heart 17–26% at peak effect (P < 0.01), but it had no effect on the Q-EG intervals in the normal zone except for a slight (1.5%) prolongation shortly after the initial intravenous bolus injection. Lidocaine also had no effect on QRS duration. Similarly, lidocaine prolonged the effective refractory period of the infarcted zone 23% (P < 0.01) at peak effect but had no effect on the effective refractory period of the normal zone. Prior to lidocaine administration, the mean effective refractory period of the normal zone was 26 msec longer than that of the infarcted zone, but at peak drug effect the disparity in refractoriness was reduced to 1 msec. The present study thus shows that lidocaine has different effects in infarcted and normal zones of the heart. In delaying activation and prolonging the effective refractory period of the infarcted zone of the heart, lidocaine has local anesthetic actions which might explain its effectiveness in curtailing ventricular arrhythmias after acute myocardial infarction.

Cost-effectiveness analysis in heart disease, part III: Ischemia, congestive heart failure, and arrhythmias

Cost-effectiveness analyses were reviewed in the following diagnostic and treatment categories: acute myocardial infarction (MI) and diagnostic strategies for coronary artery disease (CAD), coronary artery bypass graft (CABG) surgery, percutaneous transluminal coronary angioplasty (PTCA), congestive heart failure (CHF), and arrhythmias. In the case of acute MI, coronary care units, as presently used, are rather expensive but could be made much more efficient with more effective triage and resource utilization; reperfusion via thrombolysis is cost-effective, as are beta-blockers and angiotensin-converting enzyme (ACE) inhibitors post-MI in appropriate patients. Cost-effectiveness of CAD screening tests depends strongly on the prevalence of disease in the population studied. Cost-effectiveness of CABG surgery depends on targeting; eg, it is highly effective for such conditions as left-main and three-vessel disease but not for lesser disease. PTCA appears to be cost-effective in situations where there is clinical consensus for its use, eg, severe ischemia and one-vessel disease, but requires further analysis based on randomized data; coronary stents also appear to be cost-effective. In preliminary analysis, ACE inhibition for CHF dominates, ie, saves both money and lives. Cardiac transplant appears to be cost-effective but requires further study. For arrhythmias, implantable cardioverter defibrillators are cost-effective, especially the transvenous device, in life-threatening situations; radiofrequency ablation is also cost-effective in patients with Wolff-Parkinson-White syndrome apart from asymptomatic individuals; and pacemakers have not been analyzed except in the case of biofascicular block, where results were variable depending on the situation and preceding tests.

Cost-Effectiveness Analysis in Heart Disease, Part II: Preventive Therapies

Cost-effectiveness analysis of preventive therapies are reviewed in the following categories: lipid lowering, hypertension, smoking cessation, exercise, and anticoagulation. From review of 8 analyses, cost-effectiveness of primary prevention via cholesterol lowering drugs is generally expensive, whereas that of secondary prevention generally is favorable. However, targeting by age, coexisting risk factors, and gender strongly influence results that are also sensitive to drug costs. Treatment of hypertension (5 analyses) is cost-effective in virtually all patient populations and circumstances and for a wide variety of drugs. It is more so with coexisting risk. Issues relating to compliance and drug costs are important. Smoking cessation (4 analyses) is highly cost-effective and worthwhile. However, data on recidivism are incomplete, and cessation may be more difficult to achieve in the general population versus study patients. In one analysis, an exercise program was found to be cost-effective in prevention of coronary heart disease. Anticoagulants have been analyzed in various circumstances. Their cost-effectiveness is favorable for prosthetic valves, although sensitive to imprecision in monitoring. It is also favorable for mitral stenosis in the presence of atrial fibrillation but not normal sinus rhythm. Cost-effectiveness of heparinization for prosthetic valve patients undergoing surgery is rather variable and depends on type of surgery (major versus minor) and type of valve. Many topics in anticoagulant therapy remain to be explored from a cost-effectiveness point of view.

Effects of sudden change in cycle length on human atrial, atrioventricular nodal and ventricular refractory periods.

In the steady state, the refractory periods of the human atrium, atrioventricular (AV) node, and ventricle are a function of cycle length. We compared the change in refractoriness that occurred when these refractory periods were measured after eight beats at a shorter cycle length with the change that occurred when these refractory periods were measured after a single beat at the shorter cycle length. For a decrease in cycle length of 235 ± 63 msec, the atrial effective refractory period shortened 31 ± 24 msec (p < 0.01) when measured after eight beats at the shorter cycle length and 26 ± 24 msec (p < 0.01) when measured after a single beat at the shorter cycle length. Similar changes were seen in atrial functional refractory period. For a decrease in cycle length of 214 ± 63 msec, the AV nodal effective refractory period increased 30 ± 39 msec (p < 0.05) when measured after eight beats and 31 ± 34 msec (p < 0.05) when measured after a single beat. The AV nodal functional refractory period showed moderate shortening with decreases in cycle length, both when measured after eight beats and when measured after a single beat (p = NS). For both the atrium and AV node, there was no significant difference between the change in refractoriness after a single beat at the shorter cycle length and after eight beats at the shorter cycle length. For a decrease in cycle length of 175 ± 52 msec, the ventricular effective refractory period shortened 26 ± 10 msec (p < 0.01) when measured after eight beats and 16 ± 12 msec (p < 0.01) when measured after a single beat at the shorter cycle length. Thus, a single beat at the shorter interval produced 60% of the shortening of refractoriness produced by eight beats at the shorter interval (p < 0.01). These findings have implications for the performance and interpretation of stimulation studies and provide insight into the mechanism of initiation of tachycardia by premature beats.

Electrophysiological and antiarrhythmic effects of propranolol in canine acute myocardial ischemia.

To correlate the antiarrhythmic and electrophysiological effects of propranolol in acute myocardial ischemia, we examined the effects of temporary (15-minute) ligations of the left anterior descending coronary artery in studies on 15 dogs. We recorded bipolar electrograms and monophasic action potentials from the ischemic and normal zones and measured the intervals from the onset of QRS in a standard electrocardiogram lead to the major deflection of electrograms recorded from the ischemic and normal zones. We also determined monophasic action potential duration (APD) and effective refractory period (ERP). Data for control ligations were compared to those during which propranolol, 40 μg/kg, was administered intravenously immediately after ligation. Propranolol reduced the mean number of ventricular beats per minute (from 15 to 6) (P < 0.01). Propranolol slowed conduction in the ischemic zone (by 10 msec at peak effect, P < 0.01) and had no or only a very slight effect (by 1-msec at 15 minutes, P < 0.05) on conduction in the normal zone. Propranolol also prolonged APD in the ischemic (32-msec) and normal (14-msec) zones (P < 0.01), prolonged ERP in the ischemic (41-msec) and normal (20-msec) zones (P < 0.01), and reduced the APD/ERP ratio in the ischemic (1.62 to 1.47) (P < 0.01) and normal (1.62 to 1.55) (P < 0.05) zones. During the control ligation, APD in the ischemic zone was 25 msec shorter than in the normal zone (P < 0.01), but with propranolol the difference was not significant. The effects of propranolol in slowing conduction in the ischemic zone, in prolonging refractoriness, in reducing APD/ERP, and in reducing the disparity in APD between ischemic and normal zones may explain its demonstrated antiarrhythmic effects in acute myocardial ischemia.