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In 1988, the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures presented a classification of coronary lesions utilizing 26 lesion features to predict the success and complications of balloon angioplasty. Using data from the Registry of the Society for Cardiac Angiography and Interventions (SCAI) we evaluated the ability of this classification to predict success and complications. Lesion success, death in hospital, emergency cardiac bypass surgery, and major adverse events were evaluated in 41,071 patients who underwent single-vessel angioplasty from January 1993 to June 1996. Logistic models using the ACC/AHA lesion classification, vessel patency, or both, were compared. A new classification based on the interaction of the ACC/AHA classification plus lesion patency was compared with the existing ACC/AHA classification. Vessel patency, added to the ACC/AHA classification, improved prediction of lesion success (p

There are few data comparing the relative frequency of new electrocardiographic (ECG) abnormalities after coronary artery bypass grafting (CABG) compared with percutaneous transluminal coronary angioplasty (PTCA) and their association with long-term cardiac mortality. The study population consisted of 3,373 patients who were either randomized or eligible to be randomized to CABG or PTCA in the BARI trial. The frequency of new postprocedural ECG abnormalities was significantly greater after a CABG procedure than after PTCA. The incidence of new postprocedural major Q waves, ST-segment elevation, and T-wave abnormalities were significantly more frequent after CABG. After PTCA (n = 1,869), the 5-year cardiac mortality rates associated with the new development of major Q waves, ST-segment elevation, ST-segment depression, T-wave abnormalities, or no abnormality was 18.1%, 8.5%, 8.9%, 6.0%, and 5.4%, respectively. After CABG (n = 1,427), 5-year cardiac mortality rates were 8.0%, 4.2%, 3.8%, 2.8%, and 3.7%, respectively. The adjusted relative risk of 5-year cardiac mortality for new Q-wave abnormalities was 2.6 after CABG (p <0.04) and 4.6 after PTCA (p <0.01). Thus, patients who undergo CABG have more postinitial procedural ECG abnormalities than patients who undergo PTCA. Cardiac mortality is significantly increased by the new development of postprocedural Minnesota code Q-wave abnormalities regardless of whether patients undergo CABG or PTCA. [ABSTRACT FROM AUTHOR]

Cigarette smoking is linked to increased cardiac morbidity and mortality, and has been shown to affect both lipid profiles and thrombotic factors in healthy subjects. However, the influence of smoking on the atherothrombotic environment has not been studied in a large population of patients after acute myocardial infarction (AMI). Blood samples and medical history, including smoking status, were obtained from 1,045 patients at a 2-month visit after AMI. Smokers were asked to refrain 24 hours before the visit, but not all complied. Measurements included total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apolipoprotein-B, apolipoprotein-A, triglycerides, factor VII, factor VIIa, von Willebrand factor, D-dimer, and plasminogen activator inhibitor. There were 247 current, 443 past, and 349 nonsmokers. After adjustment for clinical variables, current smokers had higher levels of total cholesterol and apolipoprotein-B than past and nonsmokers (p <0.01). High-density lipoprotein cholesterol and apolipoprotein-A levels were similar between groups. Fibrinogen was elevated in current (p = 0.001) and past (p = 0.029) smokers, compared with nonsmokers. Smokers who smoked within 24 hours of blood sampling had higher apolipoprotein-B (p = 0.005), total cholesterol (p = 0.001), and fibrinogen (p = 0.015) levels than those who refrained from smoking. In conclusion, postinfarction patients, who historically have higher levels of atherogenic lipids than healthy subjects, have increased levels of these lipids attributed to active smoking. After smoking cessation, lipid profiles approach nonsmoker levels, but fibrinogen remains elevated. Smoking within 24 hours of blood sampling was associated with further adverse prothrombotic and lipogenic effects. [ABSTRACT FROM AUTHOR]

Patients who were stable 1 to 6 months after a cardiac event underwent routine exercise testing with thallium scintigraphy. The prognosis of patients with good exercise capacity (Bruce stage 3) was similar whether or not ischemia was demonstrated and similar to patients with reduced exercise capacity and no ischemia, whereas the presence of both ischemia and a reduced exercise tolerance identified patients with a significantly poorer prognosis. [ABSTRACT FROM AUTHOR]

The objective of this study was to test the hypothesis that psychological factors are determinants of anginal symptoms during positive exercise tests. The sample consisted of clinically stable patients who were enrolled in the Multicenter Study of Myocardial Ischemia 1 to 6 months after admission to a coronary care unit. Among 186 post-myocardial infarction patients, 151 developed ischemia (i.e., a stress-induced myocardial perfusion defect) without symptoms (silent ischemia) and 35 developed angina with ischemia (symptomatic ischemia) during a thallium exercise test; among 39 patients who had been hospitalized for unstable angina, 24 developed silent ischemia and 15 developed symptomatic ischemia. Two sets of psychometric tests were administered: set 1, factors that influence awareness of physical symptoms, and set 2, factors associated with biases toward or against reporting perceived symptoms. Two hundred eleven patients produced complete data in each set. Analysis of set 1 factor scores revealed significant effects of symptom status (p = 0.006) and index event (p = 0.02), but no interaction. No effects were found in set 2. Patients who are clinically stable after recovery from an acute coronary event and who experience angina during exercise testing are more aware of physical symptoms in general than are comparable patients with silent ischemia. Psychological biases toward or against reporting perceived symptoms do not differentiate these groups. Thus, it appears that silent ischemia is probably "silent" in the sense of being truly asymptomatic rather than of stoic endurance or denial of perceived symptoms.

Percutaneous transluminal coronary angioplasty (PTCA) is currently performed in many patients seeking care because of severe manifestations of multivessel coronary artery disease. Previously, the majority of such patients would have undergone coronary artery bypass grafting (CABG). No definitive evidence is available as to which initial revascularization strategy has the best long-term clinical and economic outcomes. The Bypass Angioplasty Revascularization Investigation (BARI) is the largest of several recent clinical trials that were designed to test the hypothesis that an initial strategy of PTCA in selected patients with multivessel coronary artery disease does not compromise long-term clinical outcome compared with an initial strategy of CABG. This report describes how patients were screened, selected, and recruited in BARI and how this process may influence the results and the interpretation of the trial. During the enrollment period, 25,200 patients undergoing diagnostic coronary angiography at the participating institutions or with off-site angiograms referred to BARI investigators were screened for BARI eligibility. Excluded from screening were patients without coronary artery disease, those with single-vessel disease, prior revascularization, primary congenital, valvular, or myocardial disease, and age > 80 years. Slightly more than half of the patients screened (12,670) were not clinically eligible for BARI because of left main disease, insufficient symptoms, emergency revascularization, or other logistic reasons. Thus, 12,530 patients had severe angina and/or ischemia and were clinically eligible for BARI. Nearly 33% of them (4,110) had multivessel disease, which was suitable for both PTCA and CABG.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of diltiazem on long-term outcome after acute myocardial infarction (AMI) was assessed in 2,377 patients enrolled in the Multicenter Diltiazem Post-Infarction Trial and subsequently followed for 25 +/- 8 months. The study population included 855 patients (36%) with at least 1 prior AMI before the index infarction and 1,522 patients (64%) with a first AMI, of whom 409 (27%) had a first non-Q-wave AMI, 664 (44%) a first inferior Q-wave AMI, and 449 (30%) a first anterior Q-wave AMI. This post hoc analysis revealed that, among patients with first non-Q-wave and first inferior Q-wave AMI, there were fewer cardiac events during follow-up in the diltiazem than in the placebo group, and that the reverse was true for patients with first anterior Q-wave AMI or prior infarction. The diltiazem:placebo Cox hazard ratio (95% confidence limits) for the trial primary end point (cardiac death or nonfatal reinfarction, whichever occurred first) was: first non-Q-wave AMI-0.48 (0.26, 0.89); first inferior Q-wave AMI-0.66 (0.40, 1.09); first anterior Q-wave AMI-0.82 (0.51, 1.31); and prior AMI-1.11 (0.85, 1.44). Use of cardiac death alone as an end point gave an even more sharply focused treatment difference: first non-Q-wave AMI-0.46 (0.18, 1.21); first inferior Q-wave AMI-0.53 (0.27, 1.06); first anterior Q-wave AMI-1.28 (0.68, 2.40); prior infarction-1.26 (0.90, 1.77). Further analysis revealed that these differences in the effect of diltiazem in large part reflected the different status of the 4 electrocardiographically defined subsets in terms of left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Cycle length variability (CLV), defined as the standard deviation of normal cycle length intervals, has been found to be a powerful predictor of subsequent mortality in a population of 808 survivors of acute myocardial infarction. Decreased CLV is associated with a significant increase in mortality. CLV remained an independent predictor of outcome even after adjusting for left ventricular ejection fraction, clinical risk factors, heart rate and ventricular arrhythmias. In the same population of survivors of acute myocardial infarction, the results of exercise testing also strongly predicted outcome, with those failing to take the test having the worst survival, and those completing the low-level stress test taken before discharge having the best prognosis. The hypothesis that the status of stress test (completed; did not complete; failed to take) and CLV were measuring the same factor related to mortality was tested. Although the distribution of CLV was shifted to higher CLV in patients who completed the test and to lower CLV in those who failed to take the test, both predictors of mortality remained independent predictors of long-term mortality (average of 31 months of follow-up) after controlling for each other. Moreover, subgroups with an approximate 15-fold difference in mortality were defined using both variables (CLV less than 50 ms, did not take test had a 54% mortality; CLV greater than 100 ms, completed the test had a mortality of 3.5%). CLV is a measure of autonomic tone; it is not strongly related to exercise ability and using the results of both stress testing and CLV results in the identification of subgroups of postinfarction patients with markedly disparate risks of mortality.

The value of low-level exercise testing early after acute myocardial infarction (AMI) in 207 patients taking beta-blocking drugs was evaluated in a multicenter study of prognosis after AMI. After stratifying patients according to the absence of significant rales upon admission or pulmonary congestion on the admitting chest x-ray, the results of the exercise test (ability to complete the 9-minute protocol) permitted a large cohort (108 patients, 52% of exercising patients) with no deaths from cardiac causes in the year after AMI to be identified. The results suggest that even in patients taking beta-blocking agents, low-level exercise testing together with clinical stratification has value in identifying a large group of patients with a good prognosis after AMI.

Follow-up results in 593 patients less than or equal to 7 years (mean 4.7) after hospital discharge for their first myocardial infarction (MI) are presented. Patients were grouped according to the presence or absence of Q waves on electrocardiograms after the MI and by peak serum glutamic oxalacetic transaminase (SGOT) level during hospitalization. Cardiac mortality varied. Patients with Q-wave infarcts and an SGOT level less than or equal to 240 IU/liter had a cardiac mortality of 3.1% per year, whereas patients with Q-wave MI and an SGOT level greater than 240 IU/liter had an 11% 6-month mortality and a 3.8% per year cardiac mortality thereafter. However, patients with non-Q-wave (nontransmural) MI had a excellent survival rate for 2 years (96.8%) which continued in patients aged less than or equal to 60 years thereafter. However, patients with non-Q-wave infarcts aged greater than 60 years had a 12% per year cardiac mortality in the third post-MI year and an additional 12% died each year thereafter. Early mortality was related to enzyme level, whereas late mortality was a function of type (Q-wave or non-Q-wave) and age.