To evaluate the variability in the reported diagnostic accuracy of the exercise electrocardiogram, we applied meta-analysis to 147 consecutively published reports comparing exercise-induced ST depression with coronary angiography. These reports involved 24,074 patients who underwent both tests. Population characteristics and technical and methodologic factors, including publication year, number of electrocardiographic leads, exercise protocol, use of hyperventilation, definition of an abnormal ST response, exclusion of certain subgroups, and blinding of test interpretation were analyzed. Wide variability in sensitivity and specificity was found (mean sensitivity, 68%; range, 23-100%; SD, 16%; and mean specificity, 77%; range, 17-100%; SD, 17%). The four study characteristics found to be significantly and independently related to sensitivity were the treatment of equivocal test results, comparison with a "better" test such as thallium scintigraphy, exclusion of patients on digitalis, and publication year. The four variables found to be significantly and independently related to specificity were the treatment of upsloping ST depressions, the exclusion of subjects with prior infarction or left bundle branch block, and the use of preexercise hyperventilation. Stepwise linear regression explained less than 35% of the variance in sensitivities and specificities reported in the 147 publications. There is wide variability in the reported accuracy of the exercise electrocardiogram. This variability is not explained by information reported in the medical literature.

The prevention of cardiovascular disease antedates our current preoccupation with risk factors for coronary heart disease and hypertension. Indeed, earlier preventive efforts have in part been so successful that many people have forgotten that they existed. The almost forgotten entity, beriberi heart disease, was first prevented in 1883 by Takaki of Japan. With diphtheria, it was the identification of the causative bacillus by Klebs in 1883, leading finally to the development of diphtheria toxoid by Ramon in 1923, which resulted in the disappearance of diphtheritic heart disease. Success in the attack on syphilitic heart and vascular disease began with Bordet and Gengou in 1901 with the discovery of the phenomenon of complement fixation, and with the formulation of Salvarsan by Ehrlich in 1907. The story of the prevention of rheumatic fever has a large cast of characters, but special recognition must be given to Coburn for his observations confirming the role of the hemolytic streptococcus published in 1931 and showing the prophylactic value of sulfanilamide published in 1939. The important association of maternal rubella with congenital heart malformations was revealed by Gregg in 1941. Alcoholic heart disease was identified particularly by Brigden and Evans in 1957 and 1959, respectively. In relation to coronary and hypertensive heart disease, the names of Anitschkow (1933), Leary (1935), and Keys (1948) in relation to diet, of Freis (1967) in the field of hypertension treatment, of White (1927) in relation to physical exercise, and of English, Willius, and Berkson (1940) and Hammond and Horn (1954) in the role of cigarette smoking, deserve special recognition.

We have speculated previously that the abrupt conversion from chronic stable to unstable angina and the continuum to acute myocardial infarction may result from myocardial ischemia caused by progressive platelet aggregation and dynamic vasoconstriction themselves caused by local increases in thromboxane and serotonin at sites of coronary artery stenosis and endothelial injury. Platelet aggregation and dynamic coronary artery vasoconstriction probably result from the local accumulation of thromboxane and serotonin and also relative decreases in the local concentrations of endothelially derived vasodilators and inhibitors of platelet aggregation, such as endothelium-derived relaxing factor (EDRF) and prostacyclin. With severe reductions in coronary blood flow caused by these mechanisms, platelet aggregates may increase, and an occlusive thrombus composed of platelets and white and red blood cells in a fibrin mesh may develop. When coronary arteries are occluded or narrowed for a sufficient period of time by these mechanisms, myocardial necrosis, electrical instability, or sudden death may occur. We believe that unstable angina and acute myocardial infarction are a continuum in relation to the process of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary artery stenosis is brief, unstable angina or non-Q wave infarction may occur. However, when the coronary artery obstruction by these mechanisms is prolonged for several hours, Q wave myocardial infarction results. Chronic endothelial injury and coronary artery stenosis are probably associated with the accumulation of platelets, white and red blood cells, and a fibrin mesh at the site of stenosis and endothelial injury.

The endothelium releases the powerful vasodilator and antiaggregatory substance, EDRF, both under basal conditions and upon stimulation by a wide variety of agents. Endothelial injury or dysfunction may play an important role in the spasmogenicity of the coronary artery, although other possible alterations related to atherosclerosis should also be considered. Among the possible stimuli, aggregating platelets are important as a source of vasoconstrictor substances. The endothelium may also produce the vasoactive substances EDHF and EDCF(s). Their pathophysiologic significance remains to be determined.

Three to four percent of patients who have myocardial revascularization without additional procedures have moderately severe or severe heart failure. Analysis of reported experience and data from two centers indicate that the severity of heart failure correlates poorly with left ventricular ejection fraction and other indexes of left ventricular function. Operative mortality ranges from 2.2% to 14.9% and roughly correlates with the severity of heart failure. By logistic regression, age, ejection fraction, presence of mitral regurgitation, and presence of left main coronary artery disease are identified as incremental risk factors for operative death. Long-term survival is affected by age, ejection fraction, sex, presence of left main coronary artery disease, severity of angina, and presence of mitral insufficiency.

The early and long-term results of myocardial revascularization are reviewed for four unidentified community hospitals, for Katholieke Universiteit (Leuven, Belgium), and for the University of Alabama at Birmingham at two different times. After operation, approximately 77% of patients are free from all ischemic events at 5 years and nearly 50% are free at 10 years. Over 90% of patients survive 5 years, and approximately 80% survive 10 years. Some of the incremental risk factors for early death after operation include older age; degree of left ventricular dysfunction; hemodynamic instability at the time of operation; recent myocardial infarction; number of diseased coronary vessels; associated mitral incompetence, ventricular aneurysm, or ventricular tachycardia; longer aortic cross-clamp time; and non-use of the internal mammary artery for revascularization. The number of diseased coronary arteries and the aggressiveness of the atherosclerotic process, degree of left ventricular dysfunction, older age, and non-use of the internal mammary artery are risk factors for reduced long-term survival.

We reviewed 14 reports from 1978 to 1988 of 6,136 patients with unstable angina pectoris treated by coronary artery bypass grafting (CABG). The mean age was 56.8 years, and 23% were female. Mean operative mortality in the 14 reports was 3.7% (1.2-8.5%). The mean incidence of perioperative myocardial infarction was 9.9% (3.8-17%). The mean incidence of postoperative low cardiac output was 16% (8-35%). No risk factors for morbidity or mortality different from those observed in patients with chronic stable angina were identified. Clinical subgroups of the heterogeneous group of patients with unstable angina pectoris are associated with different prognoses and treatment results. Variable pathological changes are associated with these subgroups. Reductions in morbidity and mortality of those patients undergoing CABG may require better preoperative management of the underlying pathological process and improved myocardial preservation at the time of CABG. Angina relief, improved survival, and reduction in late nonfatal myocardial infarction is similar to that observed in patients with chronic stable angina after CABG.

Over the last 20 years, operative mortality has decreased and late survival has improved for patients with chronic stable angina who have coronary artery bypass surgery. However, this favorable trend may not continue because the operation is now extended to elderly and high-risk patients. The most powerful predictors of operative mortality include indexes of left ventricular function, age, and the number of associated medical conditions. Female gender, severity of angina, and extent of coronary artery disease appear to be predictors of operative mortality in some series but not in all. Indexes of left ventricular dysfunction remain the most powerful predictors of late death, but the extent of coronary disease, older age, and presence of associated diseases (including noncardiac vascular disease) remain important determinants. Analyses of the randomized trials and registry studies reveal a consistent trend: in patients at high risk on the basis of clinical, functional, and anatomic characteristics, coronary artery bypass surgery prolongs survival in comparison with medical therapy alone. In patients determined to be at low risk, medical therapy is initially recommended with the realization that revascularization may be necessary subsequently if symptoms worsen or the severity of ischemia increases.

The internal mammary artery is the premier conduit for initial and repeat coronary artery bypass grafting and should be used as either a pedicled or free graft whenever possible. Saphenous veins from the greater and lesser systems are distinctly second choices but can serve satisfactorily as aortocoronary grafts for many years. When neither the internal mammary arteries nor the saphenous veins are available, the cardiac surgeon today must choose from a wide variety of alternative conduits that have been used periodically over the past two decades for coronary artery bypass grafting.

Because of excellent long-term patency (greater than 90% at 7 years), internal thoracic artery (ITA) bypass grafts are preferred over saphenous vein grafts for myocardial revascularization. ITA grafts can be used for up to 70% of all distal anastomoses and in up to 95% of patients. ITA grafts are more technically demanding; inadequate length, traumatic arterial injury, torsion, separation of intima and adventitia, and anastomotic stricture are important pitfalls. Postoperative problems of bleeding, phrenic nerve injury, mediastinal infection, and arm paresis or paresthesia are complications attributed to ITA grafts, but they are uncommon if meticulous technique is used.

Occlusion rate of the saphenous vein is around 12-20% during the 1st year and 2-4% annually for the next 4 or 5 years. Subsequently, this rate doubles, so that at 10 years, approximately 50% of grafts become occluded due to the occurrence of graft atherosclerosis. A similar percentage of patent grafts show atherosclerotic changes at the end of the 1st decade. Sequential vein grafts probably suffer the same fate although late follow-up is lacking. Reoperation is estimated to be 30% at 10 years, as judged by angiographic criteria. The operative risk of reoperation is at least double that of primary operation; symptomatic relief appears to be of shorter duration. Recent technical changes to better preserve medial and endothelial function and to pharmacologically inhibit platelet function may lead to longer duration of the venous conduit.

Compared with isolated coronary artery bypass grafting (CABG), the combination of valve replacement or repair with coronary revascularization generally increases operative risk. However, complete revascularization is superior to no revascularization in patients with valvular and coronary artery disease (CAD). Patients who undergo aortic valve replacement and CABG have two unrelated disease processes; these patients only infrequently have ischemic cardiomyopathy, and the operative mortality is slightly increased to 4-7% for the combined procedure versus isolated aortic valve replacement. Patients who are operated on for mitral valve disease and CAD fall into two groups: 1) where CAD and mitral valve disease are not etiologically related, and 2) where mitral valve dysfunction is the result of ischemic changes. In the latter group, operative mortality significantly exceeds that for isolated mitral valve surgery, and surgical priority increases that difference (operative mortality 7-20%). Thus, the operative risk for a mitral valve procedure plus CABG exceeds that for isolated coronary revascularization or isolated valve replacement. In the combined procedure, risk increases if valve dysfunction is caused by CAD, if severe left ventricular function is present, if the patient has been assigned to Class IV, or if emergency operation is required.

The direct surgical techniques for the treatment of refractory ischemic ventricular tachycardia have now been available for 10 years. This report assimilates the first decade's experience with these direct procedures to clarify the present indications for ventricular tachycardia surgery, the preferred method for conducting the operative procedures, the clinical results that are to be expected, the subsequent prognosis, and the role of the automatic internal cardioverter-defibrillator in the contemporary management of refractory ischemic ventricular tachycardia.

Onset of cardiogenic shock in patients with various manifestations of acute myocardial ischemia has high mortality, but use of improved hemodynamic monitoring, the intra-aortic balloon pump, and early operation have improved previously dismal results. Review of published experience spanning the last 20 years indicates that 66% of patients survive after emergency myocardial revascularization for acute myocardial infarction and cardiogenic shock. If cardiac damage is overwhelming and irreversible, selected patients may be "bridged" with mechanical biventricular circulatory assist devices and transplanted. Infarctectomy for acute myocardial infarction remains controversial and unproven; successful repair of free left ventricular wall rupture is uncommon. In patients with cardiogenic shock, operations for acute postinfarction ventricular septal defect or mitral insufficiency have operative survival rates of 45% and 54%, respectively. Long-term (greater than 2-year) survival for patients after repair of acute postinfarction ventricular septal defect is 84%. However, 5-year survival after successful operation for acute postinfarction mitral insufficiency complicated by cardiogenic shock is only 40%.

Analysis of published reports indicates that ischemic mitral insufficiency is associated with higher operative mortality (10-30%) than is nonischemic mitral valve procedures. Probable incremental risk factors include emergency operation, acute myocardial infarction, hemodynamic instability, poor left ventricular function, pulmonary hypertension, advanced age, and renal failure. Early valve repair or replacement with myocardial revascularization improves survival in patients with circulatory insufficiency due to acute postinfarction mitral regurgitation. Although the technique of repair of nonacute ischemic mitral insufficiency is not standardized, repair with revascularization is preferred. Preliminary data suggest that long-term results are primarily related to the severity of left ventricular dysfunction.

At a time when hospital mortality for adult cardiac operations is continuing to fall, the ischemic mitral regurgitation subset remains at relatively high risk. Based on analysis of available data, efforts to improve results might be directed toward a more general application of mitral valve reconstruction in this population. Other promising therapeutic measures include the liberal use of reperfusion therapy in the acute papillary muscle dysfunction group, better selection of patients for operation, and, perhaps, operative recommendation to a greater proportion of the more stable patients who previously were treated medically. Incorporating these therapeutic concepts into routine clinical practice may improve the overall prognosis of this difficult subgroup.

Thirty-one published reports (366 patients) and 48 consecutive patients treated for postinfarction ventricular septal defect at four institutions in northern California were reviewed. Overall hospital mortality was 43% in the reviewed group and was not affected by age, concomitant myocardial revascularization, date of operation, presence of cardiogenic shock, or location of the defect. Mortality for the 48 consecutive patients, all of whom had surgery within 30 days of acute infarction, was 67%. Although there were no survivors over 65 years of age, mortality was not affected by age, location of the ventricular septal defect, or concomitant myocardial revascularization.