The Starling relationship in the normal human ventricle may be different than usually portrayed. In normal, resting, supine man the ventricular function curve is at its peak at a left ventricular end-diastolic pressure of approximately 10 mm Hg. Below this point is a strong direct relation between filling pressure and stroke work, while at higher filling pressures, a plateau occurs. Limitation of ventricular response is related to a sharply rising ventricular pressure-volume curve at a normal level of filling pressure. Thus, in the supine position, the normal heart is not on the active portion of the ventricular function curve, but is in a unique position in which cardiac output is probably controlled by factors other than ventricular filling pressure. In ventricular failure, the peak of the ventricular function curve is displaced to a higher level.

This report deals with the ramifications of the concept of left axis deviation. In early life, the leftward shift of the frontal plane QRS axis is determined chiefly, if not solely, by the relative weights of the ventricles. Once adult ventricular weight ratios are reached, there is a long period of axis stability, then a gradual leftward drift of the QRS, governed principally by left anterior fascicular conduction. Thus, the normal QRS axis is age-dependent, and left axis deviation must be considered accordingly.

Changes in cardiac metabolism in myocardial failure and after alcohol ingestion are discussed. The main effect of alcohol ingestion is loss of cardiac contractility. Since heart muscle does not contain alcohol dehydrogenase, its toxicity is probably the result of a direct toxic effect of ethanol and acetaldehyde on the myocardial cell, possibly involving various membrane systems. Alcohol inhibits mitochondrial respiration and the activity of enzymes in the tricarboxylic acid cycle, and its interferes with both mitochondrial calcium uptake and binding. Ethanol profoundly affects myocardial lipid metabolism. Acetaldehyde diminishes myocardial protein synthesis and inhibits Ca++-activated myofibrillar ATPase. In myocardial failure, a series of possibilities may be responsible for the loss of contractility. Excitation-contraction coupling could be disturbed at the level of the sarcolemma, at the sarcoplasmic reticulum, at the mitochondria, and between calcium and the regulatory proteins. Deficiencies in Ca++ delivery systems of excitation-contraction coupling on the myosin ATPase activity could be responsible for the dimunition in cardiac contractility. Mitochondrial function may also be involved, since mitochondria from failing human hearts are defective with respect to respiratory control and calcium accumulation. Under certain conditions, the relationship of mitochondria to calcium sequestration is very important in influencing contractility. The involvement of contractile and regulatory proteins in myocardial failure cannot be excluded.

This study included 89 patients, 70-82 years (mean 72.8 years), who had procedures using cardiopulmonary bypass since 1955. Twenty-six patients had elective aortic valve replacement (AVR), with two hospital deaths. One patient who underwent emergency AVR for bacterial endocarditis died of septic shock. Ten patients had AVR and coronary artery bypass surgery (CABG), with one hospital death (10%). Fourteen patients had mitral valve replacement (MVR), with eight hospital deaths (57%). Two died of left ventricular rupture after leaving the operating room, and the remainder died of low cardiac output. Twenty-five patients had CABG with no early deaths. Seven patients had aneurysms of the thoracic aorta, with two early deaths. Six patients had other procedures with one death, making a total of 16 operative deaths in the 89 patients. Eighty-four of the patients (94%) were New York Heart Association (NYHA) Functional Class III or IV for congestive heart failure and/or angina, preoperatively. Of these, 12 were in extremis immediately before surgery, and six survived. There were 10 late deaths. The actuarial survival rates for one, two and five years for all patients were 69% (40 patients), 47% (20 patients) and 21% (seven patients), respectively. At recent follow-up (mean 20 months) 84% of the hospital survivors were symptomatically improved at least one NYHA Functional Class. We conclude that CABG and/or AVR can be performed in elderly patients with a low hospital mortality and with symptomatic improvement. However, MVR in the elderly carries an unusually high mortality (7.3 times greater than patients less than 70, in our experience), and this risk must be weighed when considering MVR in these patients.

In this report major risk factors in coronary heart disease (CHD) are reviewed, with particular emphasis on the role of nutrition. International and national epidemiologic data indicate that reducing or eliminating certain risk factors (e.g., a diet high in cholesterol and saturated fats) may reduce the risk of premature CHD. Most trends indicate that many Americans are more concerned about diet for health reasons. Preventive measures for CHD are also discussed.

Hemodynamically significant primary anomalies of the coronary arteries are those which alter myocardial perfusion. There are four major types: coronary artery fistulae, origin of the left coronary artery from the pulmonary artery, congenital coronary stenosis or atresia, and origin of the left coronary artery from the right sinus of Valsalva, with subsequent passage of the vessel between the aorta and right ventricular infundibulum. The angiographic features of these lesions are discussed.

Valve prostheses have played an important part in the past two decades in the management of patients with valvular heart disease. However, many of the devices used in valve replacement have introduced new clinical problems. This paper deals with some of the problems associated with valve replacement, including one not previously emphasized--valve prosthesis-patient mismatch, which may cause obstruction to ventricular outflow and/or inflow.

Intraventricular conduction defects are common following repair of various forms of congenital heart disease. Such defects may affect adversely the long-term prognosis of patients in whom cardiac hemodynamics were adequately restored. Review of previously published studies suggests that the site of the conduction defect may be the reason for the different prognoses reported for patients from different institutions. The so-called "trifascicular block" pattern which sometimes occurs following open heart surgery is probably due to a more extensive lesion to the branching and penetrating parts of the His bundle rather than additional injury to the posterior left bundle branch fibers. Transient complete heart block in the immediate postoperative period seems to be a predictor for late development of complete heart block or sudden death at least as powerful as right bundle branch block and left anterior hemiblock.

Epicardial mapping provides a method for defining antegrade and retrograde sites of pre-excitation. It is best undertaken only after a careful, detailed preoperative electrophysiological study has been performed. The potential pitfalls of the technique are many and technical expertise must be constantly available to maintain a functioning system. For these reasons, it is not likely to lend itself to widespread application. The same techniques can be applied to localization of the site of origin of atrial or ventricular dysrhythmias, localization of myocardial ischemia and infarction, as well as to differentiate between epicardial delays due to conduction delay and those caused by intramural myocardial delay.

A review is given on the use of programmed electrical stimulation of the heart in patients suffering from tachycardia. The application of this technique makes it possible to evaluate mechanisms of tachycardia directly in the human heart. By repeating the same stimulation program following drug administration the effect of drugs on arrhythmia mechanisms can be studied. There are several factors, however, that influence the amount of information on mechanism and pathway of tachycardia and selection of appropriate therapy that can be obtained during the study. These factors as well as how information obtained programmed electrical stimulation of the heart has resulted in a better use of the 12-lead electrocardiogram as a diagnostic tool are discussed.

Despite a decade of experience with aortocoronary bypass grafting embracing 300,000 or more operations, indications for its use remain controversial. The controversy persists because of a lack of adequate controls with which to compare the clinical course of operated patients; only 1248 have been reported who have been studied in a carefully controlled and random manner. Benefit has been claimed frequently by comparing the course of patients treated surgically with medically treated patients followed the decade before. Such comparisons are not valid in view of the well documented changes in the natural history of coronary artery disease that have been occurring during the last decade. Despite a low operative mortality and rate of graft closure, available data in the literature do not indicate that initial symptomatic improvement necessarily persists, or that myocardial infarctions, arrhythmias, or congestive heart failure will be prevented, or that life will be prolonged in the vast majority of operated patients.