Coronary bypass for stable angina: a prospective randomized study.

To evaluate the effects of coronary-artery bypass, 100 patients with stable, disabling angina were randomized to medical (49) or surgical (51) therapy. There was no statistical difference in major cardiac events after three years (death in five medical vs. four surgical, infarction in eight vs. 10, and unstable angina requiring operation or reoperation in eight vs. three cases). Surgical patients with three-vessel disease had fewer major events (P less than 0.05) than the comparable medical group and less unstable angina requiring operation (P less than 0.02). All unstable angina was less frequent in the surgical group (15 vs. six, P less than 0.01). Functional classification improved more in surgical patients at six months (P less than 0.01) and at late followup examination (P less than 0.05). After six months, surgical patients achieved significantly higher exercise work loads (P less than 0.01), exercise heart rates (P less than 0.05), maximum paced heart rates (P less than 0.01) and myocardial lactate extraction (P less than 0.01). On the basis of this interim report of a relatively small group of patients, we conclude that bypass results in greater functional improvement and less unstable angina than medical therapy. The likelihood of death and myocardial infarction is unchanged by operation.

Effects of ouabain on myocardial oxygen supply and demand in patients with chronic coronary artery disease. A hemodynamic, volumetric, and metabolic study in patients without heart failure.

The effects of digitalis glycosides on myocardial oxygen supply and demand are of particular interest in the presence of obstructive coronary artery disease, but have not been measured previously in man. We assessed the effects of ouabain (0.015 mg/kg body weight) on hemodynamic, volumetric, and metabolic parameters in 11 patients with severe chronic coronary artery disease without clinical congestive heart failure. Because the protocol was long and involved interventions which might affect the determinations, we also studied in nine patients using an identical protocol except that ouabain administration was omitted. Left ventricular end-diastolic pressure and left ventricular end-diastolic volume fell in each patient given ouabain, even though they were initially elevated in only two patients. Left ventricular end-diastolic pressure fell from 11.5+/-1.4 (mean+/-SE) to 5.6+/-0.9 mm Hg (P less than 0.001) and left ventricular end-diastolic volume fell from 100+/-17 to 82+/-12 ml/m2 (P less than 0.01) 1 h after ouabain infusion was completed. The maximum velocity of contractile element shortening increased from 1.68+/-0.11 ml/s to 2.18+/-0.21 muscle-lengths/s (P less than 0.05) and is consistent with an increase in contractility. No significant change in these parameters occurred in the control patients. No significant change in myocardial oxygen consumption occurred after ouabain administration but this may be related to a greater decrease in mean arterial pressure in the ouabain patients than in the control patients. We conclude that in patients with chronic coronary artery disease who are not in clinical congestive heart failure left ventricular end-diastolic volume falls after ouabain administration even when it is initially normal. Though this fall would be associated with a decrease in wall tension, and, therefore, of myocardial oxygen consumption, it may not be of sufficient magnitude to prevent a net increase in myocardial oxygen consumption. Nevertheless, compensatory mechanisms prevent a deterioration of resting myocardial metabolism.

Hemodynamic changes after valve replacement with Starr-Edwards prostheses.

A brief review of the pathophysiology of aortic and mitral valve disease and the hemodynamic results of valve replacement with caged ball prostheses are described. In most patients intracardiac pressures and restored to normal at rest, although there are small pressure gradients across mechanical valves. Severe pulmonary hypertension, if present, usually will regress. With exercise, abnormalities of left atrial pressure or left ventricular function may be found after valve replacement. The causes of failure to achieve hemodynamic improvement with surgery and the late return of congestive failure are discussed.