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The long-term results of aortic valve replacement were reviewed in all 88 patients with isolated aortic regurgitation and all 103 patients with isolated aortic stenosis who were operated upon at the National Heart and Lung Institute from 1963 to 1971. Survival curves were compared to determine whether any of 30 preoperative clinical and hemodynamic findings correlated with long-term survival. The indices that were of predictive value in patients with aortic regurgitation were found to be different from those in aortic stenosis. Symptoms, cardiac index, and cardiothoracic ratio did not influence survival in patients with aortic regurgitation. In these patients, survival was inversely correlated with the level of left ventricular end-diastolic pressure (LVEDP): six-year survival was 74% in patients with LVEDP ≤ 10 mm Hg, 41% with LVEDP 11-20 ( P < .05), and 30% with LVEDP > 20 ( P < .01). Survival also was lower in patients with aortic regurgitation who had elevated pulmonary arterial and left atrial pressures, and in patients with electrocardiographic evidence of severe left ventricular hypertrophy (LVH). Using an LVH point score method (Romhilt-Estes), 56% of patients with a score ≤ 6 survived six years; 29% with a score > 6 survived ( P < .02). Survival in aortic stenosis did not relate to any of the above, but did correlate with preoperative functional class. Five-year survival was 70% in class II, but only 40% in class III-IV ( P < .02). Moreover, cardiothoracic ratio in patients with aortic stenosis correlated with survival in an unexpected way. Eleven of 31 patients with cardiothoracic ratio ≤ .45 had sudden unexplained death postoperatively, compared to only six of 72 patients with cardiothoracic ratio > .45 ( P < .01). This difference did not correlate with postoperative hemodynamic measurements, including magnitude of the transprosthetic gradient. We conclude that certain preoperative indices are of value in predicting long-term prognosis after valve replacement for aortic regurgitation and for aortic stenosis, but that the specific predictive indices for the two groups differ.

Twenty-two patients underwent cardiac catheterization before and an average of five months after aorto-coronary bypass operation (ACBO). Two groups were examined: 10 patients with all grafts patent, and 12 patients with one or more grafts occluded. All patients improved symptomatically, regardless of graft patency. However, in the occluded group, left ventricular end-diastolic pressure (LVEDP) increased (4.4 ± 2.2 mm Hg, P < 0.05), stroke volume index fell (9.8 ± 3.1 ml/m 2 , P < 0.05), ejection fraction decreased (10 ± 4%, P < 0.05), and left ventricular stroke work index fell (12 ± 3 g-m/m 2 , P < 0.01). Qualitative analysis of segmental left ventricular contractility was performed. Of 28 segments supplied by patent grafts, six improved and nine deteriorated. Of 22 segments supplied by occluded grafts, none improved and eight deteriorated. Frequently no angiographically demonstrable basis for the segmental deterioration was evident. We concluded that while ACBO may appreciably benefit severely symptomatic patients, our results do not substantiate the claim that ACBO should be recommended when the primary surgical goal is preservation or enhancement of myocardial function.

The response of the left ventricle to a level of supine bicycle exercise that induced angina, and the effects of ouabain (0.01 mg/kg) on this response were evaluated in 14 patients with coronary arterial disease. Before administration of ouabain, exercise was associated with depressed pumping performance of the left ventricle in four patients: stroke work fell with exercise while left ventricular end-diastolic pressure (LVEDP) increased. In five patients left ventricular (LV) performance was not frankly depressed, but nevertheless was abnormal: stroke work increased, but was accompanied by an inordinately large rise in LVEDP. In the remaining five patients LV function was essentially normal. Ouabain improved LV performance at rest in only a minority of patients, but during the stress of exercise, LV hemodynamics were improved by ouabain in 12 of the 14 patients. Five patients, however, continued to show either depressed or abnormal function with exercise after they were given ouabain. As judged by the relationship of LVEDP to LV peak dp/dt, left ventricular contractility was increased by ouabain in most patients both at rest and during exercise. Despite its beneficial effects on left ventricular performance, ouabain did not consistently alter either exercise tolerance or the LV tension-time index and pressure-rate product at which angina occurred.

Glucagon has a positive inotropic effect in normal hearts but is ineffective in animals with chronic cardiac failure. To assess directly the influence of glucagon on the human myocardium, we measured contractility and activation of adenyl cyclase, the enzyme thought to mediate the inotropic action of glucagon, in left ventricular papillary muscles obtained from 12 patients at mitral valve replacement. On the basis of preoperative ventricular end-diastolic pressures and cardiac output (independent of papillary muscle data) patients were classified in three groups: normal, cardiac failure, and condition indeterminate. Concentration-response curves showed that glucagon caused a mean rise of 11% in peak papillary muscle tension and a rise of 12% in peak rate of tension development in the normal patients; myocardial adenyl cyclase activity from each normal patient rose after glucagon (average, 84%). In the papillary muscles of the patients with cardiac failure, glucagon did not augment either tension or adenyl cyclase activity. In contrast, contractility and adenyl cyclase activity increased after norepinephrine in both normal patients and those with cardiac failure. The indeterminate group had two patients whose papillary muscles responded to glucagon and two whose papillary muscles did not respond. Thus, direct study of human papillary muscles shows that chronic cardiac failure is uniformly associated with complete loss of the normal enhancement of contractility and associated activation of adenyl cyclase after glucagon. This perhaps explains the inefficacy of this drug in treating patients with chronic cardiac failure.

Long-term follow-up is described of seven patients with fistulae between a coronary artery and the right atrium or right ventricle. Left-to-right shunt flow ranged from minimal to 2.2:1. Of six patients followed 3½ to 17 years (average 10) without operation, five demonstrated symptomatic, electrocardiographic, hemodynamic, and angiographic stability. In the sixth patient, a second angiographic study, performed 15 years after the first one, showed the right coronary artery to be occluded proximal to its fistulous communication with the right ventricle, and a left-to-right shunt could no longer be detected. Four of the seven patients underwent operative closure of a fistulous opening into the right atrium, and all four have been restudied postoperatively. Right heart pressures and the degree of dilatation of the involved coronary artery were essentially unchanged following operation. One patient, who had a moderate-sized shunt preoperatively, noted alleviation of her fatigue and demonstrated electrocardiographic improvement. Analysis of flow dynamics did not suggest that the shunt predisposed to shear-induced intimal damage of the dilated feeding coronary artery, but did suggest such changes might occur in the narrow fistulous communication. We conclude that little anatomic and functional change occurs in patients with coronary artery fistulae and small-to-moderate shunts over rather prolonged medical follow-up periods, and that operative closure does not reduce the size of the dilated proximal coronary artery. Since it is unclear whether the abnormality predisposes to premature coronary atherosclerosis, a better understanding of the natural history of the disease is necessary before the precise role of operation in patients with small-to-moderate shunts can be defined.

Two patients with obstructed valve orifices secondary to infective endocarditis are described. In one patient the mitral valve orifice was obstructed by large streptococcal vegetations, and in the second, the aortic valve orifice was obstructed by fungal vegetations. The occurrence of obstructive valvular lesions secondary to infective endocarditis is rare.

The hemodynamic findings in 28 patients with small (2M uncovered, 2M and 3M covered) Starr-Edwards mitral prostheses are compared with the findings in 12 patients with larger (3M and 4M uncovered) prostheses. Although most patients with the smaller prostheses evidenced both clinical and hemodynamic improvement after operation, the majority continued to have a significant left atrial-left ventricular pressure gradient and an elevated left atrial pressure at rest. During exercise the gradient increased, and left atrial pressure was abnormally elevated in each patient. The hemodynamic findings were decidedly less satisfactory in patients with smaller prostheses than in patients in whom it had been possible to insert larger prostheses. It is concluded that the major site of obstruction to left atrial emptying in patients with smaller prostheses is the small primary orifice of the prosthesis present at the time of insertion. Further narrowing of the primary or secondary orifices by thrombus and/or tissue ingrowth probably contributes to the obstruction in some patients.

Several important indices of myocardial performance depend upon accurate and frequent measurement of ventricular volume. Studies employing such measurements have been limited because of the difficulty of manually measuring and calculating volumes frequently enough to obtain meaningful data. We, therefore, have developed an automated method for determination of ventricular volume in man. Left ventricular cineangiograms taken in the right anterior oblique position at 60 frames/sec are projected with a flickerless projector onto a Plumbicon television camera. A second television camera is used by a skilled operator for masking out noncontributory portions of the film and for shading selected areas to facilitate accurate recognition of the opacified chamber. An electronic video-tracking device then simultaneously determines the area and the maximum length of the opacified chamber in each cine frame. These data are recorded as analog signals on magnetic tape. Volumes are calculated by computer and plotted against time. When volumes determined by this automated method are compared with those obtained by manual planimetry, the correlation coefficient is 0.96. Aluminum prolate spheroids, left ventricular casts, and left ventricular cineangiograms were studied. This automated technic permits rapid and accurate measurement of ventricular volume in patients having diagnostic left ventriculograms.

From 1963 to 1971, aortic and mitral valves were replaced in 100 patients; 22 died in hospital. Follow-up in survivors is 100%. Catheterization was performed preoperatively in 99 patients and postoperatively in 85% of survivors. The influence of 19 preoperative potential risk factors on hospital mortality, postoperative symptomatic improvement, and long-term survival (assessed by monthly cohort-adjusted survival tables) was determined. Long-term survival was also assessed by comparing average values of the various risk factors in patients surviving 1, 2, and 3 years with values in patients who died during these intervals. In addition, changes induced by operation were studied 6 months postoperatively and their value in predicting subsequent longevity assessed. Significant ( P < 0.05) findings were: a higher hospital mortality in patients with left atrial pressures ≥30 mm Hg or with fabric-covered valves; less postoperative symptomatic improvement in older patients; lower long-term survival rate in men and in patients with high left atrial, right atrial, pulmonary arterial, or right ventricular end-diastolic pressures. A decrease in radiographic heart size or a New York Heart Association class I or II status 6 months postoperatively was associated with a favorable subsequent prognosis. Postoperative hemodynamic values did not predict subsequent survival.

The hemodynamic responses of nine patients with severe coronary artery disease were studied during the precipitation of angina by both supine exercise and increasing rates of atrial pacing. Tension-time index and the first derivative of left ventricular pressure pulse (LV dp/dt) at the onset of angina were significantly higher ( P P

Two women, ages 34 and 36 years, suffered an acute transmural anterior myocardial infarction accompanied by typical ECG and serum enzyme changes. At the time of selective cinecoronary arteriography 29 and 57 months later, however, neither had demonstrable narrowing of any coronary artery. Both have persistent ECG changes of an anterior infarct and markedly diminished contractions of a large segment of the anterior wall and apex on left ventriculogram. Neither before nor after infarction has either patient experienced angina pectoris. Both patients are premenopausal, and neither of them has diabetes, hypertension, obesity, valvular heart disease, a lipoprotein abnormality, or a family history of premature coronary arterial disease. Both smoke cigarettes. At the time of infarction one patient was taking an oral contraceptive and the other was 11-days postpartum. The pathogenesis of the myocardial infarcts in these patients is unknown. Embolization or in situ thrombosis of a previously normal anterior descending coronary artery with subsequent clot lysis would explain the infarcts, the normal coronary arteriograms, and the absence of prior or subsequent angina.