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Twenty-one patients with partial anomalous pulmonary venous drainage with intact atrial septum have been studied. These include 13 patients not previously reported from our laboratories and eight patients with complete hemodynamics reported by others. Methods for identification of this abnormality and for identification of an intact atrial septum are described, including differential indicator dilution curves, catheter probing of the atrial septum and pulmonary angiography. Blood flow through anomalously draining lobes of the lung is usually higher than through normally drainage lobes attributable to the higher pressure differences across the anomalous lung, right atrial pressure being uniformly lower than left atrial pressure. The pulmonary vascular resistance when "standardized" to the flow of blood normally present in different portions of the lung indicated that no significant differences existed between normally and anomalously draining lobes. Six patients had coexisting rheumatic mitral stenosis and one had congenital mitral stenosis. Its influence on the hemodynamic changes produced by PAPVD is discussed.

Autologous blood clot was used to produce pulmonary macroembolism, and lycopodium spores to produce microembolism in normal mongrel dogs. Pressures were recorded from the pulmonary artery, left atrium and femoral artery; cardiac output and pulmonary blood volume (PBV) were determined using sequential indicator dilution curves from injections into the pulmonary artery and left atrium. Macro- and microembolism caused comparable elevations of pulmonary artery pressure and total pulmonary resistance. Macroembolism with blood clots resulted in marked decreases in PBV and pulmonary vascular compliance. However, microembolism with lycopodium spores caused only small decreases in PBV despite a large reduction in pulmonary vascular compliance. Prostaglandin E 1 infusion after microembolism had no effect on pulmonary hemodynamics, but caused significant systemic hypotension. After macroembolism PGE 1 infusion decreased PBV and decreased systemic arterial pressure.

Eight patients with mixed mitral stenosis and regurgitation underwent hemodynamic and angiographic study prior to mitral valve replacement. The stenotic orifice of the mitral valve was calculated employing the total left ventricular stroke volume by cineangiography as the numerator of the Gorlin Formula. Excellent agreement with the measured orifice of the mitral valve was obtained using a value of 37.9 (0.85 X 44.5) for the constant in the Gorlin formula as recommended by Cohen and Gorlin. Recalculation of this constant independently by our data yielded a value that was almost identical. Regurgitant flows and orifice sizes were calculated for each patient using the same constant as for calculation of the stenotic orifices.

The anatomy of the mitral leaflets, a classification of the variations in pathologic morphology of rheumatic stenosis, and the evolution of a practical technic for relief of that stenosis while restoring valve action are considered. The life cycle of patients suffering from mitral stenosis is reviewed and a clinical classification of these patients is presented. Some indications and contraindications for surgery are discussed in the light of strength and weakness of present surgical methods. Results of surgical treatment are reviewed.

Sotalol (MJ 1999), a beta-adrenergic blocking agent found to have no significant intrinsic myocardial depressant effects, was administered intravenously to 20 patients with heart disease. Eight of the patients had clinical and hemodynamic evidence of chronic heart failure. Doses ranged from 0.2 to 0.6 mg/kg. In all studies, heart rate decreased significantly, accompanied by comparable decreases in cardiac index and tension-time index. There were, however, no significant changes in stroke index, mean blood pressure, or left ventricular end-diastolic pressure—even in those patients with advanced heart failure, indicating that the changes noted were primarily rate-related and could not be ascribed to myocardial depression. To confirm this, further studies were performed in which heart rate was held constant by atrial pacing in normal and catecholamine-depleted dogs. Sotalol, at doses much higher than the minimal beta-blocking dose, did not change stroke index, blood pressure, left ventricular end-diastolic pressure, or estimated maximal velocity of isotonic shortening (V max ), confirming that myocardial contractility was unaffected. It is concluded that sotalol-induced beta blockade had no observable myocardial depressant action in dogs or adverse hemodynamic effects in cardiac patients, even when advanced chronic heart failure was present.

Systolic time intervals (STI) were measured in matched patients with and without right ventricular failure (RVF). STI were calculated from brachial arterial pressure tracings obtained at cardiac catheterization in four groups of patients: 1) controls, without RVF; 2) acute pulmonary embolism with and without acute RVF; 3) mitral stenosis, with and without chronic RVF; 4) primary pulmonary hypertension, with chronic RVF. In patients with pulmonary embolism without acute RVF, STI were normal. However, patients with acute RVF due to pulmonary embolism had significantly shortened left ventricular ejection times (LVETc) and significantly increased pre-ejection periods (PEPc) and increased PEPc/LVETc ratios ( P < 0.05, P < 0.001, P < 0.001 respectively). Similar results were obtained in patients with chronic RVF. In patients with mitral stenosis without RVF, STI were normal. However, in patients with chronic RVF due to mitral stenosis or primary pulmonary hypertension, PEPc and PEPc/LVETc ratios were lengthened and LVETc was shortened ( P < 0.003, P < 0.005, and P < 0.001 respectively). PEPc/LVETc ratios increased as stroke index decreased ( r = –0.55). There was also an association between PEPc/LVETc and right atrial mean pressure ( r = 0.70). These data demonstrate that patients with acute and chronic right ventricular failure have abnormal systolic time intervals possibly secondary to left ventricular dysfunction.

Hemodynamic studies were performed before and daily for 7 to 10 days after mitral valve replacement with a discoid prosthesis in 15 patients. Left atrial mean pressure fell from a mean of 27.5 mm Hg before surgery to normal levels (mean 11 mm Hg) within 24 hours of surgery. Cardiac index reached normal levels (mean 2.97 L/min/m 2 ) within 48 hours of valve replacement, and remained in the normal range throughout the early postoperative period in 12 of the 15 patients. The association of normal left atrial pressure and cardiac output in response to the increased metabolic demands of the postoperative period has not been reported with caged-ball mitral valve replacement. Pulmonary artery mean pressure and pulmonary vascular resistance showed a sharp decrease toward normal in the early postoperative period. In seven patients with systemic pulmonary hypertension, pulmonary artery mean pressure decreased from 72 mm Hg before surgery to 38 mm Hg at 7 to 10 days. The observed hemodynamic findings in these patients are consistent with experimental evidence that discoid mitral prostheses offer less resistance to blood flow than caged-ball mitral prostheses.

Congenital pulmonic stenosis is indicated by cardiac catheterization by the finding of a higher systolic pressure in the right ventricle than in the pulmonary artery. Eight cases of uncomplicated pulmonic stenosis are studied. The findings on history, physical examination, x-ray and fluoroscopy, and electrocardiogram have been analyzed and the variations in circulatory dynamics encountered in these individuals are described in detail.