Twenty-three patients were investigated during diagnostic right and left cardiac catheterization with an electromagnetic catheter-tip velocity probe. The catheter contained a pressure lumen for simultaneous measurements of intravascular pressure. Average peak and mean blood velocities were 66 and 11 cm/sec in the ascending aorta, 57 and 10 cm/sec in the pulmonary artery, 28 and 12 cm/sec in the superior vena cava, and 26 and 13 cm/sec in the inferior vena cava. The velocity pattern in the ascending aorta was similar to that obtained by other methods. Positioning of the catheter in the ascending aorta required care; in one patient with aortic stenosis the recorded blood velocity pattern was unsatisfactory. In the pulmonary artery flicking of the catheter often produced artifacts in the records. The effect of deep respiration on blood velocity in the ascending aorta and pulmonary artery was studied. In the ascending aorta the highest velocities and stroke volumes were achieved during late expiration while in the pulmonary artery blood velocity and stroke volume were greatest in inspiration. In nine patients the cardiac outputs calculated from the product of mean velocity and radiologically measured cross-sectional area of the ascending aorta or pulmonary artery were compared with cardiac outputs determined by the indicator-dilution method; the correlation coefficient was 0.73. There were no complications, and the probe proved reliable.
The LVEDP, cardiac output, and V o o2 were measured before and during supine muscular exercise in 38 patients. The normal pattern, established in seven patients without left ventricular dysfunction, consisted of an exercise factor [see Equation in PDF File], an LVEDP during exercise of less than 12 mm Hg, and little change or a decrease in LVEDP, which was accompanied in most instances by an increase in the stroke volume. In the majority of 31 patients with various cardiac lesions, but without valvular regurgitation, measurement of the LVEDP before and during exercise permitted the definition of normal or abnormal left ventricular function when the status of the left ventricle could not have been ascertained from other measurements. Thus, in most of the patients with mitral stenosis and abnormal resting hemodynamics, the pattern of left ventricular function during exercise was considered to be normal. Among the patients with aortic stenosis or left ventricular myocardial disease and elevated resting LVEDP, two types of abnormal performance of the left ventricle were identified. In some patients, an increase in LVEDP was accompanied by an increase in stroke volume, and this response was termed "abnormal left ventricular dynamics"; in the remaining patients, an increase in LVEDP and no change or a fall in stroke volume occurred and this response was termed "depressed left ventricular function." It is concluded that determination of the LVEDP before and during exercise adds importantly to measurements of the changes in cardiac output and O 2 consumption in characterizing left ventricular performance. The method employs standard catheterization techniques and appears to provide a practical and useful means for evaluating the functional status of the left ventricle in patients with and without myocardial dysfunction.
SUMMARYThe mechanics of left ventricular contraction were studied during diagnostic cardiac catheterization using high-speed cineangiography in 11 patients with severe chronic mitral regurgitation. Compared with a group of previously studied normal subjects, most of the patients with mitral regurgitation demonstrated a reduced velocity of shortening (Vf) we utilized quantitative cineangiographic and hemodynamic technics to define left ventricular performance and to estimate myocardial contractility. MethodsEleven patients with clinical and hemodynamic evidence of severe mitral regurgitation comprised the study group. Their ages ranged from 7 to 62 years (mean 38 years). None of the patients had diastolic arterial hypertension ( > 90 mm Hg); four had systolic arterial pressures greater than 140 mm Hg at rest. Two of these (D.M. and F.W.) also had trivial aortic regurgitation. Nine were in New York Heart Association functional class III, and two were in class II.2 One patient (T.S.) was believed to have sustained rupture of mitral valve chordae tendineae 6 years prior to study. Two patients (M.R. and M.M.) had congenital mitral regurgitation, and the remaining eight patients had rheumatic heart disease. Two patients had a history suggestive of ischemic chest pain; in one patient (J.M.) coronary arteriograms were within normal limits. In the other patient (F.W.) coronary arteriograms were not performed. However, localized abnormalities of left ventricular wall motion were not observed in any of the left ventriculograms.
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