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SUMMARY End-systolic pressure (PE8), volume (VES), wall tension (TE8) and circumference (CES) of the human left ventricle were studied at cardiac catheterization in 24 subjects with varying degrees of left ventricular dysfunction. Acute alterations in systolic load con-sistently resulted in changes in VEs and CEs, with a smaller volume and circumference characterizing the lower systolic load in each subject. End systolic pressure-volume lines were constructed by plotting PEs against VEs at the higher and lower systolic load in each subject. tricular cineangiography and simultaneous left ventricular or aortic pressure recording formed the study population. In sixteen subjects afterload was reduced with an organic nitrate. Hemodynamic and angiographic measurements were made before (control), and 15 minutes after the start of an intravenous infusion of sodium nitroprusside given at a rate sufficient to lower mean aortic pressure 15-20 mm Hg (nine subjects). Similar measurements were made before and after administration of 10 mg chewable (buccal absorption) erithrityl tetranitrate (three subjects) or 20 mg isosorbide dinitrate, p.o. (four subjects). In these subjects, heart rate was comparable in both states without atrial pacing. In three subjects, measurements were made before and 15 minutes after the start of an intravenous infusion of methoxamine given at a rate sufficient to raise aortic mean pressure by greater than 20 mm Hg; in these subjects, atrial pacing was utilized to assure comparable heart rates in the two states. In each study, quantitative left ventriculography together with simultaneous left ventricular or aortic pressure measurement was carried out in two states: before and during afterload manipulation. Data were included in the analysis only when (a) ventriculograms and pressure tracings from both states were technically of high quality for quantitation of left ventricular volume and pressure, and (b) changes in mean aortic pressure for the isosorbide dinitrate and erithrityl tetranitrate studies were at least 10 mm Hg. In 19 subjects left ventricular volumes and pressures were determined at two states of systolic loading.The remaining five subjects were selected on the basis of having single ventricular extrasystolic beats during quantitative biplane left ventriculography with simultaneous recording of left ventricular or aortic pressure. In these subjects the left ventricular end-systolic pressure-volume relations of control and post-extrasystolic potentiated beats could be compared.For the total group of 24 subjects, left ventriculography was carried out using biplane 35 mm cineangiography (PA and lateral projection) in 16 subjects, and single plane 35 mm cineangiography (right anterior oblique projection) in eight subjects. Left ventricular volumes were determined by planimetry using the area-length method of Dodge and coworkers12 and Kasser and Kennedy,13 and a small computer 845

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The increased left ventricular end-diastolic pressure associated with myocardial ischemia was studied in 19 patients at cardiac catheterization. Single plane left ventriculograms were performed using high fedelity micromanometer tipped catheters before and immediately following rapid atrial pacing. Left ventricular diastolic properties were evaluated by constructing diastolic pressure-volume curves from the simultaneous pressure and volume data. In seven control patients, there was no significant change in left ventricular hemodynamics or the diastolic pressure-volume curve after atrial pacing. Twelve patients with significant coronary artery disease developed angina during pacing and had an increased left ventricular end-diastolic pressure (18 +/- 2 mm Hg, control, vs 30 +/- 2 mm Hg, angina, P less than .01) in the immediate post-pacing period. In these patients, the post-pacing ejection fraction was modestly decreased (0.63 +/- 0.03, control, vs 0.57 +/- 0.03, angina P less than 0.01), and left ventricular volumes at end systole (59 +/- 8 cc, control, vs 74 +/- 9 cc, angina, P less than 0.0125) were increased. The post-pacing diastolic pressure-volume curves in all 12 patients were shifted upward as compared with control so that for any given diastolic volume, pressure was higher during angina. The data indicate that the increased left ventricular diastolic pressure during myocardial ischemia is the result of both impaired left ventricular systolic performance and altered left ventricular diastolic properties.

Left ventricular function during sustained isometric handgrip exercise was studied at the time of cardiac catheterization in 8 normal subjects and 26 patients with heart disease. Both groups showed increases in heart rate, aortic mean blood pressure, and cardiac minute output with no change in systemic vascular resistance. Left ventricular filling pressure and stroke work were measured before and during isometric exercise in I7 cases. In 7 normal subjects, stroke work increased (8i + 8 8 to I04 ± II g m, P< O OI) without a significant change in left ventricularfilling pressure (6-8 + o 8 to 7.5 ± I-2 mmHg, NS) suggesting a shift to a higher ventricularfunction curve. Patients with heart disease, however, showedgreat variability in their stroke work response to isometric exercise (5 with increase, 3 with no change, and 2 with decrease), despite a significant increase in left ventricular filling pressure (9X6 9 mmHg to I5 5±+i6 mmHg, P< o.oi). Myocardial mechanics during isometric exercise were studied in 6 normal subjects and 8 patients with heart disease. Left ventricular pressure-velocity curves were shifted upwards and to the right in all 6 normal subjects and in 7 of the 8 patients with heart disease. Vmax (developed pressure) increased in both normal subjects (74 ±6 to I09± 5 sec-1, + 47%, P< O OI) and to a lesser extent in the patients with heart disease (59 ± 8 to 82+I2 sec + 39%,3 P< o.oi) in response to isometric exercise. Similarly, maximum left ventricular dp/dt increased in both normals (i88i + I63 to 2408+ I29 mmHg/sec, P< o oi) and patients with heart disease (I540 ± I40 to 1976 24I mmHg/sec, P < o oi). These observations suggest that the normal physiological response to isometric exertion includes a major increase in left ventricular myocardial contractility. For the normal heart, this increase appears sufficient to account completely for the increased ventricular performance associated with handgrip exercise. For the diseased heart, increased ventricular performance induced by handgrip appears also to be mediated by increased contractility, but in addition by varying degrees of reliance upon the Frank-Starling mechanism, depending upon the adequacy of inotropic (ccntractility) reserve to meet the stress imposed by isometric exercise.

An approach to the quantitative assessment of left ventricular (LV) diastolic stiffness in man has been developed utilizing strip-chart recordings of simultaneous ultrasonic LV dimensions, LV pressure, and electrocardiogram (ECG). In 23 patients without regional abnormalities of contraction, LV pressure, and LV internal diameter (D = distance between endocardial surfaces of LV posterior wall and septum at the plane of the mitral valve) were determined at the onset (P 1 , D 1 ) and peak (P 2 , D 2 ) of left atrial mechanical systole. In addition, left ventricular volumes, V 1 and V 2 , were calculated from D 1 and D 2 using a regression formula for end-diastolic volume previously determined from biplane angiographic studies. This allowed calculation of ΔP/ΔD and ΔP/ΔV associated with the "a" wave of the LV pressure trace, and these ratios were utilized as measures of LV stiffness late in diastole. Patients with LV hypertrophy by standard ECG criteria had much greater late diastolic stiffness (11 patients, ΔP/ΔD = 6.1 ± 1.1 mm Hg/mm, ΔP/ΔV = 1.0 ± 0.2 mm Hg/cc) than those without LV hypertrophy (12 patients, ΔP/ΔD = 1.8 ± 0.2 mm Hg/mm, ΔP/ΔV = 0.29 ± 0.04 mm Hg/cc, P < 0.001 for each ratio). Comparison of the stiffness ratios showed significant variation among patients with different disease states. Thus, late diastolic stiffness was highest in patients with aortic stenosis (three patients, ΔP/ΔD = 8.9 ± 2.9 mm Hg/mm, ΔP/ΔV = 1.5 ± 0.5 mm Hg/cc), lowest in mitral stenosis (four patients, ΔP/ΔD = 1.5 ± 0.5 mm Hg/mm, ΔP/ΔV = 0.23 ± 0.06 mm Hg/cc), and intermediate in patients with aortic regurgitation (three patients, ΔP/ΔD = 4.8 ± 0.7 mm Hg/mm, ΔP/ΔV = 0.83 ± 0.12 mm Hg/cc) and mitral regurgitation (three patients, ΔP/ΔD = 3.2 ± 0.7 mm Hg/mm, ΔP/ΔV = 0.5 ± 0.1 mm Hg/cc). It is concluded that the quantitative evaluation of LV diastolic stiffness obtained by this approach correlates well with the presence or absence of LV hypertrophy and with the underlying pathophysiology.

Nine patients who underwent aortic-valve replacement for acute aortic regurgitation due to infective endocarditis were studied for clinical features that may be useful in assessing the severity of this condition. The traditional physical signs of a wide pulse pressure were absent. As compared to a group of patients with chronic aortic regurgitation, the mean (plus or minus S.D.) pulse pressure (55 plus or minus 7 vs. 105 plus or minus 22 mm Hg), left ventricular end diastolic volume (146 plus or minus 28 vs. 264 plus or minus 64 ml per square meter) and stroke volume (89 plus or minus 22 vs. 163 plus or minus 57 ml per square meter) were significantly smaller in the acute group (P less than 0.01). Left ventricular pressure exceeded left atrial pressure in late diastole, causing premature closure of the mitral valve, and the degree of early closure reflected the increase in left ventricular end diastolic pressure. Premature closure of the mitral valve was demonstrated by echocardiography in all patients. Those with echocardiographic signs of very early mitral-valve closure have severely volume-overloaded ventricles and are candidates for early valve replacement.