Ventricular Isovolumic Relaxation Time Research Articles

Effect of diltiazem on left ventricular isovolumic relaxation time in patients with hypertrophic cardiomyopathy.

The effect of diltiazem on left ventricular isovolumic relaxation time was examined in 11 patients with hypertrophic obstructive and non-obstructive cardiomyopathy in a combined study using phonocardiograms and echocardiograms. Five to 10 min after intravenous injection of diltiazem (0.2 mg/kg, body weight), a prolonged isovolumic left ventricular relaxation time, which was measured from aortic component of the second heart sound to the mitral opening on the echocardiogram, decreased from 63.1 +/- 26.0 to 46.9 +/- 28.0 msec (p less than 0.01). This study suggests that diltiazem, one of the calcium blocking agents, may ameliorate the impaired left ventricular diastolic function in patients with hypertrophic cardiomyopathy.

Modification of abnormal left ventricular diastolic properties by nifedipine in patients with hypertrophic cardiomyopathy.

The effect of nifedipine on left ventricular isovolumic relaxation and diastolic filling properties and systemic and left ventricular hemodynamics was studied in 15 patients with hypertrophic cardiomyopathy. After nidefipine (10 mg sublingually), the prolonged left ventricular isovolumic relaxation time assessed by echocardiography decreased from 112 +/- 26 to 83 +/- 23 msec (p less than 0.0001), and the left ventricular pressure decay as measured by time constant T improved from 63 +/- 20 to 49 +/- 11 msec (p less than 0.05). Left ventricular filling dynamics also improved as assessed by a return toward normal in the depressed peak rate of left ventricular diastolic filling (dimension change 72 +/- 37 to 101 +/- 39 mm/sec, p less than 0.01) and the peak rate of posterior wall thinning (47 +/- 31 to 68 +/- 36 mm/sec, p less than 0.001). These changes were accompanied by hemodynamic evidence of improved diastolic function shown as a decrease in left ventricular end-diastolic pressure and a downward shift in the left ventricular diastolic pressure-dimension relationship, suggesting improved left ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic arterial blood pressure, and no depression of the left ventricular percent fractional shortening or cardiac index. These data indicate that abnormal left ventricular relaxation and diastolic filling rates in hypertrophic cardiomyopathy are dynamic and favorably modified by nifedipine, and that this effect is not related to a depression of left ventricular systolic function.

Noninvasive study of early diastole in mitral stenosis.

Cardiac events of early diastole were studied in 50 normal subjects and 46 patients with mitral stenosis (MS) by simultaneous recordings of the mitral valve echogram (MVE), phonocardiogram, and apexcardiogram (ACG). Left ventricular isovolumic relaxation time (IRT), measured between A2 and onset of the MVE opening motion, had almost the same values in normals 54 +/- 7 msec, and MS 51 +/- 16 msec. The interval between A2 and the ACG "O" point was approximately double that of IRT: 99 +/- 11 msec in normal subjects, 109 +/- 20 msec in MS. The normal MVE opening motion had a velocity 293 +/- 76 mm/sec and duration 45 +/- 6 msec, values significantly different (P less than 0.001) from 536 +/- 271 mm/sec, 23 +/- 7.5 msec found in MS patients. In atrial fibrillation the length of the cardiac cycle did not affect A2-O interval or mitral valve opening movement duration; however cycle length was clearly related to isovolumic relaxation time. This resulted in a variation in the interval between completion of the mitral valve opening (opening snap) and O point. This interval was longer after a short diastole and vice versa.

AURICULAR SYSTOLE AND ITS RELATION TO VENTRICULAR OUTPUT

AURICULAR SYSTOLE AND ITS RELATION TO VENTRICULAR OUTPUT