First Half Of Diastole Research Articles

Hepatic vein velocities in children with right ventricular hypertension

The important finding of this study was that Doppler assessment of hepatic venous velocities demonstrates reduced or negative velocities in the first half of diastole in children with right ventricular hypertension. The only other hepatic venous waveform change occurred during end-diastole and atrial contraction. At that time amplitude of reversed blood velocity in the hepatic vein increased directly with increased right ventricular pressure, but the magnitude of increase was not clinically significant.

Impaired early and intact late diastolic function in stunned myocardium induced by demand ischemia.

Changes in left ventricular diastolic properties of pacing-induced stunned myocardium were examined in 10 anesthetized dogs instrumented with a micromanometer for left ventricular pressure and sonomicrometers for left ventricular short axis, anterior and posterior segment lengths, and posterior wall thickness. After the creation of a critical stenosis on a carotid-circumflex coronary artery bypass, left ventricular pressure and dimensions were recorded simultaneously during temporary superior and inferior vena caval occlusion to allow for the construction of end-diastolic pressure-segment length curves. After 15 min of high-frequency pacing (190-220 beats/min), measurements were repeated and compared with those before pacing. The mean lengthening rate of each dimension during the first half of diastole was calculated as an index of early diastolic function. Three minutes after the end of pacing, coronary blood flow and perfusion pressure were unchanged, whereas systolic function of the posterior wall was depressed, indicating stunning of the posterior myocardium. The time constant of left ventricular pressure decay was prolonged by 14%. The mean lengthening rate during the first half of diastole decreased by 50% in the left ventricular internal short axis and by 119% in the posterior segment. Despite the significant impairment of early diastolic function, the regional end-diastolic pressure-segment length relation of the posterior wall was unchanged. Thus, in contrast to the results reported for pacing-induced ischemia that were measured immediately after pacing, the distensibility of the left ventricular wall in stunned myocardium induced by pacing was unchanged despite depressed early diastolic function.

Abbreviated Aortic Insufficiency in Aortic Dissection Caused by Prolapse of the Intimal Flap

Aortic insufficiency was identified in a patient with acute ascending aortic dissection. The aortic insufficiency was limited to the first half of diastole by prolapse of the intimal flap against the regurgitant orifice. This unusual pathophysiology was well demonstrated by two-dimensional and color flow Doppler echocardiography.

Square root sign of left ventricular diastolic pressure curve in atrial septal defect.

The square root (dip and plateau) sign was observed in 7 of 21 adult patients with atrial septal defect (ASD). This study evaluated left ventricular (LV) diastolic filling dynamics and hemodynamic findings in 7 patients (Group 1) with, and 14 patients (Group 2) without the square root sign; 10 normal subjects (Group 3) served as controls. No significant differences were observed in LV end-diastolic and end-systolic volumes, ejection fraction, or left to right shunt. In Group 1, 77% of LV filling was completed in the first half of diastole; this percentage was 49% and 53% in Groups 2 and 3, respectively (both p less than 0.01 versus Group 1). Early diastolic filling velocity (at 20% of diastole) in Group 1 was significantly greater, and late diastolic filling velocity (at 80% and 90% of diastole) was reduced in Group 1 compared to those in Groups 2 and 3 (all p less than 0.05). The average values for right and left ventricular end-diastolic pressures were significantly higher in Group 1 (11 +/- 2 and 10 +/- 4 mmHg, p less than 0.05) than Group 2 (7 +/- 2 and 7 +/- 2 mmHg, p less than 0.05). It is suggested that a constrictive pathophysiology due to 4 chambers interaction or right ventricular constraint may play a role in the genesis of the square root sign in ASD.

Radionuclide Detection of Abnormal Ventricular Filling Patterns in Rejecting Human Allografts

Parameters of systolic and diastolic function obtained from radionuclide ventriculography (RNV) were evaluated in nine cardiac allograft recipients. In 25 examinations, left end-diastolic volume (LEDV), cardiac output (CO), left ejection fraction (LEF), right ejection fraction (REF), heart rate (HR), peak filling rate (PFR), time to peak filling rate (TPFR), peak ejection rate (PER), and average filling rate for the first half of diastole (DFRH) were determined. Endomyocardial biopsy was obtained within 48 hours. Biopsies were divided into three treatment classes (0 = normal; 1 = rejection but not requiring supplemental therapy; and 2 = rejection requiring supplemental immunotherapy). Two independent variables of diastolic function proved to be significant (DFRH P less than 0.00001, and PFR P less than 0.002) predictors of the dependent variable class when regression analysis was applied to the data. Alterations in diastolic function associated with acute rejection are detectable on RNV and simulate changes anticipated in a primary restrictive cardiomyopathy.

The effect of intracoronary diltiazem on regional myocardial function and development of infarcts in porcine hearts.

The effect of intracoronary (i.c.) pretreatment with diltiazem on regional myocardial function and the development of infarcts was investigated in regionally ischemic, reperfused porcine hearts. The left anterior descending coronary artery (LAD) was distally ligated in 16 pigs for 20-90 min followed by 24 h of reperfusion. Eight pigs were treated with increasing doses of i.c. diltiazem (0.375 mg/min, 0.75 mg/min, 1 mg/min) prior to ischemia. Eight pigs served as controls. Regional myocardial function was assessed by implanted ultrasonic crystals. Infarct size was determined as ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). I.c. diltiazem mainly depressed early systolic shortening (isovolumetric contraction) and lengthening during the first half of diastole. Pretreatment with this calcium antagonist significantly delayed the development of infarcts. In control experiments, a mean infarct size of 74% was found after 45-min ischemia. At that time no infarction was observed in the treated group, where infarcts started to evolve after 60-min ischemia. It is concluded that the favorable action of i.c. diltiazem can mainly be ascribed to a reduced myocardial oxygen consumption at the onset of ischemia.

Diastolic filling dynamics in patients with aortic stenosis.

Left ventricular filling dynamics were investigated in 24 patients with aortic stenosis (AS). Biplane cineangiography was performed with simultaneous micromanometry in these 24 patients and in six control subjects. Twelve of the patients with AS had moderate hypertrophy with a left ventricular muscle mass index of less than 180 g/m2 (ASI group) and 12 had severe hypertrophy with an index of 180 g/m2 or more (AS2 group). Filling dynamics were also evaluated postoperatively in eight patients in the AS1 and six patients in the AS2 group. Preoperatively, end-diastolic and end-systolic volume indexes were larger and ejection fraction was lower in the AS2 compared with the control or AS1 group. Percent volume increase during the first half of diastole (%V1) was smaller in the AS1 than in the AS2 group. Peak filling rate in the first half of diastole (PFR 1) was higher in the AS2 than in the control or in AS1 group, while peak filling rate in the second half of diastole (PFR2) was considerably greater in the AS1 group than in the other two groups. The time constant of left ventricular pressure decline, an index of the rate of relaxation, was prolonged in the AS2 group. In contrast, mitral valve opening pressure (MVOP) was significantly higher in this group than in the other two groups. The constant of left ventricular chamber stiffness was slightly but not significantly greater in both AS groups than in the control subjects. After surgery in patients in the AS1 group, preoperatively reduced %V1 had increased and preoperatively enhanced PFR2 had decreased. In patients in the AS2 group, excluding one with a persistent low ejection fraction after surgery, preoperatively enhanced PFR1 decreased in association with a decrease in MVOP. Thus, left ventricular filling dynamics vary in patients with AS depending on the degree of left ventricular hypertrophy and systolic function. In patients with AS and moderate hypertrophy %V1 is slightly reduced but is compensated for by a forceful atrial contraction. In those with severe hypertrophy and systolic dysfunction increased driving pressure allows %V1 to remain within normal limits, despite prolonged left ventricular relaxation and decreased elastic recoil. Both changes in left ventricular filling dynamics tend to normalize after surgery in association with a reduction in left ventricular hypertrophy and/or an improvement of systolic function.

Left ventricular function before and after diltiazem in patients with coronary artery disease

Left ventricular contraction, relaxation and diastolic mechanics were investigated before and after intravenous administration of 15 mg of diltiazem in 15 patients with coronary artery disease. High fidelity left ventricular pressure measurements were performed in all 15 patients, with simultaneous biplane cineangiography in 13. The time constant of left ventricular isovolumic pressure decay was calculated from the linear relation of left ventricular pressure and its rate of change with time (negative dP/dt). Frame by frame volume analysis through one cardiac cycle was completed to construct volume-time and pressure-volume curves before and after the administration of diltiazem. After diltiazem, left ventricular peak systolic pressure decreased from 124 to 113 mm Hg (p less than 0.001), while left ventricular end-diastolic pressure and heart rate were not altered. Maximal positive dP/dt also remained unchanged. End-diastolic volume was not changed after diltiazem, but end-systolic volume increased from 48 to 52 ml/m2 (p less than 0.025); as a result, ejection fraction decreased slightly from 57 to 55% (p less than 0.025). The time constant of left ventricular pressure decay and maximal negative dP/dt decreased from 58 to 54 ms (p less than 0.025) and from -1,404 to -1,321 mm Hg/s (p less than 0.025), respectively. Peak early diastolic filling rate increased from 621 to 752 ml/s (p less than 0.01) in association with an increase in filling volume during the first half of diastole from 60 to 68% (p less than 0.005). No consistent displacement of the diastolic pressure-volume curve was observed after diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)

Alteration of diastolic filling rate during exercise radionuclide angiography: a highly sensitive technique for detection of coronary artery disease.

Diastolic and systolic parameters of left ventricular performance were characterized from high-frequency time-activity curves obtained in 10 normal volunteers (mean age 29 +/- 4 yr), in 25 patients with normal coronary arteries, and in 50 patients with coronary artery disease (CAD) at rest and during three stages of exercise radionuclide angiography. In the normal volunteers ejection fraction was 65 +/- 5% (SD) at rest and 78 +/- 5% with exercise (p less than .001). In patients with normal coronary arteries ejection fraction was 64 +/- 5% at rest and 72 +/- 8% with exercise (p less than .0001). In patients with CAD resting ejection fraction was 60 +/- 10% and that during exercise was 61 +/- 13% (p = NS). Peak diastolic filling rate in the first half of diastole, peak systolic ejection rate, and times to peak rates and to end-systole were measured. In the normal subjects resting peak diastolic filling rate was 3.1 +/- 0.6 end-diastolic counts/sec and it increased in all subjects with exercise to 3.6 +/- 0.7 (p less than .05). In patients with normal arteries and those with CAD peak diastolic filling rate was 2.3 +/- 0.8 at rest and with exercise this parameter increased to 3.2 +/- 1.1 (p less than .001) in patients with normal arteries and fell to 1.7 +/- 0.6 in those with CAD (p less than .001). Peak systolic ejection rate decreased from 2.5 +/- 0.8 to 1.9 +/- 0.8 with exercise in patients with CAD (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Dynamics of left ventricular filling at rest and during exercise.

Left ventricular filling dynamics were examined at rest and during supine bicycle exercise in 33 patients at cardiac catheterization; 23 had coronary artery disease (ischemia group), five with prior infarction had an akinetic area at rest (scar group), and five had minimal cardiovascular disease (control). Peak filling rate and mean filling rate during the first half and second half of diastole were assessed by biplane angiography. Simultaneous micromanometer pressures were used to compute the time constant of isovolumic pressure decay (T). Peak filling rate and mean filling rate during the first half of diastole increased with exercise in all groups (from 615 to 1050 and 358 to 681 ml/sec in controls and comparably in the scar group and from 697 to 1035 and 347 to 768 ml/sec in the ischemia group). However, T was greater (reduced rate of pressure decay) with exercise in the ischemia group (38 vs 26 msec in controls; p less than .05). Changes in the atrial driving pressure for filling appeared to counterbalance the difference in T. Mean filling rate during the second half of diastole increased with exercise in controls and in the scar group but only modestly in the ischemia group (from 202 to 349 ml/sec). The reduction in late diastolic filling during exercise-induced ischemia was associated with increased filling in early diastole, with a middiastolic volume increase from 160 to 186 ml and an upward shift in the diastolic pressure-volume relation. Thus left ventricular filling is not impaired at rest in patients with coronary artery disease who have normal ejection fractions. Furthermore, the augmentation of early filling induced by exercise is not blunted but is maintained during ischemia, apparently at the expense of elevated left atrial pressure. However, late filling is restricted with ischemia by an increase in impedance.

Left ventricular filling in differentiating restrictive amyloid cardiomyopathy and constrictive pericarditis

Left ventricular filling was evaluated with use of digitized left ventriculograms in patients with (1) restrictive amyloid cardiomyopathy, (2) constrictive pericarditis, and (3) a normal heart. Restrictive cardiomyopathy (four patients) was established by right and left heart hemodynamic studies and postmortem examination; all four patients had cardiac amyloidosis. Constrictive pericarditis (seven patients) was established by characteristic right and left heart catheterizatlon data and pericardial disease at operation; four patients had calcific and three had noncalcific anatomic changes. Normal subjects (seven patients) had normal intracardiac pressures and normal findings on left ventriculography and coronary arteriography. Left ventriculographic silhouettes were digitized and left ventricular volumes were calculated by computer at 16 ms intervals. Curves of left ventricular volume and ventricular filling rate were constructed for each patient and also for each group. Patients with restrictive amyloid cardiomyopathy had no plateau in the diastollc left ventricular filling volume curve, and their left ventricular filling rate was slower than normal during the first half of diastole. Patients with constrictive pericarditis had a sudden and premature plateau in the diastolic left ventricular volume filling curve. In addition, the left ventricular filling rate was faster than normal during the first half of diastole. Statistical analysis of left ventricular filling rate in patients with restrictive amyloid cardiomyopathy, patients with constrictive pericarditis and normal patients showed significant differences during the first half of diastole; those with restrictive amyloid cardiomyopathy had 45 ± 4 percent, those with constrictive pericarditis had 85 ± 4 percent and normal subjects had 65 ± 5 percent of left ventricular filling completed at 50 percent of diastole (p < 0.05). Thus, this study showed a significantly different profile of diastolic left ventricular filling volume and ventricular filling rate curves during the first half of diastole in patients with restrictive cardiomyopathy and those with constrictive pericarditis. The findings suggest the importance of these determinations in differentiating restrictive amyloid cardiomyopathy and constrictive pericarditis at cardiac catheterization.