Left Ventricular Isovolumic Contraction Research Articles

Regional cardioplegia and cardioprotection during transluminal angioplasty, which role for nifedipine?

The influx of calcium ions into the myocardial cell sets in motion a series of steps which end with contraction. Reduced intracellular calcium activity diminishes the contractile and mechanical function and thereby lowers myocardial oxygen demand. This is a beneficial effect when the myocardium is threatened by ischemia, such as occurs during transient coronary occlusion. We investigated the direct intracoronary injection of nifedipine, a known Ca2+ antagonist, immediately prior to transluminal angioplasty (PTCA). It was reasoned that the specific inhibitory action of nifedipine on contractile energy expenditure could provide temporary support for ischemic or potentially ischemic cardiac cells in that region during such induced interruption of flow. In order to test this hypothesis, the hemodynamic response was measured in 11 patients, first, to the injection of 0·2 mg nifedipine in the left main coronary artery, and second, to the transluminal occlusion of the stenosis for 45 s during PTCA. A second group of 14 patients was also studied for lactate production before and after PTCA of the left anterior descending artery (LAD) either with or without superselective intracoronary injection of nifedipine distal to the stenosis in the LAD. Coronary sinus (CSF) and great cardiac vein flow (GC yE), difference in lactate (A-GCV) and left ventricular isovolumic contraction (peak+/dP/dt, Vmax) were monitored. A 45 occlusion of LAD virtually eliminates all flow and induces severe ischemia accompanied by impairment of LV contractility and relaxation. Nifedipine i.c., while reducing the contractile and mechanical function of the anterior wall by a regional cardioplegic effect, increases the poststenotic flow. Lactate production in the great cardiac vein following (15 s) the LAD occlusion (TO) rose sharply. Such release is almost completely suppressed when transluminal occlusion was performed immediately after the i.c. administration of nifedipine (02 mg). It is postulated that the specific inhibitory action of nifedipine on contractile energy expenditure prevents ischemic cardiac cells from becoming anaerobic, during transluminal occlusion for periods lasting up to 90s. This may prevent them from acquiring damage, as a result of what otherwise must be termed a potentially beneficial procedure.

Descriptive analysis of instantaneous left atrial volume—with special reference to left atrial function

Instantaneous left atrial volume was determined in five calves by electrical integration of left atrial differential flow (pulmonary vein flow less mitral valve flow). Volume changes were classified and compared to previously described mitral valve flow phases. With the onset of left ventricular isovolumic contraction, the left atrium began to fill. There was an initial rapid filling period, followed by a slower but steady increase in volume. With reversal of the atrioventricular gradient, there was an initial decrease in left atrial volume. This decrease then reached a plateau, during which the left atrium remained isovolumic. With atrial contraction there was a further decrease in left atrial volume. Left atrial function (reservoir, pump, or conduit) was evaluated using an algorithm to emphasize major changes. Reservoir function occurred mainly during ventricular systole, but was also seen during diastole. Pump function occurred only during ventricular diastole and could be further divided into passive and active components. The passive component contributed the majority of blood transfer from the atrium into the ventricle. Active atrial contraction provided only 13% of the stroke volume but under the conditions of normal sinus rhythms occurred at the most sensitive point of ventricular filling. Conduit function was seen during ventricular diastole, was inversely related to the reservoir and pump functions, and thus produced a rate of ventricular filling smoother than expected and permitted a maximal transfer of blood from the left atrium into the ventricle.

Systolic time intervals in induced atrial fibrillation in the dog: effects of ectopic ventricular activation.

Electrocardiogram, atrial electrogram, phonocardiogram, aortic pressure, and left ventricular pressure were recorded during periods of induced atrial fibrillation in dogs anesthetized with a combination of morphine sulfate and pentobarbital sodium. Data were accumulated by selecting 50 cardiac cycles which terminated in ectopic ventricular electrical complexes, and comparing systolic time intervals (STI) following these beats with STI Following 50 normal ventricular complexes. Ectopic ventricular activation prolonged left ventricular pre-ejection period and external isovolumic contraction time, and reduced duration of left ventricular ejection time. These events resemble changes in STI observed following induction of atrial fibrillation from a sinus rhythm, but they are of significantly greater magnitude than the effects of atrial fibrillation alone.

EVALUATION OF LEFT VENTRICULAR PREEJECTION SYSTOLE IN NORMAL CHILDREN BY ECHOCARDIOGRAPHY

The period of systole prior to left ventricular (LV) ejection (PES) can be assessed from echograms (E), by measuring the interval from the onset of the electrical Q wave to: coaptation of the mitral valve (Q-M) or opening of the aortic valve (Q-AO), and to the onset of systolic excursions of the ventricular septum (Q-S) or posterior left ventricular wall (Q-LVW). Thus we studied a group of clinically normal school children to establish standards for these different PES, and to examine the Interrelationships between these normal events. Strip chart E were obtained from a LV sector containing mitral echoes, and from a plane of the aortic root in which valve motion was well recorded, using a 2.25 MHz transducer. PES intervals were measured in milliseconds and mean and standard error of mean values were: Q-M 49.4±1.6, Q-AO 74.0±2.4, Q-S 78.2±2.2 and Q-LVW 109.0±2.4. The differences between Q-M and Q-AO (25.1) was highly significant (p=<0.001) and represents LV isovolumic contraction time. The shorter duration of Q-S than Q-LVW (31.0) with p=<0.001 reflects the conduction time along the left branch from S to LVW. Thus this study demonstrates that PES can be analyzed from a variety of reference points recorded by E. In addition E analysis of PES may be utilized to evaluate Isovolumic systole and conduction velocity along the left bundle branch. These results also indicate that the aortic valve opening is not dependent on the systolic Inward excursion of S and LVW.

End-diastolic amplitude of mitral valve echogram in mitral stenosis.

By using simultaneous recordings of the mitral valve echogram and apex cardiogram, the mitral echogram amplitude was measured at the onset of left ventricular isovolumic contraction (MAIC). Twenty normal subjects and 68 patients with a reduced diastolic closure rate in the mitral valve echogram were studied. Of these patients, 53 had mitral stenosis, 6 aortic valvar stenosis, and 9 hypertrophic obstructive cardiomyopathy. In the normal subjects the MAIC ranged between 2 and 4 mm, average 2-7 mm, in the patients with aortic valvar stenosis or hypertrophic obstructive cardiomyopathy between 2 and 4 mm, average 2-9 mm, and in the patients with mitral stenosis between 6 and 17 mm, average 11-3 mm. The DE/MAIC ratio, where DE represents the opening amplitude of the mitral valve in early diastole, was between 3-3 and 6-5, average 5-1, in normal subjects; in the patients with aortic stenosis or hypertrophic obstructive cardiomyopathy the DE/MAIC ratio was between 2-7 and 6-5, average 4-2, and in the patients with mitral stenosis between 0-7 and 1-5, average 1-1. An excellent correlation was found between the DE/MAIC ratio and mitral valve area in the patients with mitral stenosis (r = 0-84, P less than 0-01) while the correlation between the diastolic closure rate and valve area was less satisfactory (4 = 0-62, P less than 0-01). These findings suggest that in cases with a reduced diastolic closure rate for reasons other than mitral stenosis, error can be avoided by using the DE/MAIC ratio.

Non-invasive assessment of left ventricular function after correction of severe aortic regurgitation.

Twenty patients were studied with simultaneous left ventricular cavity echocardiograms and apex cardiograms during the first two weeks after correction of severe aortic regurgitation. Endocardial echoes and apex cardiograms were digitized, so that left ventricular dimensions, their rates of change, and echo dimension-apex cardiogram relations could be studied. After aortic valve replacement, there was an early reduction in end-diastolic dimension, within 2 days, from 7-0 +/- 0-8 cm to 5-7 +/- 1-0 cm (P less than 0-001), while peak normalized shortening rate (peak Vcf) dropped from 1-9 +/- 0-6 to 1-4 +/- 0-6 S-1 (P less than 0-01), and remained unchanged for the remainder of the study. Immediately after operation, striking abnormalities of isovolumic contraction and, to a lesser extent, of early relaxation, could be seen, which regressed over 4 to 7 days, except in 2 patients who developed a low output state. These changes in left ventricular dimension, Vcf, and isovolumic contraction could not have been described by an single "measure" of left ventricular function.

Effects of posture on exercise performance. Measurement by systolic time intervals.

Because posture significantly influences cardiac performance, the effects of moderate supine and upright ergometer exercise were compared on the basis of proportional (+37%) rate increments over resting control. Supine exercise produced significant decreases in left ventricular ejection time (LVET), pre-ejection period (PEP), and isovolumic contraction time (IVCT). Ejection time index (ETI) and "corrected ejection time" (LVETc) did not change significantly. Upright exercise produced greater decreases in PEP and LVET, but despite the rate increase there was no change in LVET, which resulted in sharp increases in ETI and LVETc. The discordant directional effects on LVET and its rate-correcting indices between the two postures were consistent with hemodynamic studies demonstrating lack of stroke volume change during supine exercise and increased stroke volume over control during light to moderate upright exercise. Concordant effects on PEP and IVCT are consistent with the inotropic effect of exercise in both postures with an additional Frank-Starling effect postulated during upright exercise.