Effect of Ventricular Extrasystoles on Closure of Mitral Valve
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Mitral valve function was assessed by roentgen videodensitometry. Mitral reflux was rare when single ventricular ectopic systoles were produced by electronic stimulation of the right or left ventricle at various times in the cardiac cycle. It was also rare during the compensatory pause after the ectopic systole or with the following postectopic systole. Recurrent ventricular ectopic systoles interposed once per cycle were associated with minor reflux when introduced in mid-cycle. Such extrasystoles occurred late enough in the cardiac cycle for the ventricle to relax after the primary systole and for the mitral valve to open before the extrasystole. The extrasystolic contractions were, however, weak and incapable of opening the aortic valve. When interposed early in the cardiac cycle, extrasystolic potentiation of the primary ventricular contraction occurred, and no or minimal mitral reflux was observed.Keywords:
Cardiac cycle
Systole
Two postero-anterior chest roentgenograms were exposed, one during diastole and one during systole, on each of 359 patients, 35 sets of films being later discarded because of technical errors. Fifty-two per cent of the patients showed changes of 0.3 cm or less, 41 per cent showed alterations of 0.4 to 0.9 cm, and 7 per cent a variation of 1.0 to 1.7 cm in transverse cardiac diameter. It is concluded that the set of films is more useful in evaluating heart size than one film exposed at a random point along the cardiac cycle.
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Myocardial blood flow (MBF) varies throughout the cardiac cycle in response to phasic changes in myocardial tension. The aim of this study was to determine if quantitative myocardial perfusion imaging with cardiovascular magnetic resonance (CMR) can accurately track physiological variations in MBF throughout the cardiac cycle. 30 healthy volunteers underwent a single stress/rest perfusion CMR study with data acquisition at 5 different time points in the cardiac cycle (early-systole, mid-systole, end-systole, early-diastole and end-diastole). MBF was estimated on a per-subject basis by Fermi-constrained deconvolution. Interval variations in MBF between successive time points were expressed as percentage change. Maximal cyclic variation (MCV) was calculated as the percentage difference between maximum and minimum MBF values in a cardiac cycle. At stress, there was significant variation in MBF across the cardiac cycle with successive reductions in MBF from end-diastole to early-, mid- and end-systole, and an increase from early- to end-diastole (end-diastole: 4.50 ± 0.91 vs. early-systole: 4.03 ± 0.76 vs. mid-systole: 3.68 ± 0.67 vs. end-systole 3.31 ± 0.70 vs. early-diastole: 4.11 ± 0.83 ml/g/min; all p values <0.0001). In all cases, the maximum and minimum stress MBF values occurred at end-diastole and end-systole respectively (mean MCV = 26 ± 5%). There was a strong negative correlation between MCV and peak heart rate at stress (r = −0.88, p < 0.001). The largest interval variation in stress MBF occurred between end-systole and early-diastole (24 ± 9% increase). At rest, there was no significant cyclic variation in MBF (end-diastole: 1.24 ± 0.19 vs. early-systole: 1.28 ± 0.17 vs.mid-systole: 1.28 ± 0.17 vs. end-systole: 1.27 ± 0.19 vs. early-diastole: 1.29 ± 0.19 ml/g/min; p = 0.71). Quantitative perfusion CMR can be used to non-invasively assess cyclic variations in MBF throughout the cardiac cycle. In this study, estimates of stress MBF followed the expected physiological trend, peaking at end-diastole and falling steadily through to end-systole. This technique may be useful in future pathophysiological studies of coronary blood flow and microvascular function.
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A realistic model of the left ventricle of the heart was previously constructed, using a cast from a dog heart which was in diastole. Previous studies of the three-dimensional heart model were conducted in systole only. The purpose of this investigation was to extend the model to both systole and diastole, and to determine what the effect of a previous cardiac cycle was on the next cardiac cycle. The 25.8 cc ventricular volume was reduced by 40% in 0.25 seconds, then increased to the original volume in another 0.25 seconds and then allowed to rest for 0.25 seconds. Runs done with an ejection fraction of 60% showed little variation from one cardiac cycle to another after the third cardiac cycle was completed; the maximum velocity could vary by over 30% between the first and second cardiac cycles. In systole, centerline and cross-sectional velocity vectors greatly increased in magnitude at the aortic outlet. Most of the pressure drop occurred in the top 15% of the heart. The diastolic phase showed complex vortex formation not seen in the systolic contractions; these complex vortices could account for experimentally observed turbulent blood flow fluctuations in the aorta.
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