Volume conductance catheter.
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Cardiac Catheterization↗
Biomedical subjects
W C Little
Publications and source records attributed to W C Little.
Mechanism of altered pattern of left ventricular filling with aging in subjects without cardiac disease.
The mechanism whereby aging, in the absence of cardiac disease, may alter the pattern of left ventricular (LV) diastolic filling is unknown. Accordingly, this study was designed to examine the factors that may be in part responsible for aging's effect on the pattern of LV diastolic filling. The LV end-diastolic pressure-volume relation was analyzed in 11 elderly subjects (68 +/- 5 years, mean +/- standard deviation) and 15 normal young adults (31 +/- 7 years) without coronary artery disease, systemic hypertension, LV hypertrophy or abnormality of LV systolic function. After catheterization, the subjects underwent pulsed Doppler analysis of mitral flow. All had normal 2-dimensional echocardiograms without LV or valvular dysfunction. Peak early filling velocity in the elderly subjects was decreased in comparison with that in young adults (61 +/- 14 vs 83 +/- 8 cm/s, p less than 0.001) and the ratio of early and late diastolic filling velocity was reduced (0.81 +/- 0.26 vs 1.88 +/- 0.40, p less than 0.001). The isovolumic relaxation time did not differ between the elderly and young subjects (158 +/- 20 vs 146 +/- 22 ms, difference not significant). In the elderly, LV end-diastolic pressure was increased (15 +/- 7 vs 11 +/- 4 mm Hg, p less than 0.05) despite a smaller end-diastolic volume index (60 +/- 16 vs 74 +/- 18 ml/m2, p less than 0.05), indicating a shift of the passive diastolic pressure-volume relation. It was concluded that early diastolic filling is reduced in normal aged subjects, even in the absence of coronary artery disease and systolic dysfunction. This altered pattern of diastolic filling may result from a shift of the passive LV diastolic pressure-volume relation.
Aged↗
Diastolic mitral regurgitation in acute but not chronic aortic regurgitation: implications regarding the mechanism of mitral closure.
In acute aortic regurgitation, left ventricular pressure rises rapidly during diastole, which produces presystolic mitral valve closure. This does not occur in chronic aortic regurgitation. Since normal, nonregurgitant mitral valve closure may depend on properly coordinated atrial and ventricular contractions, we hypothesized that abnormal mitral valve closure occurring before systole in acute aortic regurgitation may produce diastolic mitral regurgitation detectable by Doppler echocardiography. Accordingly, we performed ultrasonic Doppler examination of seven patients with acute aortic regurgitation and 12 patients with chronic aortic regurgitation. Regurgitant aortic flow was severe in all cases. Doppler sampling within the left atrium demonstrated regurgitant mitral flow in late diastole in all patients with acute aortic regurgitation. The onset of diastolic mitral regurgitation coincided with mitral valve preclosure in patients with acute aortic regurgitation and occurred regardless of the position of the mitral leaflets at the initiation of closure. In contrast, none of the 12 patients with chronic aortic regurgitation had mitral valve preclosure or diastolic mitral regurgitation (p less than 0.05 versus acute aortic regurgitation). We conclude that diastolic mitral regurgitation accompanies mitral valve preclosure, which occurs in acute but not chronic aortic regurgitation. Thus diastolic mitral regurgitation may be a Doppler sign of acute aortic regurgitation, in the absence of a markedly prolonged PR interval. Furthermore, this observation suggests that normal, nonregurgitant mitral closure requires more than an increase in left ventricular pressure above left atrial pressure, regardless of the position of the mitral leaflets before closure.
Acute Disease↗
Reversal of dyskinesis by increased end diastolic segment length in ischaemic-reperfused myocardium.
Persistent dyskinesis is universally observed after reperfusion of a severely ischaemic segment. Although inotropic stimulation shows a latent contractile reserve, it is not known whether this reserve can be recruited by increasing end diastolic segment length (local length-tension relation). To investigate this, six anaesthetised open chest dogs were placed on right heart bypass to increase end diastolic segment length independently of mean arterial pressure. Instantaneous left ventricular pressure-segment length relations and fractional systolic shortening were determined by sonomicrometry in the centre of the region perfused by the left anterior descending coronary artery during sequential increases in end diastolic segment length. Measurements were made before occlusion of the left anterior descending coronary artery, during 1 h of occlusion, and after 2 h of reperfusion. Before ischaemia, segmental shortening increased from 11.0(SEM 1.6)% to 23.5(1.5)% (p less than 0.05) as end diastolic segment length increased. Dyskinesis developed during occlusion of the left anterior descending coronary artery [12.1(2.6)% control v -7.2(1.6)% occlusion, p less than 0.05] and was present over the entire range of end diastolic segment lengths. Following reperfusion, segmental dyskinesis [-2.5(2.4)%] persisted at the lower end of the range of end diastolic segment length, but was progressively replaced by active shortening, averaging 7.3(3.2)% (p less than 0.05) as end diastolic segment length was sequentially increased. We conclude that segmental function following reperfusion is sensitive to changes in end diastolic segment length, and that active shortening is recruited from an apparently dyskinetic segment as end diastolic segment length progressively increases.
Animals↗
Comparison of measures of left ventricular contractile performance derived from pressure-volume loops in conscious dogs.
Three measures of left ventricular (LV) performance derived from pressure (P)-volume (V) loops have been proposed: the end-systolic P-V (PES-VES) relation, the stroke work-end-diastolic V (SW-VED) relation, and maximum dP/dt-VED (dP/dtmax-VED) relation. We evaluated the variability of repeated determinations, and inotropic and load sensitivity of these relations in conscious dogs. LVV was determined from three orthogonal LV diameters measured by sonomicrometry. Three to six sets of variably loaded P-V loops were generated by transient caval occlusions before and again after increasing inotropic state by infusing dobutamine (6 +/- 1 microgram/kg/min, mean +/- SD) and after increasing PES by 49 +/- 17 mm Hg with phenylephrine following autonomic blockade. The slope (MSW) of the SW-VED relation was the least variable at constant inotropic state (coefficient of variation, 4 +/- 3%) compared with the slope (EES) of the PES-VES relation (8 +/- 3%) or the slope (dE/dtmax) of the dP/dtmax-VED relation (11 +/- 6%, p less than 0.05). The extrapolated volume-axis intercept of the SW-VED relation was much less variable than the intercepts of the PES-VES or dP/dtmax-VED relations. MSW, EES, and dE/dtmax all increased (p less than 0.05) in response to dobutamine. The extrapolated volume-axis intercepts of the PES-VES and dP/dtmax-VED relations increased with dobutamine, whereas the volume intercept of the SW-VED relation was unchanged. MSW had the smallest increase in response to dobutamine (124 +/- 22% of control) compared to EES (178 +/- 67% of control) and dE/dtmax (211 +/- 68% of control, p less than 0.05). The position of the PES-VES relation, quantified as the VES at PES = 100 (V100), showed less variability (2 +/- 1%) than the slope of the PES-VES relation (8 +/- 3%, p less than 0.05). V100 decreased from 30.8 +/- 17.4 to 26.7 +/- 13.7 ml during dobutamine (p less than 0.05). After phenylephrine, EES, MSW, and dE/dtmax decreased by less than 10% (p = NS). The PES-VES relation shifted to the left with this increased afterload and V100 decreased by 3.2 +/- 1.5 ml (p less than 0.05), whereas the position of the SW-VED and dp/dtmax-VED relations were relatively unchanged.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Mechanism of reduced cardiac output during positive end-expiratory pressure in the dog.
The decrease in left ventricular (LV) stroke volume during positive end-expiratory pressure (PEEP) has been attributed to reduced LV filling and a decreased contractile state. To assess the relative importance of each mechanism, we examined the effects of zero, 5, 10, and 15 cm H2O PEEP on LV end-diastolic volume (EDV) and end-systolic volume (ESV), and on LV contractile performance using instantaneous pressure-volume loops recorded with micromanometer-tipped and volume conductance catheters in the LV. The LV contractile state was determined using the LV end-systolic pressure-volume relations, the LV dP/dtmax-EDV relation, and the LV stroke work-EDV relation. The importance of autonomic reflexes was assessed by repeating the sequence of PEEP after beta-adrenergic blockade using metoprolol, 10 mg administered intravenously. LV EDV decreased from a baseline of 37.8 +/- 3.7 ml (+/- SEM) to 35.0 +/- 3.8, 28.7 +/- 2.9, and 25.9 +/- 2.6 ml with 5, 10, and 15 cm H2O PEEP, respectively (p less than 0.05 for each comparison), which paralleled the decline in stroke volume. In contrast, LV ESV did not change significantly with PEEP. The slope and position of the LV end-systolic pressure-volume relation and the slopes of the LV dP/dtmax-EDV relation and the LV stroke work-EDV relation (p = NS) were not altered during PEEP before or after beta-adrenergic blockade, indicating no depression of systolic contractile function. We conclude that the decreased LV stroke volume that occurs with PEEP is due to impaired LV filling (i.e., reduced LV EDV) without a concomitant depression of myocardial contractility.
Adrenergic beta-Antagonists↗
A microcomputer based automated, quantitative coronary angiographic analysis system.
Rapid and accurate assessment of coronary artery stenotic severity is important in therapy and understanding of coronary artery disease. Since automated systems minimize prejudice and variations in analysis, we developed an automated, quantitative coronary analysis system utilizing an IBM PC-XT computer. Film images (35 mm) were cine-to-video converted and subsequently digitized by an IBM PC-XT computer. Given an approximate center line, the computer automatically detected edges, corrected for X-ray magnification, and calculated arterial dimensions. On objects of known dimensional sizes, the correlation coefficient between actual and calculated dimensions was 0.996 (p less than 0.01) with a standard error of estimate of 0.07 mm and +/- 3.0% reproducibility. For objects less than 1 mm in diameter, the standard error of estimate was 0.05 mm with +/- 4.1% reproducibility. However, with minimal contrast material (25%), the standard error of estimate increased to 0.20 mm with +/- 7.2% reproducibility. The results indicate that automated, quantitative coronary angiography can be achieved using an inexpensive IBM PC-XT based system, provided that the vessels are adequately opacified.
Adult↗
Alterations in left ventricular compliance due to changes in right ventricular volume, pressure and compliance.
Because of ventricular interdependence, part of the measured left ventricular diastolic pressure can be attributed to the right ventricle. Therefore, we examined the hypothesis that left ventricular diastolic properties are modified by alterations in right ventricular compliance and pressure even without a change in right ventricular volume. To examine this hypothesis, the hearts were removed from six dogs, the coronary arteries perfused with cool cardioplegic solution, and the hearts submerged in cool cardioplegic solution. Balloons were inserted into each ventricle. Left ventricular pressure-volume curves were recorded and approximated by an exponential equation. With no fluid in the right ventricular balloon (control), the exponential coefficient and constant were 0.038 (SD 0.004) ml-1 and 2.38(0.75) mm Hg respectively. With right ventricular pressure held constant at 20 mm Hg, the exponential coefficient and constant were 0.035(0.002) ml-1 and 3.71(1.64) mm Hg (p less than 0.05 v control constant), respectively. With a fixed right ventricular volume, the exponential coefficient and constant were significantly different (p less than 0.05 v control values) at 0.040(0.006) ml-1 and 2.81(0.96) mm Hg, respectively. After decreasing right ventricular free wall compliance by injecting glutaraldehyde into the right coronary artery, the exponential coefficient and constant were significantly different (p less than 0.01 v control values) at 0.058(0.010) ml-1 and 1.86(0.60) mm Hg, respectively. Thus, even with a constant right ventricular pressure or volume, a significant upward shift in the left ventricular pressure-volume relation occurred. Decreasing right ventricular free wall compliance further increased left ventricular pressure. The results of these studies indicate that the diastolic properties of the left ventricle can be modified by changes in right ventricular pressure and compliance even without a change right ventricular volume. Thus indices of left ventricular diastolic properties may be altered by changes in the characteristics of the right ventricle.
Animals↗
A simple method for measurement of left ventricular septal-lateral dimension.
In studies of myocardial performance of the intact heart, continuous measurement of the left ventricular septal-lateral diameter provides useful information. We describe a technique for placing a piezoelectric diameter gauge on the left ventricular endocardium of the intraventricular septum. This technique is simple and relatively atraumatic. It provides a way to evaluate septal-lateral dimension in either acute or chronic experiments and produces a stable signal that represents the instantaneous septal-lateral dimension of the left ventricle.
Animals↗
Response of the left ventricular end-systolic pressure-volume relation in conscious dogs to a wide range of contractile states.
We assessed the linearity and slope of the left ventricular end-systolic pressure (PES)-volume (VES) relation over a wide range of contractile states in conscious dogs. The animals were instrumented to determine left ventricular volume from ultrasonic left ventricular internal dimensions and measure left ventricular pressure with a micromanometer. Studies were performed 1-2 weeks after instrumentation while the animals were conscious. Contractile state was increased by incremental infusion of dobutamine (0, 2, 4, 6, and 8 micrograms/kg/min i.v.) and decreased by verapamil (10 mg i.v.) given after autonomic blockade. The 44 +/- 11 mm Hg (mean +/- SD) portion of the PES-VES relation generated by bicaval occlusion demonstrated a slight but consistent nonlinearity, apparent as a concavity toward the volume axis. This nonlinearity, present at all inotropic states, did not prevent the PES-VES relation from being well approximated by a straight line (r = 0.984 +/- 0.020, SEE = 2.1 +/- 1.4 mm Hg); furthermore, the slope of the PES-VES line provided a sensitive index of contractile state, progressively increasing with incremental doses of dobutamine and decreasing in response to verapamil. The volume-axis intercept of the linear approximation of the PES-VES relation was 2.9 +/- 3.3 ml less (p less than 0.05) than the volume-axis intercept of the nonlinear quadratic fit. Thus, the linear PES-VES relation, whose slope is sensitive to a wide variety of inotropic states, is a reasonable and useful description of the left ventricle in the range of PES-VES points that can be produced by bicaval occlusion in the conscious dog. However, linear extrapolation of the relation beyond the range of data points may not be accurate.
Animals↗
Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease?
To help determine if coronary angiography can predict the site of a future coronary occlusion that will produce a myocardial infarction, the coronary angiograms of 42 consecutive patients who had undergone coronary angiography both before and up to a month after suffering an acute myocardial infarction were evaluated. Twenty-nine patients had a newly occluded coronary artery. Twenty-five of these 29 patients had at least one artery with a greater than 50% stenosis on the initial angiogram. However, in 19 of 29 (66%) patients, the artery that subsequently occluded had less than a 50% stenosis on the first angiogram, and in 28 of 29 (97%), the stenosis was less than 70%. In every patient, at least some irregularity of the coronary wall was present on the first angiogram at the site of the subsequent coronary obstruction. In only 10 of the 29 (34%) did the infarction occur due to occlusion of the artery that previously contained the most severe stenosis. Furthermore, no correlation existed between the severity of the initial coronary stenosis and the time from the first catheterization until the infarction (r2 = 0.0005, p = NS). These data suggest that assessment of the angiographic severity of coronary stenosis may be inadequate to accurately predict the time or location of a subsequent coronary occlusion that will produce a myocardial infarction.
Adult↗
Frequency of large V waves in the pulmonary artery wedge pressure in ventricular septal defect of acquired (during acute myocardial infarction) or congenital origin.
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Coronary Circulation↗
Reduction of left ventricular mass in normal rats by captopril.
To assess the influence of captopril on left ventricular mass in 24 normal Sprague-Dawley rats, 12 were given high sodium (group 1) and 12 low sodium (group 2) diets. Half the rats given each diet were treated with 30 mg.kg-1/day captopril by gavage, the others were given placebo. Mean(SEM) arterial pressure was significantly reduced in group 2 treated rats (102.3(2.0) vs 123.4(1.5) mmHg, p less than 0.0002) but not in group 1 treated rats (113.8(2.5) vs 123.7(2.9)mmHg, NS). Blood pressure response to a 200 ng.kg-1 iv dose of angiotensin I was blocked in both group 2 (8.3(2.1) increase vs 29.7(3.6) mmHg increase for controls) and group 1 treated rats (7.8(2.8) increase vs 36.5(4.0) mmHg increase for controls). In group 2 treated rats the left ventricular to body weight ratio (X 10(-3)) was reduced compared with control (2.1(0.05) vs 2.4(0.08), p = 0.026), whereas in group 1 rats this ratio was not significantly different in the treated and control groups (2.3(0.06) vs 2.5(0.18), NS), suggesting that the reduction in left ventricular mass resulted from the influence of captopril on blood pressure. It is concluded that captopril causes a reduction in left ventricular mass in normal rats as a result of a reduction in blood pressure, independent of the effects of angiotensin I converting enzyme. This supports the concept that left ventricular mass is determined primarily by wall stress and is capable of both upward and downward regulation.
Animals↗
Effects of regional ischemia and ventricular pacing on LV dP/dtmax-end-diastolic volume relation.
We investigated the effects of coronary artery occlusion and pacing from ventricular sites on the relation of the maximum rate of rise of left ventricular pressure (dP/dtmax) to the end-diastolic volume (VED) in dogs previously instrumented to measure left ventricular pressure and to determine left ventricular volume from three ultrasonically measured dimensions. The dP/dtmax-VED relation was generated by vena caval occlusion and compared with the simultaneously produced end-systolic pressure-end-systolic volume (PES-VES) relation. The dP/dtmax-VED relation was described by a straight line during all conditions. Occlusion of the left circumflex coronary artery produced a rightward shift of the dP/dtmax-VED relation, increasing the volume intercept by 11.3 +/- 5.3 (SD) ml (P less than 0.05). Compared with atrial pacing, the dP/dtmax-VED relation was shifted to the right with the volume intercept increasing by 4.8 +/- 4.4 ml (P less than 0.05) during pacing from the right ventricular free wall, 3.7 +/- 5.0 ml (P less than 0.05) during pacing from the right ventricular apex, and 3.7 +/- 2.4 ml (P less than 0.05) during pacing from the left ventricular free wall. Similar increases were observed in the volume intercepts of the PES-VES relations during coronary occlusion or ventricular pacing. These results are consistent with the predictions of the time-varying elastance model and support its use as a conceptual framework to understand left ventricular performance during isovolumic contraction and at end systole, both in the normal ventricle and the ventricle with regional abnormalities of contraction.
Animals↗
Description of LV pressure-volume relations by time-varying elastance and source resistance.
If the left ventricle (LV) behaves as a time-varying elastance [E(t)] that is independent of load, then definition of E(t) during normal ejecting beats should permit accurate prediction of LV pressure (LVP) during a maximally afterloaded (isovolumic) beat. We tested this hypothesis in six dogs preinstrumented to measure LVP and aortic flow (Q) and to determine LV volume (V) from three dimensions. LVP and V were varied by caval occlusions. These data were used to determine E(t) and minimal volume required to generate pressure (Vo) at 10-ms intervals during systole using a simple E(t) model, P(t) = E(t) [V(t)-Vo], where P(t) is LVP at any time after the onset of contraction, and V(t) is the LV volume at t. LVP was measured during isovolumic beats generated by sudden balloon occlusion of the ascending aorta. The simple E(t) model accurately predicted isovolumic LVP during the first 70 ms of systole (r = 0.99) and also the end-systolic LVP but underestimated LVP during midsystole by 48 +/- 5 (SD) mmHg (P less than 0.05). When a pressure-dependent source resistance (K = 0.0015 s/ml) was added to the model to reduce LVP in proportion to Q, such that P(t) = E(t) [V(t)-Vo] X [1 - KQ]), LVP during the isovolumic beat was accurately predicted throughout systole (r = 0.99). However, the time to develop peak isovolumic pressure was 22 +/- 7 ms less than predicted. Similar results were obtained during inotropic stimulation with dobutamine in five animals.
Animals↗
Direct assessment of right ventricular transmural pressure.
Although the measurement of transmural pressure is important, calculation of transmural pressure is complicated by the difficulties in measuring pericardial pressure. Recently, flat balloons have been proposed to measure pericardial pressure. Over a wide range of volumes, right ventricular diastolic pressure and pericardial balloon pressure were similar in diastole, suggesting that the right ventricle is unstressed at physiologic volumes and that right atrial pressure can be used to estimate pericardial pressure. To evaluate these concepts and to assess indirectly the accuracy of measuring pericardial pressure using flat balloons, six canine hearts were examined postmortem. The pericardium was removed and the hearts were submerged in cold cardioplegic solution. Balloons were inserted into the right and left ventricles, and right and left ventricular pressure-volume curves were obtained. Right ventricular transmural pressures of 2.6 +/- 0.5, 3.9 +/- 0.9, 5.9 +/- 1.4, and 8.9 +/- 2.4 mm Hg were required to distend the right ventricle to 10, 20, 30, and 40 ml, respectively. For the left ventricle, transmural pressures of 3.4 +/- 0.7, 5.4 +/- 1.2, 8.6 +/- 2.1, and 14.1 +/- 3.8 mm Hg were recorded at volumes of 10, 20, 30, and 40 ml, respectively. Although the right ventricular transmural pressures were less than the left ventricular transmural pressures over the physiologic range, right ventricular transmural pressures were always positive and increased with increments in ventricular volume. Thus the right ventricle is not unstressed over the entire range of physiologic volumes, suggesting that pericardial balloon pressures may overestimate pericardial pressure and that right atrial pressure cannot be used to estimate pericardial pressure.
Animals↗
Influence of heart rate on left ventricular performance in conscious dogs.
The effects of atrial pacing on the left ventricular end-systolic pressure-volume relation, a relatively load-insensitive index of left ventricular performance, were studied in 8 chronically instrumented, conscious dogs. Six of the dogs were studied while autonomically intact, and 2 were studied after autonomic blockade with 2 mg/kg i.v. propranolol and 0.2 mg/kg i.v. atropine. Left ventricular pressure was measured with a micromanometer and left ventricular volume was determined from 3 ultrasonic orthogonal dimensions. Pressure was varied by caval occlusions at control heart rate and after atrial pacing at 100, 120, 140, 160, 180, and 200 bpm. The end-systolic pressure-volume relation was linear in every case (r = 0.97 +/- 0.03, SD). In the autonomically intact dogs, Emax, the slope of the end-systolic pressure-volume relation, was directly and monotonically related to heart rate in every dog, increasing to 238 +/- 99% of control at peak pacing rate (p less than 0.05). V0, the zero pressure intercept of the relation was also directly related to heart rate in every dog and increased 8.6 +/- 5.5 ml from control to peak pacing rate (p less than 0.05). Autonomic blockade did not attenuate these effects. This rightward shift of the end-systolic pressure-volume relation results in a reduced stroke volume from any end-diastolic volume, modulating the hemodynamic benefits of enhanced contractility. T, the time constant of isovolumic pressure fall during ventricular relaxation, was determined from beats with matched end-systolic pressures. T was related to heart rate, falling by 20 +/- 10.3% over the range of rates studied in the autonomically intact dogs and by 23.1 +/- 6.2% in the autonomically blocked dogs. Thus, the ventricle relaxes more rapidly at higher heart rates. We conclude that the frequency of contraction is concluded as an important determinant of overall pump function throughout the cardiac cycle in conscious dogs.
Animals↗
Comparison of effects of dobutamine and ouabain on left ventricular contraction and relaxation in closed-chest dogs.
Because catecholamines and digitalis have different effects on the time course of myocardial intracellular calcium concentration, their effects on the time course of left ventricular contraction and relaxation may also be different. To study this question, dogs were instrumented to measure left ventricular pressure and determine left ventricular volume from three ultrasonic dimensions. After full recovery from the instrumentation, the effects of dobutamine (2-10 micrograms/kg), ouabain (0.5 mg i.v.) alone, and ouabain given after propranolol (2 mg/kg i.v.), or phentolamine (5 mg i.v.) and incremental doses of ouabain (0.25-0.75 mg i.v.) were assessed on different days. Left ventricular pressure and volume were varied by caval occlusions. Dobutamine significantly increased the slope of the left ventricular end-systolic pressure-volume relation (Emax) and the slope of the dP/dtmax-end-diastolic volume relation (dE/dtmax), while significantly decreasing the time from end-diastole to end-systole (tmax) and the time constant (T) of the isovolumic fall in left ventricular pressure. Ouabain also increased Emax and dE/dtmax but did not alter tmax or T. Dobutamine produced a greater increase in dE/dtmax than in Emax, whereas ouabain produced similar increases in both. These effects of ouabain were not altered by pretreatment with propranolol or phentolamine. We conclude that although dobutamine and ouabain are both positive inotropes that increase Emax, dobutamine speeds the rate of left ventricular contraction (tmax) and relaxation (T), whereas ouabain does not. These effects of ouabain and dobutamine on global parameters of left ventricular chamber performance mirror their influence on intracellular calcium availability. Furthermore, these observations are consistent with the predictions of the time-varying elastance model of the left ventricle and support its usefulness as a conceptual framework to understand and link events occurring during isovolumic contraction, end-systole, and isovolumic relaxation.
Animals↗