Function and reserve of the hypertrophic left ventricle in aortic valve disease]

Left ventricular function was analyzed by angiography in 31 patients with aortic valve disease and in 12 patients without heart disease (control group). Ejection fraction, percentage shortening of minor equator, mean velocity of fiber shortening and men left atrial pressure were considered as parameters of left ventricular function. Contractile reserve was tested by a single postextrasystolic beat. Patients with pure aortic stenosis and an increase of left ventricular muscle mass to 220% of the normal value showed no impairment of left ventricular function. Patients with pure aortic regurgitation and a left ventricular muscle mass of 260% of normal showed no significantly impaired function. Both groups increased ejection fraction and percentage shortening of the minor equator after premature beat comparable to the control group. Patients with combined lesions of the aortic valve had a left ventricular muscle mass of 360% of normal. This group showed decreased ejection fraction, percentage shortening of minor equator and mean velocity of fiber shortening as compared to the control group while mean left atrial pressure was significantly elevated. After premature beat all parameters remained depressed as compared to control group. We conclude that the degree of hypertrophy determinates cardiac function in aortic valve disease. Moderate hypertrophy shows normal function at rest, while severe hypertrophy shows impaired function.     

Arrhythmogenic effect of high blood pressure: some observations on its mechanism

An increase in aortic pressure is a reproducible way of causing ventricular ectopic rhythms. This study sought to determine whether it is the aortic pressure per se or the concommitant increase in afterload or preload that has a direct arrhythmogenic effect. Experiments were carried out in 17 anaesthetised dogs. For each 10 s period the pressure and the presence of a ventricular arrhythmia (at least one ectopic beat) were noted. In nine animals an aortic valve gradient was created (and released). The results were compared to those obtained by impeding the aortic flow at the ascending aorta. The mean systolic left ventricular pressure was significantly higher in the arrhythmia associated periods in 8/9 experiments when there was an aortic valve gradient and in 5/9 experiments when there was not. In 4/9 experiments the mean aortic pressure associated with arrhythmia was significantly lower with an aortic valve gradient than when there was no gradient and no arrhythmia. In 7/9 of these experiments, coronary sinus flow was measured volumetrically during the manoeuvres applied. The coronary flow was significantly lower when there was neither arrhythmia nor aortic valve gradient than when there was an arrhythmia (with or without an aortic valve gradient). In another eight experiments a pressure reservoir in the aorta was either raised or lowered while another pressure reservoir in the left atrium was moved in the opposite direction. Thus the mean aortic pressure could be increased while the left atrial pressure was decreased and vice versa. If the left atrial pressure was taken into account, the mean difference of the aortic pressure from its expected value, derived from the aortic v left atrial pressure regression equation, was significantly higher when there was an arrhythmia than it was when there was no arrhythmia in all eight experiments. On the other hand, the mean difference in the left atrial pressure from its expected value was significantly higher when there was an arrhythmia in 1/8, lower in 2/8 and not significantly different in 5/8 experiments. It is concluded that when the blood pressure is raised, it is the increase in afterload rather than an increase in aortic pressure itself or in the preload that has an arrhythmogenic effect on the ventricles.     

The estimation of the ventricular function by means of peak aortic flow velocity-diastolic aortic pressure relationship

Responses of the left ventricle to changes in afterload were tested in 11 open-chest dogs of which left atrial pressure was controlled arbitrarily. Maximal left ventricular dP/dt remained unchanged statistically against changes in afterload when left atrial pressure was kept constant, while it was changed with alteration of preload and by deterioration of left ventricular contractility induced by coronary ligation. Peak aortic flow velocity showed negative linear relationship against diastolic aortic pressure when left atrial pressure and left ventricular contractility were constant. This linear relation shifted downwards not only by reduction of contractility but also by lowering preload. Stroke volume also showed similar relationship, but abrupt decrease in stroke volume in higher range of aortic pressure. Effects of extracardiac factors on stroke volume which was ejected by constant ventricular contractility were considered to be complex. Peak aoratic flow velocity at 50 mmHg of aortic distolic pressure under the constant state of preload could be one of the indexes of ventricular function.     

Myocardial relaxation in atrial fibrillation

Although myocardial contractility has been known to vary from beat to beat in atrial fibrillation, myocardial relaxation in this arrhythmia has not been investigated. In this study, left ventricular relaxation was examined in seven patients with atrial fibrillation (four with mitral valve disease, one with aortic regurgitation, one with secundum type atrial septal defect and one with apical left ventricular hypertrophy). The left ventricular pressure was measured with a micromanometer-tipped catheter and the time constant of isovolumic left ventricular pressure decline (the relaxation time constant) was calculated by means of exponential curve fitting from more than 20 consecutive beats in each patient. The maximal rate of rise of left ventricular pressure (dP/dt) and the relaxation time constant were examined in relation to the preceding RR interval (RR2) and to the ratio of the RR2 interval to the pre-preceding RR interval (RR2/RR1), and the correlation coefficients were obtained. The dP/dt correlated better with RR2/RR1 than with the RR2 interval (0.82 +/- 0.05 versus 0.48 +/- 0.2), but the relaxation time constant did not show any correlation with RR2/RR1 or the RR2 interval (0.03 +/- 0.21 and 0.06 +/- 0.21, respectively). The relaxation time constant was fairly constant in each patient even when the RR2 interval and RR2/RR1 varied greatly. Thus, relaxation in atrial fibrillation is independent of changes in contractility as seen in the relation between postextrasystolic relaxation and postextrasystolic potentiation of contractility.     

Quantitative data on the afterload dependence of left ventricular dP/dtmax in isolated canine hearts

Summary In 15 canine heart-lung preparations the effect of an increase in aortic pressure on left ventricular dP/dt_max was tested. Abrupt elevation of aortic pressure by 20–80 mm Hg during diastole without change in enddiastolic pressure did not influence left ventricular dP/dt_max in the following heart beat. Left ventricular circumference increased slightly.Stepwise elevation of aortic pressure from 60 to 130 mm Hg (LVEDP maintained constant) resulted in an augmentation of the steady-state values of dP/dt_max by only 42 mm Hg/s per 10 mm Hg pressure rise.If the enddiastolic pressure was not maintained constant, the increase in dP/dt_max was 77 mm Hg/s per 10 mm Hg pressure rise.Aortic pressure alterations exhibit a slight but significant influence on left ventricular contractility in the steady-state phase, while an acute effect is not detectable, thus demonstrating that a sudden increase in coronary perfusion pressure is without immediate effect on the cardiac performance.A preliminary report was given at the 51st meeting of the German Physiological Society 1979.     

Hemodynamic correlates of late diastolic posterior motion of the aortic root

Motion of the posterior aortic root on echocardiography is related to left atrial volume change. Early diastolic posterior motion of the aortic root reflects both LA emptying and filling and has been measured as the atrial emptying index. To study late diastolic motion of the aortic root, we measured the slope of posterior motion of the aortic root after left atrial systole (following the P wave of the ECG) in 25 subjects without heart disease (Group 1), in 15 patients with left ventricular hypertrophy due to pressure overload (Group 2), and in 10 patients (Group 3) with mitral stenosis. The aortic root slope measured (mean ± SEM) 58.0 ± 1.9 mm./sec. in Group 1, 50.6 ± 4.5 mm./sec. in Group 2 (NS vs 1) and 28.8 ± 4.5 mm./sec. in Group 3, (p < 0.01 vs 1 or 2).In 16 patients (four in Group 1 and 12 in Group 2) studied at catheterization, an inverse correlation (r = ?0.74, p < 0.01) was found between the aortic root slope (over a range of 30 to 73 mm./sec.) and left ventricular late diastolic chamber stiffness measured with simultaneous left ventricular echo and high-fidelity pressure recordings. No correlation was found between this slope and either left atrial size, total aortic root excursion, left ventricular pressure pre “A” wave, height of the A wave, end-diastolic pressure, or the atrial contribution to left ventricular filling. Therefore, the aortic root slope in late diastole is decreased in mitral stenosis, and in the absence of mitral stenosis, it appears to be related to late diastolic properties of the left ventricle.     

Hemodynamic effects of acute atrioventricular sequential pacing in patients with left ventricular dysfunction

Acute atrioventricular (A-V) sequential pacing was compared with ventricular pacing in seven men with symptomatic left ventricular failure (New York Heart Association functional class III and IV) and depressed left ventricular ejection fraction (mean 29 percent, range 18 to 40). Cardiac index was higher during A-V sequential pacing than during ventricular pacing for every patient at paced rates of 75 to 100 beats/min. The mean increment was 17 percent (range 10 to 37) at a paced rate of 75 beats/ min, 23 percent (range 8 to 45) at a paced rate of 85 beats/min and 29 percent (range 19 to 55) at a paced rate of 100 beats/min. The increase in cardiac index in an individual patient did not correlate with baseline characteristics including functional class, cardiothoracic ratio, resting ejection fraction, cardiac index or balloon-occluded pulmonary wedge pressure.Arterial pressure varied from beat to beat during ventricular pacing because of the changing relation of atrial to ventricular systole. When an atrial contraction preceded a ventricular paced beat by a physiologic interval intraarterial pulse pressure uniformly increased. That increase correlated strongly (r = 0.993) with the increase in cardiac index that occurred during A-V sequential pacing. Measurement of the pulse pressure during A-V dissociation is a simple technique that may be useful for predicting the degree of improvement in cardiac output expected with methods of pacing that restore A-V synchrony.     

Correlation between myocardial structure and diastolic properties of the heart in chronic aortic valve disease: Effects of corrective surgery

Left ventricular end-diastolic properties were evaluated with cineangiography and pressure measurements before and 6 months after aortic valve replacement with a Björk-Shiley prosthesis in 10 patients with aortic stenosis, 7 patients with mixed aortic valve disease and 7 patients with aortic insufficiency. Mean left atrial pressure, left ventricular end-diastolic pressure, volume and wall thickness were measured, and the stiffness constant K_A and the elastic stiffness E_m were calculated. Myocardial cell diameter and the degree of myocardial fibrosis were determined with morphometric analysis of transmural needle biopsy specimens obtained from the left ventricular free wall at operation. Significant correlations were found between myocardial cell diameter and end-diastolic pressure (r = 0.63), mean left atrial pressure (r = 0.58), end-diastolic wall thickness (r = 0.80), K_A (r = 0.56) and E_m (r = 0.53). However, no significant correlation existed between percent fibrosis and any of these measurements. Before operation, end-diastolic left ventricular pressure, mean left atrial pressure, K_A and E_mwere significantly elevated in aortic stenosis and mixed aortic valve disease but not in aortic insufficiency. After valve replacement clinical improvement was seen in all patients. End-diastolic left ventricular pressure, mean left atrial pressure, enddiastolic volume and E_m decreased and normalized completely in all groups. End-diastolic wall thickness and K_A decreased significantly in aortic stenosis and mixed aortic valve disease (not in aortic insufficiency) but remained moderately elevated. Close correlations were found between end-diastolic wall thickness and K_A (r = 0.78) and between mean left atrial pressure and E_m (r = 0.85).

These results suggest (1) myocardial cell diameter, but not myocardial fibrosis, is a major determinant of end-diastolic properties of the left ventricle in chronic aortic valve disease. (2) Corrective surgery with a Björk-Shiley valve causes normalization of elastic stiffness of the chamber and of mean left atrial pressure, thus explaining the alleviation of congestive symptoms.     

Blood flow in pulmonary veins: III. Simultaneous measurements of their dimensions, intravascular pressure and flow

Vein flow in the large extraparenchymal pulmonary veins is pulsatile and its wave form has an inverse relationship to left atrial pressure. Extraparenchymal pulmonary veins are thin walled and collapsible. This enables them to behave as highly compliant structures. Dimensional measurements of their cross sectional area in living open chested dogs showed them to be non circular at low left atrial pressures. They rapidly assumed a circular cross section as left atrial pressure rose. Only at pressures above 1.5 kPa (11 mmHg) were the pulmonary veins circular in cross section. The aggregate volume of the large extraparenchymal pulmonary veins, when fully distended, was found to be equal to or greater than one stroke volume of the heart. The extraparenchymal pulmonary veins act as a reservoir to the left atrium so that left ventricular stroke volume can be maintained relatively unaffected by beat by beat changes in right ventricular stroke output. Their behaviour at normal mean left atrial pressures also enables them to isolate the lung capillaries from retrograde transmission of positive pressure transients from the left atrium, which could otherwise impede venous outflow of blood from the lung capillary bed.     

Atrial contribution to ventricular filling in patients with coronary artery disease as assessed by cardiac pacing

Analysis of beat to beat changes in left ventricular (LV) ejection time during cardiac pacing was utilized to assess the atrial contribution to ventricular filling in coronary artery disease. The recordings of aortic pressure were made during atrial and ventricular pacing at a rate of 5 to 10 beats/min above sinus rhythm. During ventricular pacing, LV ejection time became maximum when an atrial contraction preceded a ventricular contraction by a physiologic interval and was similar to that obtained during atrial pacing (max ET). When the atrial systole occurred with or followed the paced ventricular contraction, LV ejection time became minimum (min ET). The atrial contribution was calculated as (max ET--min ET)/max ET X 100(%). Patients with coronary artery disease had a significantly large atrial contribution. In patients without myocardial infarction, the atrial contribution was increased to compensate for impaired early diastolic filling. In patients with myocardial infarction, the atrial contribution was reduced when LV end-diastolic pressure was markedly high. The atrial contribution generally plays an important role in increasing stroke volume, but it had less effect despite the forceful atrial contraction as LV filling pressure became more elevated.     

Aortic blood flow velocity during Wenckebach periods in man

By means of the Doppler ultrasonic flowmeter catheter, phasic aortic blood flow velocity and simultaneous aortic pressure, right atrial pressure, and Lead II of the electrocardiogram were measured in 7 normal subjects and 8 patients with heart disease during right atrial pacing. At pacing rates between 110 and 170 per minute, type I, second-degree atrioventricular block appeared. The increase in peak aortic blood flow velocity was generally proportional to the preceding cycle length and inversely related to the P-R interval. These variations were more pronounced during shorter Wenckebach periods. The first beat of a period always manifested a greater peak flow velocity than did the last beat. Short cycle lengths with less ventricular diastolic filling resulted in diminished aortic systolic flow velocity, with reduction up to 80 per cent. The changes in flow velocity paralleled the changes in aortic pressure.     

Echocardiographic and hemodynamic correlates of diastolic closure of mitral valve and diastolic opening of aortic valve in severe aortic regurgitation

Acute severe aortic regurgitation (AR) is characterized by a steep increase in left ventricular end-diastolic pressure, exceeding left atrial pressure and occasionally equilibrating with aortic diastolic pressure. These pressure phenomena correlate with the M-mode echocardiographic (echo) findings of diastolic closure of the mitral valve (DCMV) and diastolic opening of the aortic valve (DOAV). Six men, aged 23 to 48 years, with recent-onset, severe AR were evaluated by M-mode echo and pressures at cardiac catheterization. DCMV was seen in all 6 patients and DOAV in 4. Near-constant time intervals from the preceding R wave of the electrocardiogram to DCMV and DOAV were seen, even in 3 patients with varying RR intervals (1 with atrial fibrillation and 2 with asynchronous and demand atrial pacing). When the RR intervals were shorter than these intervals, DCMV and DOAV did not occur. Increasing the heart rate in the 2 patients by atrial pacing resulted in a marked decrease in left ventricular end-diastolic pressure. In conclusion, DCMV and DOAV have a near constant relation to the preceding R wave of the electrocardiogram, DCMV with competence of the mitral valve must be present for DOAV to occur, DOAV indicates that the diastolic blood pressure equals left ventricular end-diastolic pressure, and heart rate is an important factor influencing the hemodynamic and echocardiographic parameters in recent-onset, severe AR.     

Comparison of echocardiographic findings in patients with nonfunctioning adrenal incidentalomas

Adrenal incidentalomas (AIs) are usually discovered incidentally after imaging unrelated to adrenal glands. We aimed to evaluate standard risk factors for systemic atherosclerosis and echocardiographic changes in patients with nonfunctioning AIs and compare them with normal subjects. We evaluated 70 patients diagnosed with AIs and 51 healthy controls. Mean levels were determined for HbA1c, LDL, uric acid, fasting plasma insulin, HOMA, and neutrophil-to-lymphocyte ratio (NLR), and these values were found to be significantly higher in the patients than the controls. The mean left atrial diameter, interventricular septum thickness, posterior wall thickness, left ventricular mass, E-wave deceleration time, isovolumetric relaxation time, and the median ratio of the early transmittal flow velocity to the early diastolic tissue velocity (E/Em) were higher in patients with AIs compared to controls. The mitral annular early diastolic velocity was lower in patients with AIs. The mean aortic diastolic diameter, stiffness index (SI), and aortic strain were higher, and aortic distensibility was lower in the patients. The mean right ventricular diameter, right atrial major-axis diameter, and right atrial minor-axis diameter were statistically higher in the patient group than the controls. A negative correlation was found between the NLR and aortic strain and aortic distensibility, while a positive correction was found between the NLR and SI. We found altered left ventricular (LV) and right ventricular (RV) echocardiographic findings in patients with AIs without known cardiovascular disease. Aortic stiffness was also increased. These changes may be related to an increase in cardiovascular risk factors in AI patients.     

Reevaluation of the role of atrial systole to cardiac hemodynamics: Evidence for pulmonary venous regurgitation during abnormal atrioventricular sequencing

Twenty open-chest dogs with experimental AV heart block were evaluated hemodynamically, angiographically, and by M-mode echocardiography to further elucidate mechanisms whereby abnormal AV sequencing results in decreased cardiac hemodynamics. During fixed-rate AV pacing, there was a consistent decrease in cardiac output, left ventricular and aortic pressures, and left ventricular dimensions with an increase in left atrial pressure as the AV interval was decreased from 100 to 0 msec, and there were further changes when the AV interval was set at ?50 and ?100 msec. The hemodynamic consequences of atrial fibrillation with regular ventricular rhythms were similar to the effects of an AV interval of 0 msec. It is important to note that retrograde blood flow into the pulmonary venous system (pulmonary venous regurgitation) was demonstrated by left atrial angiography at AV intervals of both ?50 and ?100 msec. However, left ventricular angiography failed to reveal mitral regurgitation during fixed-rate pacing at any AV interval or during atrial fibrillation with regular ventricular rates. Thus, during tachyarrhythmias characterized by abnormal AV sequencing, not only is there the loss of active atrial contribution to ventricular filling but there is also evidence for a retrograde or “negative atrial kick” further compromising cardiac hemodynamics.     

Effects of heart rate on experimentally produced mitral regurgitation in dogs

The effects of increasing heart rate (HR) on the hemodynamics of acute mitral regurgitation (MR) were studied in 8 open-chest dogs. Filling volume, regurgitant volume and stroke volume were calculated from electromagnetic probe measurements of mitral and aortic flows. The left atrial-left ventricular systolic pressure gradient was measured with micromanometers. The calculated effective mitral regurgitant orifice area varied from 10 to 128 mm², with a consequent regurgitant fraction (regurgitant volume/filling volume) of 24 to 62%. After crushing the sinus node, HR was increased stepwise from 90 to 180 beats/min by atrial pacing while maintaining aortic pressure constant. With increasing HR, filling volume, stroke volume, regurgitant volume and regurgitant time decreased; total cardiac output, forward cardiac output, regurgitant output, systolic pressure gradient, regurgitant fraction and the regurgitant orifice did not change; left ventricular end-diastolic pressure decreased; and left atrial v-wave amplitude increased. These results indicate that in acute experimental MR with a wide spectrum of incompetence, the relative distribution of forward and regurgitant flows did not change with large increases in HR. At rates >150 beats/min the atrial contraction occurs early and increases the amplitude of the left atrial v wave. This may contribute to the severity of pulmonary congestion in patients with MR.     

Assessment of the contribution of atrial systole to ventricular filling by cardiac pacing

Analysis of beat to beat changes in left ventricular (LV) ejection time during cardiac pacing was utilized to assess the atrial contribution to ventricular filling in 30 consecutive patients undergoing diagnostic cardiac catheterization. The group consisted of 9 normal subjects, 18 with coronary artery disease and 3 with congestive cardiomyopathy. The recordings of aortic pressure were made during atrial pacing and ventricular pacing at a rate 5 to 10 beats/min above each individual's sinus rhythm. During ventricular pacing, LV ejection time was the longest when an atrial contraction preceded a ventricularly paced beat by a physiologic interval and was approximately similar to that obtained during atrial pacing (maxET). When the atrial systole occurred with or followed the ventricularly paced contraction, LV ejection time was decreased (minET). Since maxET occurred in the presence of an effective atrial contraction to ventricular filling and minET in the absence of this contraction, the atrial contribution to ventricular filling was calculated as (maxET-minET)/maxET X 100 (%). LV volumes at end-systole (V1), before atrial contraction (V2) and at end-diastole (V3) were obtained according to the area-length method by tracing the silhouette of left ventriculograms using a computer system. The atrial contribution was calculated from LV volumes using the formula (V3-V2)/(V3-V1) X 100 (%). There was a good correlation (r = 0.88) between the atrial contributions calculated from LV ejection times and those calculated from LV volumes. In the patients with coronary artery disease and with congestive cardiomyopathy, the atrial contribution was significantly greater than in the normal subjects. The measurement of LV ejection time during ventricular pacing may be a clinically useful screening procedure to identify patients in whom physiologic pacing may be indicated.     

Effects of left ventricular asynchrony on time constant and extrapolated pressure of left ventricular pressure decay in coronary artery disease

To elucidate the effects of ventricular asynchrony with or without myocardial ischemia on the time constant of left ventricular pressure decay and asymptote, that is, the level to which pressure would decrease if isovolumic pressure decrease continued infinitely, left ventriculography and pressure measurements were investigated in 14 normal subjects and 25 patients with coronary artery disease. Ventricular asynchrony was quantitated by the segmental area-time curve. This study consisted of two parts. 1) After a right atrial pacing stress test, the time constant and asymptote remained unchanged in eight normal subjects. In 18 patients with coronary artery disease and pacing-induced angina, asynchrony increased, the time constant was prolonged (64 +/- 13 to 94 +/- 17 ms, p less than 0.01) and the asymptote decreased (-22 +/- 10 to -46 +/- 20 mm Hg, p less than 0.01) after the pacing. 2) During right ventricular pacing at 80, 100 and 120 beats/min in the patients, asynchrony increased and the time constant was prolonged (55 +/- 7 versus 70 +/- 10, 47 +/- 11 versus 66 +/- 19, 36 +/- 7 versus 53 +/- 13 ms, respectively, p less than 0.01 versus right atrial pacing), whereas the asymptote was unchanged in six normal subjects compared with the value during right atrial pacing at each pacing rate. In seven patients with coronary artery disease, right ventricular pacing at 80, 100 and 120 beats/min also produced an increase in the time constant, while the asymptote was unchanged. Thus, prolongation of the time constant of left ventricular pressure decay may result from ventricular asynchrony even in the absence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation between apexcardiographic a wave and posterior aortic wall motion

Left ventricular end-diastolic pressure, an apexcardiogram and an aortic root echocardiogram were recorded in 24 patients. Eleven patients (46%) had a ratio of atrial to total amplitude (a/OE ratio) greater than 14% in the apexcardiogram, and all patients had a left atrial systolic posterior aortic wall motion after the conduit period that was greater than 50% of the total posterior aortic wall excursion as measured from the O to V points (A/OV ratio) on the echocardiogram. Only 2 of 24 patients (8%) had an echographic A/OV ratio greater than 0.5 with an apexcardiographic a/OE ratio of less than 14%. There was a significantly (P less than 0.001) high degree of positive correlation between the apexcardiographic a/OE ratio and the echographic A/OV ratio (r = 0.81), the a/OE ratio and left ventricular end-diastolic pressure (r = 0.82), and the A/OV ratio and left ventricular end-diastolic pressure (r = 0.75). It is concluded that the amplitude of posterior aortic root motion during atrial systole in relation to total posterior aortic wall motion may provide a useful index for the noninvasive assessment of left ventricular compliance and end-diastolic pressure.     

Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area.

The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.     

Effects of physical training on end-diastolic volume and myocardial performance of isolated rat hearts.

We studied the performance of ventricular muscle and cardiac function of hearts from rats conditioned by swimming (CH) and from sedentary rats (SH) in an isolated working heart apparatus modified to measure end-diastolic volume by dye dilution. Instantaneous aortic flow, left ventricular (LV) pressure and oxygen consumption were measured. Heart rate and mean aortic pressure were kept constant, and atrial filling pressure was varied from 5 to 20 cm H2O. Heart weights of SH and CH were equal and end-diastolic pressures and volumes were similar at all atrial pressures. However, ejection fraction, calculated circumferential fiber velocity, peak systolic pressure, peak aortic flow, cardiac output, and stroke work were all greater in CH than in SH, and the differences increased as atrial pressure was increased. Maximal negative dP/dt was greater in CH than SH at all preloads (P less than 0.001). Oxygen consumption of CH was increased in proportion to the increase in work. These results indicate that the improved pumping performance of CH is due to a change in ventricular muscle function. Faster relaxation is a prominent effect of physical training on the rat heart and may foster more complete filling at high heart rates.