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Biomedical subjects

M R Zile

Publications and source records attributed to M R Zile.

90 records · Page 5Linked to original sources
PubMed1989

Stress-shortening relations and myocardial blood flow in compensated and failing canine hearts with pressure-overload hypertrophy.

Serial changes in left ventricular (LV) size and function during the adaptation to chronic pressure overload and the transition to pump failure were studied in 16 conscious dogs (aortic bands placed at 8 weeks of age). Echocardiographic data at baseline and at 3, 6, 9, and 12 months after banding revealed a progressive increase in LV mass in all dogs. In six dogs with LV pump failure, there was a progressive decline in circumferential fiber shortening (29 +/- 4% at 12 months); this was significantly less than that seen in five littermate controls (38 +/- 3%, p less than 0.05). The average LV to body weight ratio in this group was 9.8 +/- 2.7 g/kg. In 10 dogs without pump failure (compensated LVH group), shortening exceeded that seen in the controls (43 +/- 4%, p less than 0.05); the LV to body weight ratio was 7.7 +/- 1.0 g/kg. At 12 months (cardiac catheterization), the LV end-diastolic pressure was higher in the failure (25 +/- 15 mm Hg) than in the compensated group (8 +/- 5 mm Hg, p less than 0.05); mean systolic stress was also higher in the failure group (313 +/- 67 g/cm2) than in the compensated group (202 +/- 53 g/cm2, p less than 0.05). The transmural distribution of myocardial blood flow was measured (at 12 months) with the radioactive microsphere technique; flow data were then related to an index of demand (a stress-time index). There was preferential blood flow to the subendocardial layers in the control (endo/epi = 1.28) and compensated hearts (endo/epi = 1.10), but in the failure group there was a relative decrease in subendocardial flow (endo/epi = 0.92). However, the absolute values for subendocardial flow in the normal, compensated, and failure groups were 77 +/- 54, 125 +/- 48, and 113 +/- 64 ml/min/100 g; the stress-time indexes in the subendocardial shell were 38 +/- 11, 74 +/- 19, and 93 +/- 34 g sec.10(2)/cm2/min. Despite what appears to be a marginal balance between blood flow and the stress time index in the failure group, the myocardial high energy phosphates were not depleted and the inoptropic state was not depressed. In this model of LV hypertrophy, the observed differences in fiber shortening can be explained on the basis of the inverse afterload-shortening relation; pump failure was due to an inadequate LV hypertrophy with afterload excess.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1989

The effect of acute alterations in left ventricular afterload and beta-adrenergic tone on indices of early diastolic filling rate.

The effects of an acute increase in left ventricular systolic pressure and the effects of an intravenous isoproterenol infusion on myocardial (segment) lengthening rate and chamber (minor axis dimension) filling rate were examined in 12 anesthetized dogs. Measurements of left ventricular systolic pressure (by micromanometer) and of segment length and chamber dimension transients (by ultrasonic crystals) were made in variably afterloaded beats (three-beat descending aortic cross-clamp) before and during an isoproterenol infusion that raised (+)dP/dt by 40%. During the baseline state, we found an inverse relation between the peak rate of increase in minor axis dimension [(+)dD/dt] and systolic pressure over a wide range of systolic pressures (110-160 mm Hg) and end-systolic dimensions (25-40 mm); peak (+)dD/dt and end-systolic dimension were also inversely related. During isoproterenol infusion, end-systolic dimension fell from 29.7 +/- 3.1 to 28.0 +/- 3.1 mm and (+)dD/dt increased from 79.6 +/- 8.0 to 90.1 +/- 8.7 mm/sec; however, the slope and y intercept of the relation between (+)dD/dt and end-systolic dimension were unchanged. Peak (+)dD/dt at a common end-systolic dimension of 31 mm was nearly equal during baseline and isoproterenol states (64.2 +/- 6.3 vs. 65.1 +/- 6.6 mm/sec). Similar results were found using segment length transients. We interpret these data to indicate that (+)dD/dt is strongly influenced by changes in systolic pressure and dimension and that isoproterenol-induced changes in (+)dD/dt are mediated, at least in part, through changes in systolic pressure and dimension.

Animals↗
PubMed1987

Hemodynamic correlates of left ventricular versus right ventricular radionuclide volumetric responses to vasodilator therapy in congestive heart failure secondary to ischemic or dilated cardiomyopathy.

Previous studies have failed to demonstrate the clinical relevance of radionuclide functional measurements during treatment of congestive heart failure (CHF). In the present study, data derived before and during nitroprusside infusion were analyzed in 16 patients with CHF to compare correlations of changes in left (LV) and right ventricular (RV) radionuclide measurements with simultaneous changes in 8 hemodynamic variables. Nitroprusside infusion decreased systemic artery pressure, pulmonary arterial wedge pressure, pulmonary artery pressure, right atrial pressure, and pulmonary and systemic vascular resistance, and increased cardiac output. Nitroprusside decreased LV and RV end-diastolic and end-systolic volumes and increased LV and RV ejection fraction and stroke volume. Changes in RV volumes exceeded changes in LV volumes. LV radionuclide measurements did not correlate significantly with any hemodynamic measurement except for a weak correlation between changes in LV end-systolic volume and right atrial pressure (r = 0.51). In contrast, the combination of changes in RV end-systolic volume and stroke volume predicted changes in pulmonary artery peak systolic (r = 0.90) and mean (r = 0.89) pressures. Changes in pulmonary arterial wedge pressure correlated with changes in RV end-diastolic (r = 0.78) and end-systolic (r = 0.71) volumes. In conclusion, LV radionuclide measurements are of limited value in predicting hemodynamic responses to vasodilator therapy in CHF, whereas RV volumes are strongly influenced by load changes. Their responses to nitroprusside correlate well with changes in pulmonary artery and pulmonary arterial wedge pressures.

Adult↗
PubMed1987

Distribution of a neutral cardioplegic vehicle during the development of ischemic myocardial contracture.

During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37 degrees C) ischemia in 18 isolated blood-perfused dog hearts (isovolumic left ventricle). In the baseline state, coronary perfusion pressure was 100 mmHg. At the onset of ischemia and every 15 min throughout ischemia, we infused 100 ml of crystalloid solution (37 degrees C) at a perfusion pressure of 100 mmHg and the distribution of crystalloid solution was assessed (radioactive microsphere technique). The hearts were reperfused after 60 min (n = 9) or 90 mins (n = 9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67 +/- 1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33 +/- 0.18, the LV end diastolic pressure was 7.5 +/- 0.4 mmHg, and mean transmural myocardial adenosine triphosphate (ATP) was 16.4 +/- 1.1 microM/g DW. At the onset and throughout the first 45 mins of ischemia (n = 9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26 +/- 1.6 micron/g DW). After 75 mins of ischemia (n = 9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76 +/- 0.5 microM/g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82 +/- 2.0% and the subendocardial to subepicardial flow ratio was 1.75 +/- 0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure greater than 60 mmHg, n = 4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium.

Adenosine Triphosphate↗
PubMed1987

Right ventricular pacing reduces the rate of left ventricular relaxation and filling.

Right ventricular pacing alters left ventricular synchrony and loading conditions, each of which may independently influence left ventricular relaxation. Addition of a properly timed atrial contraction by using sequential atrioventricular (AV) pacing minimizes changes in left ventricular loading conditions, but ventricular asynchrony persists. To separate the effects of altered loading from those of asynchrony, the effects of right ventricular pacing and sequential AV pacing on the rate of isovolumic pressure decline (relaxation time constant), myocardial (segment) lengthening rate and chamber (minor axis dimension) filling rate were examined. In 12 open chest anesthetized dogs, left ventricular pressure (micromanometer) and either left ventricular free wall segment length transients (n = 6) or minor axis dimension transients (n = 6) were measured during right atrial, right ventricular and sequential AV pacing; length and dimension were measured using ultrasonic crystals. Compared with right atrial pacing, right ventricular pacing produced a decrease in systolic pressure, a reduction in fractional shortening, a prolongation of the relaxation time constant (23.5 +/- 0.7 to 29.8 +/- 0.8 ms, p less than 0.05), slower peak segment lengthening rate (6.2 +/- 0.6 to 4.6 +/- 0.8 s-1, p less than 0.05) and a slower rate of increase in chamber dimension (3.5 +/- 0.1 to 2.7 +/- 0.1 s-1, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Mechanical determinants of maximum isotonic lengthening rate in rat left ventricular myocardium.

The effects of changing loading conditions and inotropic state on maximum isotonic lengthening rate (+dL/dt, muscle lengths/sec) were examined in isolated rat myocardium. Physiologically sequenced contractions were studied in 18 left ventricular papillary muscle preparations (stimulation rate, 12/min). To study the effects of changing loading conditions, only one loading variable (preload, total load, or late load) was changed during each contraction, while the others were held constant. To study the effects of isoproterenol (10(-6) M) and temperature (28 vs. 33 degrees C) on maximum isotonic lengthening rate, preload and late load were held constant and +dL/dt was examined at a common total load. When preload was increased from 0.7 +/- 0.1 to 1.4 +/- 0.1 g/mm2, muscle length increased from 0.98 +/- 0.003 to 1.01 +/- 0.002 muscle lengths, the extent of shortening increased from 0.05 +/- 0.003 to 0.08 +/- 0.003 muscle lengths, but minimum length (0.93 +/- 0.01 muscle lengths) and +dL/dt (1.1 +/- 0.1 muscle lengths/sec) were unchanged. When total load was increased from 1.5 to 4.5 g/mm2, minimum length increased from 0.91 +/- 0.05 to 0.97 +/- 0.05 muscle lengths and +dL/dt fell from 1.4 +/- 0.1 to 0.5 +/- 0.1 muscle lengths/sec. Late load (the load borne by or applied to the muscle during isotonic lengthening) was altered by changing its magnitude (g/mm2) or time (milliseconds after stimulation) of application. As late load was increased from 1.4 +/- 0.02 to 2.1 +/- 0.3 g/mm2, +dL/dt increased from 1.3 +/- 0.2 to 2.1 +/- 0.3 muscle lengths/sec.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Contribution of reduced mitral regurgitant volume to vasodilator effect in severe left ventricular failure secondary to coronary artery disease or idiopathic dilated cardiomyopathy.

Although vasodilators improve cardiac output in severe left ventricular (LV) failure, the degree to which reduction in mitral regurgitation (MR) contributes to this response is unknown. In the present study, nitroprusside-induced changes in forward cardiac output were compared with simultaneous radionuclide LV output in 14 patients with severe LV systolic dysfunction in the absence of known primary valvular disease. Regurgitant output was estimated as LV output minus forward output and regurgitant fraction was calculated as regurgitant output/LV output. At rest, LV ejection fraction averaged 0.16 +/- 0.04 (mean +/- standard deviation). Patients were classified into 2 groups based on regurgitant fraction at rest. Group I (n = 5) had little or no detectable valvular regurgitation, with regurgitant fraction less than 0.10; group II (n = 9) had evidence of MR with regurgitant fraction greater than 0.30. Nitroprusside increased forward cardiac output in all patients in both groups, but this effect was significantly greater in group II (64 +/- 34%) than in group I (31 +/- 17%) (p less than 0.01). Nitroprusside decreased regurgitant fraction in all group II patients, with mean regurgitant fraction decreasing from 0.44 +/- 0.12 to 0.26 +/- 0.15 (p less than 0.005). Thus, a large percentage of patients with severe LV systolic dysfunction have clinically relevant MR, defined as a regurgitant fraction greater than 0.30. Nitroprusside has a greater effect on forward cardiac output in patients with LV failure and MR than in patients with comparable ventricular dysfunction in the absence of detectable MR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Left ventricular stress-dimension-shortening relations before and after correction of chronic aortic and mitral regurgitation.

Mechanical characteristics of the left ventricle in chronic aortic regurgitation (AR) differ from those in chronic mitral regurgitation (MR). The differences are thought to be responsible, in part, for the changes in left ventricular (LV) function observed after surgical correction of AR or MR. To test this hypothesis, LV stress-dimension-shortening relations were determined before and after valve replacement in patients with compensated and decompensated chronic AR and MR. Echocardiographic data from 32 patients with AR and 20 patients with MR were used; preoperatively, all 52 patients had LV enlargement. Based on postoperative data, 2 subgroups were defined for each lesion: Patients in group A achieved a normal end-diastolic dimension (less than 3.3 cm/m2) and patients in group B had persistent LV enlargement. Preoperatively, the patients in group A with AR had increased peak systolic stress, but end-systolic stress and fractional shortening were normal; the patients in group B with AR had increased peak systolic stress, increased end-systolic stress and depressed shortening. One year after aortic valve replacement the patients in group A had normal systolic wall stresses and normal shortening, whereas those in group B had persistently abnormal wall stresses and a decrease in shortening. Preoperatively, patients in group A with MR had only modest elevations of peak stress, while end-systolic stress and fractional shortening were normal; in patients in group B with MR the peak stress was similar to that seen in group A, but end-systolic stress was increased and shortening was depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗
PubMed1985

Comparison of left and right ventricular end-systolic pressure-volume relations in congestive heart failure.

A hemodynamic-radionuclide study was performed to compare the relations between end-systolic pressure and volume in the left and right ventricles in 10 patients with biventricular failure, and to correlate the end-systolic pressure-volume slope with baseline variables of systolic function. During nitroprusside or nitroglycerin infusion, or a combination of both, linear relations were found between end-systolic pressure and volume for both ventricles. In 9 of 10 patients, the end-systolic pressure-volume slope was greater for the left ventricle (mean +/- SD 1.12 +/- 0.36 mm Hg X m2/ml) than for the right ventricle (0.46 +/- 0.27 mm Hg X m2/ml) (p less than 0.001). In all 10 patients, the volume-axis intercept of the pressure-volume relation was greater for the left ventricle (82 +/- 66 ml/m2) than for the right ventricle (2 +/- 30 ml/m2) (p less than 0.005). Right ventricular pressure-volume slope correlated weakly with baseline right ventricular ejection fraction (r = 0.69, p less than 0.05), strongly with the baseline right ventricular end-systolic pressure-volume ratio (r = 0.89) and inversely with baseline right ventricular end-systolic volume (r = -0.86). In conclusion, 1) in patients with severe biventricular failure, changes in systolic pressure influence end-systolic volume more strongly in the right than in the left ventricle. 2) For the right ventricle, the slope of the end-systolic pressure-volume relation is directly related to rest indexes of systolic function. 3) The greater the end-systolic volume at rest, the greater the predicted improvement in right ventricular emptying for any vasodilator-induced reduction in pulmonary artery end-systolic pressure.

Adult↗
PubMed1985

Left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy: overestimation of fiber velocities by conventional midwall measurements.

Observations that the inner (subendocardial) half of the left ventricular wall contributes more to total left ventricular wall thickening than the outer (subepicardial) half may have important implications in the analysis of myocardial fiber length transients. Accordingly, we measured endocardial and midwall shortening and lengthening rates in normal and hypertrophic heart and compared the results obtained with conventional methods of measurement with those obtained with a modified model that does not depend on use of conventional assumptions about the midwall. This modified (two-shell) cylindrical model) method considers the substantial contribution of inner wall thickening and thus does not require the assumption of a theoretical midwall fiber that remains at the midwall throughout the cardiac cycle. Echocardiographic data from six normal subjects and six patients with concentric left ventricular hypertrophy (LVH) were examined; left ventricular wall thickness ranged from 8 to 10 mm in normal subjects and from 11 to 16 mm in the patients with LVH. By design, the standard measurements of left ventricular size (diastolic and systolic dimensions) and systolic function (fractional shortening and endocardial fiber shortening velocities) were equal in the two groups. Endocardial, conventional midwall, and modified midwall methods all indicate reduced fiber lengthening rates in patients with LVH; peak fiber lengthening rates for normal and LVH groups were 4.5 +/- 0.7 vs 3.1 +/- 0.8 sec-1 (p less than .02) at the endocardium, 2.3 +/- 0.4 vs 1.6 +/- 0.4 sec-1 (p less than .02) at the midwall (conventional method), and 2.1 +/- 0.3 vs 1.4 +/- 0.3 sec-1 (p less than .01) at the midwall (modified method).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1984

Vasodilator effect on right ventricular function in congestive heart failure and pulmonary hypertension: end-systolic pressure--volume relation.

The right ventricular (RV) end-systolic pressure-volume relation during vasodilator administration was studied in 10 patients with pulmonary arterial (PA) hypertension, most of whom had biventricular failure. RV end-systolic volumes were estimated from equilibrium radionuclide RV counts and forward cardiac output. Simultaneous radionuclide and hemodynamic values were measured at rest and during nitroglycerin and nitroprusside infusion. Vasodilator administration resulted in decreases in PA mean and systolic pressures in all 10 patients, with an average decrease in end-systolic pressure (p less than 0.001) from 48 +/- 11 to 38 +/- 9 and 35 +/- 10 mm Hg during nitroglycerin and nitroprusside administration, respectively. In each patient, a direct linear relation was observed between the vasodilator-induced decrease in PA end-systolic pressure and in RV end-systolic volume. Average RV end-systolic volume decreased (p less than 0.001), from 130 +/- 69 ml/m2 at baseline to 108 +/- 62 and 102 +/- 55 ml/m2 during nitroglycerin and nitroprusside infusion, respectively. The slope of the RV end-systolic pressure-volume relation was directly related to RV ejection fraction. Thus, the vasodilator-induced decrease in PA systolic pressure is accompanied by a linear decrease in RV end-systolic volume, with a slope which is dependent on RV systolic function. This linear relation is analogous to the left ventricular end-systolic pressure-volume relation.

Adult↗
PubMed1984

Chronic mitral regurgitation: predictive value of preoperative echocardiographic indexes of left ventricular function and wall stress.

The effect of mitral valve replacement on left ventricular volume, mass, function and clinical symptoms was examined in 20 patients with chronic mitral regurgitation. Pre- and postoperative echocardiograms demonstrated that two outcomes could be defined. Left ventricular dimension at end-diastole was reduced to normal postoperatively in the 16 Group I patients, but was unchanged in the 4 Group II patients. The Group I response was associated with a dramatic reduction in left ventricular mass and a decrease in clinical symptoms; all 16 patients reached New York Heart Association functional class I. No change in left ventricular mass was seen in the Group II patients and all four remained symptomatic despite continued medical therapy. Examination of the preoperative echocardiographic measurements indicates that these data have significant prognostic value in predicting surgical outcome. When ventricular dimension at end-systole exceeds 2.6 cm/m2 or fractional shortening is less than 31% or end-systolic wall stress index exceeds 195 mm Hg, all Group II patients are identified and there are no false positive results in Group I. It is concluded that echocardiographic measurements of left ventricular size, function and wall stress can provide important prognostic information in patients with chronic mitral regurgitation. Such data may allow improved patient selection and a better definition of an optimal time for mitral valve replacement.

Aged↗
PubMed1981

Immunologic tests of value in diagnosis. 1. Acute phase reactants and autoantibodies.

Acute phase reactants are nonspecific indicators of tissue necrosis and/or inflammation but may be helpful in determining activity of disease. Rheumatoid factor is likewise rather nonspecific, but its presence is helpful in predicting the course, severity, and complications of rheumatoid arthritis. Numerous antinuclear antibodies have been identified in collagen vascular diseases; perhaps the most specific association is between anti-Sm antibody and systemic lupus erythematosus. Anti-smooth-muscle and antimitochondrial antibodies can aid in differential diagnosis of liver disease, while antithyroid antibodies can perform a similar function in diffuse goiter. Anti-parietal-cell and anti-intrinsic-factor antibodies are quite specific for pernicious anemia.

Acute Disease↗
PubMed1981

Immunologic tests of value in diagnosis. 2. Complement.

Laboratory tests are available to assess the function of the complement pathway and to measure levels of individual complement components. The pattern of complement abnormalities is often helpful in suggesting diagnostic possibilities. For example, when when total hemolytic complement, C3, and C4 are all decreased, one of the rheumatoid diseases is likely. In addition, complement levels in spinal and synovial fluid may provide helpful diagnostic clues.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Alterations in the myocardial capillary vasculature accompany tachycardia-induced cardiomyopathy.

Changes in capillary structure and distribution within the left ventricle (LV) occur with pressure and volume overload hypertrophy. These changes may cause an impairment in myocardial blood flow (MBF) and oxygen delivery resulting in myocyte injury and LV dysfunction. However, it is unknown whether changes in the capillary vasculature accompany the development of LV dysfunction in dilated cardiomyopathies. Accordingly, this study examined the relation between LV function, MBF and capillary architecture after the development of dilated cardiomyopathy in pigs produced by chronic supraventricular tachycardia (SVT). LV function was examined by echo-catheterization, and capillary morphometrics were computed using lectin histochemistry in two groups of pigs: sham controls (n = 8); and after 3 weeks of pacing-induced SVT (n = 8). Chronic SVT resulted in significantly increased LV end-diastolic dimension and pressure with a 50% reduction in LV fractional shortening compared to CON (p less than 0.05). Although no significant change in capillary density (2180 +/- 164 vs 2402 +/- 147/mm2, p = 0.25) occurred in the SVT group compared to CON, a significant reduction in the volume fraction of capillaries (12.2 +/- 0.5 vs 9.9 +/- 0.7%, p less than 0.05) and increased capillary diffusion distance (8.4 +/- 0.5 vs 7.5 +/- 0.3 microns, p less than 0.05) was observed. Frequency distribution analysis revealed a higher percentage of smaller diameter capillaries with chronic SVT vs CON (p less than 0.05). Ultrastructural examination revealed an increased capillary-myocyte distance with chronic SVT (0.95 +/- 0.08 vs 1.95 +/- 0.12 microns, p less than 0.05). These changes were accompanied by ultrastructural evidence of significant subendocardial injury (p less than 0.05). MBF was measured using microspheres in five additional conscious pigs in each group. MBF was significantly reduced and coronary vascular resistance increased in the SVT group compared to CON (p less than 0.05). Chronic SVT caused significant remodeling of the capillary vasculature; these changes were associated with reduced MBF, myocyte injury, and LV dysfunction.

Animals↗
PubMedDate not supplied

Mechanical loads and the isovolumic and filling indices of left ventricular relaxation.

In this report we have emphasized the significant influence of loading conditions on LV relaxation. Changes in inotropic state, ischemia, hypertrophy, and a host of other factors were not discussed herein. Ventricular asynchrony is likewise beyond the scope of this review, but it should be recognized that complex loading interactions among fibers within the LV wall influence relaxation and filling in ventricles that contract and relax nonsynchronously. Intact heart and isolated muscle experiments indicate that changes in preload do not influence relaxation rates when systolic pressure or total load remains constant. It appears, therefore, that the relaxation changes that occur with volume loading are primarily due to changes in systolic pressure or load. Indeed, an increase in systolic pressure may cause a substantial decrease in isovolumic relaxation rate, especially if there is a slow rise and a late peak in LV pressure. By contrast, an abrupt increase in late systolic load augments relaxation rate. Intact heart studies indicate that an abrupt load increment near the end of ejection results in premature and more rapid isovolumic relaxation, while an increase in left atrial pressure increases the filling rate; isolated muscle studies indicate that a load increment at the end of isometric relaxation causes an increase in isotonic relaxation rate. Thus, loading conditions during the periods of ejection, isovolumic relaxation, and filling can influence relaxation parameters and should be considered in clinical and experimental studies of LV relaxation.

Animals↗