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At least 19 recordsLinked to original sources
PubMed1978

Evaluation of chamber and myocardial compliance in pressure overload hypertrophy.

The effect of pressure overload hypertrophy on isolated myocardial muscle preparations remains controversial. Moreover, the ultimate effect on the diastolic function of the left ventricle in the pressure overload states of man and the relative changes in chamber and myocardial stiffness remain incompletely studied. We review here the methods as well as results of dynamic diastolic stiffness analysis in 18 patients with valvular aortic stenosis and 5 normal subjects based upon the pressure-volume and circumferential stress-strain relations obtained by simultaneous left ventricular micromanometry and high-speed cineangiography. In addition, complementary analysis of dynamic diastolic stiffness findings in chronically instrumented animals, before and after the induction of hypertrophy, are reviewed. Increased diastolic intracavitary pressures during concentric hypertrophy were found to be attributable to both increased muscle mass as well as enhanced myocardial stiffness. However, both chamber and myocardial stiffness changes during hypertrophy were quite variable with some patients (and 2 of 6 dogs) showing no enhancement of stiffness parameters. In the chronically instrumented animals where dynamic, instantaneous stiffness changes and strain rates are more readily studied than in man, viscous (velocity dependent) effects were noted to be enhanced during hypertrophy. It is postulated that variable increases in diastolic stiffness during concentric hypertrophy in the intact heart results from varying degrees of myofiber architectural distortion and/or inconstant collagen content, and further correlative studies of morphology and mechanical function are needed.

Animals↗
PubMed1979

Ischemic myocardial injury after exercise stress in the pressure-overloaded heart.

Systemic hemodynamics and regional myocardial blood flows were determined in 18 miniswine during the development of pressure-overload hypertrophy induced by supravalvular aortic constriction. Nine miniswine served as control animals. Regional myocardial blood flows were measured at rest and during exercise stress with radioactive microspheres after 2 days and 1 month of aortic constriction. Exercise stress, causing the heart rate to increase to 85% of its maximum, was imposed twice weekly for 5 minutes on 13 pressure-overloaded animals to elicit differences between the control and experimental groups that might not occur at rest. At rest, regional myocardial blood flows of pressure-overloaded animals were similar to those of control animals. When exercise stress was imposed after 2 days and 1 month of pressure overload, endocardial blood flows decreased 45% below control exercise levels, although epicardial blood flows were unchanged. During the first 2 weeks of pressure overload epicardial and endocardial electrocardiograms showed S-T segment elevation with exercise stress but not at rest. Postmortem examinations after 1 month of pressure overload showed significant histologic evidence of myocardial injury, namely, fibrosis, which was subendocardially located. These findings indicate that the pressure-overloaded heart is at risk for ischemic injury, particularly during the early, uncompensated stage.

Animals↗
PubMed1978

Normal cardiac myosin ATPase and mechanics in pressure overload with digitalis treatment.

Cardiac muscle myosin ATPase activity is depressed and contractile function impaired when the heart is subjected to a chronic pressure overload. Administering digitalis in the presence of chronic pressure overload significantly attenuates the decline in mechanical function. The current study sought to determine if the cardiac muscle myosin ATPase activity of cats treated with digitalis in the presence of pressure overload remains normal in parallel with the mechanical function. Four groups of cats were studied: normal controls (C), animals with pressure-overload hypertrophy with or without failure (HF), normal cats that received treatment with digitalis (D), and animals that received digitalis prior to and together with pressure overload (DHF). Compared to C, the maximum myosin ATPase activity of HF was significantly (P less than 0.05) depressed, but the maximum ATPase activity of D and DHF was not altered significantly (P greater than 0.05) from C. In parallel with the enzyme maximum activity, the papillary muscle isometric rate of force development was significantly (P less than 0.005) depressed in HF compared to C; D and DHF were not significantly (P greater than 0.05) different from C. It is concluded that the depression of myosin ATPase observed in HF is not present when digitalis is administered concomitant with the pressure overload.

Adenosine Triphosphatases↗
PubMed1976

Left ventricular stiffness and chamber geometry in the pressure-overloaded hypertrophied heart.

Pressure-overloaded hypertrophy of the left ventricle (LV) was produced by coarctation of the ascending aorta in 7 dogs. The overall mean weight of the left ventricle (LVW) was 7.86 +/- 1.49 (S.D.) g/kg body weight; (normal, 5.99 +/- 0.70 g/kg: p less than 0.05). After potassium arrest, pressure-volume (P-V) relationships were examined with the left ventricles isolated from the normals and from the dogs of left ventricular hypertrophy (LVH-dogs). In both groups, the P-V relationships could be expressed by an equation deltaV=a-be-cP throughout the range of filling pressure of 2.5 to 35 cmH2O, where deltav was the actual volume change of LV, P intraventricular pressure, and a, b and c constants. A sensitive index of LV stiffness, the half-inflation pressure (h), was defined as 1n (2b/a)/c. In hypertrophied hearts, h was 10.5 +/- 0.7 cmH2O; (normal 8.0 +/- 0.4 cmH2O; P less than 0.001). The ratio of LVW to LVVp=h (the left ventricular volume at h) in hypertrophy, which was related to the LV chamber geometry, was 3.1 +/- 0.6 in contrast with the normal value of 2.0 +/- 0.3. The development of concentric hypertrophy was thus demonstrated. Moreover, h was closely correlated with LVW/LVVp=h in both the normals and the LVH-dogs (r=0.83; p less than 0.01). On the other hand, an index of LV wall stiffness h/LVW/LVVP=h was relatively constant. Therefore, the increase of LV stiffness in the LVH-dogs was attributed to the change in chamber geometry.

Animals↗
PubMed1977

Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat.

This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/g). After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.

Animals↗
PubMed1976

Adaptations of the left ventricle to chronic pressure overload.

Left ventricular (LV) function during the adaptation to chronic pressure overload produced by an ascending aortic constriction was analyzed in conscious dogs, instrumented with intraventricular micromanometers and pairs of ultrasonic crystals for measurement of LV wall thickness (WTh) and internal LV chamber diameter. During inflation of the cuff to produce LV pressures averaging 220 mg Hg, calculated peak wall stress (WSt) increased by 55% above control while percent shortening decreased by 24% and mean circumferential shortening velocity (VCF) decreased by 39% from control. By 9 days (mean) after aortic constriction, the cross-sectional area (CSA) of the LV wall increased by 10% and peak WSt fell to 37% above control. End-diastolic diameter (EDD) increased to 4% above control, while percent shortening and mean VCF remained reduced at -12% and -20% of control, respectively. During the phase of concentric hypertrophy (mean 2 1/2 weeks), CSA increased further to 15% above control and WSt fell to 22% above control, while EDD and percent shortening returned to control and mean VCF increased to -7% of control (not significant). At 24 hours after release of the cuff WSt, percent shortening, mean VCF, and peak velocity of LV pressure rise (peak dP/dt) were not significantly different from control. Rapid, partial regression of hypertrophy was observed in some dogs. Thus, the left ventricle responds to chronically elevated pressure by initial dilation with increased WSt followed by gradual wall thickening and consequent reduction of WSt to near normal. After successful adaptation to the pressure overload, hypertrophy per se did not produce intrinsic depression of the myocardial inotropic state.

Animals↗
PubMed1979

Intra- and extracellular electrolytes and sarcolemmal ATPase in the failing heart due to pressure overload in dogs.

An investigation of changes in the Mg2+ -dependent, Na+ -K+ -stimulated sarcolemmal ATPase and of intracellular electrolytes in the left failing heart due to pressure overload (aortic banding) was carried out in dogs. There was no change in the sarcolemmal Mg2+ -ATPase of the left or right ventricle for the whole duration (3 to 9 months) of left ventricular pressure overload. In the early phase (3 months) of aortic banding, when there was no haemodynamic evidence of left ventricular failure, there was also no significant change in the sarcolemmal Na+ -K+ -ATPase, extracellular space, or intra- and extracellular electrolytes. However, during 6 to 9 months of aortic binding when there was haemodynamic evidence of left ventricular failure (increased end-diastolic pressure, decreased cardiac index and (dP/dt)/IIP, enlarged heart), there was also a marked increase in the left ventricular sarcolemmal Na+ -K+ -ATPase and intracellular K+; and a decrease in the intracellular Na+ and Ca2+. The extracellular space in the left ventricle also increased significantly. Unlike the left ventricle, the right ventricle did not show any evidence of failure, not did it show any change in the sarcolemmal Na+ -K+ -ATPase and intracellular electrolytes during any period of aortic banding. These results suggest that the decrease in the myocardial contractility in failing heart due to pressure overload might be associated with a decrease in the intracellular Ca2+ as a result of an increase in the sarcolemmal Na+ -K+ -ATPase.

Animals↗
PubMed1976

Heart functional responses to pressure overload in exercised and sedentary rats.

Female rats that had been subjected to a moderate treadmill running program were compared with sedentary animals on the basis of heart weight, selected biochemical measurements, and heart function. Exercised animals maintained normal growth rate, and cardiac hypertrophy was not present. Left ventricular RNA, DNA, and cytochrome c levels were unchanged. Heart functional measurements obtained in situ were similar in sedentary and exercised animals under control conditions. When subjected to sustained (1-3 days) aortic constriction pressure overload, exercised animals maintained or increased myocardial contractility. Contractility was depressed in sedentary animals. Both sedentary and exercised animals increased left ventricular end diastolic pressure without changing contractility during acute (1-3 min) pressure overload. However, exercised animals were able to fully regain normal cardiac output when the acute overload was relieved. Cardiac output remained approximately 10% below control in sedentary animals. The improved ability of previously exercised animals to withstand pressure overload appears to be due to alterations in adaptation rather than preliminary augmentation of metabolism or function.

Animals↗
PubMed1979

Heart adaptation to acute pressure overload: an involvement of endogenous prostaglandins.

The purpose of this investigation was to study the relationships between the contractile behavior of the heart and myocardial prostaglandins. Using an open-chest model in rabbits, we assayed the left ventricular tissue content to prostaglandins (PG) E and F2 alpha at various intervals following acute pressure overload created by graduated aortic stenosis. The results suggest that the rabbits could be divided into two distinct groups based on specific hemodynamic changes following coarctation (systolic and diastolic pressure, dP/dt, and contractility index). The first group included rabbits whose adaptation to pressure overload was expressed as a gradual increase in the contractility index. The second group was comprised of rabbits that developed heart failure following coarctation. The increase in contractility in response to overload in the first group was paralleled by an increase in the content of PGE and PGF 2 alpha in the left ventricle, whereas, in rabbits with heart failure, the prostaglandin level did not rise above that of the control hearts. It is suggested that an increased endogenous prostaglandin content may be an important factor in adaptation to acute overload.

Animals↗
PubMed1979

Increased passive stiffness of short-term pressure-overload hypertrophied myocardium in cat.

The passive stress-strain relationship of right ventricular papillary muscles from 10 normal and 9 experimental cats with short-term pressure-overload right ventricular hypertrophy-failure was examined by plotting the logarithm of instantaneous stress (ln sigma) against the natural strain calculated as ln(l/l0) where l = instantaneous length and l0 = length at zero force. Such a stress-strain relationship was well approximated by a linear relationship. The slope K obtained from this linear relationship was higher in the hypertrophy-failure muscles (normal, 15.01 +/- 0.87 (SEM); hypertrophy-failure, 31.79 +/- 4.09; P less than 0.005). The value of the intercept, ln C was similar in the two groups (normal, -4.33 +/- 0.20; hypertrophy-failure, -4.71 +/- 0.10). This analysis indicates the the ln sigma-natural strain relationship is linear in the papillary muscle and the slope of this relationship, an index of stiffness, is increased in hypertrophy-failure muscles. Using a three-element muscle model, it is shown that increased diastolic stiffness may contribute to the decreased systolic performance.

Animals↗
PubMed1979

[Left ventricular relaxation and filling abnormalities in patients with HOCM and left ventricular pressure overload (author's transl)].

In order to test the hypothesis that delayed mitral valve opening (MO) with regard to endsystolic dimension (t DS-MO) is specific for hypertrophic obstructive cardiomyopathy (HOCM), LV echograms of patients with different forms of LV hypertrophy due to chronic pressure overload (CPO; aortic stenosis + arterial hypertension, n = 24) and hypertrophic obstructive cardiomyopathy (n = 24) were recorded, digitized and compared with those of normals (N :n = 28(. In patients with HOCM (93 +/- 37 ms; p less than 0.0001) and CPO (66 +/- 31 ms; p less than 0.0001) the time t DS-MO was significantly delayed compared with N (13 +/- 15 MS), due to abnormal relaxation. This prolonged relaxation time resulted in an abnormal diameter increase (delta D) during the isovolumic relaxation phase (HOCM: 4.0 +/- 2.2 MM/CPO: 3.0 +/- 1.8 mm; p less than 0.0001/N:0.6 +/- 0.5 mm) and the rapid filling phase (HOCM 7.6 +/- 2.7 mm; p less than 0.0001/CPO 9.2 +/- 2.9 mm; p less than 0.05 / N: 10.7 +/- 2.2 mm). The echocardiographical signs of an abnormal relaxation are not specific for HOCM, they can be seen in different forms of secondary LV hypertrophy and are accompanied by changes in the diastolic filling pattern.

Adolescent↗
PubMed1979

[Prostaglandins, cyclic nucleotides and heart adaptation to acute and chronic pressure overload].

The content of prostaglandins (PGs) and cyclic nucleotides was determined in the rat heart at different time following coarctation of the abdominal aorta. The animals were divided into three groups according to the rate and degree of hypertrophy. The rats with the best adaptability (the highest level of hypertrophy) showed the highest myocardial PG content. An increase in myocardial weight in response to the overload correlated with an enhancement in PGE/PGF2 ratio. The relationship between the myocardial levels of PGs and cyclic nucleotides during the period of adaptation was also observed. Prostaglandins are suggested to play an important role in the heart adaptation to pressure overloads.

Animals↗
PubMedDate not supplied

Differential responses of canine myosin ATPase activity and tissue gases in the pressure-overloaded ventricle dependent upon degree of obstruction: mild versus severe pulmonic and aortic stenosis.

Mild pulmonic stenosis, induced in dogs by banding the pulmonary artery, elevated right ventricular peak systolic pressure to 60% above the control and elevated right ventricular K+- and Ca2+- activated myosin ATPase activities. In contrast, severe pulmonic stenosis, which elevated right ventricular peak systolic pressure to 300% above the control, did not produce an increase in myosin enzymatic ATPase Vmax values but caused a decrease in myosin activity. Mild aortic stenosis, induced by banding the ascending aorta, forcing a transaortic pressure gradient of 25 mm Hg, caused an elevation in left ventricular muosin ATPase, whereas severe aortic banding, brought about by creating a transaortic pressure gradient of 55 mm Hg, never caused an elevation in left ventricular myosin enzymatic Vmax values, but, like severe pulmonic banding, caused a decrease in K+- and Ca2+- activated myosin activities. Normal left ventricular myosin Vmax values in mumol of PO4/mg-min at 37 degrees C were: K+ = 2.84 +/- 0.22, and Ca2+ = 0.97 +/- 0.14. For right ventricular myosin they were: K+ = 2.15 +/- 0.16, and Ca2+ =0.74 +/- 0.10. Analyses of tissue gases, based on mass spectrometry data, showed that the hypertrophied ventricles had an elevated tissue pCO2 and an elevation in the cGMP/cAMP ratio.

Adenosine Triphosphatases↗
PubMed1978

Redistribution in left ventricular regional flow following acute right ventricular pressure overload.

The left ventricular dysfunction following acute pulmowary hypertension remains unexplained. We wondered if acute pulmonary hypertension could alter the transmural flow distribution within the left ventricular myocardium, independent of coronary flow and perfusion pressure. We used a canine preparation in which the left coronary system was perfused at constant flow and induced a two- to three-fold increase in pulmonary artery pressure by banding the pulmonary artery. Regional myocardial blood flow of the left coronary system was measured using radioactive microspheres, injected into the left coronary system before and after 10-30 min of banding of the pulmonary artery. The left ventricular subendocardial:epicardial ratio fell by 12 and 31% (p less than 0.05) of control value, 10 and 30 min, respectively, after banding of the pulmonary artery, the total flow to the left coronary system being kept constant. Left atrial mean pressure increased from 2.9 +/- 2.4 to 3.6 +/- 1.9 and 6.0 +/- 2.1 (p less than 0.05) following banding. The mechanism of the redistribution of coronary flow may relate to inappropriate vasodilation of the right septal myocardium with consequent relative left ventricular subendocardial hypoperfusion which might aggravate left ventricular ischemia in the presence of hypotension and hypoxia.

Animals↗