Normal myocardial function and energetics after reversing pressure-overload hypertrophy

Cooper, George; Satava, Richard M.; Harrison, Carlos E.; Coleman, HN

doi:10.1152/ajplegacy.1974.226.5.1158

Cited by 39 publications

(15 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many experimental studies suggest that cardiac hypertrophy induced by various stimuli will ultimately lead to cardiac failure.28' 29 Furthermore, in many circumstances, removal of the stimulus that induced the ventricular hypertrophy will lead to its regression. 30,31 This hypothesis is in part supported by the data obtained in this study. None of the acromegalic patients that we studied who had normal growth hormone levels as a result of therapy (group I) had either cardiac enlargement or dysfunction.…”

Section: Resultssupporting

confidence: 79%

Cardiac size and function in acromegaly.

Martins¹,

Kerber²,

Sherman³

et al. 1977

Circulation

View full text Add to dashboard Cite

Sixteen acromegalic patients underwent echocardiography, phonocardiography, stress electrocardiography with Thallium perfusion scanning and gated radioisotope left ventricular angiocardiograms. Abnormalities consisting of increased echo left ventricular mass index, low velocity of circumferential fiber shortening or elevated pre-ejection period to left ventricular ejection time ratio were found in six patients with coexistent hypertension or coronary disease. Concentric left ventricular hypertrophy was also found in three patients with no known etiology other than acromegaly of greater than thirteen years' duration or with fasting growth hormone concentrations greater than 100 ng/ml. One of these three also had left ventricular dysfunction. Neither hypertrophy nor ventricular dysfunction was found in other acromegalics with shorter duration of disease or lower growth hormone concentrations or with normal growth hormone concentrations after therapy. A high prevalence of coronary artery and hypertensive heart disease is associated with acromegaly. A few patients with acromegaly have a specific, potentially reversible cardiomyopathy probably related to prolonged acromegaly or very high growth hormone concentrations.

show abstract

Section: Resultssupporting

confidence: 79%

Cardiac size and function in acromegaly.

Martins¹,

Kerber²,

Sherman³

et al. 1977

Circulation

View full text Add to dashboard Cite

show abstract

“…18 A depression in both the velocity-load and shortening-load relationship have been observed in experimental models of pressure overload. 19 By the latter relationship, shortening deficits have identified patients with either aortic stenosis or aortic insufficiency.9 20 However, the ejection fraction-afterload relationship is limited as a measure of inotropic state by the extent to which ejection fraction is dependent on resting length ("preload"). In FIGURE 1.…”

Section: Discussionmentioning

confidence: 99%

Influence of aortic valve disease on systolic stiffness of the human left ventricular myocardium.

Wisenbaugh¹,

Élion²,

Nissen³

1987

Circulation

View full text Add to dashboard Cite

The new concept of systolic myocardial stiffness was applied to the study of ejection mechanics in aortic valve disease. Frame-by-frame analysis of stress (a) and volume (V) was performed for two differently loaded beats in 26 patients who underwent simultaneous cineangiography and micromanometry: nine normal subjects, eight with isolated aortic regurgitation (AR), and nine with aortic stenosis (AS). Maximum myocardial stiffness (maxEaJ) was defined as the slope of the endsystolic (es) stress-strain relationship. End-systole was defined as the frame where stiffness was maximal, and strain was defined as E = loge (Dm/Dom)

show abstract

“…A recent study 10 has established that the contractile defect of hypertrophy due to pressure overload without heart failure, produced by experimental pulmonic constriction, is totally relieved after relief for approximately 4-5 weeks from the pulmonic stenosis.…”

Section: S~9mentioning

confidence: 99%

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

Coulson¹,

Yazdanfar²,

Rubio³

et al. 1977

Circulation Research

View full text Add to dashboard Cite

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.

show abstract

Normal myocardial function and energetics after reversing pressure-overload hypertrophy

Cited by 39 publications

References 0 publications

Cardiac size and function in acromegaly.

Cardiac size and function in acromegaly.

Influence of aortic valve disease on systolic stiffness of the human left ventricular myocardium.

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

Contact Info

Product

Resources

About