Adaptations of the left ventricle to chronic pressure overload.

Sasayama, Shígetake; Ross, John; Franklin, Dean; Bloor, C M; Bishop, Sanford P.; Dilley, R B

doi:10.1161/01.res.38.3.172

Cited by 260 publications

(52 citation statements)

References 35 publications

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“…Since this increase also was found for minimal late diastolic resistance, it probably was not due directly to increased myocardial compression in systole. If our dogs with hypertrophy were similar to those studied by Sasayama et al, 15 then the changes of minimal resistance that we observed cannot be explained by increased ventricular volumes or wall tensions, since these were normal in their study.…”

Section: Discussionsupporting

confidence: 85%

Coronary blood flow in experimental canine left ventricular hypertrophy.

O’Keefe¹,

Hoffman²,

Cheitlin³

et al. 1978

Circulation Research

160

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With maximal coronary vasodilation due to adenosine or carbochrome, mean coronary vascular resistance was 84% higher in LVH than in normal hearts; with isoproterenol, resistance was 54% higher in LVH. These changes were similar in right and left ventricles. Minimal coronary resistance at end diastole also was higher in LVH-64% and 94% for the two sets of vasodilators, respectively. There were no significant differences in capillary or large vessel proportional volumes in LVH and control dogs, but arterial capacity could not be estimated. The raised minimal coronary resistance suggests the possibility that, with stress, coronary flow, especially to subendocardial muscle, might be inappropriate and perhaps cause ischemic damage. However, the changes noted might have been due to coronary arterial responses to raised coronary pressures rather than to hypertrophy itself.LEFT ventricular hypertrophy (LVH) may impair cardiac function but the mechanisms for this change are not clear. Hypertrophy alters excitation-contraction coupling, energy utilization, and contractile proteins, 1 but it is not known whether these changes are primary or secondary to other mechanisms. One of those other mechanisms, myocardial ischemia, could occur in two ways: Roberts and Wearn 2 showed that in rabbits with left ventricular Original manuscript received February 28, 1977; accepted for publication March 7, 1978. hypertrophy the capillary-fiber ratio remained at its normal value of 1:1 so that the mean diffusion distance must have increased; these findings have been confirmed in man. 3 ' 4 Then Linzbach 3 and Woods 5 reported that, although the main coronary arteries increased in diameter in people with LVH, this increase in diameter did not match the increased heart weight. They therefore inferred that in hypertrophy there might be a reduced coronary vascular reserve that might impair cardiac function. However, no one has shown that the increased diffusion distance for oxygen does impair cardiac function nor that coronary vascular reserve is reduced in hypertrophy.We wished to test another hypothesis that involves myocardial blood flow, one which also fits in with the known vulnerability of the subendocardial muscle to is-

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Section: Discussionsupporting

confidence: 85%

Coronary blood flow in experimental canine left ventricular hypertrophy.

O’Keefe¹,

Hoffman²,

Cheitlin³

et al. 1978

Circulation Research

160

View full text Add to dashboard Cite

show abstract

“…Sasayama and colleagues assessed LV responses to ascending aortic banding in conscious dogs by utilizing intraventricular micromanometers and ultrasonic crystals for measurement of LV wall thickness and internal chamber diameter. They found that the LV initially dilates in response to elevated pressure due to increased wall stress [9]. This acute response is followed by gradual wall thickening and consequent reductions in wall stress to near normal levels, thereby preserving normal LV chamber size and inotrope [9].…”

Section: Compensatory LV Response To Asmentioning

confidence: 99%

“…They found that the LV initially dilates in response to elevated pressure due to increased wall stress [9]. This acute response is followed by gradual wall thickening and consequent reductions in wall stress to near normal levels, thereby preserving normal LV chamber size and inotrope [9].…”

Section: Compensatory LV Response To Asmentioning

confidence: 99%

Patterns of Left Ventricular Remodeling in Aortic Stenosis: Therapeutic Implications

Elmariah

2015

Curr Treat Options Cardio Med

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Aortic valve stenosis is characterized by indolent progression followed by the late development of symptoms once left ventricular compensatory mechanisms fail. In this review, we describe the left ventricular response to aortic stenosis. Specifically, we highlight the process of adaptive remodeling, which begins as a beneficial compensatory mechanism but ultimately transitions to a maladaptive process characterized by inappropriate left ventricular hypertrophy, interstitial fibrosis, and diminished contractility. Myocardial fibrosis ensues as the remodeling process progresses with potentially irreversible consequences on diastolic and systolic function and on clinical symptoms and outcomes. Recent data suggest that fibrosis is largely responsible for the development of symptoms in patients with severe aortic stenosis, which unfortunately implies that fibrosis may be advanced by the time clinical symptomatology triggers evaluation for aortic valve replacement. Interstitial fibrosis persists for years after valve replacement and, when severe, can lessen the clinical benefits of valve replacement. Further evaluation of noninvasive measures capable of assessing the extent of maladaptive left ventricular remodeling and of predicting its reversal are desperately needed in order to enhance the personalized delivery of aortic valve replacement for severe aortic stenosis. We support aggressive assessment of symptomatic status with more frequent clinical follow-up and exercise testing in asymptomatic individuals with severe left ventricular hypertrophy or impaired longitudinal contractility. However, whether early valve replacement is advantageous in patients with evidence of maladaptive left ventricular remodeling in the absence of symptoms remains unknown, but is certainly worthy of further investigation.

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“…limit wall stress and preserve systolic function [8]. However, ultimately, severe afterload causes a fall in left ventricular ejection fraction even in the presence of relatively preserved contractility.…”

Section: Opinion Statementmentioning

confidence: 99%

Low gradient, low ejection fraction aortic stenosis

Chambers

2003

Curr Treat Options Cardio Med

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Low gradient aortic stenosis can be caused by critical aortic stenosis causing left ventricular impairment or by more moderate aortic stenosis coexisting with another cause of left ventricular impairment. The main challenges are to differentiate these two states and then to determine whether the left ventricle is likely to recover after aortic valve surgery. Exhaustive echocardiography is necessary, including the use of dobutamine stress. Guideline criteria for severe aortic stenosis are given in this article. The most secure criteria are mean transaortic pressure difference greater than 30 mm Hg and effective orifice area less than 1.2 cm(2) during dobutamine stress. However, the presence of left ventricular contractile reserve more closely determines outcome after surgery than do markers of stenosis. Surgery is most clearly indicated if there is severe aortic stenosis and an increase in the systolic velocity integral by greater than 20% during dobutamine infusion. Preoperative catheterization is necessary to determine coronary anatomy, but the aortic valve should not be crossed because of the relatively high risk of death, stroke, pulmonary edema, and cardiogenic shock. In patients judged too ill for immediate surgery, a period of medical resuscitation with diuretics and dobutamine should be considered. Balloon valvotomy is not indicated.

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Adaptations of the left ventricle to chronic pressure overload.

Cited by 260 publications

References 35 publications

Coronary blood flow in experimental canine left ventricular hypertrophy.

Coronary blood flow in experimental canine left ventricular hypertrophy.

Patterns of Left Ventricular Remodeling in Aortic Stenosis: Therapeutic Implications

Low gradient, low ejection fraction aortic stenosis

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