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Journal ArticleDOI

The metabolic demand and oxygen supply of the heart: Physiologic and clinical considerations

Karl T. Weber, +1 more
- 01 Oct 1979 - 
- Vol. 44, Iss: 4, pp 722-729
TLDR
The concept of inappropriate oxygen demand relative to oxygen supply would appear to be central to the patient with coronary artery disease whose oxygen delivery may be compromised, but also to patients with chronic hemodynamic overload (for example, aortic stenosis) whose hypertrophied ventricle is now failing.
Abstract
The utilization of energy by the working heart has been studied extensively over the years. Because the conversion of chemical energy to mechanical work by the heart is highly dependent on oxygen, the oxygen required and the oxygen available for this conversion are considered to form the conceptual framework of the metabolic demand and supply of the heart, respectively. The oxygen requirement of the myocardium, as assessed by the rate of oxygen consumed (MVO 2 ), is a function of the mechanical components of ventricular contraction and include: (1) the force developed and sustained by the muscular wall during its contraction; (2) the rate of force development; and (3) the frequency of generating force in the wall per unit time. The oxygen available to the mitochondria, which satisfies this requirement, is primarily determined by the oxygen delivered per unit of time (that is, coronary flow) and the oxygen extracted. Collectively, the response in flow and oxygen extraction represent the metabolic reserve of the heart. Normally, during increments in work, coronary vascular resistance decreases permitting an increment in flow; oxygen extraction (65 to 70 percent) changes little under these circumstances. However, when the response in coronary vascular resistance is limited or at its optimal value, further increments in oxygen requirements are accompanied by an increase in oxygen extraction to 80 to 85 percent; oxygen extraction may exceed 90 percent in the presence of a reduced oxygen-carrying capacity. Stressed beyond the limits of its metabolic reserve (that is, minimum coronary vascular resistance and maximal oxygen extraction) the oxygen available to the heart becomes insufficient and, hence, an aerobic limit is reached. As a consequence, anaerobic metabolism commences, ventricular performance declines and pulsus alternans appear. The concept of inappropriate oxygen demand relative to oxygen supply would appear to be central not only to the patient with coronary artery disease whose oxygen delivery may be compromised, but also to patients with chronic hemodynamic overload (for example, aortic stenosis) whose hypertrophied ventricle is now failing. Moreover, the implications of an aerobic limit may also explain the limits of hypertrophy.

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Citations
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Effects of milrinone on coronary hemodynamics and myocardial energetics in patients with congestive heart failure.

TL;DR: Although myocardial oxygen consumption did not change, regional great cardiac venous blood flow increased significantly as a result of a 30% reduction in regional coronary vascular resistance, which is consistent with a primary coronary vasodilator effect of milrinone.
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Improved hemodynamic function and mechanical efficiency in congestive heart failure with sodium dichloroacetate.

TL;DR: Dichloroacetate administration stimulates myocardial lactate consumption and improves left ventricular mechanical efficiency and does not change with dobutamine administration, suggesting that these agents may be complementary in the treatment of congestive heart failure.
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Regional fibre stress-fibre strain area as an estimate of regional blood flow and oxygen demand in the canine heart

TL;DR: The results indicate that asynchronous electrical activation causes a redistribution of mechanical work and oxygen demand and that regional total mechanical power is a better and more general estimate of regional oxygen demand than the regional pressure‐sarcomere length area.
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Coronary risk factors and myocardial perfusion in asymptomatic adults: the Multi-Ethnic Study of Atherosclerosis (MESA).

TL;DR: Coronary vasoreactivity is reduced in asymptomatic individuals with a greater coronary risk factor burden, implying that changes in coronary vascular reactivity, in response to risk factors, may be detected in adults without symptomatic CHD.
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Mechanisms of Coronary Flow Reserve Impairment in Human Hypertension An Integrated Approach by Transthoracic and Transesophageal Echocardiography

TL;DR: It is confirmed that coronary reserve in hypertensive individuals is reduced even before the occurrence of left ventricular hypertrophy, and the reduction in coronary reserve depends on both an increase in resting coronary flow and an impairment in maximal vasodilator capacity.
References
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Journal ArticleDOI

Wall stress and patterns of hypertrophy in the human left ventricle.

TL;DR: The hypothesis that hypertrophy develops to normalize systolic but not diastolic wall stress is suggested, and it is proposed that increased syStolic tension development by myocardial fibers results in fiber thickening just sufficient to return the systolics stress (force per unit cross-sectional area) to normal.
Journal ArticleDOI

Coronary heart disease. Clinical, cinearteriographic and metabolic correlations.

TL;DR: The various methods and concepts within health psychology that have been applied to further understanding of the factors that contribute to CHD and the various prevention and intervention strategies used to reduce the risk of CHD morbidity and mortality are illustrated.
Journal ArticleDOI

Control of myocardial oxygen consumption: physiologic and clinical considerations.

TL;DR: A technique for reducing myocardial oxygen requirements by stimulating the carotid sinus nerves is described and its application to the treatment of angina pectoris demonstrated.
Journal ArticleDOI

The measurement of coronary blood flow, oxygen consumption, and efficiency of the left ventricle in man

TL;DR: The results indicate that chronic increase in the energy requirements of the heart were met, not by an increases in the oxygen consumption per unit weight, but by an increased in the total oxygen consumption due to hypertrophy.
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