Energetics in the Failing Heart

4 November, 2011 (01:01) | Heart Diseases | By: Health news

These considerations, which may explain reports of detrimental effects when inotropic drugs have been used to treat chronic heart failure, lack conclusive experimental support. Furthermore, they may not apply to the cardiac glycosides, which have only moderate inotropic effects and, by increasing baroreceptor sensitivity, may reduce afterload and slow the heart in patients with heart failure.
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Energetics in the Failing Heart

In heart failure, whether due to abnormal hemodynamic demands, as are produced by aortic stenosis, or to the loss of functional myocardial tissue, as occurs after myocardial infarction, the active myocardial cells become overloaded. The resulting increase in the rate of mechanical-energy expenditure by the overloaded heart not only is sustained from day to day, but persists when activity is curtailed by rest, and even during sleep.

Hypertrophy unloads the cells of the failing heart by adding new sarcomeres and thus has an energy-sparing effect because it decreases the rate of mechanical-energy expenditure by the overloaded sarcomeres. However, several changes in the architecture of the hypertrophied heart can exacerbate the imbalance between energy expenditure and energy production. Such changes include an increase in the distance between capillaries40 and a decrease in the density of transverse capillary profiles, which impair the diffusion of substrates, notably oxygen, essential for the production of energy by the hypertrophied heart. This imbalance is especially marked in the relatively underperfused subendocardial regions of the left ventricle and is reflected in a decrease in the coronary reserve. Cellular abnormalities also appear to contribute to energy starvation in the chronically overloaded failing heart; for example, long-standing hypertrophy increases the cell volume occupied by myofibrils, which increases the number of ATP-consuming myofibrils supplied by each ATP-generating mitochondrion, thus potentially exacerbating an energy deficit. Depressed contractility in the failing heart (see below) lessens energy demands and so may be compensatory in terms of the energetics of the individual myocardial cells. Viewed from the standpoint of the circulation, of course, depressed contractility is detrimental.

Hypertrophic Response of the Heart to Chronic Overload

It is now apparent that hypertrophy of the overloaded heart is a complex process that is both beneficial and detrimental. Like the short-term effects of salt and water retention and vasoconstriction, the effect of the benefit of an increased number of sarcomeres dominates the initial adaptation to overload. It is mainly when the overload is sustained, in chronic heart failure, that the deleterious effects of hypertrophy, referred to here as the cardiomyopathy of overload, become prominent. When hypertrophy is induced by exercise, however, its detrimental effects appear to be minimal or absent, possibly because of the intermittent rather than sustained stimulus to cell growth.