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Assessment of cardiac energetics at the level of ATP-synthesis,
chemomechanical energy transformation and whole organ dynamics as a
function of haemodynamic load, ventricular configuration and
oxygen- and substrates supply is basic to understanding cardiac
function under physiological and pathophysiological (hypertrophy,
hypoxia, ischaemia and heart failure) conditions. Moreover, cardiac
energetics should be an important consideration in the choice and
application of drugs especially in the case of vasodilators,
inotropic agents and in cardioprotective measures. Only by
considering energetics at the subcellular, cellular, and
whole-heart level we can arrive at a better understanding of
cardiac performance and ultimately better clinical judgement and
drug therapy. Quantification of myocardial energetics will also
help to determine the optimal time for surgical interventions such
as valvular replacement or aneurysm resection. The present volume
is the outcome of an international symposium on cardiac energetics
held in Gargellen/Montafon (Austria), June 1986. The contributions
will certainly help bridge the existing gap between basic research
involving isolated structures and that involving the whole organ,
on the one hand, and render the results derived from basic research
applicable to clinical problems, on the other hand.
Inotropic stimulation of the myocardium, as well as vasodilation
and diuresis as essential principles in the treatment of congestive
heart failure have recently met with considerable criticism and
reevaluation. It is generally agreed that unloading of the heart,
either through vasodilation and/or diuresis, improves the working
conditions of the dilated, failing heart. It reduces myocar dial
oxygen consumption through reduction of chamber radius and,
thereby, wall tension as the major determinants of myocardial
oxygen consumption. Inotropic stimulation, quite in contrast, does
not conserve oxygen. It rather consumes energy and that may be
disadvantageous in situations of compromised oxygen supply and
energy metabolism of the working myocardium. However, under
conditions of suf ficient oxygen supply and metabolic support
inotropic stimulation may bring about in creased pumping and
subsequent improvement of myocardial failure. In recent years it
could convincingly be demonstrated that vasodilation leads to symp
tomatic improvement of congestive heart failure, improvement of
exercise tolerance, and it prolongs life - especially in the case
of ACE-inhibitors and the combination of hydra lazine with
long-acting nitrates. Quite in contrast, equally beneficial effects
could not be demonstrated for inotropic agents in congestive heart
failure. Only for the cardiac glyco sides has it been shown that
beneficial effects can be achieved, especially if atrial fibril
lation with absolute arrhythmia is present. The influence of the
cardiac glycosides on the latter represents an effect which is
independent of the inotropic action."
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