Abstract
In the normal heart, both intrinsic mechanisms (such as coronary vascular autoregulation and Starling mechanical properties) and extrinsic (mainly neurohumoral) influences allow adaptation to a wide range of demand for output of blood (1). Even under resting conditions, oxidative metabolism is crucial to the function of the heart; indeed, mitochondria comprise one-third of the mass of the myocardial cells. Oxygen extraction is near maximal even under resting conditions at 60–70% and is only increased to 80% with severe exercise. Therefore, the increased oxygen required during exercise has to be obtained from an increase in myocardial blood flow (MBF) (2). In circumstances of cardiac disease, especially (and in the West, most commonly) coronary artery disease (CAD), the limits of adaptation are much more closely confined. Critical stenosis of an epicardial artery, whether such a stenosis is static or dynamic, sharply reduces coronary vasodilator reserve (CVR, the ratio of maximal MBF/ resting MBF) in the myocardial territory supplied by the stenosed vessel (3). [With respect to vulnerability to reduction in perfusion or to increase in demand, it is well established that the subendocardium is at greater risk than the subepicardium; this issue has been reviewed in extenso by Hoffman (2) and will not be discussed further here.] MBF and, therefore, oxygen supply cannot increase adequately to satisfy the increased myocardial demand, and aerobic metabolism can no longer be sustained downstream. The regional contractile function is compromised.
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Rosen, S.D. (2000). Neuroimaging of Heart Pain. In: Ter Horst, G.J. (eds) The Nervous System and the Heart. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-713-0_10
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