Functional Neuroimaging of Angina Pectoris

  • Stuart D. Rosen
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 202)

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 function of the heart, indeed mitochondria comprise 1/3 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 vessel3. (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 4 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. Regional contractile function is compromised.

Keywords

Myocardial Ischemia Angina Pectoris Myocardial Blood Flow Brodmann Area Silent Myocardial Ischemia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Springer Science+Business Media New York 1998

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  • Stuart D. Rosen

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