Abstract
The concept of coronary flow reserve was proposed experimentally by Lance K. Gould in 1974 [1]. Under normal conditions, in the absence of stenosis, coronary blood flow can increase approximately four- to-sixfold to meet increasing myocardial oxygen demands. This effect is mediated by vasodilation at the arteriolar bed, which reduces vascular resistance, thereby augmenting flow. Coronary reserve is the capacity of the coronary circulation to dilate following an increase in myocardial metabolic demand and can be expressed by the difference between the hyperemic flow and the resting flow curve. In most clinical applications, hyperemia is induced pharmacologically, not via an increase in oxygen demand. A combined anatomical and physiological classification can ideally identify four separate segments in the hyperemic curve (Fig. 2 of Chap. 2):
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1.
The hemodynamically silent range of o%–40% stenosis, which does not affect coronary flow reserve (>2.5) to any detectable extent.
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2.
The clinically silent zone, where stenosis ranging from 40% to 70% may marginally reduce the coronary flow reserve without reaching the critical threshold required to provoke ischemia with the usual stresses.
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3.
The severe stenosis range (70%–90%), where critical stenosis reduces coronary flow reserve less than 2.0 and myocardial ischemia is usually elicited when a stress is applied.
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4.
The very severe stenosis range (>90%), producing a marked transstenotic pressure drop at rest, with a reduction of baseline myocardial blood flow and a coronary flow reserve close to 1, or even less: in these patients, the administration of a coronary vasodilator actually decreases the poststenotic flow for steal phenomena.
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Picano, E., Rigo, F., Lowenstein, J. (2003). Coronary Flow Reserve. In: Stress Echocardiography. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-05096-5_37
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