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Stress Echocardiography pp 141–161Cite as

Coronary Flow Reserve

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Abstract

The seminal concept of coronary flow reserve (CFR) 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. 9.1): (1) the hemodynamically silent range of 0–40 % stenosis, which does not affect CFR (>2.5) to any detectable extent; (2) the clinically silent zone, where stenosis ranging from 40 to 70 % may marginally reduce the CFR without reaching the critical threshold required to provoke ischemia with the usual stresses; (3) the severe stenosis range (70–90 %), where critical stenosis reduces CFR less than 2.0 and myocardial ischemia is usually elicited when a stress is applied; and (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 CFR close to 1, or even less; in these patients, the administration of a coronary vasodilator actually decreases the poststenotic flow for steal phenomena. This experimental paradigm can be accurately reproduced clinically in highly selected series of patients with single-vessel disease, no myocardial infarction, no coronary collateral circulation, normal baseline function, no left ventricular hypertrophy, and no evidence of coronary vasospasm and who are off therapy at the time of testing. In these patients, the more severe the stenosis, the more profound the impairment in CFR. The correction of the stenosis improves CFR, and perfect dilation normalizes the CFR. The perfect, predictable relationship found in the experimental animal and in a very selected patient population [2] falls apart in the clinical arena [3], where many variables can modulate the imperfect match between epicardial coronary artery stenosis and CFR. Among others, these variables include:

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Authors and Affiliations

  1. Medical College of Wisconsin, Milwaukee, WI, USA

    Fausto Rigo PhD

  2. Department of Psychosocial Oncology and Palliative Care, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA

    Eugenio Picano PhD

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Rigo, F., Picano, E. (2015). Coronary Flow Reserve. In: Stress Echocardiography. Springer, Cham. https://doi.org/10.1007/978-3-319-20958-6_9

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