Stress Echo Without the Stress

Abstract

Exercise or pharmacological stress has long been a mainstay of diagnostic testing aimed at identifying the presence of a flow-limiting coronary stenosis. The basis for this is the well-known clinical observation that even severe coronary artery atherosclerosis does not usually cause angina or ischemia at rest. Sir William Osler observed that angina pectoris is commonly precipitated by “muscular exertion, violent mental states, stomach upsets, or cold weather.”1 However, in Osler’s time, the mechanism whereby resting myocardial perfusion was maintained despite a hemodynamically significant coronary stenosis, namely coronary autoregulation, was unknown. See p 1154 Myocardial oxygen consumption and perfusion are tightly coupled.2 Because the myocardium extracts most of the oxygen delivered to it, increases in oxygen demand (eg, exercise, tachycardia) require a prompt increase in myocardial perfusion. For example, maximal exercise can easily cause a 4-fold increase in myocardial oxygen consumption, which is matched by a 4-fold increase in myocardial perfusion.3 Such hyperemic flow is typically mediated by vasodilation of precapillary arterioles to provide increased nutrient flow at the capillary level. Under normal conditions, 40% to 50% of total coronary resistance resides at the level of these precapillary arterioles (those <100 μm in diameter).4,5 These vessels respond rapidly to complex neural and metabolic control mechanisms to maintain myocardial perfusion over a wide range of driving pressures, a process known as autoregulation.6–8 Autoregulation is able to maintain nearly constant myocardial perfusion over a pressure range of 40 to 130 mm Hg in conscious dogs.9 A similar autoregulatory pressure range has been reported in humans with an intracoronary pressure wire to measure pressure distal to a stenosis and positron emission tomography to measure myocardial perfusion.10 In the healthy dog, resting coronary flow does not decrease significantly until …