Noninvasive Assessment of Myocardial Perfusion
Noninvasive assessment of myocardial perfusion is important in the diagnosis and risk stratification of patients with known or suspected coronary artery disease (CAD). Although single-photon emission computed tomography (SPECT) is most commonly used, multiple modalities including myocardial contrast echocardiography (MCE), positron emission tomography (PET), cardiac MRI (CMR), and cardiac computed tomography (CT) have emerged as promising techniques. This article will critically evaluate the strengths and weakness of these modalities for evaluating myocardial perfusion.
Myocardial perfusion is a highly regulated process that includes epicardial vessels, resistance vessels, and the endothelium. Endothelial dysfunction is an early manifestation of vascular disease and plays a role in the development of CAD.1 In normal coronaries, sympathetic stimulation causes a flow-mediated endothelium-dependent release of nitric oxide resulting in epicardial and arteriolar vasodilation. With endothelial dysfunction, vasoconstriction from acetylcholine predominates, resulting an attenuation or absence of the normal flow-mediated vasodilation.2 When coronary arteries are narrowed by atherosclerotic disease, coronary autoregulation attempts to normalize myocardial blood flow by reducing the resistance of distal perfusion beds to preserve adequate myocardial oxygen supply.3 A stenosis must exceed 85% to 90% of luminal diameter before significant reductions in resting blood flow occur.4 However, under vasodilator stimulus, maximal coronary flow has been shown to decrease with stenosis of >45% (Figure 1).4 This has been demonstrated clinically using quantitative PET myocardial perfusion imaging (MPI).5,6 Because perfusion is an early change in the ischemic cascade,7 stress modalities that assess coronary perfusion reserve have a higher sensitivity in detecting flow-limiting stenoses than analysis of stress-induced wall motion abnormalities or ECG changes alone.8 Abnormal coronary flow reserve with vasodilator stress in the absence of a significant coronary stenosis occurs and has been attributed to microvascular and/or endothelial dysfunction.9