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INTRODUCTION

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  • Ischemic heart disease (IHD) is defined as lack of oxygen and decreased or no blood flow to the myocardium resulting from coronary artery narrowing or obstruction. It may present as acute coronary syndrome (ACS), which includes unstable angina and non–ST-segment elevation (NSTE) or ST-segment elevation (STE) myocardial infarction (MI), chronic stable exertional angina, ischemia without symptoms, microvascular angina, or ischemia due to coronary artery vasospasm (variant or Prinzmetal angina). The focus of this chapter is stable IHD.

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PATHOPHYSIOLOGY

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  • Angina pectoris usually results from increased myocardial oxygen demand (MVo2) in the setting of a fixed decrease in myocardial oxygen supply because of atherosclerotic plaque.

  • Major determinants of MVo2 are heart rate (HR), contractility, and intramyocardial wall tension during systole. A doubling in any of these individual parameters requires a 50% increase in coronary flow to maintain myocardial supply.

  • The rate–pressure product, or double product (DP), is the heart rate multiplied by the systolic blood pressure: DP = HR × SBP. This is a common, noninvasive measure of MVo2 but has limitations.

  • Coronary atherosclerotic plaques typically develop in larger epicardial (R1 or conductance) vessels, which normally offer little resistance to myocardial flow. As plaques grow and narrow the lumen, the affected vessel begins to provide considerable resistance to blood flow. Smaller endocardial (R2 or resistance) vessels provide most resistance to flow in normal coronary arteries and can contract and dilate to maintain blood flow based on metabolic demands of the myocardium (referred to as autoregulation). As a result, coronary plaques that occupy less than 50% to 70% of the vessel luminal diameter rarely produce ischemia or angina. However, smaller plaques have a lipid-rich core and thin fibrous cap and are prone to rupture and cause acute thrombosis. When the luminal diameter of epicardial vessels is reduced by 70% or more, endocardial vessels are maximally dilated, coronary flow reserve has been exhausted, and even low levels of exertion may result in a flow deficit with myocardial ischemia and often angina. When epicardial stenosis exceeds 90%, endocardial flow reserve is completely exhausted at rest (referred to as critical stenosis).

  • When coronary stenosis exceeds 70%, ischemic episodes lead to production of growth factors (eg, vascular endothelial growth factor and fibroblast growth factor) that, combined with endogenous vasodilators (eg, nitrous oxide and prostacyclin), cause native collateral vessels to increase in diameter (arteriogenesis) to maintain perfusion. New collateral vessels can also develop (angiogenesis).

  • Inflammation also plays a role in IHD; macrophages and T-lymphocytes produce cytokines, chemokines, and growth factors that activate endothelial cells, increase vasoreactivity, and cause proliferation of vascular smooth muscle cells. C-reactive protein may be elevated and correlates with adverse cardiovascular events.

  • Some patients have plaque that causes a fixed decrease in supply but also have reduced myocardial oxygen supply transiently due to vasospasm at the site of the plaque. Vasospasm is typically caused by endothelial damage induced by the plaque. ...

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