++
A 45-year-old man began having chest pressure with exertion that was relieved with rest. He did not have diabetes, high blood pressure, or high cholesterol and had never had a myocardial infarction. His examination and resting ECG were normal. On the basis of the testing modalities available, he was scheduled for exercise stress testing. After a positive test, he underwent coronary angiography that demonstrated a significant stenosis in the left coronary artery (Figure 48-1). He underwent a stenting procedure and was placed on aspirin and cholesterol-lowering medication.
++
++
In the United States, a person dies of coronary heart disease every 39 seconds. Coronary heart disease is a manifestation of atherosclerotic disease and has many modifiable risk factors. Patients with and without coronary heart disease should be advised to stop smoking, maintain normal blood pressure and cholesterol levels, exercise, achieve or maintain a normal weight, and control diabetes mellitus if present.
++
Coronary heart disease (CHD) is the leading cause of death in the United States, responsible for approximately 600,000 deaths in 2014.1 The mortality rate has steadily declined for the past 30 years.
Each year, 790,000 myocardial infarctions occur (first and recurrent) with a 14% mortality rate.1
Approximately 92.1 million U.S. adults have cardiovascular disease.1
In 2012, the prevalence of CHD among U.S. adults older than 18 years of age was higher in men than in women (12.1% vs. 9.7%) and higher in people with a less-than-high-school-diploma education (13.6% vs. 10.4% for college graduates).2
In 2014, prevalence of heart disease was similar among white (10.9%), black (10.8%), and Hispanic (7.8%) persons.2
+++
ETIOLOGY AND PATHOPHYSIOLOGY
++
CHD is one of several manifestations of atherosclerotic disease, which begins with endothelium dysfunction.3
Endothelium, when normal, balances vasoconstrictors and vasodilators, impedes platelet aggregation, and controls fibrin production.
Dysfunctional endothelium encourages macrophage adhesion, plaque growth, and vasoconstriction by recruiting inflammatory cells into the vessel walls, the initiating step of atherosclerosis.
The vessel wall lesions develop a cap of smooth muscle cells and collagen to become fibroadenomas.
The vessels with these lesions undergo enlargement, allowing progression of the plaque without compromising the lumen.
Two-thirds of acute coronary events are from plaque disruption and thrombus formation, instead of progressive narrowing of the coronary artery lumen.2
Plaques most likely to rupture (high-risk plaques) have a large core of lipids, many macrophages, decreased vascular smooth muscle cells, and a thin fibrous cap.
After plaque rupture, the exposed lipid core triggers a superimposed thrombus that occludes the vessel.
Increased thrombosis is triggered by known cardiac risk ...