Coronary Heart Disease and Stable Angina

Coronary Heart Disease and Stable Angina is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

Definition

  • Coronary artery disease (CAD) refers to the luminal narrowing of a coronary artery, usually due to atherosclerosis. CAD is the leading contributor to ischemic heart disease (IHD). IHD includes angina pectoris, myocardial infarction (MI), and silent myocardial ischemia.
  • Cardiovascular disease (CVD) includes IHD, cardiomyopathy, heart failure (HF), arrhythmia, hypertension, cerebrovascular accident (CVA), diseases of the aorta, peripheral vascular disease (PVD), valvular heart disease, and congenital heart disease.
  • Stable angina is defined as angina symptoms or angina equivalent symptoms that are reproduced by consistent levels of activity and relieved by rest.
  • American Heart Association/American College of Cardiology (AHA/ACC) guidelines provide a more thorough overview of stable IHD.1,2

Epidemiology

  • In the United States, IHD is the cause of one of every six deaths.3
  • The lifetime risk of IHD at age 40 is one in two for men and one in three for women.
  • There are more than 15 million Americans with IHD, 50% of whom have chronic angina.
  • CVD has become an important cause of death worldwide, accounting for nearly 30% of all deaths, and has become increasingly significant in developing nations.
  • Death due to CVD continues to decline in large part because of adherence to current guidelines.

Etiology

CAD most commonly results from luminal accumulation of atheromatous plaque.

Other causes of obstructive CAD include congenital coronary anomalies, myocardial bridging, vasculitis, and prior radiation therapy.

Pathophysiology

  • Stable angina results from progressive luminal obstruction of angiographically visible epicardial coronary arteries or, less commonly, obstruction of the microvasculature, which results in a mismatch between myocardial oxygen supply and demand.
  • Atherosclerosis is an inflammatory process, initiated by lipid deposition in the arterial intima layer followed by recruitment of inflammatory cells and proliferation of arterial smooth muscle cells to form an atheroma.
    • The coronary lesions responsible for stable angina differ from the vulnerable plaques associated with acute MI. The stable angina lesion is fixed and is less prone to fissuring, hence producing symptoms that are more predictable.4
    • All coronary lesions are eccentric and do not uniformly alter the inner circumference of the artery.
    • Epicardial coronary lesions causing less than 40% luminal narrowing generally do not significantly impair coronary flow.
    • Moderate angiographic lesions (40%–70% obstruction) may interfere with flow and are routinely underestimated on coronary angiograms given the eccentricity of CAD.

Risk Factors

  • Of IHD events, >90% can be attributed to elevations in at least one major risk factor.5
  • Assessment of traditional CVD risk factors includes:
    • Age.
    • Blood pressure (BP).
    • Blood sugar (note: diabetes is considered an IHD risk equivalent).
    • Lipid profile (low-density lipoprotein [LDL], high-density lipoprotein [HDL], triglycerides); direct LDL for nonfasting samples or very high triglycerides.
    • Tobacco use (note: smoking cessation restores the risk of IHD to that of a nonsmoker within approximately 15 years).6
    • Family history of premature CAD: Defined as first-degree male relative with IHD before age 55 or female relative before age 65.
    • Measures for obesity, particularly central obesity; body mass index goal is between 18.5 and 24.9 kg/m; and waist circumference goal is <40 inches for men and <35 inches for women.
  • As of 2013, AHA/ACC guidelines recommend assessing 10-year atherosclerotic cardiovascular disease (ASCVD) risk for patients aged 40–79 years using new race and age-specific pooled cohort equations.7
    • The ASCVD risk calculator is available online (http://tools.cardiosource.org/ASCVD-Risk-Estimator/).
    • If there remains uncertainty about lower risk estimates, high-sensitivity C-reactive protein (≥2 mg/dL), coronary artery calcium score (≥300 Agatston units or ≥75th percentile), or ankle–brachial index (<0.9) may be obtained to revise risk estimates upward.
    • Traditional risk factors noted above should be assessed in patients younger than age 40 and every 4–6 years after 40; 10-year ASCVD risk should be calculated every 4–6 years in patients 40–79 years of age.
    • Lifetime risk can be assessed using the ASCVD risk calculator and may be helpful in the setting of counseling patients about lifestyle modifications.

Prevention

Primary prevention: See Chapter 3, Preventive Cardiology

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