9.3 RISK FACTOR ASSESSMENT
Risk factors for the development of coronary artery disease can be broken down to modifiable and nonmodifiable risk factors. Modifiable risk factors include dyslipidemias (elevated LDL, low HDL), tobacco exposure, hypertension, and diabetes mellitus. Nonmodifiable risk factors include advanced age, male gender, and family history. Occasionally, patients with severe aortic stenosis or hypertrophic cardiomyopathy may experience angina-like pain in the absence of identifiable epicardial coronary disease. The Framingham risk score incorporates age, gender, LDL-cholesterol, HDL-cholesterol, blood pressure, smoking status, and diabetes to derive an estimated risk of having an event related to CAD.
9.4 CLINICAL MANIFESTATION
The clinical history is an important tool in identifying and managing patients with chronic CAD. Anginal symptoms are frequently classified as typical or atypical. Typical angina is described as a vice-like, crushing, or heavy sensation that is associated with exertion or stress. Patients may describe discomfort rather than “pain.” Symptoms may radiate to the jaw, the neck, or the arm (typically the ulnar aspect of the left arm). Typical angina usually begins gradually and usually reaches its maximum intensity over a period of minutes before subsiding. It is unusual for angina to reach maximum intensity over seconds. Chest discomfort while walking in the cold, uphill or after a meal also is suggestive of angina. Pre-conditioning may allow some patients who develop angina with exertion to continue exertion after a rest period without symptoms. The Canadian Cardiovascular Society (CCS) classification of effort angina provides a grading system (Table 9.1).
Class I | No angina with regular daily activity Angina after strenuous exertion |
Class II | Angina limits early physical activity, angina comes on after one flight of stairs Meals or cold may make angina worse |
Class III | Unable to perform daily activities due to pain |
Class IV | All physical activity causes angina or angina at rest |
Lipoprotein(a) | Modified form of LDL which apolipoprotein(a) covalently bound to apolipoprotein B Several studies have associated Lp(a) and CVD (Reykjavik Study) |
Apolipoprotein B | Primary apolipoprotein responsible for carrying LDL to tissue Reflects number of LDL particles rather than LDL content |
Apolipoprotein A-1 | Major protein component of HDL Reflects HDL particle number rather than HDL content |
High-sensitivity CRP | Adds to the predictive capacity of established risk factors, may even be independent risk factor In JUPITER trial, patients with LDL <130 and hsCRP >2 had modest but significant benefit with lipid-lowering therapy |
9.5 PHYSICAL EXAMINATION
As mentioned, the clinical history plays a prominent role in identifying patients with chronic CAD, but the physical exam is often normal. Indirect findings raising suspicion for coronary disease include signs of hyperlipidemia such as: corneal arcus and xanthelasma; carotid bruits; decreased peripheral pulses; an S4 or S3; or displaced apical impulse (which would suggest LV dysfunction).
9.6 LABORATORY AND ECG ASSESSMENT
Laboratory investigation focuses on metabolic abnormalities and biomarker assessment. All patients with suspected CAD should have total cholesterol, LDL, HDL, triglycerides, estimated glomerular filtration, and fasting blood glucose checked. Newer biomarkers, such as high-sensitivity CRP, have been associated with overall poorer prognosis but there is no consensus yet for recommended testing (Table 9.2).
Resting ECG may be normal in many patients with stable CAD. The presence of an abnormal ECG raises the risk for future cardiovascular events. Nonspecific ST-T wave inversions, particularly in V1–V3, are associated with increased risk. LVH, AF, LBBB and AV block convey a poorer overall prognosis in the setting of angina.
9.7 NONINVASIVE TOOLS FOR RISK STRATIFICATION
Exercise stress testing provides diagnostic and prognostic information (see Chapter 4). One of