Patients who present with chest pain can be divided into three subsets:
Nonanginal chest pain.
The incidence of coronary artery disease in these patient subsets is approximately 90%, 50%, and 16%, respectively. In many instances, the clinical-pathologic correlation is poor, such as in patients with advanced coronary artery disease who have silent ischemia or those with Prinzmetal’s angina (vasospastic) who have severe angina but usually minimal or no coronary atherosclerosis.
Compare underlying pathophysiologic mechanisms in angina and unstable angina. Stable angina is most commonly related to an increase in myocardial oxygen demand triggered by physical activity. Invariably, a fixed coronary artery obstruction is present, which limits oxygen delivery during times of increased metabolic demands. The severity of the obstruction determines the threshold for cardiac ischemia.
Recently, it has become apparent that angina also can be caused by transient decreases in oxygen delivery due to coronary vasoconstriction. Nonocclusive intracoronary thrombi are usually present in patients with unstable angina and cause acute impairment in oxygen delivery. Intracoronary thrombi and platelet aggregation occur in unstable or ruptured coronary artery plaques. The local release of vasoactive compounds, such as serotonin and thromboxane A2, is thought to mediate acute vasoconstriction in patients with unstable angina.
What role does exercise ECG have in the diagnosis of coronary artery disease (CAD)?
In patients with a chest pain syndrome of uncertain etiology and a normal resting ECG, a standard exercise test is useful in the diagnosis of CAD.
Exercise ECG testing adds little in detecting the presence or absence of CAD in patients with a high pretest probability of CAD (i.e., history of typical angina with one or more risk factors).
Exercise testing is most valuable in confirming or excluding the diagnosis of CAD in patients with an intermediate pretest probability of CAD. Typically, these are patients with some atypical anginal features and a normal ECG, who may or may not have risk factors for CAD. In such patients, if typical anginal discomfort occurs during exercise and is associated with 1-mm ST-segment depression (horizontal or downsloping in nature), the predictive value for the diagnosis of CAD is 90%. If a 2-mm ST-segment depression occurs with typical angina, this finding is virtually diagnostic of CAD. An exercise ECG test associated with a hypotensive blood pressure response carries an 80% predictive value for significant CAD.
A negative exercise test in a patient with a low pretest probability of CAD is highly reliable in excluding the diagnosis of significant CAD.