Noninvasive assessment of coronary artery disease: the role of stress echocardiography

Abstract

Echocardiography combined with either exercise or pharmacological stress is a widely used method for the noninvasive assessment of coronary artery disease. This is due to the high diagnostic accuracy that does not differ substantially among the various stress modalities. In addition, stress echocardiography has a useful role in risk stratification of patients with known or suspected coronary artery disease. In particular, evidence of inducible ischemia is predictive of an unfavorable outcome, whilst its absence is associated with a very low risk of future cardiac events. These findings have strong implications in clinical decision-making. One of the main characteristics of the echographic marker of ischemia is that it is significantly more specific than the electrocardiographic one. The higher specificity of stress echocardiography translates into increased prognostic value as compared to exercise electrocardiography. Nevertheless, exercise electrocardiography has a very high negative predictive value. Moreover, compared to stress echocardiography it is safer, simpler, less costly and requires no specific competence. Based on these data, exercise electrocardiography remains the cornerstone of the noninvasive evaluation of coronary artery disease. Stress echocardiography, on the other hand, is particularly useful in those cases when exercise electrocardiography is not feasible, non-interpretable (owing to the presence of left bundle branch block or of a pacemaker or of other electrocardiographic baseline abnormalities), or when it gives inconclusive data, or a positive result at an intermediate or high workload (in such cases, precise knowledge of the site and extension of ischemia can be of crucial importance in deciding between conservative and aggressive treatment), as well as in cases in which ischemia during the test is frequently a false positive response, as in hypertensive patients, in women and in all cases of left ventricular hypertrophy.