Therapy for Angina Pectoris Secondary to Coronary Disease

Ischemic heart disease is the world’s leading cause of mortality and also causes widespread morbidity and limitation of life-style. Coronary artery disease (CAD) is the predominant cause of ischemic heart disease and generally results from fixed coronary artery obstruction that limits myocardial oxygen delivery relative to demand. Mortality associated with CAD is relatively high and was estimated at more than 11⁄4 million deaths in industrialized countries in 2001 (Lopez et al., 2006). Of note, CAD is projected to remain the primary basis of mortality at least through year 2030 (Mathers & Loncar, 2006). The impact of CAD on quality of life is even more impressive. The symptom that most commonly limits life-style in patients with CAD is angina pectoris. Angina pectoris is a symptom characterized by (1) substernal chest discomfort that is (2) predictably provoked by exertion or emotional stress, (3) lasts up to 20 minutes after the triggering activity is stopped, and (4) is relieved within minutes by nitroglycerin or rest. If all of these criteria are met, the symptom is called “typical angina pectoris”; if only 2 are met, the symptom is called “atypical angina”. If one or none are met, the symptom probably is non-cardiac in origin (Diamond et al., 1983). Typical angina has several different causes but predominantly results from CAD. Indeed, the presence of typical angina predicts CAD with a likelihood of 90%, while the association of atypical angina with CAD is reported to be 50%. CAD with ischemia also can cause other symptoms, such as abnormal chest sensations that do not meet the criteria for angina, dizziness, palpitation, dyspnea, etc. Angina pectoris is the presenting symptom in 50% of those with CAD (O'Rourke, 2010). Most often, this symptom is “stable”, i.e., after its onset, it occurs at a relatively predictable workload, frequency and severity. By convention, stable angina manifests little change in these characteristics over 2 weeks, though some variation can be expected if change occurs in myocardial oxygen demand, physical stress or ambient temperature (Braunwald et al., 1994). In general, stable angina correlates with the stability or quiescence of an atherosclerotic plaque. Almost 20% of acute myocardial infarctions (MI) are preceded by chronic stable angina (Thom et al., 2006). This symptom must be distinguished from the less frequent “unstable angina”, considered to occur when angina first is manifest (“new onset angina”), or when angina-like discomfort is present at rest (i.e., without the activity/