Angina pectoris is chest pain caused by ischemia of the myocardium secondary to a supply/demand mismatch [1]. In most cases, myocardial ischemia is caused by one or more flow-limiting stenoses in one or more of the epicardial coronary arteries, while in a minority it is caused by coronary vasospasms (Prinzmetal’s angina) or microvascular dysfunction [2-5]. In the elective setting, PCI is performed to alleviate patients from their angina by treating flow-limiting coronary stenoses. However, ever since the introduction of coronary interventions by balloon angioplasty, clinical research evaluating PCI treatment is mostly focused on the quantification of the failure of the different techniques and devices, including the number of deaths, peri-procedural myocardial infarctions (MIs), spontaneous (recurrent) MIs, repeat (target vessel/lesion) revascularizations, and stent thrombosis (ST). In this perspective, it is quite remarkable that there has been much less focus on the success of the device in terms of quantifying the reduction of angina burden. This development was most likely driven by the difficulties to objectively assess angina in clinical trials. As the Academic Research Consortium (ARC) committee discussed in their consensus document on endpoint definitions, angina “does not lend itself as readily to objective assessment as the other proposed end points and is better measured as a stand-alone end point with the use of formal, validated health status instruments” [6]. The general thought is that it is easier to objectively assess the conventional clinical endpoints.,
Department of Cardiology

Grundeken, M., Onuma, Y., & Serruys, P. (2017). What are appropriate clinical endpoints? From device failure assessment to angina evaluation. In Bioresorbable Scaffolds: From Basic Concept to Clinical Applications (pp. 207–214). doi:10.1201/9781315380629