A Letter to our Readers: Past, Present and Future

Despite enormous advances in elucidation of mechanisms responsible for coronary artery disease, diagnostic methods, and treatment, its toll remains horrific. Coronary Artery Disease is dedicated to improving understanding of its pathophysiology and natural history, pertinent diagnostic methods, and therapy and prevention. Accordingly, in addition to its publication of timely reviews in depth, it considers and publishes papers in these three categories of original investigation.

During the past 50 years treatment of acute coronary syndromes has progressed predicated on a paradigm that clinical outcomes are determined largely by the extent to which jeopardized ischemic myocardium undergoes cell death. Efforts to minimize necrosis and improve prognosis have focused on restoration of myocardial perfusion through pharmacologically induced revascularization, percutaneous coronary interventions, and coronary artery bypass grafting. A second strategy has been enhancement of the balance between myocardial oxygen supply and myocardial oxygen demand through reduction of cardiac work with the use of pharmacologic agents to lower ventricular afterload or heart rate. Refinements in these approaches have included judicious use of anticoagulant agents, antiplatelet drugs, and ancillary measures to reduce oxidative stress and improve myocardial energetics. Although it has been recognized that a favorable local metabolic milieu can preserve jeopardized ischemic cardiomyocytes, therapy predicated on achieving such conditions has been only modestly and inconsistently effective.

Recently, many investigators have speculated that apoptosis (programmed cell death) is a major contributor to overall cardiomyocyte cell death consequent to ischemic insults. The hope has been that if this is indeed the case, anti-apoptotic interventions may prove strikingly beneficial in improving prognosis and broadening the window during which effective revascularization can be induced. Whether a major modification of the fundamental paradigm that has guided therapy for many decades will be forthcoming will depend on the fruits of the labors of many investigators exploring the possibility that in addition to oncotic (cell swelling) cell death constituting the bulk of necrosis induced by ischemia, apoptosis and possibly autophagy will turn out to be important after the onset of ischemic insults in patients.

Coronary Artery Disease is committed to facilitating the exploration of these and related issues and the rapid dissemination of knowledge relevant to them. Manuscripts stemming from basic science, clinical investigation, epidemiology, and critical reviews germane to coronary artery disease and its sequelae are welcomed. So are our readers.

Burton E. Sobel, M.D.
Editor-in-Chief, Coronary Artery Disease