Przyklenk, K. and Kloner, R.A. (1989) Reperfusion Injury by Oxygen-Derived Free Radicals? Effect of Superoxide Dismutase plus Catalase, Given at the Time of Reperfusion, on Myocardial Infarct Size, Contractile Function, Coronary Microvasculature, and Regional Myocardial Blood Flow. Circulation Research, 64, 86-96.
https://doi.org/10.1161/01.RES.64.1.86

has been cited by the following article:

• TITLE: Myocardial Infarction: An Overview of STEMI and NSTEMI Physiopathology and Treatment

  AUTHORS: J. G. Kingma

  KEYWORDS: Ischemia, Reperfusion, Infarction, Ischemia, No-Reflow, Microcirculation, Blood Flow, Ischemic Conditioning

  JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.8 No.11, November 12, 2018

  ABSTRACT: Patients with myocardial infarction resulting from acute coronary syndrome are classified by electrocardiographic presentation: 1-acute ST-segment elevation myocardial infarction (STEMI) or 2-non-ST-segment elevation myocardial infarction (NSTEMI). Prompt reperfusion of an infarct-related artery by percutaneous coronary interventions provides some relief of symptoms; long-term prognosis appears to be worse in STEMI compared to NSTEMI patients but clinical findings remain controversial. Reduced myocardial perfusion to the infarct area, caused in part by microvascular obstruction, is a privileged target for diverse pharmacologic or non-pharmacologic interventions (or combinations thereof) to improve clinical outcomes. To date, benefits of both pharmacologic and non-pharmacologic strategies to either limit microvascular obstruction and myocardial injury or improve myocardial perfusion are inconsistent. This review focuses on the physiopathological aspects of myocardial infarction in relation to development of STEMI/NSTEMI and on potential cardioprotective strategies.