Reperfusion Therapy Reduces the Risk of Myocardial Rupture Complicating ST‐Elevation Myocardial Infarction

T he debate about the advantages of fibrinolytic therapy or primary percutaneous coronary angioplasty (PCI) as a superior reperfusion strategy for ST-elevation myocardial infarction (STEMI) has continued for 30 years. In the first decade, primary PCI was limited by first-generation equipment, inadequate radiographic imaging systems, suboptimal adjunctive antithrombotic therapy, and delays in time-totreatment. Successful reperfusion rates were too low and infarct artery reocclusion and restenosis rates were too high, so fibrinolytic therapy was associated with better clinical outcomes. Since then, fibrinolytic therapy improvements have included bolus administration of newer agents, adjunctive dual antiplatelet therapy with aspirin and clopidogrel, and cardiac catheterization as soon as possible for reperfusion failure and within 24 hours after successful reperfusion to maximize sustained infarct artery patency rates. Perhaps more impressive has been the improvement in primary PCI that now makes it the preferred reperfusion strategy. The PCI wires and catheters are well engineered, radiographic and intravascular imaging capability allows excellent visualization of the coronary arteries, antithrombotic medications decrease the risk of acute closure, and drug-eluting stents assure excellent long-term infarct artery patency rates. Most importantly, pre-hospital and in-hospital systems of care have been developed to decrease time-to-treatment and offer reperfusion therapy to almost all patients with STEMI unless treatment is deemed futile. Lost in the debate over which reperfusion strategy best reduces mortality rates is the important reduction in morbidity associated with both reperfusion therapies compared with historical controls. Hemodynamic, electrical, mechanical, and thrombotic complications have all been reduced by successful reperfusion therapy that restores microvascular perfusion, limits infarct size, and improves left ventricular remodeling. A leading cause of death before reperfusion therapy was myocardial rupture, defined for the purposes of this discussion as free-wall rupture or ventricular septal rupture and excluding papillary muscle rupture or left ventricular pseudoaneurysm formation from contained free-wall rupture. The incidence of myocardial rupture is difficult to ascertain because death can occur before hospital admission, failed diagnosis is possible unless routine echocardiography is performed, and autopsy rates have been poor and variable. Some patients have certainly been misclassified as sudden cardiac death or cardiogenic shock due to myocardial necrosis. Rates as high as 6% for myocardial rupture and 3% for ventricular septal rupture were reported in the prereperfusion era. More recently, the risk in the reperfusion era appears to be approximately 2% for myocardial rupture and 0.3% for ventricular septal rupture. The clinical diagnosis of free-wall rupture is suggested by the physical findings of cardiac tamponade (Beck’s triad of hypotension, jugular venous distension, and muffled heart sounds; pulsus paradoxus), electrical mechanical dissociation in the absence of preceeding heart failure, or hypotension with at least a moderate pericardial effusion on echocardiography. The clinical diagnosis of ventricular septal rupture is suggested by a systolic murmur and confirmed by an abnormal oxygen saturation run during pulmonary artery catheterization, color flow Doppler echocardiography, or contrast left ventriculography. Pathologic confirmation of myocardial rupture can also be obtained during surgery or necropsy. Risk for myocardial rupture is increased with first myocardial infarction (MI), anterior MI, older age, female sex, absence of prior angina or MI, hypertension, no or unsuccessful reperfusion therapy, late reperfusion therapy, and one-vessel disease without collateral circulation. Prognosis is poor with mortality rates of 75% to The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Division of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI. Correspondence to: Eric R. Bates, MD, CVC Cardiovascular Medicine, University of Michigan Health System, 1500 E. Medical Center Drive, Ann Arbor, MI 48109-5869. E-mail:[email protected] J Am Heart Assoc. 2014;3:e001368 doi: 10.1161/JAHA.114.001368. a 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.