Recovery of Ventricular Function after Myocardial Infarction in the Reperfusion Era: The Healing and Early Afterload Reducing Therapy Study

Abstract

Significant myocardial stunning with subsequent improvement of ventricular function occurred in the majority of patients after Q-wave anterior myocardial infarction. A lower peak level of creatine kinase, an estimate of the extent of necrosis, is independently predictive of recovery of function. Early functional assessment (day 1 after acute myocardial infarction) had limited ability to predict recovery of ventricular function.

Wearable Cardioverter-Defibrillator Therapy for the Prevention of Sudden Cardiac Death

“…For example, partial or complete recovery of LVEF has been observed in more than half of patients at 3 months after AMI after institution of heart failure therapies or revascularization. [15][16][17][18][19][20] Guideline-directed medical therapy with β-blockade and renin-angiotensin-aldosterone system antagonism during the early period after diagnosis of nonischemic cardiomyopathy may result in improved ventricular function and decreased future risk of SCD; 50% of patients with newly diagnosed nonischemic cardiomyopathy will demonstrate a 10% improvement in LVEF with the initiation of medical therapy. 21,22 Although the rationale and reasons for postponing ICD implantation are sensible, the current evidence base is incomplete.…”

Expression and Regulation of ST2, an Interleukin-1 Receptor Family Member, in Cardiomyocytes and Myocardial Infarction

“…Details of the trial have been described. [13][14][15] Serum samples from days 1, 14, and 90 after MI from 69 randomly chosen patients in the HEART trial were assayed for soluble ST2 with a sandwich ELISA. 16 Serum ST2 levels in mice were measured with a sandwich ELISA using a rat monoclonal anti-mouse ST2 antibody (Morwell Diagnostics) and a rabbit polyclonal anti-mouse ST2 antibody.…”

Acute Heart Failure Complicating Acute Coronary Syndromes

“…Abrupt myocyte loss leading to contractile dysfunction and AHF is an obvious mechanism, and the extent of biomarker elevation correlates with prognosis and the range of functional recovery. 4 In those without extensive myocyte necrosis, postischemic left ventricular systolic dysfunction (LVSD) leading to AHF can result from transient myocardial stunning or hibernation depending on the extent of coronary reperfusion. 5 Ventricular remodeling can increase wall stress to viable regions that may be relatively underperfused, furthering ischemia and adding to this cycle.…”