Pharmacological Intervention for Prevention of Left Ventricular Remodeling and Improving Prognosis in Myocardial Infarction

Abstract

Early reperfusion of totally occluded coronary arteries with thrombolysis and/or percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) reduces infarct size, cardiac mortality, and in-hospital events. 1,2 Prompt reperfusion of epicardial blood flow reduces infarct size and mortality rates, in-hospital events, and reinfarction. Furthermore, successful reperfusion greatly affects the reduction in infarct size and left ventricular (LV) function. The reduction in infarct size and the improvement in LV ejection fraction may decrease mechanical stress on the noninfarcted myocardium, preventing LV remodeling, including changes in LV size and shape. 3 Preventing LV remodeling is of key importance after AMI because it may be related to a reduction in adverse cardiac events, including exacerbation of congestive heart failure and cardiac mortality rates. 4 -7 Although reperfusion therapy relieves and reduces ischemia and necrosis, the process of restoring coronary blood flow causes ischemiareperfusion injury in the ischemic myocardium, which limits the beneficial effects of reperfusion and may contribute to mortality despite successful reperfusion therapy. 8,9 Reperfusion injury is triggered by cellular and mitochondrial calcium overload, oxidant stress, endothelial dysfunction, reduction in nitric oxide production, and other factors. Because reperfusion injury limits the efficacy of reperfusion therapy alone, combined use with pharmacological intervention may moderate microcirculatory impairment and clinical outcomes. Such treatments may eventually reduce infarction size and prevent ischemic LV remodeling after AMI. Furthermore, medication in the chronic phase may affect LV remodeling and clinical prognoses. We undertook a systematic review of the literature based on pharmacological reductions in infarct size and prevention of LV remodeling, both of which may be associated with improved clinical outcomes, in cases of MI. In this review, searches through MEDLINE, LILACS, and SCIELO were the sources of information. Articles were selected by their content related to the theme.

The role of oxytocin in cardiovascular regulation

“…Furthermore, ANP activates reperfusion injury salvage kinase, which has been shown to mediate ischemic preconditioning and postconditioning. In several studies with a reperfusion model in vivo , ANP showed inhibition of the occurrence of reperfusion arrhythmia, preservation of ATP content in the ischemic myocardium, and inhibition of neutrophil-induced endothelial cytotoxity (48). …”

Primary Prevention of Heart Failure

“…Ventricular remodeling may continue for weeks or months until the distending forces are counterbalanced by the tensile strength of the collagen scar; this balance then determines the size, location, and transmurality of the infarct, the extent of myocardial stunning, ventricular loading conditions, and local trophic factors [143]. Although contemporary treatment attenuates remodeling [144], there is a large heterogeneity in the remodeling response after an infarction.…”

Hyperbaric Oxygen: Its Application in Cardiology

“…These include the use of erythropoietin, adenosine, hydrogen sulfide, and intracoronary KAI-9803, an inhibitor of protein kinase delta. 15,16 If any of these turn out to be more beneficial than HBO, they may be more practical to administer.…”