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A randomized, controlled trial, known as the Autologous Stem-Cell Transplantation in Acute Myocardial Infarction (ASTAMI) study, was conducted to investigate whether intracoronary injection of autologous mononuclear bone marrow (BMC) results in a clinically important improvement in left ventricular function as measured by the left ventricular ejection factor (LVEF). Results showed no effects of intracoronary injection of autologous mononuclear BMC on global left ventricular function.

Oie, Erik, Reidar Bjornerheim, Ole Petter F. Clausen, and Havard Attramadal. Cyclosporin A inhibits cardiac hypertrophy and enhances cardiac dysfunction during postinfarction failure in rats. Am J Physiol Heart Circ Physiol 278: H2115-H2123, 2000.--Calcineurin has recently been implicated as a mediator in the signaling pathways that transform intracellular calcium signals to the phenotype of myocardial hypertrophy. The present study was conducted to examine the effects of cyclosporin A (CsA), an inhibitor of calcineurin, on myocardial hypertrophy and remodeling during congestive heart failure (CHF) in rats. After ligation of the left coronary artery, rats were randomized to treatment with CsA or vehicle for 14 days. Compared with vehicle, CsA substantially attenuated myocardial hypertrophy in the CHF rats as assessed by alterations in ventricular weight-to-tibial length ratios (P [is less than] 0.05). Myocardial gene expression of skeletal [Alpha]-actin was also reduced in the failing left ventricle (LV) after treatment with CsA (P [is less than] 0.05), although the mRNA levels were still substantially elevated relative to those of sham rats. CsA-induced inhibition of compensatory myocardial hypertrophy in the CHF rats led to increased dilatation of the LV cavity and reduced fractional shortening and peak positive and negative first derivatives of LV pressure (P [is less than] 0.05). Plasma renin and endothelin-1 levels were increased in the CHF-CsA rats, providing humoral cues of aggravated cardiac function. Thus this study supports a crucial role of calcineurin-dependent pathways in the mechanisms of compensatory myocardial hypertrophy during CHF. In addition, our data indicate that inhibition of compensatory myocardial hypertrophy exerts detrimental effects on cardiac remodeling and function after myocardial infarction. calcineurin; myocardium; heart failure