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  • Title: [New aspects of ACE inhibitor treatment of heart failure].
    Author: Dietz R, Osterziel KJ.
    Journal: Z Kardiol; 1996; 85 Suppl 6():241-6. PubMed ID: 9064971.
    Abstract:
    Coronary artery disease is the underlying cause in most of our patients with heart failure nowadays. The arguments put forward for treating these patients with ACE-inhibitors would be reinforced when convincing data are reported demonstrating 1) a reduction of malignant arrhythmias, 2) a reduction in reinfarction rate and 3) a reduction of progressive deterioration in left ventricular function. 1) ACE-inhibitors and malignant arrhythmias. The prolongation of life in heart failure patients treated with ACE-inhibitors might either derive from retarding the progression of heart failure (CONCENSUS I) or from reducing sudden cardiac death (VHeFT II-trial). However, it remains to be established whether the advantage for ACE-inhibitors in reducing sudden death only exists in comparison to a group of patients treated with the combination of hydralazine plus ISDN or whether this is true also in comparison to a placebo group. 2) ACE-inhibitors and reinfarction. Retrospective analysis of data from studies of left ventricular dysfunction (SOLVD) and from the survival and ventricular enlargement (SAVE) study suggested that ACE-inhibitors may reduce the reinfarction rate by about 20%. The underlying mechanisms are not well understood but could in part be mediated by improving endothelial function and/or attenuating the inhibition of PAI-1 through the administration of ACE-inhibitors. 3) ACE-inhibitors and progressive left ventricular dysfunction. ACE-inhibitors are effective means in retarding the remodeling process after myocardial infarction. This is not only true for the progressive increase in left ventricular dimension, but also for the progressive loss of contractile function in the primarily unaffected myocardium. Both, clinical and experimental studies suggest that the observed reduction in mortality is particularly related to the attenuation of the remodeling process by ACE-inhibitors.
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