Prazosin in the Treatment of Heart Failure: Problems and Potential
The scientific rationale for the use of drugs which selectively block α-adrenoceptor antagonists in the treatment of heart failure has been convincingly expounded on a number of occasions (Braunwald 1977; Mason 1978; Taylor 1980) and repeatedly demonstrated in practice (see reviews by Taylor et al. 1982; Ribner et al. 1982; Franciosa 1983). But as with many therapies used in this dynamic circulatory situation, the results of such treatment have not lived up to the expectations (Taylor, 1983). The reasons are clear: Too much was asked of too little. This simplistic concept that modulation of one circulatory consequence of heart failure would fundamentally alter the haemodynamic profile, the symptom complex, the morbidity risk or the length of survival in this terminal pathophysiological state failed to take into account the powerful compensatory mechanisms still existing in these patients. But neither should the real clinical benefits and unproved potential of α-adrenoceptor modulation in this syndrome be totally discounted. The evidence must be carefully and sensibly sifted to determin what benefits are possible and how such therapy should be further explored. This is the attitude that will prevail in this brief review of prazosin in the treatment of heart failure.
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