Abstract
Elucidation of the primary, secondary, and tertiary pathophysiological consequences of pumping failure of the heart now allows targeting of the ways and means by which pharmacologic intervention may impede progression of the syndrome. The prime therapeutic aims must be to reduce the distending influence of the increased preload on the ventricle and to reduce the increased cardiac pressure afterload by vasodilatation, thereby enhancing contraction and relaxation of the overstretched myocytes. Improvement in pumping function of the failing heart can also be expected to reduce the magnitude of the excessive neuroendocrine responses, to relieve the clinical symptoms of breathlessness and fatigue, to reduce nonfatal morbid events, and possibly even to extend survival. Drugs, singly or in combination, which are able to primarily relieve pre- and afterload on the heart and secondarily, therefore, are able to improve cardiac pumping activity are attractive pharmacotherapeutic remedies. Ibopamine, by its powerful ability to stimulate dopaminergic adrenoceptors, appears to possess the necessary properties to fulfill this concept,and studies thus far confirm its therapeutic prospects in the treatment of heart failure.