Abstract
It is suggested that the loss of ANF activity following total heart replacement predisposes to embolic sequelae. Cerebral embolism is a frequent complication of total artificial heart implantation. Of seven patients receiving the Jarvik-7 total artificial heart before February 1986, four suffered postoperative cerebral embolism (1). The prevalence of this grave complication has blunted early optimism about the therapeutic utility of mechanical replacement of the heart (1). The purpose of this note is to suggest a possible etiological factor in this complication that may previously have been overlooked. Recent studies suggest that the cardiac hormone atrial natriuretic factor (ANF) plays an important role in the maintenance of cardiovascular homeostasis (2). ANF is a circulating peptide hormone secreted by atria1 muscle; among its physiological effects are increased urine volume, increased excretion of sodium and to a lesser extent of calcium, and antihypertensive and vasorelaxant: effects (2). Since ANF is localized in the atrial cardiocytes (l), total removal of the myocardium must cause total suppression of ANF activity. This suppression might predispose to embolic events via several mechanisms. Increased plasma osmolarity already has been suggested as an iatrogenic factor predisposing to thrombosis in such cases (2); decreased natriuresis (or decreased excretion of other osmoles) induced by loss of ANF activity could exacerbate this effect. Loss of the vasorelaxant action of ANF could contribute to relative vasoconstriction, which might predispose to embolism. Another possible effect of ANF loss is the decreased excretion of calcium, which is required for platelet aggregation (3). Increased plasma calcium might enhance clotting by restoring near-optimum plasma calcium levels for platelet aggregation, or possibly by being transported into platelets (3). Sharply elevated plasma concentrations of ANF have been observed in hamsters with cardiomyopathy and congestive heart failure (2). If elevated plasma ANF levels also are present in human end-stage heart disease, then the effects of total loss of ANF activity might be more severe in such patients than in healthy humans. If the loss of ANF activity does contribute to the etiology of strokes following artificial heart implantation, then postoperative ANF replacement therapy might help prevent this sequela. Since the human ANF gene has been cloned (2), such therapy might be carried out at relatively low cost with recombinant ANF. I also wish to suggest that ANF depletion
Published Version
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