Clinical review 36: Cardiovascular manifestations of endocrine disease.

Abstract

NDOCRINE diseases affect multiple organs, almost always involving the heart and cardiovascular system. In many cases the adaptive cardiac response is physiologically normal and the clinical findings are subtle. Conversely, cardiovascular manifestations can be the presenting or predominate finding for such diseases as hyperthyroidism, acromegaly or carcinoid syndrome. In the present review we will address the changes, including alterations in blood pressure, vascular resistance, cardiac work, cardiac growth, arrhythmias, ischemic and valvular heart disease and the cardiac related morbidity which accompanies endocrine disease (Table 1). The hypothesis that we will explore is whether these manifestations are a result of primary effects upon the heart or whether the effects are secondary as a consequence of the cardiac response to systemic perturbations mediated by endocrine disease. Emphasis will be placed on the pathophysiology of these changes and the response to palliative as well as to definitive treatment. Hyperthyroidism Since the earliest descriptions by Caleb Perry and Robert Graves (see Ref 1) the association between hyperthyroidism and a hyperdynamic cardiovascular system has been noted. As a result of the effects of thyroid hormone on the peripheral circulation and on the heart, hyperthyroidism results in a fall in systemic vascular resistance, an increase in cardiac output and cardiac work and enhanced left ventricular contractility (1). Although this is observed clinically as a rapid heart rate with a widened pulse pressure and hyperdynamic precordial activity with increased cutaneous blood flow, the physiological consequence is an increase in myocardial oxygen consumption and under certain circumstances cardiac hypertrophy. Certain symptoms, including exercise intolerance, dyspnea on exertion and heart failure have led clinicians to postulate an effect of thyroid hormone on the heart. In their studies of left ventricular ejection fraction (LVEF) with exercise, Forfar and colleagues (2) have observed that the failure to increase the LVEF in exercising hyperthyroid patients was corrected by rendering the subjects euthyroid. This observation led them to postulate a reversible form of hyperthyroid cardi