Pheochromocytoma: a cause of ST-segment elevation myocardial infarction, transient left ventricular dysfunction, and takotsubo cardiomyopathy.

OBJECTIVE: To report the case of a patient with a pheochromocytoma and apical left ventricular dysfunction that resolved after surgical resection of the pheochromocytoma, to review the effects of catecholamines on myocyte function and the concept that takotsubo cardiomyopathy (TC) is caused by excess catecholamines, and to illustrate the difficulty in the management of an acute coronary syndrome (ACS) during a hypertensive crisis attributable to a pheochromocytoma. METHODS: We present the clinical history, physical findings, laboratory results, and imaging studies in a 60-year-old man with an ACS, TC, and an incidentaloma later diagnosed to be a pheochromocytoma. The association with TC and the pertinent literature are reviewed. RESULTS: A 60-year-old man was suspected of having myocardial ischemia on the basis of symptoms of paroxysmal chest pain extending to the left shoulder, diaphoresis, ST-segment elevation on an electrocardiogram, and elevated serial levels of cardiac enzymes. Coronary angiography did not reveal substantial coronary artery obstruction but detected ballooning of the apical, anterior, and inferior cardiac walls, consistent with TC. He had a history of labile hypertension and palpitations of 3 months' duration. An adrenal mass detected on a prior computed tomographic scan and increased 24-hour urine catecholamine levels were consistent with a pheochromocytoma. Treatment with phenoxybenzamine was initiated, and he underwent a right adrenalectomy, which confirmed that the tumor was a pheochromocytoma and dramatically improved the patient's condition. CONCLUSION: Pheochromocytomas manifest with labile blood pressures and should be considered in the differential diagnosis of ACS. This case also supports the concept that TC is caused by excess catecholamines.

The diagnosis and treatment of lipid disorders in NIDDM - abstract

Dyslipidaemia in NIDDM is multifactorial due in part to diabetes mellitus and in part to the effects of aging, inactivity, obesity, late expression of genetic disorders and the use of drugs which may adversely influence lipid levels. The dyslipidaemia of NIDDM is characterized by hypertriglyceridaemia, low HDL-C and small dense LDL particles. Post-prandial lipaemia is also exaggerated in NIDDM due to impaired clearance of atherogenic particles (chylomicron remnants, small VLDL). Hypercholesterolaemia is not a typical feature of NIDDM except when the total cholesterol is increased due to increased VLDL-C. When LDL-C is increased, it is usually not due to NIDDM but to disorders or factors that commonly increase LDL-C in the adult non-diabetic population. Glycosylation of apoproteins and increased susceptibility of lipoproteins to oxidation probably also contribute to the increased risk of macrovascular disease. Treatment involves diet, exercise, weight loss, improved glycaemic control, elimination of secondary causes of dyslipidaemia and, when necessary, pharmocological lipid-lowering drugs. The response to diet may be variable. In some patients, the plasma triglyceride level may paradoxically increase in response to the NCEP diets which contain 55 - 60 per cent of calories from CHO and 45 per cent of calories from fat (saturated and polyunsaturated fat should each represent 10 per cent of calories and mono-unsaturated fat should represent 25 per cent of calories). Gemfibrozil and reductase inhibitors are the only drugs which can be consistently and safely utilized in NIDDM. Bile acid-binding resins may aggravate hypertriglyceridaemia and cause a paradoxical increase in serum total cholesterol level. Niacin is relatively contraindicated in NIDDM because it produces insulin resistance, intensifies hyperglycaemia and increases the requirement for oral sulfonylurea agents and/or insulin. Use of increased doses of an oral sulfonylurea agent may predispose to niacin-induced hepatotoxicity. Whether hyperinsulinaemia and the use of larger doses to control hyperglycaemia contribute to the risk of macrovascular disease is unresolved at this time (AU)