A 52-year-old white man presented with a small full wall thickness anterior myocardial infarct. He L was given intravenous streptokinase, aspirin, and nitrates, and his course was uncomplicated.He had suffered mild essential hypertension for 10 years and had been treated over this period with moduretic (one tablet per day). His primary physician had excluded causes of secondary hypertension, and he had been told that his blood pressure control on the diuretic was satisfactory (documented at levels between 146 and 138 mm Hg systolic and 90 and 96 mm Hg diastolic). His serum cholesterol levels had been measured on several occasions, and the last reading was 6.8 mmol/dL (205 mg%).A chest radiograph performed in the hospital showed cardiomegaly, and his electrocardiogram showed high voltage over his anterior chest leads. An echocardiogram confirmed increased posterior and septal thicknesses, with normal fractional shortening. A radionuclide ventriculogram showed a left ventricular ejection fraction of 40%. Serum creatinine concentration was within normal limits, as were serum potassium and blood glucose levels.His blood pressure on presentation to the hospital with the myocardial infarction was 160/100 mm Hg and remained at this level for the first 24 hours. On the second day, 6.25 mg captopril was given and then 12.5 mg twice daily. His blood pressure fell to 150/95 mm Hg, and his captopril dose was increased to 25 mg twice daily.On discharge from the hospital, his blood pressure was 140/82 mm Hg. Six months later, on medical review, his blood pressure was 142/84 mm Hg, his cholesterol was 5.5 mg/dL, and his left ventricular hypertrophy had regressed.This man presents with a very common clinical and management problem: a middle-aged man with longstanding treated hypertension and left ventricular hypertrophy complicated by an acute myocardial infarct.Dr Johnston was an invited speaker at