Objective-To assess the prevalence of symptomatic and silent myocardial ischaemia in patients with hypertensive left ventricular hypertrophy.Design-Cross sectional study. Setting-University department of medical cardiology.Patients-90 patients (68 men and 22 women; mean age 57 (range 25 to 79)) with left ventricular hypertrophy due to essential hypertension.Interventions-48 hour ambulatory ST segment monitoring (all patients), exercise electrocardiography (n = 79), stress thallium scintigraphy (n = 80), coronary arteriography (n = 35).Results-43 patients had at least one episode of ST segment depression on ambulatory electrocardiographic monitoring. The median number of episodes was 16 (range 1 to 84) with a median duration of 8-6 (range 2 to 17) min. Over 90% of these episodes were clinically silent. 26 patients had positive exercise electrocardiography and 48 patients had reversible thallium perfusion defects despite chest pain during exercise in only five patients. 18 of the 35 patients who had coronary arteriography had important coronary artery disease. Seven of these patients gave no history of chest pain.Conclusions-Symptomatic and silent myocardial ischaemia are common in hypertensive patients with left ventricular hypertrophy, even in the absence of epicardial coronary artery disease. Despite the large number of epidemiological studies there are few data on the objective assessment of myocardial ischaemia in individual patients with hypertensive left ventricular hypertrophy. We have shown previously that patients with hypertensive left ventricular hypertrophy may have thallium perfusion abnormalities or coronary artery disease and yet be symptom free.6 Because chest pain was an exclusion criterion for the previous study, however, the patients were not representative of all patients with hypertensive left ventricular hypertrophy. We therefore conducted the present study to assess prevalence of symptomatic and asymptomatic myocardial ischaemia in hypertensive patients with left ventricular hypertrophy attending a hospital based hypertension clinic and to determine the best non-invasive method to identify prognostically important coronary artery disease in these patients. Patients and methodsWe recruited 90 consecutive patients (68 men) (mean age 57 (range 25 to 79) years) who agreed to be in the study and fulfilled the following criteria:(a) they had essential hypertension-secondary hypertension was excluded by clinical evaluation, routine biochemical screening, chest x ray, and, where indicated, intravenous pyelography. (b) they had the electrocardiographic pattern of left ventricular hypertrophy and strain.

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Opiates and loop diuretics are the mainstay of treatment of acute pulmonary oedema, but it is now recognized that immediate response to intravenous loop diuretics is acute vasoconstriction with impaired cardiac performance. It therefore seemed appropriate to compare the effects of intravenous isosorbide 5-mononitrate and frusemide on systemic and coronary haemodynamics in a group of patients with chronic cardiac failure at cardiac catheterization. Intra-arterial blood pressure was recorded from the ascending aorta, pulmonary capillary wedge pressure and cardiac output were measured using a Swan-Ganz thermodilution catheter. Coronary venous blood flow was measured using a thermodilution technique and A-V oxygen difference across the myocardium was obtained from simultaneous blood sampling in the aorta and coronary sinus. Absolute myocardial nutrient blood flow was measured using a ¹³³Xe clearance technique.Frusemide in a dosage of 0.5 mg/kg given intravenously provoked acute vasoconstriction with falls in cardiac output and stroke volume. Pulmonary capillary wedge pressure was unchanged in the first 60 min after administration of frusemide. Isosorbide 5-mononitrate in a dosage of 15 mg intravenously, significantly reduced the pulmonary capillary wedge pressure within 5 min, and with the subsequent fall in systolic arterial blood pressure, cardiac output was maintained.These results suggest that intravenous isosorbide 5-mononitrate could well be of value in the immediate management of the patient with acute pulmonary oedema.

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In the management of the patient with chronic cardiac failure, the combination of an arteriolar vasodilator and venodilator should be beneficial. 8 patients with NYHA grade III-IV chronic cardiac failure were studied following placebo, after 4 weeks’ therapy with the arteriolar vasodilator felodipine, and with the combination of felodipine and oral isosorbide 5-mononitrate. Haemodynamic measurements were made at rest and during dynamic exercise at an individual, fixed, near maximal workload. Ejection fraction (EF) was obtained by gated radionuclide ventriculography. At rest, heart rate was unchanged 73 ± 6 at control, 72 ± 4 with felodipine and 74 ± 4 beats/min with the addition of isosorbide 5-mononitrate. Mean arterial pressure fell from 98 ± 5 to 84 ± 4 (p < 0.02) and 84 ± 3 mm Hg (p < 0.02) with nitrate. Cardiac index increased from 2.2 ± 0.1 to 2.5 ± 0.2 litres/min/m² with felodipine and further to 2.6 ± 0.2 litres/min/m² (p < 0.02) with nitrate. Exercise tachycardia and mean arterial pressure were not significantly affected by therapy. Cardiac index increased on exercise from 4.4 ± 0.3 to 4.8 ± 0.3 litres/min/m² with felodipine and 4.9 ± 0.3 litres/min/m² (p < 0.05) with the addition of nitrate. Stroke volume index increased from 35.4 ± 4 to 40.8 ± 4 beats/min/m² and further to 41.0 ± 4 beats/min/m² (p < 0.05) and EF from 14 ± 3 to 18 ± 3% with nitrate. In conclusion, in patients with chronic cardiac failure, treatment with a calcium channel blocker produced sustained haemodynamic improvement, particularly on exercise, and combination with nitrate produced further benefit.