SUMMARY Exercise thallium-201 myocardial scintigraphy was performed in 23 patients with hypertrophic cardiomyopathy. Eighteen patients presented with chest pain which was a persistent symptom in 11. Selective coronary arteriography was performed in 16 patients and showed normal coronary arteries in 15 and insignificant luminal irregularities in one patient.Eighteen patients had abnormal scintigrams. Three had an abnormal distribution of tracer entirely attributable to asymmetric septal hypertrophy, whereas 15 had discrete tracer uptake defects which could not be explained solely by myocardial hypertrophy. In this latter group of patients three scintigraphic patterns were identified: (1) in 10 patients defects were seen in scintigrams immediately after exercise but not in delayed images obtained four to six hours later. Eight of these patients had chest pain.(2) Four patients had uptake defects seen in both initial and delayed images. One patient had chest pain. (3) In three patients, one of whom had chest pain, tracer defects were seen only in delayed images and were not apparent in the initial scintigrams.Chest pain occurred in eight out of 10 patients with scintigraphic evidence of myocardial ischaemia but was present in only three out of 13 patients with non-ischaemic scintigrams.The value of exercise thallium-201 myocardial imaging as a diagnostic technique in hypertrophic cardiomyopathy appears limited. Scintigraphic evidence of regional myocardial ischaemia in the absence of significant coronary artery disease, however, contributes to an understanding of the mechanism of angina production in patients with hypertrophic cardiomyopathy.

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A study was performed in 13 patients with idiopathic mitral valve prolapse and in 21 control subjects to assess the effect of the cold pressor test on systolic motion of the mitral valve. A significant increase in blood pressure occurred in 10 patients with mitral valve prolapse and in 19 controls after immersion of one hand in ice-cold water. M-mode echocardiographic recordings from the mitral valve were obtained in all patients before, during, and after the cold pressor test, together with simultaneous phonocardiograms in selected patients. Nine out of 10 patients with mitral valve prolapse and a hypertensive response to the cold stimulus showed a significant increase in the depth of mitral valve prolapse during the cold pressor test whereas in three patients with mitral valve prolapse and no hypertensive response the depth of mitral valve prolapse did not change during cold stimulation. Three patients with previously demonstrated mitral valve prolapse had equivocal resting echocardiograms but developed diagnostic evidence of mitral valve prolapse during the cold pressor test. No evidence of mitral valve prolapse was seen in any of the control subjects before, during or after the cold pressor test. In four patients with mitral valve prolapse and a hypertensive response to cold stimulation the systolic click was delayed by the cold pressor test, whereas the time of the systolic click remained constant in the three patients whose blood pressure did not increase. It is concluded that the cold pressor test provides a stimulus sufficient to delay the onset and increase the depth of mitral valve prolapse, thereby enhancing the diagnostic sensitivity of echocardiography in this condition.

Nisoldipine coat core (CC) is a long-acting calcium channel blocker (CCB) with a slow and smooth onset of action. It is effective in the treatment of angina pectoris, increasing exercise duration, time to ST segment depression and time to onset of angina. The results of two studies reviewed here, in which patients received concomitant treatment with a β-blocker, showed that the anti-anginal efficacy of nisoldipine CC, 40 mg once daily, measured at trough was comparable with amlodipine, 10 mg once daily, and with diltiazem retard, 120 mg twice daily, and that efficacy was maintained over a 24-hour period. The third trial reviewed here showed that nisoldipine CC was at least as effective as three-times-daily treatment with diltiazem (total dose 240 mg). To date, the effects of nisoldipine CC have been investigated in over 4,000 patients with hypertension and angina pectoris. Clinical experience suggests that once-daily nisoldipine CC is at least as well tolerated as other CCBs, provides consistent efficacy and is a useful treatment in the management of patients with angina pectoris. The CCBs show promising beneficial effects in experimental atherosclerosis and a small number of clinical trials show some effect on the progression of atherosclerosis in coronary artery disease and restenosis following coronary angioplasty. An ongoing long-term trial with nisoldipine CC after coronary angioplasty is discussed.

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