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SUMMARY Ischaemic cardiomyopathy and dilated cardiomyopathy may be clinically indistinguishable and cardiac catheterisation is often required to differentiate between them. We have described the thallium-201 scintigraphic appearances both on exercise and after redistribution in 13 patients with ischaemic cardiomyopathy and 11 patients with dilated cardiomyopathy and have assessed the usefulness of this non-invasive technique in distinguishing between the two groups.All patients with ischaemic cardiomyopathy and seven of the 11 patients with dilated cardiomyopathy displayed perfusion defects. Reversible defects were equally common in the two groups, occurring in approximately 60% of patients. Reverse redistribution defects were confined to the group with ischaemic cardiomyopathy and were found in five patients, and fixed defects were also much more common in this group, being present in 92% compared with 27% of patients with dilated cardiomyopathy. In addition, fixed defects were much more extensive in the group with ischaemic cardiomyopathy and involved greater than 40% of the outer perimeter of the left ventricular image in 10 out of 12 of these patients compared with only one patient in the group with dilated cardiomyopathy.We conclude that the finding of a reversible defect on thallium imaging is non-specific as to aetiology, and does not necessarily imply ischaemic heart disease. The presence, however, of either a fixed defect involving more than 40% of the outer left ventricular perimeter or a reverse redistribution defect strongly favours an ischaemic rather than a dilated cardiomyopathy.Both dilated cardiomyopathy and ischaemic heart disease may have an identical clinical presentation with cardiomegaly, impaired left ventricular function, and congestive heart failure.' 2 Subjects with dilated cardiomyopathy have poor myocardial function associated with widely patent, non-obstructed coronary arteries, whereas when ischaemic heart disease is the underlying pathology, myocardial dysfunction results from severe atheromatous narrowing of the coronary arteries. The term ischaemic cardiomyopathy has been coined to describe this latter situation.' In view of the differing natural history, prognosis, and treatment of the two conditions accurate differentiation between them is important.At present, coronary angiography is often necessary to make the distinction, but myocardial perfusion scintigraphy using thallium-201 (T1) has been suggested by Bulkley et al.3 as a useful non-invasive alternative. These authors performed imaging only at rest but were able to differentiate correctly between dilated cardiomyopathy and ischaemic cardiomyopathy in the majority of patients studied.Received for publication 23 March 1981 290The aim of the present study was to establish the Ti scintigraphic appearances on exercise and after redistribution in patients with dilated cardiomyopathy and to evaluate the usefulness of sequential imaging with TI as a non-invasive means of distinguishing this group from patients with a similar ...

Nine patients with stable angina (group 1) underwent maximal treadmill stress testing and thallium-201 (201T1) myocardial scintigraphy after intravenous propranolol hydrochloride, and after placebo. Though seven of the nine patients exercised longer after propranolol than after placebo, this difference did not reach statistical significance. Propranolol, however, significantly reduced the mean maximum rate pressure product. Comparison of the perfusion scans on and off propranolol showed that in 36 out of 90 of the myocardial segments recorded (nine patients, five segments scanned twice per patient), only one of the scans showed a defect. In 24 out of 36 of these the propranolol scan was negative, the defect appearing in the placebo scan. Defects present on both scans but differing significantly in size occurred in 22 out of 54 view pairs (nine patients, three views after exercise and three views after redistribution on propranolol and on placebo), and in 19 of these the smaller defect was seen in the propranolol scan. In one of the nine patients, the propranolol scan was normal (false negative), whereas defects corresponding to angiographically proven coronary artery lesions were seen on the placebo scan. Six patients (group 2) were maximally exercised after propranolol and then re-exercised to the same rate pressure product on placebo. Again 16 out of 60 of the segment pairs disagreed and in 10 of these the unmatched defect was present on the placebo scan. In 10 out of 14 discrepant view pairs, the smaller defect occurred on the propranolol scan. Thus in patients taking propranolol, negative results do not exclude coronary artery disease, and perfusion defects (if present) though accurately reflecting the presence of disease may underestimate its true extent.

SUMMARY Intravenous administration of the vasodilator sodium nitroprusside has beneficial haemodynamic effects in subjects with severe aortic regurgitation while acute digitalisation can produce unwanted effects associated with an increase in systemic vascular resistance. This study compares the haemodynamic effects of the vasodilator prazosin and digoxin in eight patients with isolated severe aortic regurgitation. Prazosin 5 mg orally resulted in a 12±3 (SE) per cent increase in cardiac index (thermodilution), maintained over four to six hours, while digoxin 075 mg intravenously did not change the cardiac index. Prazosin reduced mean arterial pressure by 9±3 mmHg and systemic vascular resistance by 18±4 per cent while digoxin resulted in a 6±2 per cent increase in the latter. Mean pulmonary capillary wedge pressure fell 3 mmHg with prazosin. In this group of patients with severe aortic regurgitation but without severe cardiac failure, the changes with either drug, studied in doses conventionally used, were small but those with prazosin were directionally more desirable than those resulting from digoxin.This study describes and compares the haemodynamic effects of the orally active vasodilator drug prazosin and digoxin in a group of patients with severe chronic aortic regurgitation.Corrigan," writing in 1832, believed that when digitalis glycosides were administered in the treatment of heart failure resulting from aortic regurgitation, the patients were "always worse".He attributed the harmful effects he observed to bradycardia which "allowed more time for regurgitation". In 1908, Stewart2 predicted harmful effects from digitalis in aortic regurgitation because of a rise in the systemic vascular resistance. Objective evidence of the haemodynamic effects of the digitalis glycosides in the presence of aortic regurgitation is sparse. Kloster and associates3 found that ouabain resulted in a fall in cardiac output in patients with aortic regurgitation without cardiac failure while Hopkins and Taylor4 found that ouabain and acetylstrophanthidin increased the regurgitant fraction in dogs with experimentally *