These data confirm our initial observation of familial aggregation of LMD. Moreover, in apparently healthy siblings of patients with LMD, this heritable component results in a risk increase for future events that is greater than that of a strong positive family history by itself.
The effect of 2.5 mg prazosin orally was monitored for one hour by cardiac catheterisation in 11 patients with cardiac insufficiency as a result of primary cardiomyopathy. Mean pressures of the pulmonary capillary bed and pulmonary artery decreased on average by 9 mm Hg, of the right atrium by 2.5 mm Hg and systemically by 8 mm Hg. Judging by the increase of cardiac index patients were divided into a group of 7 "responders", all showing congestive cardiomyopathy, and a group of 4 "nonresponders" with various cardiomyopathies. During prazosin treatment cardiac index increased by 23% and pulmonary arteriole resistance decreased by 4% and pulmonary arteriole resistance increased by 41%. It is concluded that not all forms of left ventricular failure respond favourably to prazosin. Divergent effects of prazosin may possibly be caused by unequal effects on pre- and after-load of both ventricles and on variable behaviour of lung arteriole resistance.
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