We describe an analysis of 227 patients with lacunar infarcts; 177 were inpatients and the remaining 50 were outpatients. The group comprised 11% of all inpatients with cerebrovascular pathology and 16% of all consecutive inpatients with brain infarcts studied at the Department of Neurology of the Hospital de la Santa Creu i Sant Pau. The main risk factors identified in these patients were arterial hypertension in 164 (72%), diabetes mellitus in 64 (28%), and heart disease in 58 (26%). The most common clinical syndromes were pure motor hemiparesis in 125 (55%), pure hemisensory stroke in 42 (18%), the sensorimotor deficit syndrome in 34 (15%), ataxic hemiparesis in seven (3%), and the dysarthria-clumsy hand syndrome in four (2%); atypical syndromes were observed in 15 patients (7%). Lacunes were demonstrated by computed tomography in 100 patients (44%) and by magnetic resonance imaging in 35 (78%) of the 45 patients in which it was applied. Magnetic resonance imaging was significantly better (p< 0.001) than computed tomography for imaging lacunes, especially those located in either the pons (p<0.005) or the internal capsule (/xO.001). After the acute phase, mild or no neurologic disability was detected in 178 patients (78.4%), moderate disability persisted in 48 patients (
The present study suggests that early detection of allograft coronary vasculopathy is feasible with surveillance myocardial perfusion or coronary angiographic studies. When identified early after transplantation, immunosuppressive treatment may result in regression of coronary disease.
The haemodynamic effects of a single dose of intravenous molsidomine were assessed in 12 patients with severe coronary disease. The investigation was carried out at rest during angina induced by pacing and after molsidomine during pacing at the rate at which angina had been produced. During angina, left ventricular systolic and end-diastolic pressure rose, left ventricular stroke work fell and coronary flow and myocardial oxygen consumption increased by 58.3% above the control levels. After the administration of molsidomine, atrial stimulation was not followed by angina and there were no significant changes in systolic blood pressure. Left ventricular end-diastolic pressure fell sharply and coronary flow and myocardial oxygen consumption were only 38% and 33% higher, respectively, than the control levels. The beneficial effects of molsidomine in ischaemic heart disease, therefore, are the result of peripheral vasodilation which, by reducing the preload and afterload, lowers the oxygen requirements of the myocardium and thus increase the threshold for angina. A direct action on the coronary network can not be excluded but if such an action does exist it must be very small in the light of the marked systemic effect.
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