To evaluate the possibility of quantitatively diagnosing carotid and cerebral atherosclerosis noninvasively, we measured common carotid flow volume in 60 sides (30 patients), using an ultrasonic quantitative flowmeter, and then compared these findings to the severity score of carotid and cerebral atherosclerosis as determined at autopsy. Stenosis decreased common carotid flow volume in the carotid and cerebral arteries. Increases in the severity score varied inversely with reduced flow volume, which was high in inverse correlation (r= -0.696). Patients with flow volumes of 8.5 ml/sec or greater did not have stenosis greater than or equal to 75%, whereas all patients with flow volumes of 6.4 ml/sec or less had stenosis greater than or equal to 50%, with 45% of these having stenosis greater than or equal to 75%. These pathological findings confirm that the common carotid flow volume reflects the degree of carotid and cerebral atherosclerosis present and that the lower limit of common carotid flow volume in healthy subjects is 6.5 ml/sec (Stroke 1991^22:319-323) U ltrasound has advanced the noninvasive diagnosis of carotid and cerebral atherosclerosis, but quantitative measurement only recently has been possible. Our ultrasonic quantitative flow measurement system has made it possible to measure noninvasively and quantitatively the absolute blood flow volume in the common carotid artery that constitutes the input end of the cerebral arteries.

It has been reported that coronary diseases in patients with Fabry's disease are induced by deposits in endothelial cells and coronary smooth muscle cells. Most of those are ischemia due to stenosis. This report describes a case of patient with Fabry's disease who showed severe vasospasms without coronary artery stenosis during acetylcholine loaded coronary angiography. In this case, a myocardial biopsy revealed that the deposits in the endothelial cells of the myocardial capillaries were lamellated appearance. Recently, it is reported that endothelial cell damage could be an important cause of coronary vasospasm. This case suggests that the some sort of functional disorder was induced by glyco-sphingolipid deposits in the coronary endothelial cells, and that this might have led to coronary artery spasms without the organic stenosis of coronary arteries.

No abstract

To investigate the clinical significance of interactions between cisapride and sustained-release nifedipine, we comparedthe plasma nifedipine concentration and blood pressure after administration of nifedipine alone (20 mg) with those obtained after administration of nifedipine with cisapride (2.5 mg) in 20 patients with hypertension. The plasma nifedipine level was not altered by cisapride at one hour after administration, but was significantly increased at two (p<0.01), three (p<0.01), and four (p<0.05) hours when compared with the level measured after nifedipine alone. Cisapride significantly decreased the mean blood pressure at three hours (p<0.05) after administration ofnifedipine. The acetaminophen method was used to determine gastric emptying time. The plasma concentration of acetaminophenat 45 minutes after administration was significantly increased by cisapride, suggesting that enhanced gastrointestinal motility might be the basis for the increase in the plasma nifedipine concentration. These results suggest that enhancement of the antihypertensive effect ofnifedipine can occur when the drug is prescribed with cisapride, and that caution is needed whenusing such a combination therapy. (Internal Medicine 35: 941-945, 1996)

SUMMARYParoxysmal tachycardia with widened QRS complexes was found in a 46-year-old woman.In sinus rhythm, the patient had electrocardiographic evidence of type B preexcitation with a left bundle branch block pattern.The resting PR interval (160msec) and A-H interval (100 msec) were within normal limits, but the H-V interval (10msec) was abnormally short. Programmed atrial extrastimuli at progressively shorter coupling intervals resulted in sudden prolongation of the A-H interval from 120msec to 250msec, and the His bundle activities became incorporated just after initiation of the QRS complexes.The QRS morphology was changed but the change was minimal, and atrial echo beats or sustained tachycardia with wide and preexcited QRS complexes were elicited. It is postulated that the site of reentry is within the AV node with preexcitation occurring as the result of conduction in an anomalous nodoventricular pathway.