These electrophysiological features, which are manifestations of the abnormal atrial electrophysiology, would favor production of atrial reentry in chronic lone AF.

No abstract

Abstract. Koga N, Kurashige Y, Sato T (Koga Hospital, Kurume, Japan). Long-term effects of LDL apheresis on carotid arterial atherosclerosis in familial hypercholesterolaemic patients. J Intern Med 246: 35]43.Objectives. To assess the long-term effect of LDL apheresis on carotid arterial atherosclerosis in severe familial hypercholesterolaemic (FH) patients. Design. Changes in existing plaque, new plaque formation and annual progression rate of carotid early plaque were evaluated by B-mode ultrasonography. Subjects. LDL apheresis group: two homozygous FH and nine heterozygous FH patients received a combination of LDL apheresis and cholesterol-lowering drug therapy for a mean of 7.8 years. Control group: 10 heterozygous FH patients were maintained by medication only for a mean of 5.5 years. Results. As a result of LDL apheresis treatment, LDL cholesterol levels reduced from 16.0 6 3.60 to 6.43 6 0.07 mmol L 21 in homozygous FH patients and from 11.5 6 2.46 to 4.32 6 1.2 mmol L 21 in heterozygous FH patients. During the long-term treatment period, the existing plaque tended to progress and new plaque formation in carotid arteries was also observed in both groups. The annual progression rate of mean maximum intima]media thickness in the common carotid artery was a mean of ]0.0023 6 0.0246 mm year 21 in heterozygous FH patients in the LDL apheresis group, suggesting regression. This was significantly lower when compared with the control group, which had a mean of 0.0251 6 0.0265 mm year 21 . Conclusion. The results suggest that the long-term treatment with combined LDL apheresis and drugs may delay the progression of the atherosclerotic process and prompt the stabilization of atheromatous plaque in severe FH patients.

Losartan, an angiotensin II receptor antagonist with no bradykinin potentiating property, provides the opportunity to study the consequences of blocking angiotensin II. The objective of this study was to evaluate the antiarrhythmic responses of reperfusion arrhythmia to losartan in dogs. The effects of losartan on ventricular tachyarrhythmias induced during occlusion and reperfusion of the left anterior descending coronary artery were investigated in 30 dogs. The animals were randomized to receive either losartan (n = 15) or saline (n = 15). The VF inducing threshold was measured before occlusion and after reperfusion. Losartan (50 micrograms/kg per min) or saline was intravenously administered 5 minutes before occlusion and continued throughout the entire study period. The incidence of ventricular tachyarrhythmias during reperfusion was lower in the losartan group than in the control group (4/15 vs 6/15). There was no significant change in VF inducing threshold between the period before occlusion and during reperfusion in the losartan group [10.9 +/- 5.7 vs 11.1 +/- 5.7 mA, P = NS), whereas there was a significant decrease in the control group (15.5 +/- 4.4 vs 7.7 +/- 3.9 mA, P < 0.01). Blockade of the angiotensin II receptor has beneficial effects on reperfusion arrhythmias.

Light and electron microscopic examinations were performed on 20 coronary artery sites from nine patients who had undergone percutaneous transluminal coronary angioplasty. Twelve successfully dilated sites without prior thrombosis showed evidence of a tear in the luminal surface (with or without fracture of an atheroma) even at 140 days after angioplasty. The tear split through a relatively undistensible intima in 9 (75%) of the 12 sites. Two successfully dilated sites with prior thrombosis showed an intraintimal tear with a widely lacerated fibrous cap and thin mural thrombus. After dilation, the occluded prior nonthrombosed site showed marked protrusion of a separated plaque. An occluded prior thrombosed site after dilation revealed intraintimal canal-like hematoma. Four sites that occluded after balloon passage revealed a dissecting hematoma in three and plaque disruption in the other.