ABSTRACT
Prevention of restenosis after percutaneous transluminal coronary angioplasty (PTCA) continues to be a significant problem. Recent controlled studies have demonstrated that cilostazol suppresses restenosis after PTCA. The effects of ticlopidine, another antiplatelet agent, were compared in terms of outcomes of patients randomized for treatment with the two drugs after PTCA. A total of 35 patients (47 lesions) were assigned prospectively and randomly to ticlopidine (17 patients, 24 lesions) and cilostazol (18 patients, 23 lesions) groups. Minimal luminal diameter (MLD) and percentage of stenosis to reference diameter were estimated before PTCA, just after the procedure and after 4 months follow-up. All patients underwent 4 months angiographic follow-up, at the end of which MLD was 2.03+/-0.71 mm in the ticlopidine group and 2.05+/-0.68 mm in the cilostazol group (p = 0.95), and the percentage of stenosis to reference diameter was 31.4+/-16.7% and 30.0+/-17.0%, respectively (p = 0.78). The restenosis rate was 12.5% in the ticlopidine group and 17.4% in the cilostazol group (p = 0.69), relatively low as compared to the 20% to 30% reported in previous studies. Adverse drug reactions during the follow-up period were observed in two of the ticlopidine group and none of the cilostazol group. We conclude that both ticlopidine and cilostazol are effective for the prevention of restenosis after PTCA, however the former may be associated with slight side effects.
Subject(s)
Angioplasty, Balloon, Coronary , Coronary Disease/drug therapy , Platelet Aggregation Inhibitors/therapeutic use , Tetrazoles/therapeutic use , Ticlopidine/therapeutic use , Aged , Angioplasty, Balloon, Coronary/adverse effects , Cilostazol , Coronary Angiography , Coronary Disease/diagnostic imaging , Coronary Disease/therapy , Female , Follow-Up Studies , Humans , Male , Middle Aged , Prospective StudiesABSTRACT
We recently studied two patients with cerebral embolism, in whom transesophageal echocardiography revealed protruding atherosclerotic plaques with freely mobile projections in the aortic arch. Ultrasonic imaging showed that the carotid artery was normal, and transthoracic and transesophageal echocardiography did not reveal a cardiac embolic source in either case. In one patient, we observed that an atherosclerotic plaque became ulcerated and developed mobile projections over the course of a year. More consideration should be given to the thoracic aorta as a source of embolism in patients with unexplained stroke.
