Angioscopic Evaluation of Stabilizing Effects of an Antilipemic Agent, Bezafibrate, on Coronary Plaques in Patients with Coronary Artery Disease.

Abstract

SUMMARYTo evaluate the stabilizing effects of an antilipemic agent, bezafibrate, on coronary plaques, we carried out a prospective angioscopic and angiographic open trial. From April 1997 to December 1998, 24 patients underwent coronary angioscopy of plaques in nontargeted vessels during coronary interventions and then again 6 months later. The patients were divided into control (10 patients, 14 plaques) and bezafibrate (14 patients, 21 plaques) groups. Oral administration of bezafibrate (400 mg/day) was started immediately after the intervention and was continued for 6 months. The vulnerability score was determined based on the angioscopic characteristics of plaques and compared before and 6 months later. Six months later, the vulnerability score was reduced (from 1.6 to 0.8; P<0.05) in the bezafibrate group and unchanged (from 1.4 to 1.3; NS) in the control group. In the bezafibrate group, the changes in the vulnerability score were not correlated with those in % stenosis or minimal lumen diameter. The plasma total cholesterol level (T-C) was unchanged, triglyceride level (TG) was decreased, and high density lipoprotein cholesterol level (HDL-C) was increased in the bezafibrate group, but were unchanged in the control group. In the bezafibrate group, T-C and TG were decreased and HDL-C was increased in patients with a reduced vulnerability score but were unchanged in those with an unchanged score. These results indicate that 6 month administration of bezafibrate stabilizes coronary plaques and that the stabilization is not correlated with angiographic changes. (Jpn Heart J 2002; 43: 319-331)

Increased serum triglyceride clearance and elevated high-density lipoprotein 2 and 3 cholesterol during treatment of primary hypertriglyceridemia with bezafibrate

“…30,31 From these reports, it can be supposed that the development of atherosclerosis may be suppressed because of a reduction of systemic inflammation or through other mechanisms involving increases in both HDL 2 -C and HDL 3 -C by bezafibrate administration. 24,32 …”

Coronary Angioscopic Evaluation for Serial Changes of Luminal Appearance After Pharmacological and Catheter Interventions

“…8,16,[41][42][43] The culprit plaque of ACS or ischemia-related plaque with severe stenosis is usually treated by catheter intervention. Although disrupted and thrombotic yellow plaque is located in not only the culprit lesion, but also non-culprit lesion showing no significant stenosis on the angiograms, 8,[41][42][43][44] such angioscopically vulnerable plaque generally receives pharmacological intervention. Non-culprit plaques are therefore selected as targets for angioscopic analysis in the assessment of pharmacological intervention.…”

“…8 A similar phenomenon is recognized after 6-month follow-up of bezafibrate therapy without any angiographic regression on the target plaques. 41 In control participants receiving only diet therapy, the angioscopic scores are unchanged or increased. 8,41 Statin therapy also has favorable potency for healing over subclinical ruptured plaque in nonculprit lesions (Figure 2).…”

“…41 In control participants receiving only diet therapy, the angioscopic scores are unchanged or increased. 8,41 Statin therapy also has favorable potency for healing over subclinical ruptured plaque in nonculprit lesions (Figure 2). 42 A serial combination study using …”

Multiple Yellow Plaques Assessed by Angioscopy With Quantitative Colorimetry in Patients With Myocardial Infarction

“…19,20 The angioscopic finding of multiple yellow plaques in the coronary arteries does not necessarily represent the presence of multiple coronary regions that have a higher probability of plaque rupture, because it is the subtype of yellow plaque, such as glistening yellow plaque, 5,8 deep yellow or yellow-red plaque, 6 dark yellow plaque, 21 intense yellow plaque 22 or plaque with a high yellow color saturation, 9 that is specifically associated with a lipid core underneath a thin fibrous cap. Such coronary regions are associated with plaque rupture.…”