Impact of coronary artery remodeling on clinical presentation of coronary artery disease: an intravascular ultrasound study.

OBJECTIVES: We examined the association between the features of the culprit lesion in coronary artery disease (CAD) and clinical presentation as shown by intravascular ultrasound (IVUS). BACKGROUND: The association between coronary remodeling pattern and clinical presentation of CAD is unclear. METHODS: We analyzed 125 selected patients who underwent preintervention IVUS. Acute myocardial infarction (AMI) and unstable angina pectoris (UAP) were categorized as an acute coronary syndrome (ACS), and stable angina pectoris (SAP) and old myocardial infarction (OMI) as stable CAD. Coronary remodeling patterns and plaque morphology of the culprit lesion obtained by IVUS were analyzed in terms of their association with clinical presentation or angiographic morphology. RESULTS: Angiographically complex lesions were associated with ACS and OMI. In patients with a complex lesion, positive remodeling was observed more frequently than in those with a simple lesion. In AMI and UAP, positive remodeling was observed more frequently than in SAP and OMI (82% vs. 78% vs. 33% vs. 40%, respectively, p < 0.0001). The remodeling ratio was greater in AMI and UAP than in SAP and OMI (1.26 +/- 0.15 vs. 1.11 +/- 0.10 vs. 0.94 +/- 0.11 vs. 0.96 +/- 0.13, respectively, p < 0.0001). Furthermore, within ACS, the remodeling ratio was greater in AMI than in UAP (1.26 +/- 0.15 vs. 1.11 +/- 0.10, respectively, p < 0.05), whereas the frequency of positive remodeling was not different. CONCLUSIONS: Positive remodeling was more frequently observed in ACS than in stable CAD. Moreover, the degree of positive remodeling was greater in AMI than in UAP. These results may reflect the impact of remodeling types and its degree in the culprit lesion of CAD on clinical presentation.

Late development of an aneurysm of a saphenous vein used as an aortocoronary conduit.

A case of a large saphenous vein aortocoronary aneurysm that developed late after coronary artery bypass grafting is presented. This is the first case of a large saphenous vein aortocoronary aneurysm identified by serial angiography and 3-dimensional computed tomographic scanning.

Probucol therapy in the prevention of restenosis after successful percutaneous transluminal coronary angioplasty.

The effect of probucol, a drug that inhibits the secretion of smooth muscle cell-derived growth factor, was evaluated in the prevention of restenosis after percutaneous transluminal coronary angioplasty (PTCA). In 67 patients who successfully underwent prospective PTCA for the first time, the effects obtained in 31 patients given 750 mg or 1000 mg of probucol daily (group P) were compared with those in 36 patients given 150 mg of dipyridamole daily (group D). Drug treatment was initiated at least 7 days before PTCA and was continued for 3 to 6 months after PTCA, at which time a follow-up angiography was performed. There were no significant differences in patient characteristics (age, sex, pre-PTCA severity of angina pectoris), the number of affected vessels undergoing dilatation, or the residual degree of stenosis. The restenosis rate was significantly lower in group P (6 cases, 19.4%) than in group D (15 cases, 41.7%). In the nonrestenosis subgroup, the degree of stenosis progressed from 28.0 +/- 13.9% just after PTCA to 32.4 +/- 20.5% at follow-up angiography in group P, while it progressed significantly from 28.6 +/- 15.6% to 40.1 +/- 21.2% in group D (P < 0.05). A significant drop in serum cholesterol was observed in group P. The restenosis rate was lower in patients with high cholesterol levels at PTCA. No adverse reactions were noted in any patient. We conclude that probucol is effective in preventing restenosis after PTCA.

Effects of trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, in preventing restenosis after percutaneous transluminal coronary angioplasty.

Trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, is a potential inhibitor of intimal proliferation after percutaneous transluminal coronary angioplasty (PTCA). To study its efficacy, 72 patients were randomized to receive Trapidil (600 mg/day orally for 1 week before PTCA and for 4 to 6 months after PTCA; n = 36) or aspirin and dipyridamole (aspirin, 300 mg/day, and dipyridamole, 150 mg/day; n = 36). At entry, both groups were comparable with regard to age, sex, dilated vessels, severity of pre-PTCA stenosis, residual stenosis after PTCA, and prevalence of coronary risk factors. Repeat coronary angiography was performed 6 months after PTCA. Restenosis, defined as the loss of at least 50% of the gain in luminal diameter accomplished by dilation, was present in seven patients (19.4%) in the trapidil group and 15 patients (41.7%) in the aspirin-dipyridamole group (p less than 0.05). The progression of stenosis in patients with less than 30% residual stenosis was significant in both groups. Furthermore, in the patients with residual stenosis of more than 30%, progression of stenosis was less in the trapidil group than in the aspirin-dipyridamole group. Thus trapidil was useful in preventing intimal proliferation after PTCA, especially in patients with more than 30% residual stenosis after PTCA.

[Development of severe mitral regurgitation following percutaneous transvenous mitral valve commissurotomy].

The purpose of this study was to analyze the risk factors of unexpected occurrence of mitral regurgitation (MR) following percutaneous transvenous mitral valve commissurotomy (PTMC) in patients with mitral stenosis. The analyzed factors were clinical pictures, hemodynamic findings, echocardiographic findings and balloon inflation techniques during PTMC. Among 24 patients undergoing successful PTMC using an Inoue's balloon, severe MR developed in five patients (21%). No significant correlation in the occurrence of MR was observed in clinical findings, hemodynamic data and balloon inflation techniques including the times and size of ballooning. Echocardiographic findings of the mitral valve including the pliability of the mitral leaflet and localized calcification of the mitral orifice were the most contributory factors to the occurrence of severe MR. The localized alternation of valve stiffness produced localized tear or excessive dilatation of the mitral leaflet during PTMC, resulting in severe MR. Hemodynamic results and calculated mitral valve areas after PTMC showed significant improvement in both groups with and without MR. However, symptomatic improvement in patients with severe MR was less prominent when compared to the patients without MR. Thus, the complete echocardiographic evaluation of the mitral valve apparatus before PTMC is important to prevent severe MR.