Fumiyuki Ishibashi

Detection and treatment of vulnerable plaques and vulnerable patients: novel approaches to prevention of coronary events.

There is growing interest in the possibility that identification and treatment of vulnerable plaques and vulnerable patients can enhance the progress made against coronary artery disease. Innovations in medical therapy—statins and other agents—and novel interventional cardiology techniques—eg, drug-eluting stents—have significantly decreased the morbidity and mortality caused by coronary atherosclerosis. However, coronary events continue to be the leading cause of death in the United States, accounting for >479 000 deaths (1 in 5) in 2003.1 Improved preventive measures are needed because, for many individuals, sudden coronary death is the first sign of the disorder. And even those who survive an acute coronary syndrome remain at high risk. After successful treatment of the initial culprit lesion by a percutaneous coronary intervention (PCI), the risk of a coronary event from a new lesion is ≈10% in the following year and 5% in each of the subsequent 4 years2,3 (Figure 1). Figure 1. Occurrence of coronary events (revascularization, death, MI, acute coronary syndromes, or congestive heart failure) after PCI in 4 studies of bare-metal stents. In addition to events resulting from stented lesions (solid line), many events are caused by nontarget (vulnerable) plaques (dashed line). Modified from Cutlip et al2 with permission from the American Heart Association. Copyright 2004. These substantial levels of ongoing morbidity and mortality have led to heightened interest in new methods to prevent coronary events. For primary prevention, the effort has focused on plasma markers and noninvasive testing to identify vulnerable individuals. For secondary prevention, interest has focused on vulnerable patients and the vulnerable plaques they may possess that might be identified and treated during the catheterization for their initial event. ### Definitions of the Vulnerable Plaque and the Vulnerable Patient The terminology to describe vulnerability has become relatively standardized.4–10 The term “vulnerable plaque” is used to designate a plaque at high risk of disruption leading …

Elevated Troponin T Levels and Lesion Characteristics in Non–ST-Elevation Acute Coronary Syndromes

Background—Elevated troponin T levels in non–ST-elevation acute coronary syndromes (NSTE-ACS) have been shown to predict an adverse outcome. Furthermore, it has been reported that troponin T could help improve the effectiveness of such new antithrombotic drugs as platelet GPIIb/IIIa antagonists and low-molecular-weight heparins. We hypothesized that such elevated troponin T levels in NSTE-ACS indicate the presence of thrombus at culprit lesions, and this hypothesis was verified through the use of coronary angioscopy. Methods and Results—We studied 57 consecutive patients with NSTE-ACS who underwent preinterventional angioscopy. Before catheterization, we obtained blood samples to determine troponin positivity, and the patients were then classified as either troponin-positive or troponin-negative groups (diagnostic threshold, 0.1 ng/mL). Using angioscopy at the culprit lesions, we examined the presence of coronary thrombus, yellow plaque, and complex plaque. Moreover, we compared the preinterventional angiographic parameters (thrombus and complexity of the culprit lesion, and TIMI flow) between the two groups. Twenty-two patients were troponin-positive and 35 patients were troponin-negative. Univariate analyses indicated that the TIMI flow and the incidence of coronary thrombus detected with angioscopy correlate with the elevated troponin T levels. A multivariate logistic regression analysis showed the presence of coronary thrombus detected with angioscopy to be the only independent factor associated with elevated troponin T levels in patients with NSTE-ACS (odds ratio, 22.1; 95% CI, 2.59 to 188.42; P =0.0046). Conclusions—Using angioscopy, the elevated troponin T levels in NSTE-ACS were confirmed to be strongly associated with the presence of coronary thrombus.

Outcome of target sites escaping high-grade (>70%) restenosis after percutaneous transluminal coronary angioplasty

This study examined the fate of target sites that escaped high-grade restenosis (> or = 70% diameter narrowing) after percutaneous transluminal coronary angioplasty. Although favorable long-term prognosis after successful percutaneous transluminal coronary angioplasty is well documented, little is known about the stability of target sites. Long-term follow-up (mean 6.5 years, range 1.0 to 12.0) was performed in 693 patients with 948 narrowings (stenosis <70% in diameter at follow-up coronary angiography). Among them, 249 patients (36%) with 303 target sites received late follow-up coronary angiography. The relation of target sites to the culprit lesions for coronary events or newly developed angina was angiographically reviewed and progression/regression was also examined, focusing on the target sites. Regression was observed in 16 of 255 target sites in subjects with <50% stenosis and in 21 of 48 sites in the group with midgrade stenosis of 50% to 69% luminal narrowing (16 of 255, 6.3% vs 21 of 48, 43.8%, p <0.001). Progression was observed in 33 and 4 sites (33 of 255, 12.9% vs 4 of 48, 8.3%; p = NS) in each group, respectively. The rest remained within the same range of stenosis. Culprit lesions for 2 acute myocardial infarctions, 7 unstable anginas, and 17 newly developed anginas were related to the original target sites. Three lesions developed in the midgrade stenosis group. Those 26 lesions were a component of 8.6% of 303 angiographically confirmed sites and 2.7% of total target sites. Target sites that escape high-grade restenosis frequently regress and become stable plaques and rarely trigger coronary events.

Are multiple plaque disruptions more common in patients with acute coronary syndrome than in patients with stable ischemic heart disease

Background Plaque disruption with or without thrombus plays a key role in acute ccrcnary syndrome(ACS) and sudden progression of coronary lesions. Previous cur study demonstrated that plaque disruptions in culprit lesion is mere ccmmcn in patients with ACS than stable ischemic heart disease(SIHD). We investigated whether the prevalence of plaque disruptions in non ischemic related arteries is different between in patients with ACS and SIHD in living subjects. Methods We performed coronary angioscopy in non ischemic related artery on coronary angiography in 32 patients with ACS and 30 patients with SIHD. Forty-one arteries were explored in each groups. Results At least one plaque disruption was found somewhere other than on the culprit artery I” 31 patients(50%). Plaque disruption was found mere frequently in ACS group(Zlpts.65.6%) than in SIHD group(lOpts.33.3%)(pcO.O01). Conclusion Multiple plaque disruptions were mere ccmmcn in patients with acute ccrcnary syndrome than in patient with stable ischemic heart disease. These results indicate that acute coronary syndrome is not a local vascular accident but a pancoronary process.