Evaluation of Need for Implantable Cardioverter-Defibrillator by Thallium-201 Scintigraphy Among Japanese Patients With Prior Myocardial Infarction.

BACKGROUND: Identifying who among current Japanese patients with prior myocardial infarction (MI) would benefit from an implantable cardioverter-defibrillator (ICD) is imperative. Accordingly, this study seeks to determine whether single-photon emission computed tomography (SPECT) can help identify such patients. Methods and Results: This retrospective study enrolled 60 consecutive patients with prior MI who underwent stress thallium-201 SPECT and ICD implantation from February 2000 to October 2014. Occurrence of arrhythmic death and/or or appropriate ICD therapy, defined as shock or antitachycardia pacing for ventricular fibrillation or tachycardia, was identified until November 2016. During the median follow-up interval of 6.6 years, 18 (30%) patients experienced arrhythmic death and/or appropriate ICD therapy. Multivariate Cox proportional hazard regression analysis revealed that the summed stress score (SSS) [hazard ratio (HR)=1.14; P=0.005] and left ventricular ejection fraction (LVEF) at rest (HR=0.92; P=0.038) were significantly associated with the occurrence of arrhythmic events. Patients with SSS ≥21 and LVEF ≤30%, which were determined to be the best cutoff points, had significantly higher incidence of the arrhythmic events than the other patients (64% vs. 11%; HR=7.18; log-rank P=0.001). CONCLUSIONS: SSS using stress thallium-201 SPECT in combination with LVEF can help determine the need for ICD therapy among current Japanese patients with prior MI.

Fibrillatory pattern of dissociated venous activity after pulmonary vein isolation: Novel characteristics for remnant foci of a trigger ectopy for atrial fibrillation.

BACKGROUND: Dissociated pulmonary vein activity (DPVA), defined as isolated intrinsic ectopic beats observed after successful pulmonary vein (PV) isolation, indicates the presence of remnant foci of trigger ectopy but has yet to be extensively studied. We investigated the correlation between DPVA and the PV triggers of atrial fibrillation (AF). METHOD AND RESULTS: Consecutive 110 patients undergoing AF ablation were enrolled. We defined trigger ectopy as documented ectopic foci observed to spontaneously initiate AF. Trigger ectopy was detected in 62 (56%) patients. DPVA in at least one PV was detected in 95 (86%) patients. Of the 440 isolated PVs, we recognized trigger ectopy in 73 (16%) PVs (culprit PVs) and DPVA in 184 (42%) PVs. DPVA was more frequently observed in culprit PVs than in non-culprit PVs [59% vs. 39%; odds ratio (OR)=2.3; p=0.001]. The concordance ratio of culprit PV was 67% (8/12) in PV with fibrillatory DPVA, 20% (35/172) in PV with non-fibrillatory DPVA, and 12% (30/256) in PV without DPVA. Fibrillatory DPVA was more frequently observed in culprit PVs than non-fibrillatory DPVA (OR=7.8; p=0.001). Non-PV foci were observed in 10 (11%) of the 95 patients with DPVA and 5 (33%) of the 15 patients without DPVA (OR=4.3; p=0.02). No significant difference in the frequency of AF recurrence was observed between them. CONCLUSIONS: Fibrillatory DPVA was found to be strongly associated with trigger ectopy of AF. Non-fibrillatory DPVA might merely indicate the existence of bystander ectopic foci located inside PVs. Non-PV ectopic foci were frequently observed in patients without DPVA.

Bacterial Contamination During Pacemaker Implantation Is Common and Does Not Always Result in Infection.

BACKGROUND: Bacterial cultures of cardiovascular implantable electronic devices removed from patients without clinical infection are often positive, and the cultured bacteria are different from those at the time of clinical infection. This discrepancy has not been adequately explained. We hypothesized that the cause is bacterial contamination at operation and compared the results of bacterial cultures between patients with de novo pacemaker implantation and those with pacemaker replacement. METHODS AND RESULTS: We prospectively enrolled consecutive 100 patients who underwent cardiac pacemaker implantation (49 de novo implantations, 51 replacements). We took swab cultures from inside the generator pocket (1) immediately after the creation of new pocket or removal of old generator, (2) after connection of leads to new generator, and (3) after pocket lavage. Swab cultures were positive in 272 (45%) of 600 samples. The majority of the cultured bacteria were Propionibacterium species. No statistical difference was detected between de novo implantations and replacements in the positive ratio of swab cultures. The positive ratio was not correlated with the number of previous device replacements. CONCLUSIONS: The positive ratio of swab cultures was not different between new implantations and replacements, suggesting that a positive culture merely indicates contamination of bacteria during operation rather than colonization.

In-Stent Yellow Plaque at 1 Year After Implantation Is Associated With Future Event of Very Late Stent Failure: The DESNOTE Study (Detect the Event of Very late Stent Failure From the Drug-Eluting Stent Not Well Covered by Neointima Determined by Angioscopy).

OBJECTIVES: This study examined whether coronary angioscopy-verified in-stent yellow plaque at 1 year after drug-eluting stent (DES) implantation is associated with future event of very late stent failure (VLSF). BACKGROUND: Atherosclerosis detected as yellow plaque by angioscopy has been associated with future events of acute coronary syndrome. Development of in-stent neoatherosclerosis is a probable mechanism of VLSF. METHODS: This study included 360 consecutive patients who received successful angioscopic examination at 1 year after implantation of a DES. They were clinically followed up for VLSF defined as cardiac death, acute myocardial infarction or unstable angina, or need for revascularization associated with the stent site. RESULTS: The follow-up interval was 1,558 ± 890 days (4.3 ± 2.4 years). The incidence of VLSF was significantly higher in the patients with yellow plaque than in those without (8.1% vs. 1.6%; log rank p = 0.02). Multivariable analysis revealed the presence of yellow plaque (hazard ratio [HR]: 5.38; p = 0.02) and absence of statin therapy (HR: 3.25; p = 0.02) as risks of VLSF. CONCLUSIONS: In-stent atherosclerosis evaluated by yellow plaque at 1 year after the implantation of DES and the absence of statin therapy were risks of VLSF. The underlying mechanism of VLSF appeared to be the progression of atherosclerosis as demonstrated by the yellow plaque.

Association of target lesion characteristics evaluated by coronary computed tomography angiography and plaque debris distal embolization during percutaneous coronary intervention.

BACKGROUND: The slow-flow or no re-flow phenomenon has been associated with distal embolization, especially of plaque debris, and with unfavorable clinical outcomes. Therefore, we examined the association between the coronary computed tomography angiography (CCTA) findings of the target lesion and distal embolization during percutaneous coronary intervention (PCI). METHODS AND RESULTS: Consecutive patients (n=55: 18 unstable angina, 19 stable effort angina, 18 silent ischemia) who underwent PCI with a filter-type distal protection device after evaluation of the target lesion by CCTA were analyzed. CCTA examined low-attenuation plaque (LAP), positive remodeling (PR), and ring-like enhancement of the target lesion. Distal embolization of thrombus and plaque debris was evaluated by pathological examination of material collected in the filter.Any distal embolization and distal embolization of plaque debris were respectively detected in 75% and 0% of patients with LAP or PR alone, in 95% and 17% of patients with both LAP and PR, and in 100% and 27% of patients with all of LAP, PR and ring-like enhancement. The sensitivity and specificity to predict plaque debris embolization by having both findings of LAP and PR was 100% and 46%, respectively. CONCLUSIONS: The CCTA findings of the target lesion were associated with distal embolization and were very sensitive for predicting plaque debris embolization.

Atherosclerotic change at one year after implantation of Endeavor zotarolimus-eluting stent vs. everolimus-eluting stent.

BACKGROUND: Atherosclerosis progression is thought to be one of the mechanisms of late stent failure. Atherosclerosis progression is detected as yellow plaque formation on angioscopy. Cypher sirolimus-eluting stent has been reported to accelerate atherosclerosis progression, but the influence of Endeavor zotarolimus-eluting stent (Endeavor-ZES) or Xience everolimus-eluting stent (Xience-EES) on atherosclerosis has not been clarified. Therefore, we examined the serial changes in extent of atherosclerosis after the implantation of Endeavor-ZES or Xience-EES. METHODS AND RESULTS: Consecutive patients who received implantation of Endeavor-ZES (n=25) or Xience-EES (n=30) at de novo lesion of native coronary artery and who had successful angioscopy immediately after stent implantation (baseline) and at 1-year follow-up were included in the study. Change in the maximum yellow color grade (grade 0-3) of the stented segment from baseline to follow-up was examined and was compared between Endeavor-ZES and Xience-EES. The maximum yellow color grade decreased significantly from baseline to follow-up in Endeavor-ZES (1.6±1.1 vs. 0.4±0.8, P<0.001), but it did not change in Xience-EES (1.7±1.0 vs. 1.4±0.7, P=0.23). Although the maximum yellow color grade was not different between Endeavor-ZES and Xience-EES at baseline (P=0.72), it was significantly lower in Endeavor-ZES than in Xience-EES at follow-up (P<0.001). CONCLUSIONS: Atherosclerosis evaluated by yellow color of the plaque was significantly reduced at 1 year after Endeavor-ZES implantation, but was not changed after Xience-EES implantation.

Detection of yellow plaque by near-infrared spectroscopy - Comparison with coronary angioscopy in a case of no-flow phenomenon during coronary intervention.

Yellow plaques detected by coronary angioscopy have been regarded as vulnerable plaques and associated with distal embolization or slow/no-flow phenomenon during coronary intervention. This is the first report that compared the findings of angioscopy and near-infrared spectroscopy (NIRS) in a patient who suffered no-flow phenomenon during coronary intervention. A 41-year-old male patient with silent myocardial ischemia received coronary intervention. Coronary angiogram revealed diffuse stenosis in the distal right coronary artery. Target lesion was examined by NIRS and angioscopy. NIRS can detect lipid core plaque, which is presented as an yellow area in contrast to the normal red area. Target segment was filled with lipid core plaques. On the other hand, angioscopy revealed a ruptured yellow plaque with a thrombus in the target segment. The distribution of yellow plaques detected by angioscopy appeared well corresponded to the yellow areas detected by NIRS. After the insertion of filter-type distal protection device, balloon pre-dilatation and stent implantation were performed. Then, no-flow phenomenon occurred. Coronary flow was finally recovered in the protected vessel but was still disturbed in the non-protected vessel. The filter was filled with much plaque debris. The correlation between the yellow area detected by NIRS and the yellow plaques detected by angioscopy appeared very well. .

Regression of luminal stenosis at the site of silent plaque disruption in the era of optimal medical therapy. Low high-density lipoprotein cholesterol level isa potential risk of stenosis progression.

BACKGROUND: Plaque disruption and its healing is thought to be the major mechanism of atherosclerosis, but the contribution of silent plaque disruption to luminal stenosis progression has not been fully clarified. The aim of this study was therefore to examine the change in luminal stenosis at the site of silent plaque disruption. METHODS AND RESULTS: Consecutive patients (n=36) who received coronary angiography and angioscopy that identified silent plaque disruption (baseline) and had repeated coronary angiography later (follow-up) were included for analysis. Silent plaque disruption was defined as plaque with thrombus detected in non-culprit segments. Diameter stenosis of the site was angiographically measured at baseline and at follow-up, and their difference was defined as stenosis change. Statin was used in 89% of study patients, and serum low-density lipoprotein cholesterol level was 91 ± 21 mg/dl. The diameter stenosis decreased significantly from baseline to follow-up at 12 ± 4 months (32 ± 14% vs. 27 ± 14%, P<0.001), and the stenosis change was -5.6 ± 7.9%. High-density lipoprotein cholesterol (HDL-C) was significantly associated with stenosis change (r=-0.51, P=0.001) and was the only factor significantly associated with stenosis change. CONCLUSIONS: In the era of optimal medical therapy with statin, the site of silent plaque disruption showed significant regression of luminal stenosis. Nevertheless, serum HDL-C was inversely associated with stenosis change, and its low level remained as a potential risk of luminal stenosis progression at the site of silent plaque disruption.

Ruptured plaque and large plaque burden are risks of distal embolisation during percutaneous coronary intervention: evaluation by angioscopy and virtual histology intravascular ultrasound imaging.

AIMS: Slow flow and no flow phenomena have been associated with distal embolisation, especially of plaque debris, and with unfavourable clinical outcomes. However, patients at high risk of distal embolisation for whom distal protection might be beneficial have not been adequately identified. We examined the frequency of distal embolisation and its predicting factors, including both ACS and non-ACS patients. METHODS AND RESULTS: Consecutive patients (n=98) with or without ACS who had received PCI with a filter-type distal protection device and successful angioscopic and VH-IVUS examination were prospectively enrolled. The presence of yellow plaque and plaque rupture was evaluated by angioscopy. Tissue classification and plaque burden was evaluated by VH-IVUS. Distal embolisation was evaluated by pathological examination of material collected in the filter. Distal embolisation of plaque debris was more frequently detected in patients with ACS (48% vs. 25%, p=0.02), in those with ruptured plaque (86% vs. 13%, p<0.001), in those with large (>75%) plaque burden (50% vs. 23%, p=0.006), and in those with grade 2/3 yellow plaque (52% vs. 7%, p<0.001), as compared to those without it. CONCLUSIONS: The presence of ruptured yellow plaque and of large plaque burden, rather than the setting of ACS, was highly predictive of distal embolisation of plaque debris.

The level of blood thrombogenicity was not elevated in stable patients with disrupted coronary plaque.

BACKGROUND: Although extremely high blood thrombogenicity has been reported in patients with acute myocardial infarction, it has not been clarified if the increased blood thrombogenicity is a cause of acute myocardial infarction or a mere result induced by thrombus formation at the disrupted plaque. Therefore, we examined if blood thrombogenicity is extremely increased as in acute myocardial infarction patients when disrupted plaque is present in patients with stable coronary artery disease. METHODS AND RESULTS: Consecutive patients (n=38) with stable coronary artery disease who received angioscopic examination were included. Patients were divided into two groups according to presence or absence of disrupted plaque that accompanied thrombus. Blood thrombogenicity was evaluated by blood vulnerability index and compared between the patients with and without disrupted plaque. Among 38 study patients, 16 had disrupted plaque and 22 did not. Blood vulnerability index was not different between the patients with and without disrupted plaque (2395 ± 612 vs. 3013 ± 1476, p=0.12). Multivariate analysis revealed no significant association between blood vulnerability index and the presence of disrupted plaque. CONCLUSION: The presence of disrupted plaque, in comparison with its absence, was not associated with higher blood thrombogenicity evaluated by blood vulnerability index.

A higher colour grade yellow plaque was detected at one year after implantation of an everolimus-eluting stent than after a zotarolimus-eluting stent.

OBJECTIVE: Neoatherosclerosis or atherosclerosis progression is one of the mechanisms of long-term stent failure. Yellow plaque detected by angioscopy has been associated with advanced atherosclerosis and the future risk of a coronary event. We compared the yellow colour of the stented segment between zotarolimus-eluting stents (ZES) and everolimus-eluting stents (EES) at 1 year after implantation. DESIGN: Cross-sectional study. PATIENTS: Consecutive patients underwent angioscopic examination 1 year after the implantation of ZES (n=45) or EES (n=45) at a de novo native coronary lesion. MAIN OUTCOME MEASURES: The maximum yellow colour grade (grade 0-3) of the stented segment, maximum and minimum neointima coverage grade (grade 0-2) and the presence of thrombus were examined. The neointima heterogeneity index was calculated as maximum - minimum coverage grade. RESULTS: Maximum yellow colour grade was higher in EES than in ZES (1.3±0.9 vs 0.4±0.8, p<0.001) and maximum (2.0±0.2 vs 1.2±0.5, p<0.001) and minimum (1.5±0.6 vs 0.7±0.5, p<0.001) coverage grade was higher in ZES than in EES. The neointima heterogeneity index was not different between ZES and EES (0.4±0.5 vs 0.5±0.6, p=0.42). The incidence of thrombus was very low and was not different between ZES and EES (2% vs 4%, p=0.55). CONCLUSIONS: Although both ZES and EES had good healing with homogeneous neointima coverage and a low incidence of thrombus, EES had more advanced atherosclerosis as shown by the presence of higher grade yellow plaque than ZES at 1 year after implantation.

Vasospasm-induced acute myocardial infarction-Thrombus formation without thrombogenic lesion at the culprit.

Although plaque rupture is the major cause of acute myocardial infarction, vasospasm is also known as a potential cause of acute myocardial infarction. However, it is very rare and is sometimes difficult to diagnose correctly. A 30-year-old male patient with suspected unstable angina pectoris who received catheterization in 1999 had normal coronary artery but positive result in the provocation test of vasospasm. Although his angina had been suppressed by medications, he suffered ST-elevation acute myocardial infarction after the discontinuation of medication. The initial angiogram showed total occlusion of the proximal left anterior descending coronary artery. Thrombolysis and nitroglycerin achieved recanalization of the culprit lesion with only mild residual stenosis. Angioscopy revealed normal white luminal wall without any thrombogenic lesion. Therefore, the cause of coronary occlusion was diagnosed as vasospasm. However, since the repeated vasospastic occlusion of the culprit lesion regardless of repeated intra-coronary injection of nitroglycerin was observed, a stent was implanted and vasospasm was successfully prevented. It is not easy to judge from the angiogram that the cause of coronary occlusion in the patients with acute myocardial infarction is vasospasm. It is important to think routinely about the possibility of vasospasm as a cause of acute myocardial infarction. .

Systemic and local factors associated with coronary plaque disruption.

INTRODUCTION: Yellow plaques are regarded vulnerable; and disrupted yellow plaques are the major cause of acute coronary syndrome. We examined the factors associated with the disruption of yellow plaques among patients and lesion characteristics. MATERIALS AND METHODS: Consecutive 161 patients with ischemic heart diseases who received coronary angioscopic examination were analyzed. Yellow plaques in the segments to which intervention had never been performed were included, and their yellow color grade and presence/ absence of disruption were examined. Associated factors for plaque disruption were examined among patients and lesion characteristics. RESULTS: In 161 patients, 392 yellow plaques were included for analysis and 70 of them were disrupted. Frequency of plaque disruption (=disrupted / all yellow plaques) was significantly higher at the segments of severer stenosis (stenosis≥75% vs. 75-25% vs. <25%: 34% vs. 21% vs. 14%, p=0.006). Multivariate analysis revealed angiographic stenosis (odds ratio [OR], 1.014; 95% confidence interval [CI], 1.005-1.023; p=0.003), yellow color grade (OR, 3.297; 95% CI, 2.062-5.273, p<0.001), LDL-cholesterol (OR, 1.012; 95% CI, 1.004-1.020, p=0.003), male gender (OR, 3.608; 95% CI, 1.538-8.465; p=0.003), and hypertension (OR, 2.552; 95% CI, 1.094-5.953; p=0.030) as significant associated factors for plaque disruption. CONCLUSION: Angiographic stenosis, yellow color grade, LDL-cholesterol, male gender, and hypertension were significantly associated with the disruption of yellow plaques.

Very late stent thrombosis at 2.5 years after sirolimus-eluting stent implantation with prior angioscopic image of culprit lesion: A case report.

Although very late stent thrombosis after drug-eluting stent implantation is a critical event, its cause has not been clarified. This is the first report of a case with very late stent thrombosis after drug-eluting stent implantation for which prior angioscopic image of the culprit lesion is available. A 54-year-old Japanese male patient with stable angina who received implantation of sirolimus-eluting stent at the culprit lesion and 1-year follow-up angiographic and angioscopic examinations came back with chest pain at rest at 2.5 years after the stent implantation. Very late stent thrombosis was diagnosed by emergent angiographic and angioscopic examinations and was treated by zotarolimus-eluting stent. One-year angiographic and angioscopic follow-up examinations after zotarolimus-eluting stent were performed. Angioscopy revealed uncovered stent strut, yellow plaques, and thrombus at 1-year follow-up after sirolimus-eluting stent implantation, and it confirmed the thrombotic occlusion inside the sirolimus-eluting stent at the time of emergent catheterization. This is a case of very late stent thrombosis in the drug-eluting stent where uncovered stent strut, yellow plaques, and thrombus had been detected by angioscopy 1.5 years before the onset. Those thrombogenic sources might be the cause of stent thrombosis.

Chronic kidney disease and coronary artery vulnerable plaques.

BACKGROUND AND OBJECTIVES: Chronic kidney disease (CKD) is a risk factor of cardiovascular disease. The number of yellow plaques is a predictor of future cardiovascular events. We assumed that CKD might raise the risk of cardiovascular events by increasing the number of yellow plaques. Therefore, we compared the number of yellow plaques between patients with and without CKD. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Consecutive 136 patients with acute myocardial infarction who received percutaneous coronary intervention (PCI) and angioscopic examination were analyzed. The infarct-related artery was angioscopically examined. The number of yellow plaques, maximum yellow color grade of detected yellow plaques, and prevalence of disrupted yellow plaques in nonculprit segments were compared between patients with and without CKD. RESULTS: The number of yellow plaques was significantly larger in CKD than in non-CKD patients (median [interquartile range]: 4.0 [2.0 to 6.0] versus 2.0 [1.0 to 4.0], P = 0.001). Maximum yellow color grade and prevalence of disrupted plaques in the nonculprit segments were not different between patients with and without CKD. Multivariate logistic regression analysis revealed CKD as an independent risk of multiple yellow plaques per vessel (odds ratio 3.49, 95% confidence interval 1.10 to 11.10, P = 0.03). CONCLUSION: CKD was an independent risk factor of multiple coronary yellow plaques, suggesting that patients with CKD would have a higher risk of coronary events because they had more yellow plaques than patients without CKD.

Relationship between coronary plaque vulnerability and serum n-3/n-6 polyunsaturated fatty acid ratio.

BACKGROUND: A low ratio of serum eicosapentaenoic acid to arachidonic acid (EPA/AA) has been associated with cardiovascular events. Higher-grade yellow color coronary plaques are associated with higher plaque vulnerability and higher thrombogenic potential. Therefore, the association between EPA/AA ratio and yellow color grade of coronary plaques was examined. METHODS AND RESULTS: Consecutive patients (n=54) who underwent percutaneous coronary intervention were enrolled in this study. The serum EPA/AA ratio was examined on admission. All patients underwent an angioscopic examination of the culprit vessel to examine the color grade of yellow plaques (0, white; 1, slight yellow; 2, yellow; and 3, intense yellow) and the presence of thrombus. Excluding 16 patients with acute coronary syndrome (ACS), 38 patients with stable angina were divided into 2 groups according to their EPA/AA ratio: the low EPA/AA group (n=19, EPA/AA ratio <0.37 [median]) and the high EPA/AA group (n=19, EPA/AA ratio ≥0.37). The maximum color grade (2.5 ± 0.5 vs. 1.9 ± 0.9; P=0.01) of yellow plaques was significantly higher and the number of non-culprit yellow plaques with thrombus (1.7 ± 0.8 vs. 1.2 ± 1.1; P=0.06) tended to be higher in low EPA/AA than in high EPA/AA stable angina patients. Multivariate analysis revealed that the serum EPA level (odds ratio=0.98, 95% confidence interval=0.96-0.99, P=0.03) was associated with the presence of grade-3 yellow plaques. CONCLUSIONS: A low serum EPA level and a low EPA/AA ratio was associated with high vulnerability of coronary plaques.

Detection of disrupted plaques by coronary CT: comparison with angioscopy.

BACKGROUND: Disrupted plaques are the major cause of acute coronary syndrome (ACS). Although the detection of vulnerable plaques by coronary CT (CCT) has been examined and reported, there has been no report on the detection of disrupted plaques by CCT. OBJECTIVES: To test the ability of CCT to detect disrupted coronary plaques. METHODS: 32 consecutive patients with suspected ischaemic heart disease who underwent successful coronary angioscopic examination and CCT were analysed. Yellow plaques of colour grade 1-3 and disrupted yellow plaques were examined by angioscopy. CCT findings (low attenuation, positive remodelling and ring-like enhancement) were examined for each site of yellow plaques. RESULTS: In the 32 patients, 65 yellow plaques were detected. Higher-colour-grade yellow plaques and disrupted yellow plaques had a significantly higher incidence of CCT findings: low attenuation (grade 1 vs grade 2 vs grade 3, 18% vs 59% vs 69%; non-disrupted vs disrupted, 36% vs 66%), positive remodelling (24% vs 59% vs 75%; 33% vs 75%), and ring-like enhancement (0% vs 19% vs 25%; 6% vs 44%). Positive and negative predictive values for ring-like enhancement to detect disrupted plaque were 88% and 63%, respectively; those for the combined CCT findings (low attenuation, positive remodelling and ring-like enhancement) to detect disrupted plaque were 90% and 58%, respectively. CONCLUSION: CCT findings were associated with disrupted plaques confirmed by angioscopy. Ring-like enhancement had a high positive predictive value for detecting disrupted plaque.

Risk of in-stent thrombus formation at one year after drug-eluting stent implantation.

INTRODUCTION: Although very late stent thrombosis is an important problem with drug-eluting stents, risks for in-stent thrombus formation have not been clarified. Therefore, we examined the risks among patient and lesion characteristics by direct visualization of the stented lesion by angioscopy. MATERIALS AND METHODS: Consecutive patients (n=118) who received successful angioscopic examination of drug-eluting (sirolimus- or paclitaxel-eluting) stents at 1-year after implantation were included. Presence or absence of thrombus directly on the area of each condition determined by the combination of lesion color (white or yellow) and neointima coverage (grade 0-2) was evaluated for each stent; and the factors associated with the presence of thrombus were analyzed. RESULTS: Multivariate logistic regression analysis revealed lesion color (=yellow; odds ratio [OR] 5.5, 95% confidence interval [CI] 3.0-10, p<0.001), neointima coverage (=grade 0 or 1; OR 5.5, 95% CI 2.4-13, p<0.001), and stent type (=paclitaxel-eluting stent; OR 7.6, 95% CI 3.9-15, p<0.001) as independent contributors for in-stent thrombus formation. CONCLUSION: Yellow color of the lesion, poor neointima coverage, and use of paclitaxel-eluting stent were the risks of in-stent thrombus formation at 1 year after DES implantation.

Patients with more coronary yellow plaques have higher risk of stenosis progression within 7 months.

BACKGROUND: Disruption of vulnerable plaques causes acute coronary syndrome and stenosis progression. Yellow plaques are regarded as vulnerable and the number of yellow plaques per vessel (NYP) has been reported as a marker of vulnerable patients. Therefore, we examined if patients with more yellow plaques would have higher risk of stenosis progression. METHODS AND RESULTS: A series of patients (n = 70) who received percutaneous coronary intervention (PCI) and angioscopy was included. Patients were divided into 2 groups according to NYP: group 1 (NYP <4, n = 32) and group 2 (NYP ≥ 4, n = 38). Coronary artery stenosis progression in any segment excluding target lesion of PCI was examined by angiography at 7 months. Maximum yellow color grade of yellow plaques (2.7 ± 0.7 vs. 1.7 ± 1.2, p < 0.0001) and the number of non-target disrupted yellow plaques was larger in group 2 than in group 1 (1.1 ± 1.5 vs. 0.2 ± 0.6, p=0.0017). Progression of coronary stenosis was detected more frequently in group 2 than in group 1 (29% vs. 9%, p = 0.041). The number of sites with stenosis progression was larger in group 2 than in group 1 (0.47 ± 0.98 vs. 0.09 ± 0.30 sites/patient, p = 0.036). CONCLUSIONS: Vulnerable patients with more yellow plaques had higher incidence of stenosis progression. Approximately 30% of vulnerable patients with NYP ≥ 4 had stenosis progression within 7 months.