Shunta Sakai

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.

Extended Follow-Up by Serial Angioscopic Observation for Bare-Metal Stents in Native Coronary Arteries: From Healing Response to Atherosclerotic Transformation of Neointima

Background— Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. Methods and Results— Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P <0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P <0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P =0.011). Conclusions— This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing. Received January 29, 2009; accepted April 15, 2009. # CLINICAL PERSPECTIVE {#article-title-2}Background—Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. Methods and Results—Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P<0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P<0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P=0.011). Conclusions—This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing.

Rapid data acquisition protocol in ECG-gated myocardial perfusion SPECT with Tc-99m-tetrofosmin

Into 25 patients with heart disorders,99mTc-tetrofosmin 555–740 MBq was injected intravenously at rest. After 40 minutes, ECG-gated myocardial perfusion SPECT was performed with a two detector gamma camera VERTEX (ADAC), setting up two detectors to form a 90-degree angle. Sixteen frames per R-R interval were acquired during a 180° rotation from the RAO 45° to the LPO 45°. A pair of data sets with standard (SDA) and rapid data acquisition (RDA) protocols was collected. In an SDA protocol, SPECT imaging was performed for 50 sec per step in 5° angular steps (total acquisition time; 15 minutes). An RDA protocol was conducted with 12 sec per step, 6° angular steps (acquisition time, 3 minutes). LVEF (%) and LVEDVml quantitated automatically with a QGS program showed excellent correlations between two protocols with correlation coefficients of 0.980 (p < 0.01) and 0.983 (p < 0.01), respectively. Subsequently visual assessment of regional wall motion based on a four-point grading system was carried out with a 3-D cine LV display. High complete agreement was gained with 158 (90.3%) out of total 175 segments, so that assessment of the global and regional LV function with the RDA protocol demonstrated high reliability and feasibility.

Analysis of ST-segment shift in lead AVR improves short-term prognostic risk stratification in acute coronary syndrome

0.5 mm ST segment displacement was assessed in the 12-lead ECG at baseline for the remaining 3,657 pts. Results were correlated to &month mortality. Results: There were 442 (11.5%) pts who had STEz1.00 mm in lead aVR. The B-month mortality rates were 29.2% (129/442) in pts with STE 21 .OO mm in lead aVR vs 4.6% (165/3,415) in pts without STE 21 .OO mm in lead aVR (pcO.001). The 6-month mortality rates were 29.4% (1211412) in pts with STE 51.00.~2.00 mm I” lead aVR and 26.7% (6/ 30) in pts with STE ZOO mm in lead aVR (p=O.92). All pts with STE >I.00 mm in lead aVR had ST segment depression (STD) to.5 mm in other leads. There was a strong correlation between STE in lead aVR and the sum of STD in other leads (r=O.63, p l .OO mm in lead aVR were 7.2% (1 Oll1407) if STD was present vs 3.2% (64/2,006) if STD was absent (p

Extended Follow-Up by Serial Angioscopic Observation for Bare-Metal Stents in Native Coronary Arteries

Background— Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. Methods and Results— Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P <0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P <0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P =0.011). Conclusions— This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing. Received January 29, 2009; accepted April 15, 2009. # CLINICAL PERSPECTIVE {#article-title-2}Background—Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. Methods and Results—Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P<0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P<0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P=0.011). Conclusions—This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing.

Visualized plaque debris as a cause of distal embolization after percutaneous coronary intervention in patient with unstable angina.

Procedural complications of percutaneous transluminal coronary angioplasty for unstable angina are higher than for stable angina. We report a case in which coronary angioscopy proved the dislodgment of a large plaque fragment after Cutting Balloon angioplasty and confirmed our suspicion that plaque fragmentation can cause distal embolization. Cathet Cardiovasc Intervent 2002;55:113–117.

Extended Follow-Up by Serial Angioscopic Observation for Bare-Metal Stents in Native Coronary ArteriesCLINICAL PERSPECTIVE: From Healing Response to Atherosclerotic Transformation of Neointima

Background— Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. Methods and Results— Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P <0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P <0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P =0.011). Conclusions— This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing. Received January 29, 2009; accepted April 15, 2009. # CLINICAL PERSPECTIVE {#article-title-2}Background—Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. Methods and Results—Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P<0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P<0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P=0.011). Conclusions—This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing.

Extended Follow-Up by Serial Angioscopic Observation for Bare-Metal Stents in Native Coronary ArteriesCLINICAL PERSPECTIVE

Background— Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. Methods and Results— Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P <0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P <0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P =0.011). Conclusions— This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing. Received January 29, 2009; accepted April 15, 2009. # CLINICAL PERSPECTIVE {#article-title-2}Background—Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. Methods and Results—Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P<0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P<0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P=0.011). Conclusions—This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing.

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.