Koji Seimiya

Changes in coronary plaque color and morphology by lipid-lowering therapy with atorvastatin: serial evaluation by coronary angioscopy

OBJECTIVES Changes in coronary plaque color and morphology by statin therapy were evaluated using coronary angioscopy. BACKGROUND Coronary plaque stabilization by statin therapy has not been clarified in humans. METHODS Thirty-one patients with coronary artery disease were divided into either the comparison group (n = 16) or the atorvastatin group (n = 15). Before treatment and 12 months after, the color and complexity of 145 coronary plaques were determined according to angioscopic findings. The yellow score of the plaque was defined as 0 (white), 1 (light yellow), 2 (yellow), or 3 (dark yellow), and its disrupted score was defined as 0 (smooth surface) or 1 (irregular surface) and as 0 (without thrombus) or 1 (with thrombus). In each patient, the mean yellow score and mean disrupted score were calculated. RESULTS Mean low-density lipoprotein cholesterol (LDL-C) decreased by 45% in the atorvastatin group, whereas an increase of 9% was seen in the comparison group. The mean yellow score decreased from 2.03 to 1.13 in the atorvastatin group, whereas it increased from 1.67 to 1.99 in the comparison group. There was a good correlation between the change in the mean yellow score and the change in LDL-C levels (r = 0.81, p < 0.0001). The change in the mean yellow score and mean disrupted score differed significantly between the two groups (p = 0.002 and p = 0.03, respectively). CONCLUSIONS This is the first report clarifying detailed changes in coronary plaque by statin in humans. This study indicated that lipid-lowering therapy changes plaque color and morphology and should then lead to coronary plaque stabilization.

In Vivo Comparison of Optical Coherence Tomography and Angioscopy for the Evaluation of Coronary Plaque Characteristics

Atherosclerotic yellow plaques identified by coronary angioscopy are considered as vulnerable plaques. However, characteristics of yellow plaques are not well understood. Optical coherence tomography (OCT) provides accurate tissue characterization in vivo and has the capability to measure fibrous cap thickness covering a lipid plaque. Characteristics of yellow plaques identified by angioscopy were evaluated by OCT. We examined 205 plaques of 41 coronary arteries in 26 patients. In OCT analysis, plaques were classified as fibrous or lipid. Minimal lumen area of the plaque, arch of the lipid, and fibrous cap thickness on the lipid plaque were measured. Yellow grade of the plaque was defined as 0 (white), 1 (light yellow), 2 (medium yellow), or 3 (dark yellow) based on the angioscopy. A total of 149 plaques were diagnosed as lipid plaques. Neither the minimal lumen area nor the arch of the lipid was related to the yellow grade. There was an inverse relationship between color grade and the fibrous cap thickness (grade 0 [n = 45] 218 +/- 89 microm, grade 1 [n = 40] 101 +/- 8 microm, grade 2 [n = 46] 72 +/- 10 microm, and grade 3 [n = 18] 40 +/- 14 microm; p <0.05). Sensitivity and specificity of the angioscopy-identified yellow plaque for having a thin fibrous cap (thickness <or=110 microm) were 98% and 96%, respectively. In conclusion, angioscopy-identified yellow plaques frequently were lipid tissue with an overlying thin fibrous cap. Fibrous caps of the intense yellow plaques were very thin, and these plaques might be structurally vulnerable.

Long-Term Follow-Up Evaluation After Sirolimus-Eluting Stent Implantation by Optical Coherence Tomography: Do Uncovered Struts Persist?

To the Editor: Presently, occurrence of late stent thrombosis (LST) after drug-eluting stent implantation is a major clinical concern. Although LST is an infrequent complication, LST can lead to serious results. A long-term follow-up study revealed recently that LST occurs at a constant rate of 0.6

Comparison of neointimal coverage by optical coherence tomography of a sirolimus-eluting stent versus a bare-metal stent three months after implantation.

No detailed data regarding neointimal coverage of bare-metal stents (BMSs) at 3 months after implantation was reported to date. This investigation was designed to evaluate the neointimal coverage of BMSs compared with sirolimus-eluting stents (SESs) using optical coherence tomography. A prospective optical coherence tomographic follow-up examination was performed 3 months after stent implantation for patients who underwent BMS (n = 16) or SES implantation (n = 24). Neointimal hyperplasia (NIH) thickness on each stent strut and percentage of NIH area in each cross section were measured. Malapposition of stent struts to the vessel wall and the existence of in-stent thrombi were also evaluated. There were 5,076 struts of SESs and 2,875 struts of BMSs identified. NIH thickness and percentage of NIH area in the BMS group were higher than in the SES group (351 +/- 248 vs 31 +/- 39 mum; p <0.0001; 45.0 +/- 14% vs 10.0 +/- 4%; p <0.0001, respectively). The frequency of uncovered struts was higher in the SES group than the BMS group (15% vs 0.1%; p <0.0001). Malapposed struts were observed more frequently in the SES group than the BMS group (15% vs 1.1%; p <0.0001). In conclusion, there was no difference in incidence of in-stent thrombus between the 2 groups (14% vs 0%; p = 0.23). The present study showed almost all BMS struts to be well covered at a 3-month follow-up, suggesting that patients receiving BMS stents may not require dual-antiplatelet therapy >3 months after implantation.

Serial long-term evaluation of neointimal stent coverage and thrombus after sirolimus-eluting stent implantation by use of coronary angioscopy

Objective: Progression of neointimal stent coverage (NSC) and changes in thrombus were evaluated serially by coronary angioscopy for up to 2 years after sirolimus-eluting stent (SES) implantation. Methods: Serial angioscopic observations were performed in 20 segments of 20 patients at baseline, at 6 months and at 2 years after SES implantation. NSC was classified as follows: 0, uncovered struts; 1, visible struts through thin neointima; or 2, no visible struts. In each patient, maximum and minimum NSC was evaluated. Existence of thrombus was also examined. Results: The maximum NSC increased from 6 months to 2 years (mean (SD) 1.2 (0.4) vs 1.8 (0.4), respectively, p = 0.005), while the minimum NSC did not change (0.7 (0.5) vs 0.8 (0.4), respectively, p = 0.25). The prevalence of patients with uncovered struts did not decrease from 6 months to 2 years (35% vs 20%, respectively, p = 0.29). Although there were no thrombus-related adverse events, new thrombus formation was found in 5% of 6-month, and in 20% of 2-year follow-up evaluations. The prevalence of thrombus inside the SES at baseline, 6 months and 2 years was similar (40%, 40% and 30%, respectively; p = NS). Conclusions: Neointimal growth inside the SES progressed heterogeneously. Uncovered struts persisted in 20% of the patients for up to 2 years and subclinical thrombus formation was not uncommon.

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.

Lack of association between large angiographic late loss and low risk of in-stent thrombus: angioscopic comparison between paclitaxel- and sirolimus-eluting stents.

Background— It recently has been hypothesized that a larger late loss may have a protective role against stent thrombosis. The relationship between angiographic late loss and the presence of thrombus based on angioscopic findings within paclitaxel-eluting stents (PES) and sirolimus-eluting stents (SES) was investigated in this study. Methods and Results— Prospective 6-month follow-up angiographic and angioscopic examinations were performed on 18 patients for PES and on 20 patients for SES. Late loss was measured by quantitative coronary angiography. Angioscopic neointimal stent coverage (NSC) grade was classified as follows: 0=uncovered struts without neointima, 1=visible struts through thin neointima, and 2=no visible struts. In each patient, maximum NSC, minimum NSC, and the existence of thrombus were evaluated. Late loss and maximum NSC were greater in PES than in SES (0.38±0.43 versus 0.10±0.23 mm; P =0.02 and P =0.0004, respectively). Late loss was correlated with maximum NSC (grade 0, 0.06±0.01 mm; grade 1, 0.10±0.05 mm; and grade 2, 0.48±0.46 mm), whereas there was no correlation between late loss and minimum NSC. The prevalence of patients with uncovered struts did not differ (44% of PES, 40% of SES; P =0.78). In-stent thrombus was found more frequently in PES than in SES (72% versus 40%, P =0.046) despite no occurrence of stent thrombosis. Only within PES were thrombi found in the segments of NSC grade 2 associated with large late loss. Conclusion— The present study suggests that angiographic large late loss was not associated with a low risk of in-stent thrombus. Received January 27, 2008; accepted May 30, 2008. # CLINICAL PERSPECTIVE {#article-title-2}Background—It recently has been hypothesized that a larger late loss may have a protective role against stent thrombosis. The relationship between angiographic late loss and the presence of thrombus based on angioscopic findings within paclitaxel-eluting stents (PES) and sirolimus-eluting stents (SES) was investigated in this study. Methods and Results—Prospective 6-month follow-up angiographic and angioscopic examinations were performed on 18 patients for PES and on 20 patients for SES. Late loss was measured by quantitative coronary angiography. Angioscopic neointimal stent coverage (NSC) grade was classified as follows: 0=uncovered struts without neointima, 1=visible struts through thin neointima, and 2=no visible struts. In each patient, maximum NSC, minimum NSC, and the existence of thrombus were evaluated. Late loss and maximum NSC were greater in PES than in SES (0.38±0.43 versus 0.10±0.23 mm; P=0.02 and P=0.0004, respectively). Late loss was correlated with maximum NSC (grade 0, 0.06±0.01 mm; grade 1, 0.10±0.05 mm; and grade 2, 0.48±0.46 mm), whereas there was no correlation between late loss and minimum NSC. The prevalence of patients with uncovered struts did not differ (44% of PES, 40% of SES; P=0.78). In-stent thrombus was found more frequently in PES than in SES (72% versus 40%, P=0.046) despite no occurrence of stent thrombosis. Only within PES were thrombi found in the segments of NSC grade 2 associated with large late loss. Conclusion—The present study suggests that angiographic large late loss was not associated with a low risk of in-stent thrombus.

Lack of Association Between Large Angiographic Late Loss and Low Risk of In-Stent ThrombusCLINICAL PERSPECTIVE

Background— It recently has been hypothesized that a larger late loss may have a protective role against stent thrombosis. The relationship between angiographic late loss and the presence of thrombus based on angioscopic findings within paclitaxel-eluting stents (PES) and sirolimus-eluting stents (SES) was investigated in this study. Methods and Results— Prospective 6-month follow-up angiographic and angioscopic examinations were performed on 18 patients for PES and on 20 patients for SES. Late loss was measured by quantitative coronary angiography. Angioscopic neointimal stent coverage (NSC) grade was classified as follows: 0=uncovered struts without neointima, 1=visible struts through thin neointima, and 2=no visible struts. In each patient, maximum NSC, minimum NSC, and the existence of thrombus were evaluated. Late loss and maximum NSC were greater in PES than in SES (0.38±0.43 versus 0.10±0.23 mm; P =0.02 and P =0.0004, respectively). Late loss was correlated with maximum NSC (grade 0, 0.06±0.01 mm; grade 1, 0.10±0.05 mm; and grade 2, 0.48±0.46 mm), whereas there was no correlation between late loss and minimum NSC. The prevalence of patients with uncovered struts did not differ (44% of PES, 40% of SES; P =0.78). In-stent thrombus was found more frequently in PES than in SES (72% versus 40%, P =0.046) despite no occurrence of stent thrombosis. Only within PES were thrombi found in the segments of NSC grade 2 associated with large late loss. Conclusion— The present study suggests that angiographic large late loss was not associated with a low risk of in-stent thrombus. Received January 27, 2008; accepted May 30, 2008. # CLINICAL PERSPECTIVE {#article-title-2}Background—It recently has been hypothesized that a larger late loss may have a protective role against stent thrombosis. The relationship between angiographic late loss and the presence of thrombus based on angioscopic findings within paclitaxel-eluting stents (PES) and sirolimus-eluting stents (SES) was investigated in this study. Methods and Results—Prospective 6-month follow-up angiographic and angioscopic examinations were performed on 18 patients for PES and on 20 patients for SES. Late loss was measured by quantitative coronary angiography. Angioscopic neointimal stent coverage (NSC) grade was classified as follows: 0=uncovered struts without neointima, 1=visible struts through thin neointima, and 2=no visible struts. In each patient, maximum NSC, minimum NSC, and the existence of thrombus were evaluated. Late loss and maximum NSC were greater in PES than in SES (0.38±0.43 versus 0.10±0.23 mm; P=0.02 and P=0.0004, respectively). Late loss was correlated with maximum NSC (grade 0, 0.06±0.01 mm; grade 1, 0.10±0.05 mm; and grade 2, 0.48±0.46 mm), whereas there was no correlation between late loss and minimum NSC. The prevalence of patients with uncovered struts did not differ (44% of PES, 40% of SES; P=0.78). In-stent thrombus was found more frequently in PES than in SES (72% versus 40%, P=0.046) despite no occurrence of stent thrombosis. Only within PES were thrombi found in the segments of NSC grade 2 associated with large late loss. Conclusion—The present study suggests that angiographic large late loss was not associated with a low risk of in-stent thrombus.

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.