Tomotaka Dohi

Non-Fibroatheroma Lesion Phenotype and Long-Term Clinical Outcomes : A Substudy Analysis From the PROSPECT Study

OBJECTIVESnThe purpose of this study was to determine the clinical impact of non-fibroatheroma lesion phenotype in patients presenting with an acute coronary syndrome (ACS).nnnBACKGROUNDnAlthough fibroatheromas (FAs) are known to be clinically unstable, the impact of non-FA lesion phenotype on clinical outcomes has not been studied.nnnMETHODSnIn the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study, patients presenting with an ACS underwent 3-vessel grayscale and virtual histology intravascular ultrasound (VH-IVUS) after successful percutaneous intervention for all culprit lesions and were followed for 3 years. Patients were divided into those who had only the non-FA phenotype (pathological intimal thickening or fibrotic and/or fibrocalcific lesions) versus those who had at least 1 nonculprit FA.nnnRESULTSnAmong 2,880 nonculprit lesions identified by VH-IVUS, 39.8% were non-FAs (1,042 pathological intimal thickening, 72 fibrotic, and 33 fibrocalcific). Nonculprit major adverse cardiac events (MACE) (death, myocardial infarction, or urgent rehospitalization for progressive or unstable angina) were attributed to only 7 non-FA lesions (0.7%) versus 43 FA lesions (2.7%, p < 0.001) during 3 years follow-up. Of 609 patients, 67 (11.0%) patients had only non-FA lesion phenotypes. Patients with only non-FAs tended to be younger and more often female, have fewer nonculprit lesions and less overall plaque burden and necrotic core, and fewer nonculprit lesion MACE compared with patients with at least 1 FA. In the adjusted Cox proportional hazards model, absence of a FA was a significant predictive of a lower 3-year nonculprit MACE rate (hazard ratio: 0.23; 95% confidence interval: 0.06 to 0.95).nnnCONCLUSIONSnNon-FA lesions were clinically stable and were rarely associated with clinical events during 3 years of follow-up. The intermediate-term prognosis in patients presenting with ACS in whom all nonculprit lesions are non-FAs is favorable. (nnnPROSPECTnAn Imaging Study in Patients With Unstable Atherosclerotic Lesions; NCT00180466).

Utility of Peak Creatine Kinase-MB Measurements in Predicting Myocardial Infarct Size, Left Ventricular Dysfunction, and Outcome After First Anterior Wall Acute Myocardial Infarction (from the INFUSE-AMI Trial)

Infarct size after ST-segment elevation myocardial infarction (STEMI) is associated with long-term clinical outcomes. However, there is insufficient information correlating creatine kinase-MB (CK-MB) or troponin levels to infarct size and infarct location in first-time occurrence of STEMI. We, therefore, assessed the utility of CK-MB measurements after primary percutaneous coronary intervention of a first anterior STEMI using bivalirudin anticoagulation in patients who were randomized to intralesion abciximab versus no abciximab and to manual thrombus aspiration versus no aspiration. Infarct size (as a percentage of total left ventricular [LV] mass) and LV ejection fraction (LVEF) were evaluated by cardiac magnetic resonance imaging at 30 days and correlated to peak CK-MB. Peak CK-MB (median 240 IU/L; interquartile range 126 to 414) was significantly associated with infarct size and with LVEF (r = 0.67, p <0.001; r = -0.56, p <0.001, respectively). A large infarct size (greater than or equal the median, defined as 17% of total LV mass) and LVEF ≤40% were more common in the highest peak CK-MB tertile group than in the other tertiles (87.6% vs 49.5% vs 9.1%, p <0.001; 43.2% vs 14.0% vs 4.6%, p <0.001, respectively). Peak CK-MB of at least 300 IU/L predicted with moderate accuracy both a large infarct size (area under the curve 0.88) and an LVEF ≤40% (area under the curve 0.78). Furthermore, CK-MB was an independent predictor of 1-year major adverse cardiac events (hazard ratio 1.42 per each additional 100 IU/L [1.20 to 1.67], p <0.001). In conclusion, CK-MB measurement is useful in estimating infarct size and LVEF and in predicting 1-year clinical outcomes after primary percutaneous coronary intervention for first anterior STEMI.

Mechanisms and Patterns of Intravascular Ultrasound In-Stent Restenosis Among Bare Metal Stents and First- and Second-Generation Drug-Eluting Stents

The most common causes of in-stent restenosis (ISR) are intimal hyperplasia and stent under expansion. The purpose of this study was to use intravascular ultrasound (IVUS) to compare the ISR mechanisms of bare metal stents (BMS), first-generation drug-eluting stents (DES), and second-generation DES. There were 298 ISR lesions including 52 BMS, 73 sirolimus-eluting stents, 52 paclitaxel-eluting stents, 16 zotarolimus-eluting stents, and 105 everolimus-eluting stent. Mean patient age was 66.6 ± 1.1xa0years, 74.2% were men, and 48.3% had diabetes mellitus. BMS restenosis presented later (70.0 ± 66.7xa0months) with more intimal hyperplasia compared with DES (BMS 58.6 ± 15.5%, first-generation DES 52.6 ± 20.9%, second-generation DES 48.2 ± 22.2%, pxa0= 0.02). Although reference lumen areas were similar in BMS and first- and second-generation DES, restenotic DES were longer (BMS 21.8 ± 13.5xa0mm, first-generation DES 29.4 ± 16.1xa0mm, second-generation DES 32.1 ± 18.7xa0mm, pxa0= 0.003), and stent areas were smaller (BMS 7.2 ± 2.4xa0mm(2), first-generation DES 6.1 ± 2.1xa0mm(2), second-generation DES 5.7 ± 2.0xa0mm(2), p <0.001). Stent fracture was seen only in DES (first-generation DES 7 [5.0%], second-generation DES 8 [7.4%], pxa0=xa00.13). In conclusion, restenotic first- and second-generation DES were characterized by less neointimal hyperplasia, smaller stent areas, longer stent lengths, and more stent fractures than restenotic BMS.

The relationship among extent of lipid-rich plaque, lesion characteristics, and plaque progression/regression in patients with coronary artery disease: a serial near-infrared spectroscopy and intravascular ultrasound study.

AIMSnTo evaluate the relationship between lipid content and plaque morphometry as well as the process of lesion progression and regression in patients with significant coronary artery disease.nnnMETHODS AND RESULTSnThe present study, using data from the YELLOW trial, was conducted in patients having significant coronary lesions (fractional flow reserve <0.8) who underwent serial intravascular ultrasound (IVUS) and near-infrared spectroscopy (NIRS) at baseline and after 7 weeks. For each coronary plaque (≥50% plaque burden that was ≥5 mm in length), we evaluated plaque characteristics and the extent of lipid-rich plaque [LRP, defined as the 4 mm long segment with the maximum lipid-core burden index (maxLCBI4 mm)] on NIRS. Among 66 patients (age 63.0 ± 10.1 years; 82% statin use at baseline), 94 plaques were identified. The extent of LRP at baseline was positively correlated with IVUS plaque burden (r = 0.317, P = 0.002). A large LRP (maxLCBI4 mm ≥500) was present only in plaques with a large plaque burden (≥70%). Multivariate analysis demonstrated that plaque burden was the best predictor of the extent of LRP (P < 0.001). In lesions with a large plaque burden and a large amount of LRP at baseline, a reduction in LRP was seen in all lesions in patients receiving intensive statin therapy (P = 0.004) without a significant change in plaque burden.nnnCONCLUSIONSnCoronary lesions containing a large amount of LRP also had a large plaque burden. Short-term regression of LRP (without a change in plaque burden) was observed mainly in plaques with a large plaque burden and a large amount of LRP at baseline.nnnCLINICAL TRIAL REGISTRATIONnhttp://www.clinicaltrials.gov. Unique identifier: NCT01567826.

Prevalence and anatomical features of acute longitudinal stent deformation: An intravascular ultrasound study.

We report the prevalence and anatomical features of longitudinal stent deformation as detected by intravascular ultrasound (IVUS)

Serial Intravascular Ultrasound Findings After Treatment of Chronic Total Occlusions Using Drug-Eluting Stents

Morphologic changes after chronic total occlusion (CTO) treatment with drug-eluting stents (DESs) have not been assessed in detail. Our aim was to use both baseline and follow-up intravascular ultrasound studies to evaluate the morphologic changes and, especially, the changes in distal vessel size and the effect of subintimal stenting after treatment of CTOs with DES. We analyzed serial follow-up intravascular ultrasound (baseline and follow-up at 9 ± 2 months) after DES implantation into 40 CTOs. Overall, 33 CTOs were treated by the anterograde approach; and 7 were treated by the retrograde approach. Minimum lumen cross-sectional area (CSA) trended toward a decrease from baseline to follow-up (4.8 ± 1.7 vs 4.5 ± 1.7 mm(2), p = 0.10), although the minimum stent CSA (4.8 ± 1.7 vs 4.9 ± 1.7 mm(2), p = 0.26) did not change. The distal reference, but not the proximal reference lumen CSA, increased significantly at follow-up (3.8 ± 2.0 to 5.1 ± 2.3 mm(2), p = 0.0004). Late-acquired stent malapposition was seen in 17 patients (42.5%). In 8 CTOs (20%), a part of the stent was implanted into a subintimal space; in these 8 patients, maximum percent neointimal hyperplasia and minimum lumen area was similar in the subintimal segment compared with the adjacent intraplaque segment. The frequency of late-acquired stent malapposition was similar. In conclusion, after CTO treatment with DES, distal vessel enlargement was detected. Subintimal stenting after recanalization of CTO was not inferior compared with stenting within the plaque in terms of long-term morphologic impact.

Etiology, Frequency, and Clinical Outcomes of Myocardial Infarction After Successful Drug-Eluting Stent Implantation Two-Year Follow-Up From the ADAPT-DES Study

Background—The frequency, causes, and impact of myocardial infarction (MI) after successful percutaneous coronary intervention have not been well studied. Methods and Results—The Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents (ADAPT-DES) study was a prospective, multicenter registry study of 8582 patients undergoing successful drug-eluting stent implantation at 11 centers in the United States and Germany. After excluding 128 patients with periprocedural MI, we investigated the pathogenesis, frequency, and long-term consequences of non-periprocedural MI in 8454 patients. MI during 2-year follow-up developed in 263 patients (3.3%) at a median (25th and 75th percentiles) time of 318 (129, 503) days. The 263 MIs were subclassified as spontaneous MI (n=78; 29.7%), secondary or indeterminate MI (n=64; 24.3%), stent thrombosis–related MI (n=63; 24.0%), and in-stent restenosis–related MI (n=58; 22.1%). Multivariable predictors of MI included clinical and angiographic factors (acute coronary syndromes presentation, diabetes mellitus, current smoker, multivessel disease, treatment of an in-stent restenotic lesion), laboratory findings (low baseline hemoglobin and reduced creatinine clearance), antiplatelet agent–related factors (higher on-treatment platelet P2Y12 receptor reactivity and premature thienopyridine discontinuation), and not being on a statin at discharge. Patients who experienced an MI during the follow-up period had significantly greater 2-year mortality than those without MI (17.3% [42 deaths] versus 3.4% [265 deaths], P<0.001). By multivariable analysis, the adjusted hazard ratio (95% confidence interval) for subsequent mortality during follow-up was 2.17 (1.06, 4.45) in patients with versus without a non-periprocedural MI (P=0.03). Conclusions—The occurrence of a non-periprocedural MI within 2 years after successful drug-eluting stent implantation is relatively infrequent, but has numerous etiologies and is significantly associated with subsequent mortality. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT00638794.

THE IMPACT OF NON–FIBROATHEROMA LESION PHENOTYPE ON LONG–TERM CLINICAL OUTCOMES: A SUBSTUDY ANALYSIS FROM PROSPECT

While fibroatheromas (FA) are known to be clinically unstable, the impact of non–FA lesion phenotype on clinical outcomes has not been studied.nnIn the PROSPECT, pts presenting with acute coronary syndrome underwent 3–vessel grayscale and virtual histology intravascular ultrasound (VH–IVUS)