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Despite the known association of cardiac rupture with acute myocardial infarction (AMI), it is still unclear whether the clinical characteristics are associated with the risk of in-hospital mortality in patients with AMI complicated by cardiac rupture. The purpose of this study was to investigate the association between the time of cardiac rupture occurrence and the risk of in-hospital mortality after AMI. We conducted a retrospective analysis of multicenter registry data from eight medical universities in Eastern Japan. From 10,278 consecutive patients with AMI, we included 183 patients who had cardiac rupture after AMI, and examined the incidence of in-hospital deaths during a median follow-up of 26 days. Patients were stratified into three groups according to the AMI-to-cardiac rupture time, namely the > 24-h group (n = 111), 24–48-h group (n = 20), and n = 52). Cox proportional hazards regression analysis was used to estimate the hazard ratio (HR) and the confidence interval (CI) for in-hospital mortality. Around 87 (48%) patients experienced in-hospital death and 126 (67%) underwent a cardiac surgery. Multivariable Cox regression analysis revealed a non-linear association across the three groups for mortality (HR [CI]; 48 h: 2.25 [1.22–4.15]) after adjustments for age, sex, Killip classification, percutaneous coronary intervention, blood pressure, creatinine, peak creatine kinase myocardial band fraction, left ventricular ejection fraction, and type of rupture. Cardiac surgery was independently associated with a reduction in the HR of mortality (HR [CI]: 0.27 [0.12–0.61]) and attenuated the association between the three AMI-to-cardiac rupture time categories and mortality (statistically non-significant) in the Cox model. These data suggest that the AMI-to-cardiac rupture time contributes significantly to the risk of in-hospital mortality; however, rapid diagnosis and prompt surgical interventions are crucial for improving outcomes in patients with cardiac rupture after AMI.

BACKGROUND The pathophysiology and chronological course of atherosclerosis seems to be different between men and women due to biological differences, and age and gender differences in plaque composition of coronary lesions remain to be elucidated.Methods and Results:A total of 860 consecutive patients with a median age of 69 years (IQR, 60-78 years) who underwent optical coherence tomography (OCT) of culprit lesions was included. The composition of culprit plaque on OCT was compared between female (n=171) and male (n=689) subjects in younger (

Introduction: Low eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio is associated with an increased risk of cardiovascular events in patients with coronary artery disease (CAD). However, the association between EPA/AA ratio and the characteristics of non-culprit coronary plaque in statin-treated patients with CAD remains to be elucidated. Hypothesis: Lower EPA/AA ratio is associated with a higher prevalence of vulnerable characteristics in non-culprit coronary plaque in statin-treated patients with CAD. Methods: A total of 367 consecutive stain-treated patients with stable coronary disease, who underwent percutaneous coronary intervention for the culprit lesion and optical coherence tomography (OCT) imaging of a non-culprit plaque in a culprit vessel were included. The characteristics of non-culprit plaque assessed by OCT were compared between the lower EPA/AA group (EPA/AA Results: The prevalence of lipid-rich plaque (58.8 vs. 42.0%, p=0.004) and plaque with macrophage (56.1 vs. 32.1%, p Conclusions: Lower EPA/AA ratio was associated with a higher prevalence of vulnerable characteristics in non-culprit plaque. The present results may partly explain the impact of low EPA/AA ratio on the increased incidence of recurrent events in patients with CAD.

Introduction: High body mass index (BMI) is associated with increased incidence of type 2 diabetes (T2D) and subsequent cardiovascular disease (CVD). However, the association between the BMI and the characteristics of coronary plaque in younger T2D patients with CVD remains to be elucidated. Hypothesis: Higher BMI is associated with a higher prevalence of vulnerable coronary plaque in younger T2D patients with CVD. Methods: A total of 140 consecutive younger (2 , n=70) or the lower BMI group (BMI 2 , n=70) according to the median of BMI. The characteristics of culprit plaque assessed by OCT were compared between the two groups. Results: The prevalence of thin-cap fibroatheroma (TCFA) (34.8 vs. 17.4%, p =0.020) and lipid-rich plaque (44.9 vs. 26.1%, p =0.021) was significantly higher in the higher BMI group than in the lower BMI group (Panel A). The prevalence of TCFA was further compared according to the tertile of LDL-C levels. A significant trend toward higher prevalence of TCFA according to the increase in LDL-C levels was observed in patients with higher BMI ( p =0.017) (Panel B), although the trend was not significant in patients with lower BMI ( p =0.487) (Panel C). Conclusions: Higher BMI was associated with a higher prevalence of TCFA in younger T2D patients with CVD. Higher LDL-C level was associated with a higher prevalence of TCFA among patients with higher BMI although the association was not significant among patients with lower BMI.

High triglyceride (TG) levels have been demonstrated to be a risk factor for coronary artery disease. This study aimed to clarify the impact of TG levels on the characteristics of coronary plaques.A total of 850 consecutive patients who underwent optical coherence tomography (OCT) imaging of the culprit lesion were included. The morphologies of culprit plaques were compared between the higher TG group (nonfasting TG levels ≥150 mg/dL, n = 337) and the lower TG group (nonfasting TG150 mg/dL, n = 513).The prevalence of lipid-rich plaques (43% vs. 33%, p = 0.005), thin-cap fibroatheromas (TCFAs) (24% vs. 17%, p = 0.015) and macrophages (40% vs. 31%, p = 0.006) was significantly higher in the higher TG group than in the lower TG group. In addition to a high low-density lipoprotein cholesterol (LDL-C) level (≥140 mg/dL), high TGs (≥150 mg/dL) were identified as an independent factor for the presence of TCFAs (odds ratio 1.465, 95% confidence interval 1.004-2.137, p = 0.048). Among patients with lower LDL-C levels (100 mg/dL), the prevalence of macrophages (38% vs. 26%, p = 0.007) and layered plaques (48% vs. 38%, p = 0.019) was significantly higher in the higher TG group than in the lower TG group.Higher TG levels were associated with a higher prevalence of TCFAs in culprit coronary lesions. The prevalence of macrophages and layered plaques was more frequently observed in patients with higher TGs than those with lower TGs among patients with LDL-C 100 mg/dL.

Reducing low-density lipoprotein cholesterol (LDL-C) levels with statins slows the progression of atherosclerotic plaques and reduces cardiovascular events. The 2019 European Society of Cardiology/European Atherosclerosis Society guidelines recommend absolute LDL-C treatment targets of100 mg/dL,70 mg/dL and55 mg/dL according to coexisting patient risk factors.To clarify the difference in the plaque characteristics of coronary lesions associated with these LDL-C levels in statin-treated patients.A total of 685 consecutive statin-treated patients with coronary artery disease (CAD) who underwent optical coherence tomography (OCT) imaging of culprit lesions were enrolled. The characteristics of culprit plaques evaluated by OCT were compared among the high LDL-C group (≥100 mg/dL, n=247), the moderate LDL-C group (70-100 mg/dL, n=289), the low LDL-C group (55-70 mg/dL, n=106) and the very low LDL-C group (55 mg/dL, n=43).A significant trend toward a lower prevalence of thin-cap fibroatheroma (TCFA) associated with the LDL-C groups was observed (23.1, 18.3, 9.4 and 11.6%, respectively, in each group; p=0.002). A trend toward a lower prevalence of TCFAs associated with the LDL-C groups was also observed among patients with lower hemoglobin A1c (6.2%; p=0.003). LDL-C70 mg/dL (the low/very low group) was independently associated with the lack of TCFAs (odds ratio, 0.50; 95% confidence interval, 0.27-0.87, p=0.014).Lower LDL-C levels were associated with a lower prevalence of TCFAs in culprit plaques among statin-treated patients with CAD.

Background Tendon xanthomas are accumulations of collagen and macrophages, which contain cholesterol esters and a marker of high risk for coronary artery disease (CAD). Objective The aim of the article was to clarify whether the presence of Achilles tendon thickening (ATT) was associated with disease severity and plaque vulnerability in patients with CAD. Methods A total of 241 consecutive patients who underwent percutaneous coronary intervention and ATT assessment were analyzed. ATT was defined as Achilles tendon thickness of ≥9 mm on radiograph. The severity of CAD and plaque vulnerability was assessed by the findings on angiogram and optical coherence tomography, respectively. Results ATT was found in 44 patients (18.2%). The frequency of multivessel disease (79.6% vs 58.4%, P = .009) and left main lesion (13.6% vs 3.1%, P = .004) was significantly higher in patients with ATT (ATT group) than in patients without ATT (no ATT group). Multivariate logistic regression analyses demonstrated that the presence of ATT was independently associated with the presence of multivessel disease (odds ratio, 2.33; 95% confidence interval, 1.08–5.46; P = .031). The ATT group had a higher prevalence of intimal vascular channels (50.0% vs 24.7%, P = .018) and macrophage accumulation (58.3% vs 33.3%, P = .028) in culprit plaque than the no ATT group. Conclusions Patients with the presence of ATT had a higher prevalence of multivessel coronary disease and left main coronary artery disease than with patients without ATT. The presence of ATT was also associated with vulnerable features, including intimal vascular channels and macrophage accumulation in culprit plaques.

Plaque erosion (PE) is a major underlying mechanism of acute coronary syndrome (ACS). Patients with PE may have less systemic atherosclerosis. We aimed to clarify the status of carotid atherosclerosis in patients with PE. A total of 115 consecutive patients with ACS who underwent optical coherence tomography (OCT) imaging of the culprit lesion were enrolled. Patients were classified into PE (n = 26), plaque rupture (n = 56) or calcified plaque (CP, n = 33) based on OCT findings of the culprit lesions. The status of carotid atherosclerosis was assessed by the findings of carotid echography. The mean IMT was the lowest in the PE group (1.5 ± 0.6 mm) among the three groups (p = 0.004) with a significant difference between the PE group and the CP group (2.1 ± 0.6 mm, p

Introduction: The impact of high triglyceride (TG) level on the characteristics of coronary plaque remains to be elucidated. Hypothesis: Higher TG level is associated with higher prevalence of vulnerable coronary plaque in patients with coronary artery disease (CAD). Methods: A total of 865 consecutive patients who underwent optical coherence tomography (OCT) imaging of the culprit lesion were included. Patients were classified into either the higher TG group (non-fasting TG ≥ 200 mg/dL, n=150) or the lower TG group (non-fasting TG < 200 mg/dL, n=715). The morphologies of culprit plaque assessed by OCT were compared between the two groups. Results: The median (interquartile range) of TG in the 2 groups was 265.5 (221.5 – 314.8) mg/dL and 115.0 (84.0 – 152.0) mg/dL, respectively. The frequency of macrophage accumulation was significantly higher in the higher TG group than the lower TG group (41 vs. 33%, p=0.043) (Panel A), whereas the prevalence of other plaque components including thin-cap fibroatheroma (22 vs. 19%, p=0.386), microchannel (24 vs. 25%, p=0.907) and cholesterol crystal (23 vs. 23%, p=0.862) was comparable between the two groups. The incremental frequency of macrophage accumulation according to TG levels was observed (p=0.015, Panel B). Although the frequency of macrophage accumulation was comparable between the 2 groups among patients with a higher HDL cholesterol (HDL-C) level (>35 mg/dL), macrophage accumulation was significantly more frequent in the higher TG group than in the lower TG group (71 vs. 41%, p=0.032) among patients with a lower HDL-C level (≤35 mg/dL). Conclusions: Higher TG level was associated with higher frequency of macrophage accumulation in culprit plaques in patients with CAD. The present results may partly explain the role of TG on the development of culprit plaque in coronary artery.

Introduction: Factors for adverse cardiac events after drug-eluting stent (DES) implantation among patients with hemodialysis (HD) remain to be elucidated. Hypothesis: Suboptimal DES implantation is associated with the increased incidence of adverse events in patients with HD. Methods: A total of 109 consecutive patients with HD who underwent optical coherence tomography (OCT)-guided DES implantation were included. The impact of post-stent OCT findings on the incidence of device-oriented clinical endpoints (DoCE) at 1 year was investigated. DoCE included cardiac death, target vessel-related myocardial infarction, target lesion revascularization, and stent thrombosis. Results: There was no significant difference in baseline clinical characteristics and pre-stent lesion characteristics between patients with DoCE (n=15) and those without DoCE (n=94). Significant hazard ratio (HR) for the incidence of DoCE was not observed in the presence of edge dissection, irregular protrusion, or incomplete stent apposition (Panel A). In receiver operating characteristic curve analyses, the best cutoff of minimum stent cross-sectional area (MSA), %stent expansion [MSA / mean reference lumen cross-sectional area х 100], and eccentricity index (minimum stent diameter / maximum stent diameter) at MSA site for detecting DoCE was 3.4 (mm 2 ), 72.0 (%), and 0.71, respectively. Significant HR for the incidence of DoCE was observed in the presence of MSA< 3.4 (HR 3.58, 95% confidence interval [CI] 1.04 - 12.4, p=0.035) and eccentricity index< 0.71 (HR 6.68, 95% CI 1.94 - 23.0, p=0.001) (Panel B). Conclusions: Smaller stent area and eccentric expansion were associated with increased incidence of DoCE after DES implantation in patient with HD, although the presence of other post-stent suboptimal findings were not associated with the incidence of DoCE. The present results suggest the importance of larger stent area and concentric stent expansion in patients with HD.

Background Previous studies have demonstrated that plaque erosion is associated with less atheromatous plaque at both culprit and non-culprit lesion than other plaque types of acute coronary syndrome (ACS). However, the status of systemic atherosclerosis in patients with plaque erosion remains to be elucidated. Purpose To clarify if plaque erosion is associated with less systemic atherosclerosis than other plaque types of ACS. Methods A total of 239 consecutive patients with ACS who underwent optical coherence tomography (OCT) imaging of the culprit lesion were enrolled. Patients were classified into either plaque erosion (PE, n=45) or non-plaque erosion (non-PE, n=194) including plaque rupture and calcified nodule based on OCT findings of the culprit lesions. The status of systemic atherosclerosis was assessed by the findings of carotid echography, the severity of aortic arch calcification (AAC; grade 0–3) on chest X-ray, brachial-ankle pulse wave velocity (baPWV) and ankle-brachial pressure index (ABPI). Results The maximum intima media thickness (IMT) was significantly thinner in the PE group than in the non-PE group (1.9±0.8 vs. 2.3±0.9 mm, p=0.023) (Panel A). The prevalence of heterogeneous plaque and calcified plaque was significantly lower in the PE group than in the non-PE group (25.0 vs. 50.4%, p=0.010, 18.8 vs. 38.5%, p=0.037, respectively). The prevalence of AAC grade was significantly different between the two groups with a tendency toward lower AAC grade in the PE group than the non-PE group (Panel B). The mean baPWV (1588.1±420.6 vs. 1686.5±363.5 cm/sec, p=0.186) and ABPI (1.1±0.1 vs. 1.1±0.1, p=0.270) was comparable between the two groups. Conclusion Plaque erosion was associated with less atherosclerosis in carotid artery and aortic arch than non-plaque erosion. These findings may help further clarify the distinct pathophysiology of plaque erosion. Funding Acknowledgement Type of funding source: None

Background The association between the level of high sensitivity C-reactive protein (hsCRP) and coronary plaque characteristics in patients with acute coronary syndrome (ACS) remains to be elucidated. Purpose To clarify the morphological characteristics of culprit lesion in patients with ACS according to the hsCRP levels using optical coherence tomography (OCT). Methods A total of 215 consecutive patients with ACS, who underwent OCT imaging of culprit lesions were included. The patients were classified into either the higher hsCRP group (hsCRP ≥0.14 mg/dL, n=108) or the lower hsCRP group (hsCRP Results The higher hsCRP group had higher prevalence of insulin therapy (14 vs. 6%, p=0.037) and current smoker than the lower hsCRP group (37 vs. 18%, p=0.002). The prevalence of long lesion (≥25 mm, 67 vs. 53%, p=0.041) and fibrocalcific plaque (53 vs. 33%, p=0.003) was significantly higher in the higher hsCRP group than in the lower hsCRP group (Figure). On the other hand, the prevalence of plaque rupture (36 vs. 46%, p=0.174) and lipid-rich plaque (47 vs. 64%, p=0.011) was rather lower in the higher hsCRP group than in the lower hsCRP group (Figure). In a multivariate analysis, fibrocalcific plaque (odds ratio [OR]: 2.098, 95% confidence interval [CI]: 1.125–3.913, p=0.019), lesion length (mm, OR: 1.036, 95% CI: 1.010–1.061, p=0.004) and current smoker (OR: 2.757, 95% CI: 1.388–5.476, p=0.003) was independently associated with higher hsCRP level. Conclusions ACS patients with high hsCRP levels had more fibrocalcific plaque and longer lesion than those with low hsCRP levels. The association between high hsCRP levels and vulnerable characteristics of culprit plaque was not demonstrated. Funding Acknowledgement Type of funding source: None

Background Lowering low-density lipoprotein cholesterol (LDL-C) with statins slows progression of atherosclerotic plaques and reduces cardiovascular events. The 2019 European Society of Cardiology guideline for the management of dyslipidaemias recommends the absolute LDL-C treatment target as Purpose To investigate plaque morphologies according to LDL-C levels in statin-treated patients with coronary artery disease (CAD). Methods A total of 685 consecutive statin-treated patients with CAD, who underwent optical coherence tomography (OCT) imaging of culprit lesions were enrolled. The prevalence of vulnerable compositions in culprit plaques evaluated by OCT was compared among the groups of patients classified by LDL-C levels ( Results LDL-C levels Conclusions Lower LDL-C level was associated with a trend toward lower prevalence of thin-cap fibroatheroma and thrombus in statin-treated patients with CAD. Funding Acknowledgement Type of funding source: None

The ultra-short dual antiplatelet therapy (DAPT) followed by P2Y

Background Diabetes mellitus is a risk for increased incidence of adverse clinical events after percutaneous coronary intervention. However, the difference in the incidence of adverse clinical events according to stent type in patients with diabetes remains to be elucidated. In the present study, we aimed to compare the clinical outcomes between patients treated with the biodegradable polymer sirolimus-eluting stents (BP-SES) and the durable polymer everolimus-eluting stents (DP-EES) among patients with diabetes. Methods Among 631 lesions in 510 consecutive patients treated with either BP-SES or DP-EES, 165 lesions in 141 patients with diabetes mellitus and stable angina pectoris were identified and classified into the BP-SES group (48 lesions in 44 patients) and the DP-EES group (117 lesions in 100 patients). The incidence of adverse clinical events after stent implantation was compared between the 2 groups. Results There was no significant difference in the prevalence of conventional risk factors, lesion characteristics, and procedural characteristics between the 2 groups. During median 386 [334–472] days follow-up, the incidence of target lesion revascularization (11.4 vs. 2.0%, p = 0.003) and device-oriented clinical endpoint (13.6 vs. 6.0%, p = 0.035) in the BP-SES group was significantly greater than that in the DP-EES group. A univariate model demonstrated that the BP-SES usage was significantly associated with the higher incidence of target lesion revascularization (odds ratio, 6.686; 95% confidence interval, 1.234–36.217; p = 0.028). Conclusion BP-SES was associated with the greater incidence of TLR than the DP-EES in patients with diabetes mellitus. Further studies with larger cohorts and longer follow-up are required to confirm the present results.

Achilles tendon thickening (ATT) is a marker of high risk for coronary artery disease (CAD). However, the association between the presence of ATT and the incidence of cardiovascular events in patients with CAD is unclear. A total of 406 consecutive patients who underwent percutaneous coronary intervention (PCI) and ATT assessment were analyzed. ATT was defined as the Achilles tendon thickness of 9 mm or more on radiography. The incidence of major adverse cardiovascular events (MACE) at 1-year was compared between patients with ATT and those without ATT. MACE included cardiac death, non-fatal myocardial infarction, stroke, target vessel revascularization (TVR), and non-TVR. ATT was found in 67 patients (16.5%). The incidence of cardiac death (3.2 vs. 0.0%, p = 0.001), TVR (12.7 vs. 4.0%, p = 0.005) and MACE (20.6 vs. 9.6%, p = 0.011) was significantly higher in the ATT group than the no ATT group. Patients with ATT had significantly higher incidence of cardiac death (5.6 vs. 0%, p

OBJECTIVES To assess the clinical significance of a novel optical coherence tomography (OCT)-derived volumetric parameter of stent expansion by comparing it with the conventional parameters in real-world practice. BACKGROUND The clinical significance of novel parameters in real-world practice including longer and smaller stents remains to be elucidated. METHODS A total of 226 de novo lesion treated with drug-eluting stents in 208 consecutive patients were enrolled. Stent expansion was retrospectively assessed on the final OCT images after stent implantation. The novel parameter was the minimum expansion index (MEI) calculated using a novel algorithm that yields the ideal lumen area in each frame by taking into account vessel tapering. The device-oriented clinical end point (DoCE) included cardiac death, target vessel-related myocardial infarction, ischemia-driven target lesion revascularization. RESULTS The MEI in the lesions with a DoCE (n = 22) at 2 years and cases without a DoCE (n = 204) was 64.3 ± 12.0% and 78.5 ± 14.6%, respectively (p

Distinct clinical characteristics have been demonstrated in patients with plaque erosion as compared with those with plaque rupture. We reasoned that greater physical activity might influence the onset of plaque erosion. In total, 97 consecutive patients with non ST-segment elevation acute coronary syndrome (ACS) who underwent optical coherence tomography (OCT) imaging of the culprit lesion were enrolled. OCT-determined culprit plaque characteristics were plaque erosion (18.6%), calcified plaque (26.8%), plaque rupture (32.0%) and other (22.7%). The physical activity evaluated by estimated metabolic equivalents (METs) at ACS onset was significantly greater in the plaque erosion group than in the plaque rupture group (3.3 ± 1.7 vs. 2.1 ± 1.0, p = 0.011). The rate of ACS onset outdoors was the highest (61.1%) in the plaque erosion group. The combination of greater physical activity (> 3 METs), outdoor onset and higher body mass index (> 25.1 kg/m2) had a significant odds ratio for the incidence of plaque erosion (odds ratio 15.0, 95% confidence interval 3.81 to 59.0, p

Background and aims Endothelial glycocalyx covers the endothelium and maintains vascular integrity. However, its association with the severity and vulnerability of coronary artery disease (CAD) remains to be elucidated. Methods A total of 259 consecutive patients with stable CAD requiring percutaneous coronary intervention (PCI) were prospectively enrolled. Patients were classified into 2 groups according to the median value of serum syndecan-1, which is a core component of the endothelial glycocalyx (lower syndecan-1 group [syndecan-1 Results There was no significant difference in clinical characteristics between the lower syndecan-1 group and the higher syndecan-1 group other than the prevalence of family history of CAD (19 vs. 32%, p = 0.022), prior PCI history (45 vs. 60%, p = 0.015) and estimated glomerular filtration rate (57.8 ± 17.2 vs. 50.9 ± 25.6 ml/min/1.73 m2, p = 0.011). Although disease severity on angiogram was comparable between the 2 groups, the prevalence of lipid-rich plaque (40 vs. 19%, p = 0.004) and thin-cap fibroatheroma (20 vs. 6%, p = 0.006) was significantly higher in the lower syndecan-1 group than the higher syndecan-1 group. Lower syndecan-1 level was independently associated with higher prevalence of lipid-rich plaque (odds ratio 3.626, 95% confidence interval 1.535–8.566, p = 0.003). Conclusions Lower syndecan-1 level was associated with higher prevalence of vulnerable plaque in patients with CAD. This finding suggests the association between impaired endothelial glycocalyx and the development of vulnerable plaque.

Cognitive impairment is frequently represented in elderly patients with cardiovascular disease (CVD); yet, the mechanism is uncertain. Recent studies have suggested the association between the vascular endothelial dysfunction and cognitive impairment. The aim of this study was to clarify the association between endothelial dysfunction and cognitive impairment in elderly patients with CVD.A total of 80 elderly patients (> 70 years old) with CVD were included. Patients who had already pharmacologically intervened for cognitive impairment were excluded. The endothelial dysfunction was assessed by the reactive hyperemia-peripheral arterial tonometry (RH-PAT). Cognitive impairment was diagnosed by the Mini-mental state examination.The RH-PAT index was significantly lower in cognitive impairment (median 1.60 [interquartile range (IQR) 1.34 to 1.89], n = 51) as compared with non-cognitive impairment (median 1.75 [IQR 1.55 to 2.30], n = 29, P = 0.005). By a multivariate analysis, the RH-PAT index was independently associated with cognitive impairment (odds ratio: 0.89; 95% confidence interval: 0.81 to 0.97; per 0.1, P = 0.044). In the receiver-operating characteristic analysis, the best cut-off of the RH-PAT index to identify cognitive impairment was 1.65 (area under the curve 0.67; P = 0.011) with limited the sensitivity (63%) and specificity (66%).A lower RH-PAT index was significantly associated with the presence of cognitive impairment in elderly CVD patients. Further studies are required to clarify the mechanism and the causal relationship between the endothelial dysfunction and cognitive impairment in patients with CVD.

Aim: Fractional flow reserve (FFR) reflects on the diffuse atherosclerosis per coronary artery. It is unknown whether the statin therapy affects long term FFR after stenting. The aim of this study was to evaluate the long term FFR after stent implantation in patients who are intaking fixed-dose rosuvastatin. Methods: A total of 22 patients with stable angina pectoris were enrolled. The values of FFR were measured before, immediately after, and 18 months after (follow-up day) the implantation of everolimus eluting stent (EES; Promus Element™ or Promus Element Plus™). A fixed dose of rosuvastatin at 5 mg/day was administrated to all patients. Results: Of the 22 patients, 2 were excluded because of adverse effect of rosuvastatin and in-stent total occlusion after EES implantation. Overall, the values of FFR immediately after and 18 months after EES implantation did not show significant change (from 0.90 ± 0.05 to 0.88 ± 0.06, p = 0.16). However, there was a significant negative correlation between low density lipoprotein (LDL) cholesterol level at follow-up day and changes in the value of FFR (p = 0.01, r = −0.74). There was an increase in the FFR value after stenting in 8 out of 9 patients with LDL cholesterol level below 75 mg/dl (area under the curve 0.92, p = 0.0005). Conclusions: LDL cholesterol level was associated with the change in the FFR value in patients following stent implantation. Lower LDL cholesterol tended to improve in the long-term FFR, underscoring the importance of lowering LDL cholesterol to prevent the progression of coronary atherosclerosis.

The ultra-short dual antiplatelet therapy (DAPT) followed by P2Y12 inhibitor monotherapy might be promising after percutaneous coronary intervention (PCI). However, CYP2C19 loss-of-function (LOF) alleles have been reported to diminish the effect of clopidogrel, and clopidogrel monotherapy has a concern about the increased ischemic risk for patients with such alleles. STOPDAPT-2 is the multicenter prospective open-label, but adjudicator-blinded randomized control study comparing 1-month DAPT followed by clopidogrel monotherapy with the standard 12-month DAPT after PCI with cobalt–chromium everolimus-eluting stents. Among the participants of STOPDAPT-2, selected patients participated in a substudy of the CYP2C19 gene test. Patients with two CYP2C19*2 or *3 alleles were defined as the poor metabolizer (PM), one allele as the intermediate metabolizer (IM), and no allele as the extensive metabolizer (EM). The primary endpoint was the composite of cardiovascular and bleeding events, as defined in STOPDAPT-2. Among 750 (24.9%) patients with known CYP2C19 genotypes, 129 (17.2%) were PM, 367 (49.0%) were IM, and 254 (33.9%) were EM. The hazard ratios of 1-month DAPT relative to 12-month DAPT for the primary endpoint in PM, IM, and EM strata were 0.66 (95% CI 0.11–3.94), 1.94 (95% CI 0.60–6.31), and 0.21 (95% CI 0.02–1.78), respectively (P interaction = 0.17), and those for cardiovascular composite endpoint were 1.00 (95% CI 0.14–7.10), 6.10 (95% CI 0.75–49.55), and 0.26 (95% CI 0.03–2.34), respectively (P interaction = 0.12). In conclusion, for the selected patients in STOPDAPT-2 trial, CYP2C19 LOF alleles had no significant, consistent interaction with the effect of 1-month DAPT relative to 12-month DAPT for clinical outcomes, although the study was overtly underpowered. STOPDAPT-2 ClinicalTrials.gov number, NCT02619760.

Key Clinical Message Major aortopulmonary collateral arteries branching from coronary arteries may cause coronary steal. The careful follow‐up is needed irrespective of symptoms because increasing physical activities and oxygen demand along with the age may induce myocardial ischemia. Transcatheter intervention by well‐trained physician would be a treatment option in patients with myocardial ischemia.

Background Previous studies demonstrated the impact of concomitant cancer on the increased risk of adverse cardiac and bleeding events after percutaneous coronary intervention (PCI). However, the impact in this 2nd- and 3rd-generation drug-eluting stent (DES) era remains to be elucidated. Purpose To clarify the impact of cancer on clinical outcomes in patients after 2nd- or 3rd -generation DES implantation. Methods A total of 932 patients who underwent PCI with 2nd- or 3rd -generation DES were included. Patients who were diagnosed with cancer after PCI were excluded from the present cohort. The incidence of major adverse cardiac events (MACE) including cardiac death, myocardial infarction and target or non-target vessel revascularization, and bleeding events was compared between the patients with cancer or the history of treatment for cancer (cancer group, n=140) and the patients without cancer (no cancer group, n=792). Bleeding events were evaluated according to the Thrombolysis in Myocardial Infarction definition. Further comparisons were performed between the 2 groups (cancer group, n=126; no cancer group, n=252) after the adjustment of baseline clinical characteristics using 1:2 propensity score-matching analysis. Results The incidence of MACE at median 577 [340–1043] days after the PCI was comparable between the 2 groups in both unadjusted (15.0% vs. 15.0%, p=0.984) (Panel A) and adjusted cohorts (14.3 vs. 13.1%, p=0.796), although the incidence of all cause death in the cancer group was significantly greater than the no cancer group (15.1 vs. 9.5%, p=0.007, in the adjusted cohort). The increased risk of MACE was not observed in any types of cancer or treatment (Panel B). The incidence of bleeding events was also comparable between the 2 groups (4.0 vs. 2.0%, p=0.297, in the adjusted cohort). Conclusion The increased incidence of MACE and bleeding events in patients with cancer was not demonstrated after the 2nd- or 3rd-generation DES implantation. Further studies are required to clarify the safety and efficacy of PCI in patients with cancer.

Background Among several parameters for stent expansion, which is better for predicting adverse events remains to be elucidated. Purpose To assess the predictive significance of several parameters for stent expansion on the incidence of adverse cardiac events. Methods A total of 183 consecutive patients with de novo lesion treated with drug-eluting stent (DES) under optical coherence tomography (OCT) guidance were enrolled. The stent expansion was retrospectively assessed on the final OCT images after the stent implantation by both conventional and novel parameters. The conventional parameters included the minimum stent cross-sectional area (MSA) and %stent expansion defined as [MSA/mean reference lumen cross-sectional area × 100]. The novel parameter was the minimum expansion index (MEI) calculated by using a novel algorhythm which yields the ideal lumen area in each frame by taking into account vessel tapering. The expansion index was calculated by [actual lumen area/ideal lumen area × 100] in each frame through the stented segment. The MEI was the minimum value of expansion index through the stented segment. The both conventional and novel parameters were compared between cases with and without device-oriented cardiac events (DoCE). Receiver operating characteristics (ROC) curves were constructed to assess the ability of those parameters to predict DoCE. Results The MSA and MEI in the DoCE group (n=12) were significantly smaller than the no DoCE group (n=171) (3.29±0.72 vs. 4.45±1.97 mm2, p Conclusion Among several parameters for stent expansion, a novel MEI was better to predict device-oriented cardiac events after DES implantation.

Introduction Syndecan-1 is a component of endothelial glycocalyx which maintains vascular integrity. Thus, it may be impaied in patients with coronary artery disease (CAD). Purpose To assess the association between serum syndecan-1 level and the severity and vulnerability of CAD. Methods A total of 259 consecutive patients with stable angina requiring percutaneous coronary intervention (PCI) were prospectively enrolled. Patients were classified into 2 groups according to the median syndecan-1 value (Lower syndecan-1 group [syndecan-1 Results There was no significant difference in baseline clinical characteristics between the lower syndecan-1 group and the higher syndecan-1 group other than the prevalence of family history of ischemic heart disease (19 vs. 32%, p=0.022) and prior PCI history (45 vs. 60%, p=0.015). The prevalence of multivessel disease (70 vs. 68%, p=0.627), left main disease (4 vs. 5%, p=0.748) and chronic total occlusion (15 vs. 15%, p=0.959) was comparable between the 2 groups. On the other hand, the prevalence of lipid-rich plaque (40 vs. 19%, p=0.004) and TCFA (20 vs. 6%, p=0.006) was significantly higher in the lower syndecan-1 groupthan the higher syndecan-1 group (Figure). The lower syndecan-1 was independently associated with the higher prevalence of lipid-rich plaque (Table). Table 1. Multivariate analysis for lipid-rich plaque Odds ratio 95% CI pvalue Lower syndecan-1 2.981 1.448–6.411 0.003 Dyslipidemia 1.693 0.738–4.142 0.218 Chronic kidney disease 1.354 0.669–2.765 0.400 Smoking 0.975 0.453–2.154 0.951 Diabetes mellitus 0.819 0.400–1.661 0.580 Conclusions Lower syndecan-1 level was associated with higher prevalence of vulnerable plaque in patients with CAD. Serum syndecan-1 may have a potential as a marker for the presence of vulnerable coronary plaque.

Optical coherence tomography (OCT)-guided percutaneous coronary intervention (PCI) may increase contrast volume. However, the impact of OCT-guided PCI on the decline in kidney function (DKF) in actual clinical practice remains unclear.Among 1,003 consecutive patients who underwent either OCT-guided or intravascular ultrasound (IVUS)-guided PCI in our institute, we identified 202 propensity score-matched pairs adjusted by baseline factors. The incidence of DKF was compared between the OCT-guided PCI group and the IVUS-guided PCI group. DKF was defined as an increase in serum creatinine level of ≥ 0.5 mg/dL or a relative increase of ≥ 25% over baseline within 48 hours (acute DKF) or 1 month (sustained DKF) after PCI.Baseline characteristics, including the prevalence of chronic kidney disease (54% versus 46%, P = 0.09), were comparable between the OCT- and IVUS-guided PCI groups except for the age. The contrast volume was comparable between the two groups (153 ± 56 versus 144 ± 60 mL, P = 0.09), although it was significantly greater in the OCT-guided PCI group in patients with acute coronary syndrome (ACS; 175 ± 55 versus 159 ± 43 mL, P = 0.04). The incidence of acute DKF (0.5% versus 2.5%, P = 0.22) and sustained DKF (5.0% versus 10.4%, P = 0.31) was comparable between the two groups. Multivariate analysis demonstrated that ACS (odds ratio 4.74, 95% confidence interval 2.72-8.25, P < 0.001) was a predictor of sustained DKF.Compared with IVUS-guided PCI, OCT-guided PCI did not increase the incidence of DKF in actual clinical practice, although the increased contrast volume was observed in ACS cases.

The association between endothelial function, evaluated using flow-mediated dilatation (FMD), and the severity of coronary artery disease remains to be elucidated.A total of 245 consecutive patients with stable angina were prospectively enrolled. FMD was evaluated in the brachial artery before percutaneous coronary intervention. Patients were divided into 2 groups according to the FMD value (lower FMD group [FMD < 2.0], n = 82; higher FMD group [FMD ≥ 2.0], n = 163). The severity of coronary artery disease was evaluated using findings of angiography and optical coherence tomography, and compared between the 2 groups.The prevalence of left main (LM) disease was significantly higher in the lower FMD group than in the higher FMD group (8.5% versus 2.5%, P = 0.046), although the prevalence of multivessel disease was comparable between the groups. Lower FMD was independently associated with a higher prevalence of LM disease (odds ratio, 3.89; 95% confidence interval, 1.12-15.5; P = 0.033). A general linear model with multiple variables revealed that the minimal lumen area (MLA) in the culprit lesion was significantly smaller in patients with lower FMD than in those with higher FMD (regression coefficient b, -0.249 mm2; 95% confidence interval, -0.479--0.018 mm2; P = 0.035). The prevalence ofvulnerable plaque characteristics was comparable between the 2 groups.Patients with lower FMD had a higher incidence of LM disease and a smaller MLA in the culprit lesion. FMD may be a useful, noninvasive indicator for identifying patients with severe coronary artery disease.

Background High lipoprotein (a) [Lp(a)] levels are an independent factor for worse prognosis in patients with coronary artery disease (CAD). However, the association between serum Lp(a) level and coronary plaque vulnerability remains to be determined. Methods A total of 255 consecutive patients with CAD who underwent optical coherence tomography imaging of culprit lesions were included. Patients were divided into 2 groups according to their Lp(a) levels (the higher Lp(a) group [≥25 mg/dL], n = 87; or the lower Lp(a) group [, Highlights • High Lp(a) (≥25 mg/dL) was observed in 34% of patients requiring PCI. • Higher Lp(a) was associated with the higher prevalence of thin-cap fibroatheroma. • High LDL-C enhanced the association between Lp(a) and thin-cap fibroatheroma.

Ezetimibe reduces plasma levels of low-density lipoprotein cholesterol by inhibiting Niemann–Pick C1-like protein 1 (NPC1L1). A recent study demonstrated that NPC1L1 plays an important role in absorption of fat-soluble vitamins including vitamin K. We evaluated whether the add-on treatment of ezetimibe affects anticoagulation in patients taking warfarin. Between October 2007 and March 2015, the administration of ezetimibe was started to a total of 101 outpatients who were already on oral anticoagulation with warfarin. We retrospectively analyzed blood lipid levels, prothrombin time international normalized ratio (PT-INR) and time in therapeutic INR range (TTR). Seventy-one patients (70 %) showed increase in PT-INR after ezetimibe treatment (1.96 ± 0.45 to 2.20 ± 0.61, p

Background and aims Intraplaque cholesterol crystal (CC) is recognized as a component of vulnerable plaques. However, the clinical characteristics of patients with CC and the impact of CC on clinical events remain unknown. Methods A total of 340 consecutive patients who underwent optical coherence tomography (OCT) imaging of culprit lesions were included in the study. CC was defined as a thin linear structure with high reflectivity and low signal attenuation on OCT images. The incidence of major adverse cardiovascular events (MACE) at 1-year was compared between patients with CC (CC group) and those without CC (non-CC group). MACE included cardiac death, non-fatal myocardial infarction, target vessel revascularization (TVR), and non-TVR (NTVR). Results CC was observed in 29% (n = 98) of the patients. There was no significant difference in baseline clinical characteristics between the CC and non-CC groups, other than in eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio (0.39 ± 0.29 vs. 0.47 ± 0.33, p = 0.047) and hemoglobin A1c (HbA1c) levels (6.51 ± 0.97 vs. 6.25 ± 0.87%, p = 0.016). The incidence of MACE and NTVR at 1-year was significantly higher in the CC group than in the non-CC group (15.3 vs. 7.9%, P = 0.038; 8.1 vs. 2.5%, p = 0.017). The presence of CC was significantly associated with a higher rate of 1-year MACE (odds ratio 4.78, confidential interval 2.02–10.10, p Conclusions Patients with CC in the culprit lesion had higher HbA1c and lower EPA/AA than patients without CC. The 1-year clinical outcomes in patients with CC in the culprit lesion were worse than in those without CC.

Cognitive impairment is frequently represented in elderly patients with cardiovascular disease (CVD); yet, the mechanism is uncertain. Recent studies have suggested the association between the vascular endothelial dysfunction and cognitive impairment. The aim of this study was to clarify the association between endothelial dysfunction and cognitive impairment in elderly patients with CVD.A total of 80 elderly patients (70 years old) with CVD were included. Patients who had already pharmacologically intervened for cognitive impairment were excluded. The endothelial dysfunction was assessed by the reactive hyperemia-peripheral arterial tonometry (RH-PAT). Cognitive impairment was diagnosed by the Mini-mental state examination.The RH-PAT index was significantly lower in cognitive impairment (median 1.60 [interquartile range (IQR) 1.34 to 1.89], n = 51) as compared with non-cognitive impairment (median 1.75 [IQR 1.55 to 2.30], n = 29, P = 0.005). By a multivariate analysis, the RH-PAT index was independently associated with cognitive impairment (odds ratio: 0.89; 95% confidence interval: 0.81 to 0.97; per 0.1, P = 0.044). In the receiver-operating characteristic analysis, the best cut-off of the RH-PAT index to identify cognitive impairment was 1.65 (area under the curve 0.67; P = 0.011) with limited the sensitivity (63%) and specificity (66%).A lower RH-PAT index was significantly associated with the presence of cognitive impairment in elderly CVD patients. Further studies are required to clarify the mechanism and the causal relationship between the endothelial dysfunction and cognitive impairment in patients with CVD.

The aim of this study was to investigate whether the underlying plaque type affects the neointimal coverage after drug-eluting stent implantation.A total of 1793 struts in 22 zotarolimus-eluting stents were assessed using optical coherence tomography imaging within 3 months of implantation. Neointimal coverage was evaluated within 5 mm from each stent edge on cross-sectional optical coherence tomography images at every 1-mm interval. The percentage of struts covered by neointima was compared among the normal segment group, the fibrous plaque group, and the lipid plaque group on the basis of the underlying plaque type.The percentage of covered strut was significantly lower in the normal segment group than in the fibrous plaque group (35.9±30.2 vs. 57.1±31.0%, P0.05) and the lipid plaque group (vs. 64.7±23.5%, P0.01). The neointima was significantly thinner in the normal segment group than in the lipid plaque group (19.0±22.3 vs. 32.0±18.8 μm, P0.01). The percentage of struts on the normal segment was significantly higher in cross-sections with a ratio of uncovered to total struts per section more than 0.3 than in cross-sections with a ratio up to 0.3 (32.4±31.7 vs. 19.5±33.8%, P0.01).Struts on the normal segment were less covered and had thinner neointima than struts on the lipid plaque at the stent edge within 3 months after zotarolimus-eluting stent implantation. Caution should be exercised when implanting longer drug-eluting stents to achieve uniform strut coverage in the early phase.

The irregular protrusion has been reported as an independent predictor of 1-year adverse cardiac events. However, the impact of stent type on the incidence of irregular protrusion remains to be elucidated. A total of 308 consecutive patients with stable angina, who underwent optical coherence

Background Stroke prevention by warfarin, a vitamin K antagonist, has been an integral part in the management of atrial fibrillation. Vitamin K-dependent matrix Gla protein (MGP) has been known as a potent inhibitor of arterial calcification and osteoporosis. Therefore, we hypothesized that warfarin therapy affects bone mineral metabolism, vascular calcification, and vascular endothelial dysfunction. Methods We studied 42 atrial fibrillation patients at high-risk for atherosclerosis having one or more coronary risk factors. Twenty-four patients had been treated with warfarin for at least 12 months (WF group), and 18 patients without warfarin (non-WF group). Bone alkaline phosphatase (BAP) and under carboxylated osteocalcin (ucOC) and receptor activator of nuclear factor-kappa B ligand (RANKL) were measured as bone metabolism markers. Reactive hyperemia-peripheral arterial tonometry (RH-PAT) index measured by Endo-PAT2000 was used as an indicator of vascular endothelial function. Results There were no significant differences in patient background characteristics and other clinical indicators between the two groups. In WF group, the ucOC levels were significantly higher than those in the non-WF group (10.3 ± 0.8 vs. 3.4 ± 0.9 ng/mL; P, Highlights • Stroke prevention by warfarin has been an integral part in the management of atrial fibrillation. • Warfarin prevents the activation of vitamin K-dependent proteins, MGP and Gas-6. • Long-term warfarin therapy increases the serum levels of ucOC and RANKL. • Long-term warfarin therapy is associated with vascular endothelial dysfunction.

Incretin hormones have been reported to have cytoprotective actions in addition to their glucose-lowering effects. We evaluated whether teneligliptin, a novel dipeptidyl peptidase-4 (DPP-4) inhibitor, affects left ventricular (LV) function in patients with type 2 diabetes mellitus (T2DM). Twenty-nine T2DM patients not receiving any incretin-based drugs were enrolled and prescribed with teneligliptin for 3 months. Compared to baseline levels, hemoglobin A1c levels decreased (7.6 ± 1.0 % to 6.9 ± 0.7 %, p < 0.01) and 1,5-anhydro-d-glucitol levels increased (9.6 ± 7.2 μg/mL to 13.5 ± 8.7 μg/mL, p < 0.01) after treatment. Clinical parameters, including body mass index and blood pressure, did not show any difference before and after treatment. Three months after treatment, there were improvements in LV systolic and diastolic function [LV ejection fraction, 62.0 ± 6.5 % to 64.5 ± 5.0 %, p = 0.01; peak early diastolic velocity/basal septal diastolic velocity (E/e′) ratio, 13.3 ± 4.1 to 11.9 ± 3.3, p = 0.01]. Moreover, there was an improvement in endothelial function (reactive hyperemia peripheral arterial tonometry [RH-PAT] index; 1.58 ± 0.47 to 2.01 ± 0.72, p < 0.01). There was a significant negative correlation between changes in the E/e’ ratio and RH-PAT values. Furthermore, circulating adiponectin levels increased (27.0 ± 38.5 pg/mL to 42.7 ± 33.2 pg/mL, p < 0.01) without changes in patient body weight. Teneligliptin treatment was associated with improvements in LV function and endothelial functions, and an increase in serum adiponectin levels. These results support the cardio-protective effects of teneligliptin in T2DM patients and increase in serum adiponectin levels.

The target lesion revascularization of paclitaxel-eluting stents (PES) has been reported to be lower than that of sirolimus-eluting stents in patients on hemodialysis (HD). However, the comparison of PES and second generation drug-eluting stents in CKD patients has not been fully investigated. We compared clinical outcomes of everolimus-eluting stents (EES) and PES in CKD patients.Hundred and forty seven CKD patients (eGFR60mLmin(-1)1.73m(-2)) treated with PES (n=74, from May 2007 to December 2009) and EES (n=73, from January 2010 to January 2013) were enrolled in the study. Major adverse cardiac events (MACEs) were defined as death, non-fatal myocardial infarction, and ischemia driven target lesion revascularization.The incidence of 36-month MACE was significantly lower in EES, non-HD group compared to PES, non HD group (0% in EES group and 13.5% in PES group, respectively, P0.01). There was no significant difference in MACE between EES and PES in HD patients (5.4% in PES group and 5.5% in EES group, P=0.98). In multivariate analysis, PES group and PES ISR were independent factors for worse incidence of MACE.In CKD patients, PES was associated with worse clinical outcomes in non-HD patients as compared with EES.

Cell migration, proliferation, and differentiation of cardiac fibroblasts (CFs) play a central role in cardiac fibrosis. Factor Xa (FXa)-dependent protease-activated receptor (PAR)-1 and PAR-2 have been reported as important targets in proinflammatory and fibroproliferative diseases. From this viewpoint, we aimed to investigate whether treatment of rivaroxaban, an approved oral direct FXa inhibitor, attenuates functional changes in angiotensin (Ang) II-induced mouse CFs.Confluent cultured mouse CFs were pretreated with or without rivaroxaban. Ang II-induced cell migration was decreased by 73% in rivaroxaban induced cells. Rivaroxaban inhibited Ang II-induced cell proliferation by 27% at 0.01 μg/ mL, 69% at 0.1 μg/mL, 71% at 1 μg/mL, and 69% at 5 μg/mL. In mouse cytokine array measuring 40 cytokines, the productions of interleukin-16, TIMP-1, and tumor necrosis factor-α (TNF-α) were significantly reduced with 0.1 μg/mL of rivaroxaban pretreatment (all P < 0.05). TIMP-1 levels in the culture supernatant measured by ELISA were also decreased by rivaroxaban pretreatment in Ang II-induced CFs (35% decrease at 0.01 μg/mL, 47% at 0.1 μg/mL, 47% at 1 μg/mL, and 57% at 5 μg/mL). In the dual reporter assay analysis, rivaroxaban inhibited various inflammatory signal pathways, including the nuclear factor-kappa B (NF-κB), active protein-1 (AP-1), and mitogen-activated protein kinase (MAPK) pathways (decreases of 82%, 78%, and 75%, respectively).These data suggest that rivaroxaban inhibits Ang II-induced functional activation in cultured mouse CFs via inhibiting NF-κB and MAPK/AP-1 signaling pathways, which may be a possible target of heart failure, through the antifibrotic and anti-inflammatory efficacy of rivaroxaban in Ang II-stimulated cardiac fibroblasts.

In recent years, direct oral anticoagulants (DOACs) of dabigatran, rivaroxaban, apixaban, edoxaban, which are all alternatives to warfarin, have been released. The use of DOACs is becoming more widespread in the clinical management of thrombotic stroke risk in patients with atrial fibrillation (AF). In large-scale clinical trials of each drug, DOACs were reported to inhibit intracranial hemorrhage, stroke, and death compared to warfarin. Warfarin is an endogenous vitamin K antagonist; therefore, patients who are taking warfarin must be prohibited from taking vitamin K. Vitamin K is an essential cofactor required for the ɤ-carboxylation of vitamin K-dependent proteins including coagulation factors, osteocalcin (OC), matrix Gla protein (MGP), and the growth arrest-specific 6 (GAS6). OC is a key factor for bone matrix formation. MGP is a local inhibitor of soft tissue calcification in the vessel wall. GAS6 prevents the apoptosis of vascular smooth muscle cells. Therefore, decrease of blood vitamin K levels may cause osteoporosis, vascular calcification, and the inhibition of vessels angiogenesis. This study aimed to evaluate the effects of changing from warfarin to rivaroxaban on bone mineral metabolism, vascular calcification, and vascular endothelial dysfunction. We studied 21 consecutive patients with persistent or chronic AF, who were treated with warfarin at least for 12 months. Warfarin administration was changed to rivaroxaban (10 or 15 mg/day) in all patients. Osteopontin (OPN), bone alkaline phosphatase (BAP), and under-carboxylated osteocalcin (ucOC) were measured. Pulse wave velocity (PWV) and augmentation index (AI) were also measured as atherosclerosis assessments. All measurements were done before and six months after the rivaroxaban treatment. There was a significant increase in serum level of BAP compared to baseline (12.5 ± 4.6 to 13.4 ± 4.1 U/L, P

Incomplete neointimal coverage and malapposed struts after stenting are associated with increased risk of stent thrombosis. We aimed to evaluate neointimal coverage early after Resolute zotarolimus-eluting stent (R-ZES) implantation using optical coherence tomography (OCT). A total of 20 patients with de novo native coronary lesions with R-ZES were enrolled. Among these patients, 20 stented lesions in 19 patients were evaluated at 1, 2, and 3 months after R-ZES implantation. The strut apposition and neointimal coverage were evaluated by OCT. Neointimal hyperplasia (NIH) thickness and percentage of covered struts and the proportion of incompletely apposed struts were measured at 1-mm intervals. The mean percentages of covered stent struts were over 85 % within 3 months (88.4 ± 6.3 % at 1 month, 95.5 ± 5.5 % at 2 months, 93.6 ± 3.5 % at 3 months). The percentages of incompletely apposed struts were not significantly different among the groups (4.4 ± 4.2 % at 1 month, 1.9 ± 1.9 % at 2 months, 3.1 ± 2.2 % at 3 months, p = 0.51). Mean NIH thickness (38.9 ± 8.1 μm at 1 month, 70.6 ± 18.8 μm at 2 months, 54.1 ± 5.9 at 3 months, p = 0.0016) was thickest in the 2 months group. Most of all OCT findings within 2 months demonstrated neointimal coverage with low signal intensity. The neointimal coverage of ZES-R was over 85 % within 3 months. These data may support shorter requirement of dual antiplatelet therapy duration with R-ZES.

A 70-year-old man underwent percutaneous coronary intervention (PCI) for a diffuse lesion at proximal right coronary artery. Optical coherence tomography (OCT) showed an additional 15-mm-length stent would be suitable to cover a residual lesion with irregular cavities ([Figure 1A][1]). However, on

Previous studies demonstrated the comparable results of post-stent minimal lumen diameter (MLD) between optical coherence tomography (OCT)-guided and intravascular ultrasound (IVUS)-guided stenting. However, the difference in MLD between OCT-guided and IVUS-guided stenting in chronic total occlusion