Search

Background Right ventricular (RV) pacing causes left ventricular (LV) dyssynchrony sometimes resulting in pacing‐induced cardiomyopathy. However, RV pacing for hypertrophic obstructive cardiomyopathy is one of the treatment options. LV flow energy loss (EL) using vector flow mapping (VFM) is a novel hemodynamic index for assessing cardiac function. Our study aimed to elucidate the impact of RV pacing on EL in normal LV function and hypertrophic cardiomyopathy (HCM) patients. Methods A total of 36 patients with dual‐chamber pacemakers for sick sinus syndrome or implantable cardioverter defibrillators for fatal ventricular tachyarrhythmias were enrolled. All patients were divided into two groups: 16 patients with HCM (HCM group) and others (non‐HCM group). The absolute changes in EL under AAI (without RV pacing) and DDD (with RV pacing) modes were assessed using VFM on color Doppler echocardiography. Results In the non‐HCM group, the mean systolic EL significantly increased from the AAI to DDD modes (14.0 ± 7.7 to 17.0 ± 8.6 mW/m, P = .003), whereas the mean diastolic EL did not change (19.0 ± 12.3 to 17.0 ± 14.8 mW/m, P = .231). In the HCM group, the mean systolic EL significantly decreased from the AAI to DDD modes (26.7 ± 14.2 to 21.6 ± 11.9 mW/m, P, In non‐HCM patients, the RV pacing decreased the vortex area and the circulation and in HCM patients, it increased the vortex area and the circulation. The RV pacing significantly increased systolic energy loss in the non‐HCM group (P = .003), but it significantly decreased in the HCM group (P

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: The reduced incidence of cardiovascular events in patients with direct oral anticoagulant (DOAC) has been demonstrated. However, the association between taking DOAC and the characteristic of coronary plaque remains to be elucidated. Hypothesis: Taking DOAC is associated with a lower prevalence of vulnerable plaque in patients with coronary artery disease (CAD). Methods: A total of 2168 coronary plaques in consecutive 1439 patients who underwent optical coherence tomography imaging of the culprit or non-culprit lesion were analyzed. The prevalence of thin-cap fibroatheroma (TCFA) were compared between patients with DOAC (149 plaques in 105 patients) and those without (2019 plaques in 1334 patients). Results: The prevalence of TCFA was significantly lower in patients with DOAC than those without in both culprit lesion (27.3% vs. 15.4%, p=0.002) and non-culprit lesion (22.1% vs. 5.2%, p Conclusions: Taking DOAC was associated with a lower prevalence of TCFA in patients with CAD. The present results may partly explain the efficacy of DOAC on the reduced incidence of cardiovascular events in patients with CAD.

A 92-year-old man with acute heart failure due to severe aortic stenosis underwent transcatheter aortic valve implantation (TAVI). Computed tomography demonstrated severe stenosis of the right common iliac artery, occlusion of the left external iliac artery, and stenosis of the left subclavian artery. Severe calcification was observed in the sinotubular junction, which was considered a risk factor for aortic dissection with transapical TAVI using a balloon-expanding bioprosthetic valve. Therefore, transaortic (TAo) access was the only option for this high-risk surgical patient. As the maximum distance from the aortic valve annulus to the sheath insertion point was less than 60 mm, TAVI was performed transaortically using a vascular graft that extended this distance, in order to avoid sheath dislocation. Our experience demonstrates that vascular graft application is a viable option in patients with an inadequate distance between the aortic valve annulus and the puncture site in TAo-TAVI.

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.

BACKGROUND The details and consequences of a small aortic annulus among transcatheter aortic valve replacement (TAVR) patients remain uncertain. This study investigated the short-term outcomes in patients with small annular size and compared the 30-day outcome between intra- and supra-annular devices, with similar outer casing diameter in this subgroup.Methods and Results:Cases registered in the Japanese national TAVR registry between August 2013 and December 2017 were analyzed. Among a total of 5,870 registered patients, 647 (11.0%) had small annulus (area ≤314 mm2) measured by multi-detector computed tomography. Patients with a small annulus had a significantly smaller indexed effective orifice area (iEOA, 1.10 cm2/m2[0.92-1.35] vs. 1.16 cm2/m2[0.96-1.39], P

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

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 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

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.

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 Right ventricular (RV) pacing causes left ventricular (LV) dysfunction. On the other hand, RV pacing for hypertrophic obstructive cardiomyopathy (HOCM) is an established treatment. LV flow energy loss (EL) is a new hemodynamic index for assessing cardiac function. However, the impact of RV pacing on EL remains unknown. Objective The objective of this study was to investigate the EL by RV pacing on normal LV function and hypertrophic cardiomyopathy (HCM). Methods A total of 28 patients underwent echocardiography for EL assessment under AAI (without RV pacing) and DDD (with all RV pacing) mode. Among them, 16 were sick sinus syndrome (SSS) patients with normal LV function, and 12 were HCM patients. EL was calculated from color Doppler images using a vector flow mapping. Results There were no significant difference in patients' background parameters between the SSS and the HCM groups. In the SSS group, mean systolic EL was significantly increased from AAI to DDD mode (14.9 to 19.2 mW/m, P Change of flow energy loss Conclusion RV pacing increased mean systolic EL in normal LV function, but decreased in HCM with or without LV outflow obstruction. In the patients with HCM, the impact of RV pacing on EL is different compared with normal LV function.

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

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.

Background: Transcatheter aortic valve implantation (TAVI) is effective in treating severe aortic stenosis in inoperable or high-risk surgical patients, however, the little is known about outcomes after Sapien 3 20 mm transcatheter heart valve (THV) implantation. The purpose of this study was to investigate the short term outcomes of Sapien 3 20 mm THV implantation in Japanese people with a small body size. Methods: We retrospectively collected the hospital records of consecutive patients who underwent TAVI using the Sapien 3 20 mm THV between October 2016 and March 2017. Clinical and echocardiographic data from before and one week after TAVI were collected. Results: Six Japanese patients (all female, mean age 89 ± 5 years, body surface area [BSA] 1.29 ± 0.16m2) received a Sapien 3 20 mm THV. All the procedures were feasible and successful, and the 30-day mortality rate was 0%. The functional class and the echocardiographic findings significantly improved (aortic valve area, 0.5 ± 0.1 cm2 to 0.8 ± 0.1cm2; mean pressure gradient, 55 ± 15 mmHg to 19 ± 7 mmHg; P = .043, respectively). However, the values of the indexed effective orifice area in all patients after Sapien 3 20 mm THV implantation were less than 0.85 cm2/m2, suggesting prosthesis-patient mismatch (PPM). Conclusions: The implantation of a Sapien 3 20 mm THV was safe and effective in high surgical risk elderly Japanese patients with a small body size. PPM after Sapien 3 20mm THV may be prevalent among Asians with small body sizes. Careful clinical follow-up will be necessary after Sapien 3 20 mm THV implantation.

A 74-year-old female was admitted for the treatment of complete atrioventricular block. Echocardiography showed thickening of interventricular septum and a slight thinning in the basal region with normal left ventricular (LV) function. She was clinically diagnosed with cardiac sarcoidosis accompanied by active inflammation from the findings of blood test, nuclear scanning, and magnetic resonance imaging. After pacemaker implantation, we recommended corticosteroid therapy, which she refused for the fear of side effects. Three years later, she was re-admitted to our hospital due to heart failure. Echocardiography showed severe LV systolic dysfunction and dilatation with wall thinning. Even though we started corticosteroid therapy and continued it for one year, LV function was not improved. In patients with cardiac sarcoidosis accompanied by active inflammation, LV dysfunction, and dilatation may rapidly progress. Early diagnosis and treatment with corticosteroid may be important to preserve cardiac function. .

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

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

High lipoprotein (a) [Lp (a)] level is an independent factor for the worse prognosis in patients with coronary artery disease (CAD). However, the association between serum Lp (a) level and coronary plaque vulnerability remains to be elucidated. A total of 255 consecutive patients with CAD who

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 0.01). In contrast, there was a significant decrease in the serum level of ucOC (9.5 ± 5.0 to 2.7 ± 1.3 ng/ml, P 0.01). Also, in the ucOC levels, there was a significant negative correlation between baseline values and baseline to 6-months changes in high ucOC group (r = -0.97, P 0.01). The atherosclerosis- and osteoporosis-related biomarker, serum level of OPN were significantly decreased compared to baseline (268.3 ± 46.8 to 253.4 ± 47.1 ng/ml, P 0.01). AI and PWV were significantly decreased after 6 months of treatment with rivaroxaban (33.9 ± 18.4 to 24.7 ± 18.4%, P = 0.04; 1638.8 ± 223.0 to 1613.0 ± 250.1 m/s, P = 0.03, respectively). Switching to rivaroxaban from warfarin in patients with atrial fibrillation was associated with an increase of bone formation markers and a decrease of bone resorption markers, and also improvements of PWV and AI.

Achilles tendon xanthoma (ATX) is a marker at high risk for coronary artery disease (CAD) among patients with heterozygous familial hypercholesterolemia. However, the association of ATX with the disease severity among CAD patients is unclear. A total of 241 consecutive patients who underwent

Intraplaque cholesterol crystal (CC) is recognized as a component of vulnerable plaques. However, the impact on the future clinical event remains unknown. A total of 349 consecutive patients who underwent optical coherence tomography (OCT) of culprit lesion were included. CC was defined as as a

A 75-year-old woman underwent percutaneous coronary intervention (PCI) for her tight calcified lesion at proximal left anterior descending artery ([Figure 1A][1]). After debulking the thick calcified lesion using rotational coronary atherectomy, further dilation using a noncompliant balloon was