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Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia due to inadequate insulin secretion, resistance, or both. The cardiovascular complications of DM are the leading cause of morbidity and mortality in diabetic patients. There are three major types of pathophysiologic cardiac remodeling including coronary artery atherosclerosis, cardiac autonomic neuropathy, and DM cardiomyopathy in patients with DM. DM cardiomyopathy is a distinct cardiomyopathy characterized by myocardial dysfunction in the absence of coronary artery disease, hypertension, and valvular heart disease. Cardiac fibrosis, defined as the excessive deposition of extracellular matrix (ECM) proteins, is a hallmark of DM cardiomyopathy. The pathophysiology of cardiac fibrosis in DM cardiomyopathy is complex and involves multiple cellular and molecular mechanisms. Cardiac fibrosis contributes to the development of heart failure with preserved ejection fraction (HFpEF), which increases mortality and the incidence of hospitalizations. As medical technology advances, the severity of cardiac fibrosis in DM cardiomyopathy can be evaluated by non-invasive imaging modalities such as echocardiography, heart computed tomography (CT), cardiac magnetic resonance imaging (MRI), and nuclear imaging. In this review article, we will discuss the pathophysiology of cardiac fibrosis in DM cardiomyopathy, non-invasive imaging modalities to evaluate the severity of cardiac fibrosis, and therapeutic strategies for DM cardiomyopathy.

Little is known about the association between deep vein thrombosis (DVT) and arterial complications in patients with type 2 diabetes (T2DM). The aim of this retrospective cohort study was to assess the influence of prior DVT on major adverse limb events (MALEs) and major adverse cardiovascular events (MACEs) in T2DM. A total of 1,628,675 patients with T2DM with or without a history of DVT from 2001 to 2013 were identified in the National Health Insurance Research Database of Taiwan. Before matching, the patients in the DVT group (n = 2020) were older than the control group (66.3 vs. 58.3 years). Patients in the DVT group were more likely to be female than the control group (54.3% vs. 47.5%). Before matching, the DVT group had higher prevalence of most comorbidities, more prescription of antiplatelet, antihypertensive agents and insulins, but less prescription of metformin and sulfonylurea. During a mean follow-up of 5.2 years (standard deviation: 3.9 years), the matched DVT group (n = 2017) have a significantly increased risk of MALE (8.4% vs. 5.2%; subdistribution hazard ratio [SHR] 1.60, 95% CI 1.34–1.90), foot ulcer (5.2% vs. 2.6%, SHR 1.96, 95% CI 1.57–2.45), gangrene (3.4% vs. 2.3%, SHR 1.44, 95% CI 1.10–1.90) and amputation (2.5% vs. 1.7%; SHR 1.42, 95% CI 1.03–1.95) than the 10,085 matched controls without DVT. They also tended to have a greater risk of all-cause mortality (38.1% vs. 33.1%; hazard ratio [HR] 1.18, 95% CI 1.09–1.27) and systemic thromboembolism (4.2% vs. 2.6%; SHR 1.56, 95% CI 1.22–1.99), respectively. We showed the presence of DVT may be associated with an increased risk of MALEs, major amputation, and thromboembolism, contributing to a higher mortality rate in T2DM.

Background Enhancing detection of unrecognized atrial fibrillation among acute ischemic stroke patients is crucial for secondary stroke prevention. Aim To evaluate whether the detection rate of new atrial fibrillation in acute ischemic stroke patients without known atrial fibrillation could be improved by doing serial 12-lead electrocardiograms once daily for five days, compared with conventional 24-h Holter monitoring (24-h Holter). Methods We conducted a randomized clinical trial to compare the detection rates of paroxysmal atrial fibrillation between serial electrocardiograms versus 24-h Holter from October 2015 to October 2018 at six hospitals. Eligible participants were acute ischemic stroke patients with aged ≥65 years, with neither atrial fibrillation history nor any presence of atrial fibrillation on baseline electrocardiogram at admission. The primary outcome was newly detected electrocardiogram in the serial electrocardiograms and 24-h Holter group. Results Among 826 patients, baseline characteristics were similar between both groups. In the intention-to-treat analysis, there was no statistical difference between serial electrocardiograms versus 24-Holter to detect atrial fibrillation (8.4% vs. 6.9%; adjusted odds ratio 1.17, 95% confidence interval 0.69–2.01). Stepwise multivariate logistic regression revealed age ≥80 years and history of heart failure were associated with detection of paroxysmal atrial fibrillation whereas patients with lacunar infarction had lower odds for detection of paroxysmal atrial fibrillation. Conclusions Serial electrocardiograms had comparable detection rate of paroxysmal atrial fibrillation compared with 24-h Holter and might be a viable alternative to 24-h Holter as a first-line approach to survey for potential paroxysmal atrial fibrillation among elderly patients with acute ischemic stroke. Clinical Trial Registration: URL https://clinicaltrials.gov/ct2/show/NCT02578979 Unique Identifiers: NCT02578979

BACKGROUND: Pacing-induced cardiomyopathy is an undesired outcome in patients with atrioventricular block (AVB), and our animal model showed lipotoxic cardiomyopathy after pacing.OBJECTIVES: The purpose of this study was to explore the mechanisms and clinical outcomes of statins in AVB patients receiving pacing.METHODS: Rat ventricular cardiomyocytes were treated with atorvastatin, liver X receptor (LXR) agonist, and LXR antagonist during pacing. Pigs were divided into 3 groups: right ventricular pacing, pacing with concomitant atorvastatin treatment, and sham control. Clinically, we enrolled 1717 AVB patients who had received a permanent pacemaker from Chang Gung Memorial Hospital Medical database. The primary outcome (cardiovascular death or heart failure [HF] hospitalization) and individual outcome were compared between statin and nonstatin groups after inverse probability of treatment weighting.RESULTS: Lipid accumulation in rat cardiomyocytes by pacing was significantly reduced by treatment with LXR agonist and atorvastatin, whereas LXR antagonist counteracted the atorvastatin effect on lipid expression. Left ventricular ejection fraction (LVEF) was significantly lower in the AVB pig pacing group compared to the group concomitantly treated with atorvastatin. Moreover, lipid accumulation and fibronectin expression were significantly ameliorated by concomitant treatment with atorvastatin. In the clinical study, the statin group had a significantly lower risk of the primary outcome event (hazard ratio [HR] 0.69; 95% confidence interval [CI] 0.56-0.84), less HF hospitalization (HR 0.45; 95% CI 0.30-0.67), and higher LVEF than the nonstatin group.CONCLUSION: In experimental models, atorvastatin ameliorated lipid accumulation in cardiomyocytes and fibrosis in left ventricular myocardium induced by pacing. Clinically, treatment with statins was associated with less HF hospitalization and cardiovascular death in AVB patients receiving pacemaker therapy.

Background and aims Intracerebral hemorrhage (ICH) has a higher mortality than ischemic stroke. Statin is beneficial for stroke, but high potency statin treatment has been associated with the risk of hemorrhagic stroke. The aim of this study was to assess the impact of initiating statin therapy after ICH on cardiovascular outcomes. Methods Dyslipidemic patients were retrieved from the ICH population from the National Health Insurance Research Database in Taiwan. We retrospectively compared patients prescribed with and without statin treatment after ICH. Outcomes of interest were mortality, myocardial infarction, ischemic stroke, and hemorrhagic stroke during 5 years of follow-up. Results Of 17,980 adult patients with ICH and dyslipidemia, 8927 were eligible for analysis over the study period, including 1613 patients receiving statin therapy and 7314 patients not taking statins. After propensity score matching, the mean age was 61.2 ± 12.2 years in the statin group and 61.6 ± 13.0 years in the non-statin group. Hypertension was dominant, followed by diabetes mellitus, and the mean estimated NIHSS score was 12.9. The patients who received statin therapy were associated with lower risks of all-cause mortality (12.7% vs . 21.3%; hazard ratio [HR], 0.54; 95% confidence interval [CI], 0.45–0.65), cardiovascular death (4.0% vs . 7.1%; HR, 0.54; 95% CI, 0.39–0.75) and ICH (5.4% vs . 8.5%; HR, 0.62; 95% CI, 0.46–0.83) compared to those who did not receive statins. Conclusions Initiating statin therapy after ICH was associated with a decreased risk of recurrent ICH and mortality for dyslipidemia patients.

Little is known about whether venous thromboembolism (VTE) causes worse critical limb events in populations with atrial fibrillation (AF). A retrospective cohort study using claims data from Taiwan’s National Health Insurance program between 2001 and 2013 compared AF patients with or without VTE. Outcomes were percutaneous transluminal angioplasty (PTA), amputation, systemic thromboembolism, all-cause mortality, cardiovascular death, ischemic stroke, and acute myocardial infarction. Patients ( n = 316,817) with newly diagnosed AF were analyzed; of those, 2514 (0.79%) had VTE history. After inverse probability of treatment weighting, a history of VTE was significantly associated with higher risks of PTA (3.3 vs 2.2%; subdistribution hazard ratio [SHR] 1.47; 95% confidence interval [CI] 1.17–1.84); above knee amputation (0.7 vs 0.3%; HR 2.15; 95% CI 1.10–4.21); systemic thromboembolism (5.8 vs 3.9%; SHR 1.48; 95% CI 1.21–1.80); all-cause mortality (53 vs 46.4%; HR 1.20, 95% CI 1.12–1.29); and cardiovascular death (34.8 vs 29.4%; HR 1.25, 95% CI 1.14–1.36). In conclusion, VTE might increase the risk of critical lower limb events (PTA and above-knee amputation), systemic thromboembolism, and mortality in the AF population. However, current data cannot confirm a causal relationship between VTE and clinical outcomes in this population.

Background: Hepatitis C virus (HCV) infection is related to a higher risk of chronic kidney disease (CKD). This study aimed to investigate the relationships between unhealthy behaviors, metabolic indices, and HCV with CKD.Methods: This cross-sectional study was conducted as part of a community health promotion program in the HCV hyperendemic area of Taiwan between March and December 2019. Multivariable logistic regression analyses adjusted for demographic and clinical characteristics were performed to investigate the association between CKD and HCV seropositivity.Results: A total of 2,387 patients completed the examination. HCV was related to a lower estimated glomerular filtration rate (eGFR), unhealthy dietary behaviors, and multiple metabolic indices including higher systolic blood pressure (SBP), glycosylated hemoglobin (HbA1c), and triglycerides (TG), and lower high-density lipoprotein (HDL). HCV was associated with a 44% higher risk of CKD compared to non-HCV (OR 1.44, 95% confidence interval [CI] 1.05-1.98). Irregular exercise, waist circumference (WC), and higher HbA1c were significantly associated with a higher risk of CKD after multivariable analysis. A low eGFR was significantly associated with the severity of metabolic syndrome (MetS) in the HCV group (median eGFR of 86.4, 77.1, and 64.5 mL/min/1.73 m2 for individuals with one, three, and five MetS components, respectively).Conclusions: HCV seropositivity, metabolic distortion, and irregular exercise are significantly associated with CKD. Effective treatment of HCV and aggressive health promotion of physical activity may prevent the occurrence of CKD.

A retrospective cohort study was conducted using claims data from Taiwan's National Health Insurance program to assess the effect of diabetic pay-for-performance (P4P) program on major adverse limb events (MALE) and major adverse cardiovascular events (MACE) in patients with type 2 diabetes mellitus (T2DM). This study included patients with T2DM who had completed or not completed a 1-year P4P program from 2002 to 2013. Propensity-score matching was used to balance the baseline characteristics between groups. The Cox proportional-hazard model and Fine and Gray subdistribution hazard model were used to examine the association between P4P and the risks of MALE, MACE, systemic thromboembolism (ST), heart failure (HF) hospitalization, and all-cause mortality. Patients who underwent the P4P program had a significantly decreased incidence of MALE (2.0% vs. 2.6%, subdistribution hazard ratio [SHR] 0.73, 95% CI 0.71-0.76). Regarding the individual components, the P4P group demonstrated lower risks for foot ulcer (1.1% vs 1.3%, SHR 0.80, 95% CI 0.77-0.84), gangrene (0.57% vs 0.93%, SHR 0.59, 95% CI 0.56-0.63), percutaneous transluminal angioplasty (0.61% vs 0.79%, SHR 0.72, 95% CI 0.68-0.77), and amputation (0.46% vs 0.75%, SHR 0.58, 95% CI 0.55-0.62). In addition, the risks of MACE, ST, HF hospitalization, and all-cause mortality were remarkably lower in the P4P group. The P4P program might significantly reduce critical events of MALE, MACE, ST, HF, and mortality in the diabetic population.

Background Little is known about the association between deep vein thrombosis (DVT) and arterial complications in patients with type 2 diabetes. The aim of this retrospective cohort study was to assess the influence of prior DVT on major adverse limb events (MALEs) and major adverse cardiovascular events (MACEs) in patients with type 2 diabetes. Methods Patients with type 2 diabetes with or without a history of DVT hospitalization from 2001 to 2013 were identified in the National Health Insurance Research Database of Taiwan and included in this study. Propensity score matching was used to balance the baseline characteristics between groups. Cox proportional and Fine and Gray subdistribution hazard models were used to examine association a between history of DVT and the risks of MALEs and MACEs. Results During a mean follow-up of 5.2 years (standard deviation: 3.9 years), the DVT group (n = 2017) had a higher risk of MALE composite outcome (8.4% vs. 5.2%; subdistribution hazard ratio [SHR] 1.60, 95% CI 1.34–1.90). Among the individual components, the DVT group had higher risks of foot ulcer (5.2% vs. 2.6%, SHR 1.96, 95% CI 1.57–2.45), gangrene (3.4% vs. 2.3%, SHR 1.44, 95% CI 1.10–1.90) and amputation (2.5% vs. 1.7%; SHR 1.42, 95% CI 1.03–1.95). Conclusions The presence of DVT may be associated with an increased risk of MALEs, major amputation, and thromboembolism, contributing to a higher risk of mortality in patients with type 2 diabetes.

To investigate which types of β-blockers have better efficacy and safety profiles in patients with concomitant chronic obstructive pulmonary disease (COPD) and myocardial infarction (MI) to address concerns about use of β-blockers in COPD.We identified 65,699 patients with COPD prescribed β-blockers after first MI in the Taiwan National Health Insurance Research Database between January 1, 2001, and December 31, 2013. Comparisons were performed using the inverse probability of treatment weighting method. The primary outcome was all-cause mortality; secondary outcomes were heart failure hospitalization, major adverse cardiac and cerebrovascular event (MACCE), and major adverse pulmonary event (MAPE).A total of 14,789 patients prescribed β-blockers were enrolled, of whom 7247 (49.0%) used cardioselective β-blockers and 7542 (51.0%) used nonselective β-blockers. The cardioselective group had lower incidence rates of mortality (hazard ratio [HR], 0.93; 95% CI, 0.89 to 0.96), MACCE (HR, 0.96; 95% CI, 0.93 to 0.998), heart failure hospitalization (subdistribution HR, 0.84; 95% CI, 0.78 to 0.91), and MAPE (HR, 0.94; 95% CI, 0.90 to 0.98) at the end of follow-up after weighting. Similar results were also found in subgroup analysis between those prescribed bisoprolol and those prescribed carvedilol.Patients prescribed a cardioselective β-blocker may have a lower incidence of all-cause mortality, MACCE, heart failure hospitalization, and MAPE than those prescribed a nonselective β-blocker. Cardioselective β-blocker treatment during hospitalization and continuing after discharge appears to be superior to nonselective β-blocker treatment in patients with COPD after MI.

BACKGROUND: Interactions between endothelial cells and vascular smooth muscle cells (VSMCs) through the Notch signal pathway causing diabetic microvasculopathy have been reported. OBJECTIVES: The purpose of this study was to investigate whether the effect of high glucose on VSMCs through the Notch-2 signaling pathway could induce extracellular matrix (ECM) accumulation, VSMC proliferation and migration and thus directly mediate diabetic macrovasculopathy. METHODS: Rat smooth muscle cells (SV40LT-SMC Clone HEP-SA cells) were cultured in different concentrations of D-glucose to evaluate the impact of high glucose on ECM accumulation including fibronectin and collagen I measured by Western blot analysis, and on VSMC proliferation and migration evaluated by MTT assay and wound healing assay. The expression of Notch-2 intra-cellular domain (Notch-2 ICD) protein was also checked in high glucose-stressed VSMCs. N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT), an inhibitor of γ-secretase, was used to modulate the Notch-2 signaling pathway. RESULTS: High glucose (D-glucose 25 mM) induced fibronectin and collagen I expressions in VSMCs, promoted VSMC proliferation/migration, and enhanced the expression of Notch-2 ICD. DAPT inhibited Notch-2 signal to abolish the expressions of fibronectin and collagen I in VSMCs, and also prevented the proliferation/migration of VSMCs under high glucose (D-glucose 25 mM) stress. CONCLUSIONS: Our study suggests that high glucose can enhance the Notch-2 signaling pathway thereby directly mediating diabetic macrovasculopathy. Blocking the Notch-2 signaling pathway decreased fibronectin and collagen I expressions secreted by VSMCs, and reduced the proliferation and migration of VSMCs under high glucose stress. Inhibition of Notch-2 signaling represents a promising target for treating diabetic macrovasculopathy.

Background High-dose steroids and intravenous immunoglobulin (IVIG) are controversial treatments for pediatric patients with acute myocarditis. This study aimed to investigate their efficacies in the Taiwanese pediatric population. Methods This study evaluated 5563 acute myocarditis patients from the Taiwan’s National Health Insurance Research Database and identified 1542 pediatric patients hospitalized for acute myocarditis between January 1, 2001 and December 31, 2011. The exclusion criteria were age of > 11 years, associated cardiovascular comorbidities, autoimmune disease, malignancy before the index hospitalization, extracorporeal membrane oxygenation, intra-aortic balloon pumping, and dual therapy using IVIG and high-dose steroids. Results After 2:1 propensity score matching, we identified 208 subjects without steroid therapy and 104 subjects who received high-dose steroids. The mean age in that cohort was 2.6 ± 2.9 years, and high-dose steroid therapy had no significant effects on major in-hospital complications and post-discharge outcomes. After 2:1 propensity score matching, we identified 178 subjects without IVIG therapy and 89 subjects who received IVIG. The mean age in that cohort was 2.0 ± 2.1 years, and IVIG had no significant effects on the major outcomes. Conclusions The present study revealed that high-dose steroid or IVIG therapy had no significant effects on major in-hospital complications, late heart failure hospitalization, and long-term mortality.

Background and aims Statins improve clinical outcomes in patients with ischemic stroke but there is no evidence of the effect of continuing long-term statin therapy in patients with intracerebral hemorrhage (ICH). The aim of this study was to evaluate the impact of continuing statin after ICH. Methods Data on patients with ICH was retrieved from the National Health Insurance Research Database of Taiwan. The final population was separated into two groups according to those who continued and those who discontinued statin treatment. All-cause mortality and cardiovascular outcomes were analyzed after a 3 year follow-up after propensity score matching (PSM). Results Of the 114,101 patients with ICH, who were initially enrolled, 2468 patients with dyslipidemia and ICH were included. After PSM, the benefit of statin therapy on mortality appeared from 1 year to the end of the 3-year follow-up period after discharge (statin group versus non-statin group: 4.9% vs.12.3% at 1 year (hazard ratio [HR], 0.38; 95% confidence interval [CI], 0.26–0.57) and 12.9% vs. 25.3% at the end of the 3 year follow-up period (HR, 0.45; 95% CI, 0.35–0.58). Compared with the patients using lipophilic statins, those using hydrophilic statins had a significantly lower incidence of all-cause mortality (HR = 0.65, 95% CI = 0.43–0.99). There were no differences between those prescribed moderate-intensity statins and those prescribed high-intensity statins in terms of stroke and all-cause mortality (HR = 0.76; 95% CI = 0.40–1.46). Conclusions There was a lower risk of all-cause mortality following ICH in patients who continued statin treatment compared with those without statin treatment, especially in those treated with hydrophilic statins.

Background: Enhancing detection of undiagnosed atrial fibrillation (AF) in hospitalized patients with a recent ischemic stroke is important because of the treatment implications; especially since presence of paroxysmal AF may not be picked up in a single 12-lead electrocardiogram (ECG) test. While several trials have shown improved detection of AF with prolonged ECG monitoring, this strategy is associated with relatively high cost, labor intensity, and patient inconvenience, thereby making it challenging to routinely implement in all hospitals. Fortunately, conventional 24-h Holter monitoring and repeated 12-lead ECGs are readily available to detect paroxysmal AF in all hospitals, but is unclear which is the better strategy for evaluating undiagnosed AF. The objective of his study is to conduct a randomized trial of serial 12-lead ECGs vs. 24-hour Holter monitoring in the detection of AF in ischemic stroke patients without known AF. Methods and analysis: We plan to enroll 1200 participants from six hospitals in Taiwan. Patients will be eligible for enrollment if they are admitted for an acute ischemic stroke within 2 days, are ≥65 years of age, and have no known AF by history or on baseline ECG at admission. We will randomly assign participants in a 1:1 ratio to undergo daily 12-lead ECG once daily for 5 days (intervention group) or 24-h Holter monitoring (control group). Primary outcome is newly detected AF on a 12-lead ECG or AF lasting ≥30 s on Holter monitoring. Trial registration number: ClinicalTrials.gov Identifier: NCT02578979.

Purpose The aim is to determine whether serial post-systolic shortening (PSS) using speckle tracking echocardiography (STE) could predict major adverse cardiovascular events (MACE), especially symptom-driven infarct-related artery (IRA) revascularization and improvement in segmental function in post-myocardial infarction patients. Methods/Results Ninety-four patients (average age 61.1 ± 12.5 y, 84 [84.9%] male) with new-onset acute myocardial infarction were enrolled. Serial echocardiography was performed during the initial presentation, and at 3, 6 and 12 months after admission. PSS, strain and systolic strain rate were calculated using STE. Improvement in segmental function was defined as a decrease of ≧1 grade in wall motion score. During the follow-up (29.4 ± 12.7months), 22 patients (23.4%) had MACE and 17 patients had symptom-driven IRA revascularization. In multivariate model, PSS at 3 months was independently predictive for symptom-driven IRA revascularization (Hazard ratio (HR) = 0.5, 95% CI = 0.26–0.97) and for MACE (HR = 0.4, 95% CI = 0.24–0.67) (p < 0.05). Segmental function improvements were found in 255 segments (66.1%) and ROC curve analyses showed that AUC (95% CI) of the initial PSS was 0.7(0.65–0.77) (cut-off values = -1.08, sensitivity = 58%, specificity = 73% specificity). Conclusions Post-systolic shortening at 3 months is an independent predictor for symptom-driven IRA revascularization and MACE. Regional wall motion recovery also could be predicted by initial PSS. Serial assessment of two-dimensional STE should be investigated in post-myocardial infarction patients in the future.

Background: Previous studies reported that patients who had an acute myocardial infarction (AMI) have found that measuring B-type natriuretic peptide (BNP) during the subacute phase of left ventricular (LV) remodeling can predict the possible course of LV remodeling. This study assessed the use of serial BNP serum levels combined with early creatine kinase-MB (CK-MB) to predict the development of significant LV remodeling in AMI patients. Methods: Nighty-seven patients with new onset AMI were assessed using serial echocardiographic studies and serial measurements of BNP levels, both performed on day-2 (BNP1), day-7 (BNP2), day-90 (BNP3), and day-180 (BNP4) after admission. LV remodeling was defined as >20% increase in biplane LV end-diastolic volume on day-180 compared to baseline (day-2). Results: Patients were divided into LV remodeling [LVR(+)] and non LV remodeling [LVR(-)] groups. No first-week BNP level was found to predict remodeling. However, the two groups had significantly different day-90 BNP level (208.1 ± 263.7 pg/ml vs. 82.4 ± 153.7 pg/ml, P = 0.039) and significantly different 3-month BNP decrease ratios ( R BNP13) (14.4 ± 92.2% vs. 69.4 ± 25.9%, P < 0.001). The appropriate cut-off value for R BNP13 was 53.2% (AUC = 0.764, P < 0.001). Early peak CK-MB (cut-off 48.2 ng/ml; AUC = 0.672; P = 0.014) was another independent predictor of remodeling. Additionally, combining peak CK-MB and R BNP13 offered an excellent discrimination for half-year remodeling when assessed by ROC curve (AUC = 0.818, P < 0.001). Conclusion: R BNP13 is a significant independent predictor of 6-month LV remodeling. The early peak CK-MB additionally offered an incremental power to the predictions derived from serial BNP examinations.

The thrombolytic effect of platelet glycoprotein IIb/IIIa inhibitors (GP IIb/IIIa inhibitors) in myocardial infarction has been well established. Nevertheless, data on the mechanism of the cardioprotective effect of GP IIb/IIIa inhibitors in ischemic-reperfusion injury (IR) are lacking. Sprague-Dawley rats received 120 min of coronary ischemia and 180 min of reperfusion. A GP IIb/IIIa inhibitor was given via continuous intravenous infusion at a rate of 2 μg/kg/min 30 min prior to reperfusion with/without inhibitors of PKCe (chelerythrine), PI3 kinase and Akt (wortmannin), p38 MAPK (SB203582), p42/44 MAPK (PD98059) and ERK1/2 (u0126) 15 min prior to the GP IIb/IIIa inhibitor. Protein isolation and analysis were performed by Western blot analysis. The cardioprotective effects were measured as the ratio of myocardial necrotic area to the area at risk (AAR) and the apoptotic index (AI) calculated as the percentage of myocytes positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling of all myocytes stained by 4′, 6-diamidino-2-phenylindole. The GP IIb/IIIa inhibitor reduced the ratio of myocardial necrotic area to AAR and AI, and also exerted an immediate cardioprotective effect by activating multiple signaling pathways including phosphorylation and activation of PKCe, PI3 kinase, Akt, p38 MAPK, p42/44 MAPK and ERK1/2. However, there were no significant increases in the phosphorylation of Raf and MEK1/2. We concluded that the GP IIb/IIIa inhibitor reduced the extent of cardiac IR and significantly ameliorate the apoptosis of myocytes in the rats. In addition, the cardioprotective effect was mediated through the activation of multiple signal transduction pathways.

BACKGROUND Although hepatitis C virus (HCV) is a known risk factor for cardiovascular disease, whether antiviral therapy (AVT) can reduce heart failure (HF) hospitalizations is unknown.Methods and Results:In this population-based cohort study, we used data from the Taiwan National Health Insurance Research Database to evaluate the effect of interferon-based therapy (IBT) on cardiovascular events in patients with chronic HCV infection. Clinical outcomes evaluated included HF hospitalizations; a composite of acute myocardial infarction, ischemic stroke, and peripheral artery disease; all-cause death; and cardiovascular death. Of 83,229 eligible patients with chronic HCV infection, we compared 16,284 patients who received IBT with untreated subjects after propensity score matching. Patients who received IBT were less likely to be hospitalized for HF compared with untreated subjects (incidence density.ID, 0.9 vs. 1.5 events per 103person-years; hazard ratio.HR, 0.58; 95% confidence interval.CI, 0.42-0.79; P=0.001). Compared with untreated subjects, the treated group had significantly lower risk of composite vascular events (ID, 3.7 vs. 5.0 events per 103person-years; P

Objective: Non-alcoholic fatty liver disease (NAFLD) is an established risk factor for diabetes, cardiovascular disease, antiviral treatment resistance, and progression of chronic hepatitis C virus (HCV) infection to fibrosis. Apolipoprotein-B 100 (ApoB-100) is a dyslipidemia marker and steatosis predictor. We assess the correlation between ApoB-100 and hepatosteatosis. Methods: This cross-sectional study enrolled 1,218 HCV-seropositive participants from a 2012-2013 health checkup in Taiwan. NAFLD was detected using ultrasound. All anthropometric and laboratory studies that included ApoB-100 were evaluated whether or not ApoB-100 predicts NAFLD. Logistic regression was also used to examine the association between ApoB-100 and NAFLD. Results: Participants were 47.16 ± 16.08 years old (mean age). The overall prevalence of NAFLD was 35.8% (n = 436; 32.8% men, 38.1% women). Participants with ApoB-100 ≥ 8 had a significantly higher incidence of NAFLD (39.4 vs. 29.4%; 95% CI 0.044-0.156; p < 0.001). After confounding factors had been adjusted for, ApoB-100 was significantly associated with NAFLD (OR 5.45; 95% CI 1.64-18.06; p = 0.006) and high-grade hepatosteatosis (OR 7.73; 95% CI 1.74-34.35; p = 0.007). Conclusion: ApoB-100 is strongly associated with NAFLD in people with non-genotype 3 HCV; greater ApoB-100 content is significantly correlated with higher-grade hepatosteatosis.

Background Estimated glomerular filtration rate (eGFR) is used for diagnosis of chronic kidney disease (CKD). The eGFR models based on serum creatinine or cystatin C are used more in clinical practice. Albuminuria and neck circumference are associated with CKD and may have correlations with eGFR. Aim We explored the correlations and modelling formulates among various indicators such as serum creatinine, cystatin C, albuminuria, and neck circumference for eGFR. Design Cross-sectional study. Methods We reviewed the records of patients with high cardiovascular risk from 2010 to 2011 in Taiwan. 24-hour urine creatinine clearance was used as the standard. We utilized a decision tree to select for variables and adopted a stepwise regression method to generate five models. Model 1 was based on only serum creatinine and was adjusted for age and gender. Model 2 added serum cystatin C, models 3 and 4 added albuminuria and neck circumference, respectively. Model 5 simultaneously added both albuminuria and neck circumference. Results Total 177 patients were recruited in this study. In model 1, the bias was 2.01 and its precision was 14.04. In model 2, the bias was reduced to 1.86 with a precision of 13.48. The bias of model 3 was 1.49 with a precision of 12.89, and the bias for model 4 was 1.74 with a precision of 12.97. In model 5, the bias could be lower to 1.40 with a precision of 12.53. Conclusions In this study, the predicting ability of eGFR was improved after the addition of serum cystatin C compared to serum creatinine alone. The bias was more significantly reduced by the calculation of albuminuria. Furthermore, the model generated by combined albuminuria and neck circumference could provide the best eGFR predictions among these five eGFR models. Neck circumference can be investigated potentially in the further studies.

There are many published articles on the effects of the antithrombolytic function of platelet glycoprotein IIb/IIIa inhibitors (GP IIb/IIIa inhibitors) in myocardial infarction. However, few studies have explored the effects and optimal concentration of tirofibans in diminishing the extent of myocardial reperfusion injury (RI).Rats received 120 minutes of coronary ligation and 180 minutes of reperfusion. The rats were then divided into 7 groups based on the concentration of tirofiban administered intravenously 30 minutes prior to coronary reperfusion to the end of reperfusion. The ratio of myocardial necrotic area to area at risk (AAR), and myocardial malondialdehyde (MDA) and plasma myeloperoxidase (MPO) activities were measured. The apoptotic index (AI) was the percentage of myocytes positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) out of all myocytes stained by 4', 6-diamidino-2-phenylindole (DAPI).The ratio of myocardial necrotic area to AAR significantly decreased in all tirofiban subgroups. The MDA activity for tirofiban concentrations of 2 and 5 ug/kg/minute showed a slight reduction. MPO activity was significantly decreased at a tirofiban concentration of 2 ug/kg/minute. The AI was significantly decreased at a tirofiban concentration of ≥ 0.4 ug/kg/minute.The results indicate that a tirofiban can significantly ameliorate the cardiac RI and myocyte apoptosis in rats.

Background Hepatitis C virus (HCV)-infected patients with chronic kidney disease (CKD) have rarely been studied because they rarely accept interferon-based therapy (IBT) and have been difficult to follow up. We investigated long-term outcomes of IBT on the population. Methods This population-based cohort study used the Taiwan National Health Insurance Research Database as its data source. HCV patients diagnosed with CKD between Jan. 1, 2003, and Dec. 31, 2013, were selected. They were then divided into two groups based on whether they had undergone IBT. All-cause mortality, acute myocardial infarction (AMI), ischemic stroke (IS), hemorrhagic stroke, and new-onset dialysis were evaluated using a Cox proportional hazard regression analysis after propensity score matching. Results We enrolled 9872 HCV patients with CKD: 1684 patients in the treated cohort and 8188 patients in the untreated cohort. The annual incidence of all-cause mortality (19.00 vs. 42.89 events per 1000 person-years; p

Background Evidences support the benefits of moderate- to high-intensity statins for patients with acute myocardial infarction (AMI) except for those with type 2 diabetes mellitus (T2DM) on dialysis after AMI. This study was aimed to investigate the safety and efficacy of secondary prevention of cardiovascular diseases using moderate- to high-intensity statins in T2DM patients on dialysis after AMI. Methods A simulated prospective cohort study was conducted between January 1st, 2001 and December 31st, 2013 utilizing data from the Taiwan National Health Insurance Research Database. A total of 882 patients with T2DM on dialysis after AMI were selected as the study cohort. Cardiovascular efficacy and safety of moderate- to high-intensity statins were evaluated by comparing outcomes of 441 subjects receiving statins after AMI to 441 matched subjects not receiving statins after AMI. The primary composite outcome included cardiovascular death, non-fatal myocardial infarction and non-fatal ischemic stroke. Results The Kaplan–Meier event rate for the primary composite outcomes at 8 years was 30.2% (133 patients) in the statin group compared with 25.2% (111 patients) in the non-statin group (hazard ratio [HR], .98; 95% confidence interval [CI] .76–1.27). Significantly lower risks of non-fatal ischemic stroke (HR, .58; 95% CI .35–.98) and all-cause mortality (HR, .70; 95% CI .59–.84) were found in the statin group. Conclusions In T2DM patients on dialysis after AMI, the use of moderate- to high-intensity statins has neutral effects on composite cardiovascular events but may reduce risks of non-fatal ischemic stroke and all-cause mortality. Electronic supplementary material The online version of this article (doi:10.1186/s13098-017-0272-7) contains supplementary material, which is available to authorized users.

Background and aims Statin is not beneficial for dialysis patients but moderate to high intensity statin is beneficial for patients after acute myocardial infarction (MI). The aim of this study was to evaluate the effect of moderate to high intensity statin on mortality, cardiovascular outcomes in dialysis patients after acute MI. Methods Data on dialysis patients were retrieved from the National Health Insurance Research Database in Taiwan. Dialysis patients admitted for MI were selected and divided into two groups according to statin prescription or not after MI. All-cause mortality and cardiovascular outcomes after a 4-year follow-up were analyzed after propensity score matching (PSM). Results We identified 790 patients who received moderate to high intensity statin therapy and 1788 patients who did not receive any statins after acute MI and clinical outcomes were analyzed after 1:1 PSM. The benefit of statin on mortality therapy appeared from 1 year to the end of the 4-year follow-up period after hospitalization (statin group versus non-statin group: 22.9% vs. 31.1% at 1 year (HR: 0.70; 95% CI: 0.58–0.85); 48.0% vs. 55.1% at the end of the 4 years (HR: 0.76; 95% CI: 0.67–0.88)). In addition, the impact of statin therapy was stronger in patients with shock at admission (p = 0.035). There were no differences in any individual cardiovascular outcome or adverse event. Conclusions Moderate to high intensity statin therapy might lower all-cause mortality in dialysis patients after acute MI, especially those with shock, but not influence cardiovascular outcomes and any adverse events.

Background The tendency for haemorrhagic stroke in patients with chronic HCV infection has emerged recently but the finding may be confounded by comorbidities. Proving the causality between HCV infection and haemorrhagic stroke is mandatory. Our study was designed to investigate the incidence of intracranial haemorrhage in HCV-infected patients with and without treatment. Methods In the 11-year and population-based retrospective study, we acquired data from the Taiwan National Health Insurance Research Database. The patients with major comorbidities were excluded and 97,198 HCV-infected patients were included for analysis. Treated and untreated cohorts were matched with propensity score to make the confounding factors in two groups comparable. Cox proportional hazard regression analysis was performed to evaluate the hazard ratio of haemorrhagic stroke in the cohorts. We applied survival analysis to compare the cumulative incidence of outcome events between the two cohorts. Results After matching, the incidence density (ID) of haemorrhagic stroke in the untreated cohort is significantly higher than in the treated cohort (ID: 1.0 versus 0.6 events per 1,000 person-years; P=0.0014). The adjusted hazard ratio (aHR) of haemorrhagic stroke is significantly reduced in the treated group ( PConclusions The study demonstrates that antiviral therapy significantly reduces the events of intracranial haemorrhage in HCV-infected patients and consolidates the novel concept that chronic HCV infection is a risk factor for haemorrhagic stroke.

Chang-Min Chung,1,2 Hui-Wen Cheng,2 Jung-Jung Chang,2 Yu-Sheng Lin,2 Ju-Feng Hsiao,2 Shih-Tai Chang,1 Jen-Te Hsu2,31School of Traditional Chinese Medicine, College of Medicine, Chang Gung University, 2Division ofCardiology, Chang Gung Memorial Hospital, Chiayi, 3Department ofMedicine, College of Medicine, Chang Gung University, Taoyuan County, TaiwanBackground: Resistant hypertension (RH) is a common clinical condition associated with increased cardiovascular mortality and morbidity in older patients. Several factors and conditions interfering with blood pressure (BP) control, such as excess sodium intake, obesity, diabetes, older age, kidney disease, and certain identifiable causes of hypertension are common in patients resistant to antihypertensive treatment. Arterial stiffness, measured by brachial-ankle pulse wave velocity (baPWV), is increasingly recognized as an important prognostic index and potential therapeutic target in hypertensive patients. The aim of this study was to determine whether there is an association between RH and arterial stiffness. Methods: This study included 1,620patients aged ≥65years who were referred or self-referred to the outpatient hypertension unit located at a single cardiovascular center. They were separated into normotensive, controlled BP, and resistant hypertension groups. Home BP, blood laboratory parameters, echocardiographic studies and baPWV all were measured. Results: The likelihood of diabetes mellitus was significantly greater in the RH group than in the group with controlled BP (odds ratio 2.114, 95% confidence interval [CI] 1.194–3.744, P=0.010). Systolic BP was correlated in the RH group significantly more than in the group with controlled BP (odds ratio 1.032, 95% CI 1.012–1.053, P=0.001). baPWV (odds ratio 1.084, 95% CI 1.016–1.156, P=0.015) was significantly correlated with the presence of RH. The other factors were negatively correlated with the existence of RH.Conclusion: In patients aged ≥65years, the patients with RH have elevated vascular stiffness more than the well controlled hypertension group. baPWV increased with arterial stiffness and was correlated with BP levels. Strict BP control is necessary to prevent severe functional and structural vascular changes in the course of hypertensive disease.Keywords: arterial stiffness, brachial-ankle pulse wave velocity, resistant hypertension

Introduction Arterial stiffness may contribute to left ventricular hypertrophy (LVH). This study was conducted to evaluate the independent factor of LVH and the quantification of LVH by electrocardiogram (ECG) to predict the degree of aortic stiffness using brachial-ankle pulse wave velocity (baPWV) in subjects with hypertension. Materials and Methods A total of 984 consecutive patients who were diagnosed as having essential hypertension were entered into the study. baPWV determination, ECG and blood sampling were performed after a 12-hour overnight fast. LVH was diagnosed using electrocardiography; Romhilt-Estes point score was subsequently calculated. Participants were separated into LVH and non-LVH groups. Additional factors associated with LVH were examined using multivariate analyses. Results The non-LVH groups were younger (P = 0.001), had less men (P = 0.001), lower systolic and diastolic blood pressure and pulse pressure (P 0.001 for each) and lower baPWV (P 0.001). Stepwise multiple logistic regression analysis demonstrated that sex, age, systolic blood pressure and baPWV are independent factors. Using a baPWV value of 1825 cm/sec, the area under the receiver operating characteristic curve was 0.644 and the highest discriminating sensitivity and specificity were 60% and 65%, respectively. Conclusion Aortic stiffness may be related to electrocardiographically determined LVH in patients with hypertension. Thus, stiffening of large arteries, together with increased systolic blood pressure, seems to significantly contribute to the pathogenesis of LVH. Quantification of LVH by ECG can also predict the degree of aortic stiffness.

This study analyzed the corrected QT dispersion (cQTd) before and at 24 hours after successful primary percutaneous coronary intervention (PCI) in 81 patients with single coronary artery disease and acute ST elevation myocardial in-farction. Major cardiovascular events (MACE) at 1 year were defined as death, nonfatal myocardial infarction, life-threatening arrhythmias, and heart failure hospitalization. The cQTd before primary PCI was significantly longer in patients without MACE than in patients with MACE (73.1 ± 29.3 versus 56.3 ± 25.2 msec, P = 0.026). The cQTd at 24 hours after primary PCI was significantly shorter in patients without MACE than in patients with MACE (38.4 ± 20.8 versus 50.8 ± 28.7 msec, P = 0.045). Thus, the absolute cQTd change was significantly higher in patients without MACE compared to patients with MACE (P = 0.001). By multivariate analysis, absolute cQTd change was an independent predictor for the development of MACE, with an odds ratio of 1.498 for each 10-msec decrement in absolute cQTd change (95 percent confidence interval, 1.157 to 1.939, P = 0.002). In conclusion, the absolute cQTd change after primary PCI was an independent predictor of the development of MACE in patients with single vessel disease and acute ST elevation myocardial infarction.

Introduction The association between the arterial stiffness and the severity of left ventricular (LV) diastolic function in hypertension has not been fully evaluated. This study was conducted to evaluate the relationship of aortic stiffness by brachial-ankle pulse wave velocity (baPWV) to parameters reflecting the atherosclerosis and the severity of LV diastolic function in patients with hypertension. Methods LV ejection fraction, the ratio of peak velocity of early rapid filling and peak velocity of atrial filling ( E / A ratio) and LV mass index were determined with echocardiography in 800 patients with hypertension. LV diastolic function was estimated by pulsed-tissue Doppler imaging (TDI) echocardiography, averaging diastolic mitral annular velocity measurements ( Em av , Am av and Em av / Am av ratio) from 2 separate sites (basal septal and lateral). The baPWV was measured by the volume rendering method. Results Stepwise multiple logistic regression analysis demonstrated that the independent factors of LV diastolic function were deceleration time, baPWV, age and Em av / Am av ratio. The receiver- operator characteristic curve demonstrated a baPWV of 1566 cm/sec was useful to discriminate mild LV diastolic dysfunction (sensitivity, 78%; specificity, 78%), and that a baPWV of 1730 cm/sec was useful to discriminate moderate LV diastolic dysfunction (sensitivity, 73%; specificity, 57%). Conclusions Increased baPWV relates not only to the parameters reflecting atherosclerosis but also to those reflecting LV diastolic dysfunction. TDI-detected LV diastolic dysfunction is accompanied by increased aortic stiffness in essential hypertension. Therefore, quantification of aortic stiffness can predict the degree of LV diastolic function.

Accumulated evidence shows that erectile dysfunction (ED) may be a precursor of coronary artery disease (CAD).The purpose of this study was to explore the differences in coronary phenotypes between patients with ED and patients with angina pectoris.The study enrolled 30 ED patients (study group) and 120 age-matched angina patients who had no ED (control group). All patients had angiographically documented CAD.The differences in demographic characteristics, biochemical profiles and coronary characteristics between the study and control groups were compared.Diabetes mellitus (DM) and obesity defined by body mass index were more common in the study group than in the control group. The mean number of lesions and mean number of vessels with evidence of CAD were significantly different between the study and control groups (2.3 ± 0.1 vs. 2.2 ± 0.1, P0.001; 2.0 ± 0.2 vs. 1.8 ± 0.1, P0.001). The distribution of vessel involvement was similar between the groups, except for more common involvement of the ramus in the study group. There were no differences in distribution of lesion sites between the two groups. The control group had a higher percentage of type A stenotic lesions than the study group (16.3% vs. 2.9%, P = 0.004). Significant differences were also observed in type C lesions (52.9% in study group vs. 38.0% in control group, P = 0.026). Fewer calcified, irregular, and bifurcated lesions were present in the study group compared to control.This study documented coronary phenotypes in ED patients without symptomatic CAD. Although the artery size hypothesis and ED had well been thought to be a precursor of CAD, the severity of coronary lesions in these patients was not more benign than that observed in angina pectoris patients who have no ED.

IntroductionThere is growing evidence of a link between erectile dysfunction (ED) and coronary artery disease (CAD).AimsThe purpose of this study was to explore the independent determinants of CAD in ED outpatients.MethodsThis study enrolled 243 patients, ranging in age from 21 to 81 years old, suffering from ED as diagnosed by the International Index of Erectile Function (IIEF) scores. All patients underwent exercise stress tests or thallium-201 single-photon emission computed tomography perfusion imagings. Based on examination results, patients were divided into study (22 patients with a positive finding) and control groups (221 patients with a negative finding).Main Outcome MeasuresThe differences of demographic characteristics, biochemical profiles, pro-inflammatory and inflammatory markers, and echocardiographic characteristics between study and control group were compared.ResultsThe age, presence of DM and current smoking status were significant high in the study group. A significant lower high-density lipoprotein (HDL) cholesterol level, a higher percentage of HDL cholesterol levelConclusionsThis study first shows the independent determinants of CAD in ED outpatients. This novel finding may improve the screening of low-risk ED patients for CAD.

Previous studies have reported a close correlation between low ankle-brachial pressure index (ABPI) and various cardiovascular risk factors. However, despite the well-established potential hazards of consequent coronary artery disease (CAD), no data exist on the relationship between ABPI and the severity of CAD, particularly in patients with diabetes mellitus (DM).A total of 840 patients ranging from 35 to 87 years of age (mean [+/- SD] 63.9+/-10.2 years) with suspected CAD in a clinical practice were enrolled. All patients underwent ABPI measurements and coronary angiography. Patients were divided into four groups according to the results of ABPI measurements and the presence or absence of DM: group A had an ABPI value of at least 0.9 but no DM (A-/D-); group B had an ABPI value of at least 0.9 and DM (A-/D+); group C had an ABPI of less than 0.9 but no DM (A+/D-); and group D had an ABPI value of less than 0.9 and DM (A+/D+).Age was significantly higher in the A+ (groups C and D) than the A- patients (groups A and B). Moreover, men predominated in all four groups. Comparisons of sex distribution among the four groups revealed that group D had the highest percentage of women, while group A had the lowest. Total cholesterol level did not differ among the four groups, although group D tended to have the highest result. Patients in group D had the highest percentages of hypertension, hypercholesterol, hypertriglyceride, low high-density lipoprotein cholesterol and high low-density lipoprotein cholesterol among the four groups. Group D exhibited the highest triglyceride and uric acid levels, the lowest high-density lipoprotein cholesterol level, and the highest metabolic syndrome criteria number and percentage of metabolic syndrome. Furthermore, group D had the highest mean lesion numbers, mean numbers of target vessel involvement, stenoses with type C classification and complex morphology lesions (chronic total occlusion, diffuse or calcified lesions) among the four groups. There were still significant differences in lesion numbers (P0.001) and numbers of target vessel involvement (P0.001) for ABPI predicting CAD severity after controlling for the effects of DM and age. The sensitivity, specificity, positive predictive value and negative predictive value of using an ABPI of less than 0.9 to predict CAD differed significantly between patients with and without DM.ABPI is a useful noninvasive tool for predicting CAD severity, even in patients with DM.

Obesity is a risk factor for all-cause mortality. The obesity incidence depends on different definitions. Among patients with high-risk coronary heart disease (HRCA), we have studied differences in obesity incidence, according to different anthropometric indices.Based on the definitions of the International Guidelines Committees for body mass index (BMI), waist circumference (WCF), and waist-hip ratio (WHR), we have classified 487 CAD patients into 3 groups: normal (group 1), overweight (group 2), and obese patients (group 3). Among men, obesity criteria BMI, WCF and WHR were positive in 17.5%, 14.2%, and 66.4% of the subjects. Among male subjects65 years, the incidence of HRCA (%), for the 3 groups (normal, overweight, obese) were for BMI (2.4, 21.5, 28.9, P = 0.005); WCF (17.9, 12.1, 37.9, P = 0.012); WHR (0, 15.4, 30.4, P = 0.024). In male subjects65 years, for the HRCA incidence (%), only WHR showed a significant difference between the 3 groups (0, 15.4, 30.4, P = 0.024). Among women, 30.6%, 63.6%, and 87.6% were obese by the BMI, WCF, and WHR criteria, respectively. We did not find any significant differences in the HRCA distribution between age groups and degrees of obesity.HRCA distribution varied among obese male patients. According to the different methods of measurement, obesity percentages varied from 4- to 5-fold among men and 3-fold among women. In our view,WHR measurement is the method of choice for the determination of obesity among patients with CAD.

Background: This retrospective study evaluated the feasibility and efficacy of trans-radial intervention for upper arm dialysis access. Methods: This study retrospectively reviewed 165 trans-radial interventions performed for upper arm dialysis access in 101 patients. Sixty-nine patients had arteriovenous graft (AVG), and 32 had arteriovenous fistula (AVF). Balloon angioplasty was performed in 66 stenotic dialysis accesses and 99 thrombosed dialysis accesses. Thrombosed dialysis access was further managed by additional balloon thrombectomy with or without urokinase injection. Results: Procedural time was 46.7 ± 25.5 minutes. Anatomic and clinical success rates were 89.7% and 84.2%, respectively. The rate of complications, most of which involved lesion rupture with contrast-media extravasation and distal embolism, was 9.7%. Pretreatment stenosis was more severe (p = 0.01) and the prevalence of total occlusion was higher (p

This study attempts to compare the risks and benefits of provisional stenting with drug eluting stents and bypass surgery for left main coronary artery (LMCA) stenosis. Recent improvements in interventional technologies have increased interest in percutaneous treatment of LMCA stenosis. However, application of percutaneous techniques to LMCA has been sporadic and controversial. In-hospital and one year outcomes of coronary artery bypass graft (CABG) and percutaneous coronary intervention (PCI) cases were compared. From September, 2003 to June, 2005, a total of 59 consecutive patients with de novo unprotected LMCA stenosis were treated with either CABG or PCI. Twenty patients received non-intravascular ultrasound-guided PCI with a stent in the LMCA. Thirty-nine patients underwent CABG. At 30-day follow-up, the major adverse cardiac and cerebrovascular event (MACE) rates of mortality, myocardial infarction, cerebral vascular accident, and target vessel revascularization were 25.6% in the CABG group and 5% in the PCI group (P = 0.054). At one year follow-up, the MACE rates were 33.3% in the CABG group and 5% in the PCI group. One year MACE for the CABG group significantly differed from that of the PCI group (P = 0.015). The odds ratio (OR) of one year MACE-free survival was 0.75 (P < 0.001) in the CABG group versus the PCI group. Further analysis demonstrated there was a significant difference in in-hospital MACE and one year MACE between the elective CABG group and elective PCI group (P = 0.045). However, there was no significant difference between the emergent CABG group and emergent PCI group (P = 1.000 for in-hospital MACE; P = 0.486 for one year MACE). PCI on unprotected LM offers an alternative option in patients with high surgical risk and appropriate lesion morphology.

Objectives Left ventricular remodeling after acute myocardial infarction increases cardiovascular events and mortality. But few study was done in patients with preserved ejection fraction (EF > 40%). We investigate whether the strain and strain rate by 2D speckle tracking echocardiography could predict left ventricular remodeling after acute myocardial infarction in this cohort. Methods The 83 patients (average age 60.7 ± 12.3 y, 75 [90.4%] male) with new-onset acute myocardial infarction receiving echocardiography immediately, and 6 months after admission were grouped by the presence or absence of left ventricular remodeling. Strain and strain rate including longitudinal, circumferential, and radial direction were calculated. The average of strain and strain rate of which segmental longitudinal strains > – 15% were defined as the injury longitudinal strain (InjLS). Results Left ventricular remodeling occurred in 24 of 83 patients (28.9%). In univariate logistic regression analyses, gender, peak CK-MB, log BNP, use of statin before discharge, wall motion score index, and InjLS were significantly associated with left ventricular remodeling (p < 0.05). In multivariate analysis using the forward stepwise method, gender, CK-MB, and InjLS were independent predictors. The hazard ratio for InjLS was 1.48 (p = 0.04). Receiver operating characteristic curve (ROC) analyses showed the area under the curve (AUC) of InjLS was largest (AUC = 0.75, cut-off value = –11.7%, sensitivity = 81%, specificity = 71%, p < 0.01). In ST-segment elevation myocardial infarction subgroup, InjLS was the only predictor according to ROC analysis (AUC = 0.79, p < 0.01, cut-off value = –11.4%, sensitivity = 88%, specificity = 77%) and multivariate logistic regression analysis (hazard ratio = 1.88, 95% CI: 1.22–2.88, p < 0.01). Conclusions InjLS was an excellent predictor for left ventricular remodeling after acute myocardial infarction in patient with preserved ejection fraction.

Most tumor invasion into the heart is nonspecific and clinically silent. Myocardium metastasis rarely mimics a myocardial infarction. In this case, a cardiac metastasis from a squamous cell carcinoma presented with both persistent ST elevation and paroxysmal supraventricular tachycardia. The secondary lesion was located in the anterior wall and lateral wall of the left ventricle and induced electrocardiographic changes imitating an acute myocardial infarction.