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Cardiac remodeling is common in the athletes. Little data is available regarding the cardiac remodeling on the recently proposed 4 sport disciplines among the elite university athletes.A total of 7639 athletes participated in the 2017 Taipei Summer Universiade. Cardiac evaluation via history, ECG, and echocardiography were performed in 826 athletes who signed up for Check Up Your Heart. Athletes were grouped into one of 4 sport disciplines Skill, Power, Mixed, and Endurance.After excluding 66 participants with missing demographic data, 13 missing echocardiographic data, and 24 inadequate echocardiographic images, a total number of 723 university athletes (mean age 23 ± 3 years, 419 males) from 99 countries engaging in 25 different sporting events were analyzed. Electrocardiograms showed that Endurance group had a slower heart rate and higher percentage of left ventricular (LV) hypertrophy (39%). Echocardiograms showed there were significant differences in LV mass index (P < .001), LV geometry (P < .001), left atrial (LA) dilatation (P = .026), right ventricular (RV) dilatation (P < .001), right atrial (RA) dilatation (P < .0001), and tricuspid annular plane systolic excurse (P = .006). LV ejection fraction, LV strain, RV strain, and LV diastolic function showed no difference in 4 sport disciplines.Eccentric LV hypertrophy was the most common type of cardiac remodeling in the university athletes participated in 2017 Taipei Summer Universiade. Adaptive changes in chamber size were more commonly seen in Endurance sport. RA dilatation was the most sensitive to hemodynamic demand, followed by RV dilatation, LA dilatation, and LV dilatation.

Acute statin therapy reduces myocardial ischemia/reperfusion (IR) injury-induced ventricular fibrillation (VF), but the underlying electrophysiological mechanisms remain unclear. This study sought to investigate the antiarrhythmic effects of a single bolus rosuvastatin injection in failing rabbit hearts with IR injury and to unveil the underlying molecular mechanisms. Rabbits were divided into rosuvastatin, rosuvastatin + L-NAME, control, and L-NAME groups. Intravenous bolus rosuvastatin (0.5 mg/kg) and/or L-NAME (10 mg/kg) injections were administered 1 hour and 15 minutes before surgery, respectively. Heart failure was induced using rapid ventricular pacing. Under general anesthesia with isoflurane, an IR model was created by coronary artery ligation for 30 minutes, followed by reperfusion for 15 minutes. Plasma NO end product levels were measured during IR. Then, hearts were excised and Langendorff-perfused for optical mapping studies. Cardiac tissues were sampled for Western blot analysis. Rosuvastatin increased plasma NO levels during IR, which was abrogated by L-NAME. Spontaneous VF during IR was suppressed by rosuvastatin (P < 0.001). Intracellular calcium (Cai) decay and conduction velocity were significantly slower in the IR zone. Rosuvastatin accelerated Cai decay, ameliorated conduction inhomogeneity, and reduced the inducibility of spatially discordant alternans and VF significantly. Western blots revealed significantly higher expression of enhancing endothelial NO-synthase and phosphorylated enhancing endothelial NO-synthase proteins in the Rosuvastatin group. Furthermore, SERCA2a, phosphorylated connexin43, and phosphorylated phospholamban were downregulated in the IR zone, which was attenuated or reversed by rosuvastatin. Acute rosuvastatin therapy before ischemia reduced IR-induced VF by improving SERCA2a function and ameliorating conduction disturbance in the IR zone.

Calcium homeostasis plays an important role in development of early afterdepolarizations (EADs) and torsade de pointes (TdP). The role of sodium-calcium exchanger (NCX) inhibition in genesis of secondary Ca rise and EAD-TdP is still debated. Dual voltage and intracellular Ca optical mapping were conducted in 6 control and 9 failing rabbit hearts. After baseline electrophysiological and optical mapping studies, E4031 was given to simulate long QT syndrome. ORM-10103 was then administrated to examine the electrophysiological effects on EAD-TdP development. E4031 enhanced secondary Ca rise, EADs development, and TdP inducibility in both control and failing hearts. The results showed that ORM-10103 reduced premature ventricular beats but was unable to suppress the inducibility of TdP or EADs. The electrophysiological effects of ORM-10103 included prolongation of action potential duration (APD) and increased APD heterogeneity in failing hearts. ORM-10103 had a neutral effect on the amplitude of secondary Cai rise in control and heart failure groups. In this model, most EADs generated from long-short APD junction area. In conclusion, highly selective NCX inhibition with ORM-10103 reduced premature ventricular beat burden but was unable to suppress secondary Ca rise, EADs development, or inducibility of TdP. The possible electrophysiological mechanisms include APD prolongation and increased APD heterogeneity.

Peripartum cardiomyopathy (PPCM) is the development of heart failure during late pregnancy to months postpartum with potential fatal outcome. However, the disease is not well-studied in Asia.We aimed to investigate the epidemiology and clinical outcomes of PPCM in Taiwan.Electronic medical records were retrieved from Taiwan National Health Insurance Research Database from 1997 to 2011. Patients with PPCM were separated into 3 groups based on the timing of diagnosis. Early: PPCM diagnosed first to ninth month of pregnancy. Traditional: PPCM diagnosed last month of pregnancy till fifth month post-delivery. Late: PPCM diagnosed sixth to twelfth month post-delivery. Primary outcomes defined as cardiac death, all-cause mortality, and major adverse cardiovascular events (MACE) within 1 year.A total of 3,506,081 deliveries during 1997 to 2011 were retrieved and 925 patients with PPCM were identified. Overall incidence of PPCM was 1:3,790 during the 15 years. Early, Traditional, and Late group each had 88, 742, and 95 patients. Cardiac death occurred in 31 patients, all-cause mortality in 72 patients, and MACE in 65 patients. Late group had 2- to 3-fold event rates in cardiac death, all-cause mortality, and MACE compared with Early and Traditional groups. Cumulative incidence showed significant differences for cardiac death (P = .0011), all-cause mortality (P = .0031), and MACE (P = .0014) among 3 groups. Multivariate Cox model showed Late group had significantly worse outcomes after adjusted for clinical variables compared with 2 other groups.Our study is the largest national cohort among Asian countries that showed timing of diagnosis of PPCM had different outcomes. Late diagnosis portended significantly increased morbidity and mortality, even after adjusted for clinical variables.

Early type 2 diabetes mellitus (DM) may only require lifestyle modifications for glycemic control without the need for oral hypoglycemic agents (OHAs). Metformin is believed to improve cardiovascular outcomes in patients with DM, and it is considered to be a first-line therapy. However, it is unclear whether metformin is beneficial for patients with a new diagnosis of DM compared to those who do not need OHAs for glycemic control.Data were obtained from a population-based health care database in Taiwan. Patients with a new diagnosis of DM were enrolled if they received metformin monotherapy only between 1999 and 2010. A 4:1 propensity score-matched cohort of patients with a new diagnosis of DM who did not take OHAs or insulin during follow-up was also enrolled. The primary study endpoint was the occurrence of major adverse cardiovascular events (MACEs). The time to the endpoints was compared between groups using Cox proportional hazards models.A total of 474,410 patients with DM were enrolled. During a mean 5.8 years of follow-up, the incidence of MACEs was 1.072% (1072 per 100,000 person-years) in the metformin monotherapy group versus 1.165% in the lifestyle modification group (those who did not take OHAs) (P < .001). After adjusting for confounders, metformin independently protected the DM patients from MACEs (hazard ratio: 0.83, P < .001). The metformin group also had an improved MACE-free survival profile from year 1 to year 12 (P < .001).In addition to lifestyle modifications, the patients with a new diagnosis of DM treated with metformin monotherapy had a lower MACE rate than those who did not take OHAs. Our findings suggest that metformin may be given early to patients with a new diagnosis of DM, even when they do not need OHAs for glycemic control.

Peripartum cardiomyopathy (PPCM), often classified as a form of dilated cardiomyopathy (DCM), is the myocardial dysfunction that occurs in late pregnancy and through the first few postpartum months.The aim of this study is to investigate the differences in the clinical outcomes of PPCM and DCM.Electronic medical records from 1997 to 2011 were retrieved from the Taiwan National Health Insurance Research Database. Patients with PPCM were compared with age- and clinical characteristics-matched patients with DCM. Primary outcomes were 1- and 3-year heart failure (HF) readmission, cardiac death, all-cause mortality, and major adverse cardiovascular events. Secondary outcomes were myocardial infarction, new onset of dialysis, heart transplant, and cerebrovascular accident. Follow-up period was divided into "within the first year" and "after the first year."A total of 527,979 patients (253,166 females) were hospitalized with a principal diagnosis of HF during 1997 to 2011 period. After excluding patients aged <18 and >50 years, patients with other forms of HF, and those with a history of cerebrovascular accidents or coronary artery disease, 797 patients with PPCM and 1267 patients with DCM were evaluated. Propensity score matching yielded 391 patients in each group. Patients with DCM had a significantly worse prognosis compared to those with PPCM for all primary and secondary outcomes at the 1- and 3-year follow-ups. After 1 year, the HF readmission rate did not significantly differ between the 2 diseases, suggesting that HF medications should be aggressively instituted in patients with PPCM.This is the first study to directly compare the clinical outcomes between age-matched patients with PPCM and DCM. Patients with PPCM had a significantly better prognosis across all cardiovascular endpoints compared to patients with DCM.

The cerebrovascular safety and efficacy of sitagliptin, a dipeptidyl peptidase-4 inhibitor, in patients with type 2 diabetes mellitus (T2DM) with ischemic stroke remains uncertain. The aim of this study was to assess the efficacy and safety of sitagliptin in patients with T2DM with recent ischemic stroke. We analyzed data from the Taiwan National Health Insurance Research Database between March 1, 2009, and December 31, 2011. Ischemic stroke patients were identified from individuals with T2DM. Patients who received sitagliptin were compared with those who did not to evaluate the cardiovascular safety and efficacy of sitagliptin. The primary outcome was a composite of ischemic stroke, myocardial infarction, or cardiovascular death. A total of 5145 type 2 diabetic patients with ischemic stroke met our inclusion criteria and were followed for up to 2.83 years (mean, 1.17 years). Overall, 1715 patients (33.3%) received sitagliptin and 3430 patients (66.7%) did not. The primary composite outcome occurred in 190 patients in the sitagliptin group (11.1%) and in 370 patients in the comparison group (10.8%) (hazard ratio [HR] = 1.02; 95% confidence interval [CI], 0.85-1.21). Patients treated with sitagliptin had a similar risk of ischemic stroke, hemorrhagic stroke, and all-cause mortality with an HR of 0.95 (95% CI, 0.78-1.16, P = 0.612), 1.07 (95% CI, 0.55-2.11, P = 0.834), and 1.00 (95% CI, 0.82-1.22, P = 0.989), respectively, compared with patients not treated with sitagliptin. Treatment with sitagliptin in type 2 diabetic patients with recent ischemic stroke was not associated with increased or decreased risks of adverse cerebrovascular outcomes.