Radiofrequency catheter ablation (RFCA) is a useful treatment for drug-refractory atrial fibrillation. RFCA can cause cerebral infarction that remains the neurologic deficit if prompt managements are delayed. We report on 3 patients who developed cerebral infarctions immediately after RFCA. Periprocedural anticoagulation such as warfarin should be continued for patients, even if they are at low risk for cerebral infarction.
Atrial Fibrillation* ; Catheter Ablation* ; Cerebral Infarction* ; Humans ; Neurologic Manifestations ; Warfarin

No abstract available.
Endarterectomy, Carotid

Benzylideneacetophenone derivative (1E)-1-(4-hydroxy-3-methoxyphenyl) hept-1-en-3-one (JC3) elicited cytotoxic effects on MDA-MB 231 human breast cancer cells-radiation resistant cells (MDA-MB 231-RR), in a dose-dependent manner, with an IC₅₀ value of 6 μM JC3. JC3-mediated apoptosis was confirmed by increase in sub-G1 cell population. JC3 disrupted the mitochondrial membrane potential, and reduced expression of anti-apoptotic B cell lymphoma-2 protein, whereas it increased expression of pro-apoptotic Bcl-2-associated X protein, leading to the cleavage of caspase-9, caspase-3 and poly (ADP-ribose) polymerase. In addition, JC3 activated mitogen-activated protein kinases, and specific inhibitors of these kinases abrogated the JC3-induced increase in apoptotic bodies. JC3 increased the level of intracellular reactive oxygen species and enhanced oxidative macromolecular damage via lipid peroxidation, protein carbonylation, and DNA strand breakage. Considering these findings, JC3 is an effective therapy against radiation-resistant human breast cancer cells.
Apoptosis* ; bcl-2-Associated X Protein ; Breast Neoplasms* ; Breast* ; Caspase 3 ; Caspase 9 ; Chalcone* ; DNA ; Extracellular Vesicles ; Humans* ; Lipid Peroxidation ; Membrane Potential, Mitochondrial ; Mitogen-Activated Protein Kinases ; Oxidative Stress* ; Phosphotransferases ; Protein Carbonylation ; Reactive Oxygen Species

BACKGROUND: To estimate and compare the trends of all-cause and cause-specific mortality rates for subjects with and without diabetes in South Korea, from 2003 to 2013. METHODS: Using a population-based cohort (2003 to 2013), we evaluated annual mortality rates in adults (≥30 years) with and without diabetes. The number of subjects in this analysis ranged from 585,795 in 2003 to 670,020 in 2013. RESULTS: Age- and sex-adjusted all-cause mortality rates decreased consistently in both groups from 2003 to 2013 (from 14.4 to 9.3/1,000 persons in subjects with diabetes and from 7.9 to 4.4/1,000 persons in those without diabetes). The difference in mortality rates between groups also decreased (6.61 per 1,000 persons in 2003 to 4.98 per 1,000 persons in 2013). The slope associated with the mortality rate exhibited a steeper decrease in subjects with diabetes than those without diabetes (regression coefficients of time: −0.50 and −0.33, respectively; P=0.004). In subjects with diabetes, the mortality rate from cardiovascular disease decreased by 53.5% (from 2.73 to 1.27 per 1,000 persons, P for trend < 0.001). Notably, the decrease in mortality from ischemic stroke (79.2%, from 1.20 to 0.25 per 1,000 persowns) was more profound than that from ischemic heart disease (28.3%, from 0.60 to 0.43 per 1,000 persons). CONCLUSION: All-cause and cardiovascular mortality rates decreased substantially from 2003 to 2013, and the decline in ischemic stroke mortality mainly contributed to the decreased cardiovascular mortality in Korean people with diabetes.
Adult* ; Cardiovascular Diseases ; Cohort Studies ; Diabetes Mellitus* ; Humans ; Korea* ; Mortality* ; Myocardial Ischemia ; Stroke

BACKGROUND AND PURPOSE: To compare the efficacy and safety of antiplatelet agents for the secondary prevention of ischemic stroke based on cytochrome P450 2C19 (CYP2C19) polymorphisms. METHODS: This study was a prospective, multicenter, randomized, parallel-group, open-label, blind genotype trial. First time non-cardiogenic ischemic stroke patients were enrolled and screened within 30 days. Participants were randomized to receive either triflusal or clopidogrel for secondary stroke prevention. The primary outcome was the time from randomization to first recurrent ischemic stroke or hemorrhagic stroke. RESULTS: The required sample size was 1,080 but only 784 (73%) participants were recruited. In patients with a poor CYP2C19 genotype for clopidogrel metabolism (n=484), the risk of recurrent stroke among those who received triflusal treatment was 2.9% per year, which was not significantly different from those who received clopidogrel treatment (2.2% per year; hazard ratio [HR], 1.23; 95% confidence interval [CI], 0.60–2.53). In the clopidogrel treatment group (n=393), 38% had good genotypes and 62% poor genotypes for clopidogrel metabolism. The risk of recurrent stroke in patients with a good CYP2C19 genotype was 1.6% per year, which was not significantly different from those with a poor genotype (2.2% per year; HR, 0.69; 95% CI, 0.26–1.79). CONCLUSIONS: Whilst there were no significant differences between the treatment groups in the rates of stroke recurrence, major vascular events, or coronary revascularization, the efficacy of antiplatelet agents for the secondary prevention of stroke according to CYP2C19 genotype status remains unclear.
Cytochrome P-450 CYP2C19 ; Cytochrome P-450 Enzyme System* ; Cytochromes* ; Genotype ; Humans ; Metabolism ; Platelet Aggregation Inhibitors ; Prospective Studies ; Random Allocation ; Recurrence ; Sample Size ; Secondary Prevention* ; Stroke*