In our hemodialysis patients, AF was a common comorbidity and was independently associated with all-cause death and major bleeding, but not with increased risk of ischemic stroke.

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SUMMARYRelative increases in unsaturated fatty acids (USFA) in the diet are considered to exert beneficial effects on coronary risk factors (CRF). However, detailed analysis of the relationships between serum USFA and CRF are scanty and there is no report of the relationship between nervonic acid (NA) and CRF. The objective of the present study was to analyze the relationships between serum USFA and CRF.Body height and weight, blood pressure, fasting serum total cholesterol (TC), triacylglycerol (TG), HDL cholesterol (HDLc), fasting blood sugar (FBS), total fatty acid composition, leptin, and high-sensitivity C-reactive protein (CRP) were measured in 31 men (age, 41-78 years) and 11 women (age, 54-77 years). The relationships between serum USFA, and body mass index (BMI), leptin, systolic blood pressure (SBP), diastolic blood pressure (DBP), TC, TG, HDLc, FBS, and CRP were analyzed using multiple regression analysis. The final results were summarized using coronary risk factor scores (CRFS) in order to assess the correlations between USFA with CRF.Oleic acid (OA), linoleic acid (LA), and eicosapentaenoic acid (EPA) were positively related to coronary risk factors (total CRFS = 2, 3, and 4, respectively), while nervonic acid (NA) exerted negative effects on these risk factors (total CRFS = −6 ). It is concluded NA may have preventive effects on obesity-related metabolic disorders. (Int Heart J 2005; 46: 975-985)

SUMMARYThe relation between n-3 polyunsaturated fatty acid (PUFA) and nonfatal myocardial infarction is still controversial.A multicenter case-control pilot study on n-3 PUFA as a negative risk factor for myocardial infarction was performed in Niigata prefecture. Seventy-three patients with acute myocardial infarction (AMI) and age and gender matched controls (n = 84) were recruited. Serum leptin levels were significantly higher in patients with AMI than the controls (8.1 ± 6.7 ng/mL versus 5.8 ± 3.7 ng/mL, P < 0.01), and serum high-density lipoprotein cholesterol (HDLc) levels were significantly lower in patients with AMI than the controls (46 ± 10.5 mg/dL versus 60 ± 15 mg/dL, P < 0.00001). Statistically significant differences were preserved in leptin and HDLc when the data were analyzed separately by gender. Serum levels (%weight) of linolenic acid (C18:3:n3), eicosapentaenoic acid (C20:5:n3), docosapentaenoic acid (C22:5:n3), and total n-3 PUFA were significantly lower in patients with AMI than the control group (P < 0.000001, < 0.05, < 0.05, < 0.05, respectively). The serum n-3 PUFA/saturated fatty acid (SF) ratio and n-3 PUFA/n-9 monounsaturated fatty acid (MUFA) ratio were significantly lower in patients with AMI than the controls (P < 0.05 and < 0.01, respectively). When the subjects were separated into two categories according to an n-3/n-6 PUFA ratio below 0.3 or above 0.3, patients with AMI were more frequently in the former while the controls were more frequently in the latter (P < 0.05).N-3 PUFA may be a negative risk factor for AMI. The results suggest leptin is a risk factor for AMI irrespective of ethnicity and gender. (Int Heart J 2005; 46: 583-591)

Hyperthyroidism is associated with low exercise tolerance despite high cardiac output and sometimes with the development of heart failure. L-type calcium channels may play a role in the mechanism, but this has not been fully understood. We examined the effects of thyroid hormone on gene expression and function of L-type calcium channels in rat ventricles by the ribonuclease protection assay and whole-cell patch-clamp technique, respectively. The effects of bisoprolol, beta-blocking agent, on the regulation of calcium channel by thyroid hormone was also studied. In hyperthyroid animals, the mRNA of the calcium channel alpha1c subunit was reduced on day 4, compared with that in euthyroid animals, and remained low on day 8. Bisoprolol did not affect the thyroid hormone mediated decrease in alpha1c subunit mRNA. While L-type calcium current was greater in hyperthyroid than euthyroid myocytes on day 4, it was smaller on day 8. In addition, the isoproterenol-induced increase in calcium current in euthyroid rats was attenuated in hyperthyroid rats. Acetylcholine decreased calcium current in hyperthyroid myocytes, but not in euthyroid myocytes. In conclusion, L-type calcium current was increased by thyroid hormone in rat ventricular myocytes by the activation of the adenylate cyclase cascade, despite a decreased calcium channel gene expression. These genomic and non-genomic modifications may play an important role in the association of high cardiac output with low exercise tolerance, and in the development of heart failure in hyperthyroidism.