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We previously reported that administration of fish oil rich in docosahexaenoic acid (DHA) increased the plasma ratio of epinephrine to norepinephrine (NE) at rest in young adults who were under chronic stress and that this effect was achieved mainly through depression of NE. However, not many reports have documented the effects of eicosapentaenoic acid (EPA) and DHA on blood catecholamine levels in healthy humans. Therefore, we performed another intervention study to test their effect on catecholamines with healthy subjects under no chronic stress.Twenty-one healthy young adults (15 men and 6 women) were randomly assigned to an omega-3 group (n = 9) or a control group (n = 12) in a double-blind manner. Twenty capsules of shellfish-derived lipids containing 762 mg of EPA plus DHA per day were administered to the omega-3 group for 2 mo. The controls took the same amount of placebo capsules. Fasting blood samples after a 30-min rest with a catheter in a forearm vein were obtained at the start and the end of the study for catecholamine measurements.EPA but not DHA concentrations in red blood cells significantly increased in the omega-3 group compared with the control group (P0.001). Plasma NE concentrations were significantly decreased in the omega-3 group (from 1.49 +/- 0.39 nmol/L to 1.05 +/- 0.14 nmol/L) compared with the control group (from 1.12 +/- 0.24 nmol/L to 1.39 +/- 0.32 nmol/L) with analysis of covariance (P0.001). The differences remained significant (P = 0.01) even after deletion of three subjects in the omega-3 group who had the highest baseline NE values and one in the control group who had the lowest baseline NE value to nullify a significant baseline differences in NE between groups.This study demonstrated that EPA plus DHA supplementation lowered plasma NE concentrations in normal volunteers even at the small dose of 762 mg of EPA plus DHA per day. This effect of EPA plus DHA to lower plasma NE concentrations may be important to understand some of the effects of fish oils on diseases.

BACKGROUND: Patients with inherited dilated cardiomyopathy (DCM) frequently die with severe heart failure (HF) or die suddenly with arrhythmias, although these symptoms are not always observed at birth. It remains unclear how and when HF and arrhythmogenic changes develop in these DCM mutation carriers. In order to address this issue, properties of the myocardium and underlying gene expressions were studied using a knock-in mouse model of human inherited DCM caused by a deletion mutation ΔK210 in cardiac troponinT. METHODOLOGY/PRINCIPAL FINDINGS: By 1 month, DCM mice had already enlarged hearts, but showed no symptoms of HF and a much lower mortality than at 2 months or later. At around 2 months, some would die suddenly with no clear symptoms of HF, whereas at 3 months, many of the survivors showed evident symptoms of HF. In isolated left ventricular myocardium (LV) from 2 month-mice, spontaneous activity frequently occurred and action potential duration (APD) was prolonged. Transient outward (I(to)) and ultrarapid delayed rectifier K(+) (I(Kur)) currents were significantly reduced in DCM myocytes. Correspondingly, down-regulation of Kv4.2, Kv1.5 and KChIP2 was evident in mRNA and protein levels. In LVs at 3-months, more frequent spontaneous activity, greater prolongation of APD and further down-regulation in above K(+) channels were observed. At 1 month, in contrast, infrequent spontaneous activity and down-regulation of Kv4.2, but not Kv1.5 or KChIP2, were observed. CONCLUSIONS/SIGNIFICANCE: Our results suggest that at least three steps of electrical remodeling occur in the hearts of DCM model mice, and that the combined down-regulation of Kv4.2, Kv1.5 and KChIP2 prior to the onset of HF may play an important role in the premature sudden death in this DCM model. DCM mice at 1 month or before, on the contrary, are associated with low risk of death in spite of inborn disorder and enlarged heart.

A 14 year-old boy was admitted for evaluation of recurrent syncope. His ECG on admission revealed a sinus rhythm with an undetermined QRS axis, T wave inversion in leads V3, V4 and abnormal q leads I, aVL, V5 and V6. However, no underlying disease could be detected by any morphological examination. Programmed ventricular stimulation also induced no ventricular tachycardia or fibrillation (VF). Only signal-averaged ECG showed ventricular late potential and the cause of syncope was not clarified. As his brother with similar ECG had died suddenly, he was prophylactically treated with an ICD. However, 14 month later he died suddenly after playing a video game. The ICD recorded VF, which was not converted despite 6 cardioversion attempts by the ICD with 30 J. Progression of myocardial damages and/or elevation of defibrillation threshold may have been the cause of unsuccessful cardioversion.

We have observed 3 cases of Brugada like ECG findings after the resection of esophageal cancer. Case 1. A 63 years-old male who had atrial fibrillation (AF) was diagnosed as affected byesophageal cancer and underwent the resection of esophagus with subsequent reconstruction using stomach into retro-sternum. Post-operative ECG showed coved type ST elevation in lead V1-4. This finally gradually reverted in ten days after operation and normalized within 2 weeks. Case 2. A 69 year-old male, who had paroxysmal AF and esophageal cancer, received the same procedure as in case 1. His ECG revealed abnormal ST elevation in V1. In thoracic CT image, right ventricle (RV) was compressed by the reconstructed stomach. Case 3. A 68 year-old male underwent the same operation as described above. His post-operative ECG showed Brugada like ST elevation in V1-3. This ST change disappeared within 3 weeks. In none of these 3 cases, there was a family history of sudden death or syncope, and the previous ECG showed no ST segment elevation. The compression of the RV by lifted stomach was considered to induce the precordial ST elevation mimicking Brugada syndrome.