on behalf of the J-RHYTHM Registry Investigators* Background--To clarify the influence of hypertension and blood pressure (BP) control on thromboembolism and major hemorrhage in patients with nonvalvular atrial fibrillation, a post hoc analysis of the J-RHYTHM Registry was performed.

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ACE (angiotensin converting enzyme) gene genotypes have been shown to be a risk factor for development of left ventricular hypertrophy and cardiomyopathy, upon the assumption that the DD genotype is linked to higher cellular ACE activity leading to myocardial fibrosis. To test an analogous hypothesis that the DD genotype favors myocardial fibrosis in the atrium and thus promotes atrial fibrillation without any structural heart diseases, we determined the distribution of the ACE gene genotypes in 77 patients with lone atrial fibrillation and investigated the effects of the ACE genotypes on the clinical characteristics of atrial fibrillation. The distribution of ACE genotypes was not significantly different between the patients and healthy volunteers. Also, the ACE gene genotypes did not affect the types of atrial fibrillation and the age at the onset of atrial fibrillation. Thus, these results refuted the hypothesis of possible relationships between ACE genotypes and lone atrial fibrillation through myocardial fibrosis, and indicated some unknown differences between the atrium and ventricle.

SUMMARYAn asymptomatic 35 year-old man was referred to our hospital because of abnormal ECG findings. The ECG showed complete right bundle branch block and left anterior hemiblock. Echocardiography revealed a moderately enlarged right ventricle (RV) and an apical aneurysm. RV wall motion showed diffusely moderate impairment, while the systolic function of the left ventricle (LV) was slightly decreased. The ejection fractions (EF) of the RV and LV were calculated as 28.1% and 41.9% by Simpson's method using multiple cardiac computed tomography (CT) scans. A 24 hour ambulatory ECG showed only 372 single premature ventricular contractions (PVC). Cardiac catheterizaion revealed that the RV was enlarged with prominent trabeculation and decreased motion. In an electrophysiologic study, neither electrical stimulation of the RV nor electrical stimulation plus isoproterenol infusion could induce ventricular tachycardia. Pathological examination of a biopsy from the interventricular septum of the RV revealed fibrofatty change in the myocardium. Based on these results, we made a diagnosis of arrhythmogenic right ventriclular cardiomyopathy (ARVC) and administered 5 mg of carvedilol. Sixty days after the initiation of carvedilol therapy, we performed repeat cardiac CT. The EF of the LV was markedly improved from 41.9% to 62.0%, although the EF of the RV was not changed. The number of PVCs showed no change. This case suggests that carvedilol is not only useful for controlling arrhythmia but also for improving left ventriclular function in some patients with ARVC. Sympathetic overactivity is reported to cause sudden death, so carvedilol may be a first-line drug for some patients with ARVC. (Jpn Heart J 2004; 45: 169-177)