Atrial natriuretic peptide (ANP) suppresses acute atrial electrical remodeling in the canine rapid atrial stimulation model.

OBJECTIVES: Atrial electrical remodeling is considered to play an important role in the appearance of atrial fibrillation. The effect of atrial natriuretic peptide (ANP) on atrial electrical remodeling was evaluated in a canine atrial stimulation model. METHODS: In 15 beagle dogs, electrodes for pacing and recording were fixed on the atrial surface. In 10/15 dogs, rapid atrial stimulation (400 bpm) was performed for 7 h at the right atrial appendage (RAA) and the remaining 5 were used as the sham without rapid pacing. In 5/10 dogs with rapid pacing, human atrial natriuretic peptide (ANP) was infused (1.0 microg/kg/min). The effective refractory period (ERP) and the monophasic action potential duration (MAP) were evaluated at 0, 3, and 7 h after rapid pacing. The expression levels of mRNAs of ion channels or transporters were evaluated from the atrial samples of sham and after a 7 hour pacing. RESULTS: In the control group with rapid pacing (n=5), the atrial ERP and MAP duration were shortened at all atrial sites, e.g., ERP from 148+/-14 ms to 109+/-8 ms at RAA, P=0.006. In contrast in the ANP group, neither the ERP nor MAP duration showed a significant shortening and the effect of ANP on hemodynamic parameter was relatively small. Expression levels of the mRNA were not significantly different between the control and ANP groups. CONCLUSIONS: Administration of ANP prevented the shortening of the ERP and MAP duration in the rapid atrial stimulation model. The effect of ANP on atrial electrical remodeling was considered to be due to its direct action on the myocardium.

A young girl with vasospastic angina associated with mutation in endothelial nitric oxide synthase gene--a case report.

A 13-year-old girl was successfully recuperated from cardiopulmonary arrest shortly after running 80 m in a competition. The electrocardiogram, echocardiogram and 123I-MIBG myocardial scintigraphic imaging indicated myocardial ischemia in the anteroseptal wall of the left ventricle. Coronary angiography during the recovery phase revealed no stenotic lesions, and spasms of the left anterior descending artery and the left circumflex artery could be provoked by acetylcholine. The endothelial nitric oxide synthase gene abnormality associated with coronary spasms was examined. The patient had the T-786 --> C, A-922 --> G, and T-1468 --> A mutations in the 5'-flanking region on one allele of the endothelial nitric oxide synthase gene. To the authors' knowledge, she represents the first case of life-threatening coronary spasms in childhood associated with mutations in the endothelial nitric oxide synthase gene.