Background-The ionic basis of acquired QT prolongation and torsade de pointes (TdP) unrelated to drugs is not fully understood. Methods and Results-We created a rabbit model with chronic complete atrioventricular block (AVB) (nϭ34), which showed prominent QT prolongation (by 120%), high incidence of spontaneous TdP (71%), and cardiac hypertrophy. Patch-clamp experiments were performed in left ventricular myocytes from 9 rabbits (8 with TdP, 1 without TdP) at Ϸ21 days of AVB and from 8 sham-operated controls with sinus rhythm. Action potential duration was prolonged in AVB myocytes compared with control (ϩ61% at 0.5 Hz, ϩ21% at 3 Hz). Both rapidly and slowly activating components of the delayed rectifier K ϩ current (I Kr and I Ks ) in AVB myocytes were significantly smaller than in control by 50% and 55%, respectively. There was no significant difference in Ca 2ϩ -independent transient outward current (I to1 ). L-type Ca 2ϩ current (I Ca,L ) in control and AVB myocytes was similar in peak amplitude, but the half voltage for activation was shifted to the negative direction (5.9 mV) in AVB myocytes. Voltage dependence of I Ca,L inactivation was not different in control and AVB myocytes. The inward rectifier K ϩ current (I K1 ) significantly increased in AVB myocytes compared with control. Conclusions-In the rabbit, chronic AVB leads to prominent QT prolongation and high incidence of spontaneous TdP. Downregulation of both I Kr and I Ks in association with altered I Ca,L activation kinetics may underlie the arrhythmogenic ventricular remodeling.

, and Itsuo Kodama. Ca v3.2 subunit underlies the functional T-type Ca 2ϩ channel in murine hearts during the embryonic period.

On-pump beating-heart coronary artery bypass grafting is the preferred method of emergency myocardial revascularization for patients with acute myocardial infarction who might tolerate cardioplegic arrest poorly. It has lower postoperative mortality and morbidity than conventional coronary artery bypass grafting.

Abstract. Re-expression of fetal genes has been considered to underlie ionic remodeling in diseased heart. T-type Ca 2+ channels have been reported to be functionally expressed in embryonic hearts. In this review, we summarize developmental changes of T-type Ca 2+ channels in mouse ventricles from 9.5 days postcoitum (dpc) to adulthood, using patch clamp and quantitative PCR. In addition, we introduced T-type Ca 2+ channel expression in hypertrophied ventricles caused by myocardial infarction (MI) and aortic banding (AOB). Substantial T-type Ca 2+ channel current was recorded at both 9.5 and 18 dpc. The currents were inhibited by Ni 2+ at low concentrations. The current was not detectable in the adult stage. Ca v 3.2 (α 1H ) mRNA is expressed dominantly at both 9.5 and 18 dpc. Ca v 3.1 (α 1G ) increases from 9.5 to 18 dpc, but remains at low level compared with Ca v 3.2. In contrast, Ca v 3.1 is greater than Ca v 3.2 at the adult stage. In MI, Ca v 3.1 mRNA correlates negatively with brain natriuretic peptide (BNP) mRNA, whereas Ca v 3.2 mRNA correlates positively with BNP mRNA. In AOB, these correlations are weak. We also analyzed the neuron-restrictive silencer factor (NRSF) in these hearts because it is the suppressor of transcription of the fetal cardiac gene program. The negative correlation between NRSF and BNP was stronger in MI than in AOB. Our findings show that Ca v 3.2 underlies the functional T-type Ca 2+ channel in embryonic heart and suggest that NRSF may regulate Ca v 3.2 expression in diseased hearts.

Complete implementation of simple multidisciplinary prevention measures as a bundle can greatly decrease the incidence of DSWI.

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A 51-year-old man who had been suffering from depression stabbed himself in the chest with an ice pick. At presentation, an ice pick lodged in the left fifth intercostal space was moving synchronously with his heartbeat. Echocardiography revealed that the tip was penetrating the anterior wall of the right ventricle. Because the patient was tamponading, an emergency operation was carried out. The ice pick was removed following the establishment of a cardiopulmonary bypass and pericardiotomy. The perforation of the right ventricle was closed with a pledget-reinforced mattress stitch. On postoperative day 12, a holosystolic murmur was detected on auscultation. Transthoracic echocardiography revealed a ventricular septal defect 5 mm in diameter located near the apex. The pulmonary-tosystemic flow ratio was 1.1 by echocardiographic measurement. No sign of heart failure was present. Although it was agreed to manage the ventricular septal defect conservatively, careful echocardiographic follow-up is mandatory.

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