In the past 4 years, 34 asymptomatic patients with the Wolff-Parkinson-White (WPW) pattern underwent electrophysiologic study. The effective refractory period (ERP) of antegrade conduction over the accessory pathway was 288 +/- 29 msec. In three asymptomatic patients (9%), the antegrade ERP of the accessory pathway was shorter than 250 msec. The antegrade ERP of the accessory pathway became shorter than 250 msec in an additional 12 of 22 (55%) patients after isoproterenol administration. Nineteen (56%) of the asymptomatic patients showed the absence of retrograde conduction over the accessory pathway even after isoproterenol administration. The rate of induction of orthodromic reciprocating tachycardia in the asymptomatic WPW patients was 15% (5/34), which was significantly lower than that in the symptomatic patients. These data suggest that in the asymptomatic patients, the absence of retrograde conduction over the accessory pathway is the reason they remained asymptomatic, free of reciprocating tachycardia. However, even in the asymptomatic patients, some had the accessory pathway in which antegrade ERP was shorter than 250 msec. They may result in rapid ventricular conduction over the accessory pathway when atrial fibrillation develops.

V entricular fibrillation (VF) can occur in patients without structural heart diseases; when it does, it is called idiopathic VF.1,2 Among primary electric diseases, Brugada syndrome (BS) is characterized by unique ECG patterns of J/ ST/T waves.3 This ECG pattern has been shown to be associated with an increased risk of sudden cardiac death compared with control subjects, 4 and an ECG diagnosis of BS is very important for risk stratification. 5,6 Clinical Perspective on p 1054Recently, we observed a case in which the characteristic ECG phenotype of BS was unmasked by relief of complete right bundlebranch block (CRBBB); when CRBBB resolved spontaneously, the characteristic ECG pattern of BS was found to be underlying. 7A similar case was reported by others. [8][9][10] The goal of this study is to discuss patients with BS that were complicated by CRBBB and to present evidence for the presence of BS in CRBBB patients. Methods PatientsThe study consisted of 11 patients who had CRBBB with the diagnosis of BS.5 Structural heart diseases were excluded by ECG, transthoracic echocardiography, and cardiac catheterization. Coronary spasm was excluded as the cause of VF by provocation tests using acetylcholine or ergonovine maleate at catheterization. Definitions of CRBBB and BSCRBBB was defined as a late R (R′) wave presenting in V 1 or V 2 , with a slurred, wide S in leads I and V 5 /V 6 and with prolonged duration of QRS ≥120 milliseconds. 11,12 If CRBBB was seen on the baseline ECG, we divided the patients into 2 groups. One group consisted of the patients in whom ECG revealed BS and CRBBB occurred subsequently during the follow-up (n=7). The other group consisted of the patients who had CRBBB on the baseline ECG but in whom BS was diagnosed in the following situations (n=4). First, resolution of CRBBB resulted in normal ventricular conduction, in which the characteristic ECG pattern for BS could be seen. The resolution of Background-The characteristic ECG of Brugada syndrome (BS) can be masked by complete right bundle-branch block (CRBBB) and exposed by resolution of the block or pharmacological or pacing maneuvers. Methods and Results-The study consisted of 11 patients who had BS and CRBBB. BS was diagnosed before the development of CRBBB, on the resolution of CRBBB, or from new characteristic ST-segment changes that could be attributable to BS. Structural heart diseases were excluded, and coronary spasm was excluded on the basis of a provocation test at catheterization. In 7 patients, BS was diagnosed before the development of CRBBB. BS was diagnosed when CRBBB resolved spontaneously (n=1) or by right ventricular pacing (n=3). The precipitating cause for the spontaneous resolution of CRBBB, however, was not apparent. On repeated ECGs, new additional upward-convex ST-segment elevation was found in V 2 or V 3 in 3 patients. In 2 patients, new ST-segment elevation was induced by class I C drugs. The QRS duration was more prolonged in patients with BS and CRBBB compared with age-and sex-matched controls: 170±13 versus 14...

BackgroundWe conducted a randomized, controlled trial to determine whether supplementation with oral branched-chain amino acids (BCAAs) improves serum albumin and clinical outcomes in heart failure (HF) patients with hypoalbuminemia.Methods and resultsWe randomly assigned 18 in-hospital HF patients with serum albumin < 3.5 g/dL to receive oral BCAA granules (LIVACT®) for 28 days during their hospital stay or until discharge (BCAA group; N = 9) or to receive no supplementation (controls; N = 9), in addition to recommended HF therapy. The primary endpoints were changes from baseline in serum albumin and cardiothoracic ratio (CTR). Sixteen patients completed the study. The mean (± standard deviation) period of BCAA supplementation was 18.4 ± 8.4 days. Serum albumin significantly increased in the BCAA group [mean difference vs baseline, 0.44 g/dL; 95% confidence interval (CI) 0.13–0.76; P = 0.014] and did not change in controls (0.18 g/dL; 95% CI − 0.05 to 0.40; P = 0.108). CTR significantly decreased in the BCAA group (− 2.3%; 95% CI − 3.8 to − 0.8; P = 0.014) and did not change in controls (− 1.0%; 95% CI − 2.3 to 0.3; P = 0.111).ConclusionIn-hospital HF patients with hypoalbuminemia supplemented with BCAAs showed increased serum albumin and decreased CTR.Clinical trial registration number UMIN000004488 [http://www.umin.ac.jp/ctr/index.htm]

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SUMMARYUsing anesthetized dogs, the coronary vascular effects of neuropeptide Y (NPY) were studied and the action of alpha-or serotonergic receptor blockade on the action of NPY was evaluated.To demonstrate the biological significance of the action of NPY, the vasoconstrictor potencies of NPY and norepinephrine were compared. One to 5 nmol of intracoronary NPY reduced coronary flow in a dose-dependent manner.The action started rather gradually and lasted for 10 min or more. Since perfusion pressure and central venous pressure were unchanged, the decrease in coronary flow should be a result of coronary vasoconstriction. Intracoronary norepinephrine infusion caused vasodilatation but when dogs were pretreated with 0.5 to 1.0 mg/kg of systemic propranolol, a vasoconstrictor effect was observed at a 5 times higher dose than with NPY.Furthermore, the action of NE was only transient, lasting for 30 sec or less. The vasoconstrictor action of NPY was not antagonized by phentolamine or by ketanserin.Since NPY is an endogenous polypeptide found in the sympathetic nerve terminals around coronary arteries, it may participate in the regulation of coronary flow.