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To evaluate the short term effects of inhalation of oxygen at night in 51 patients with congestive heart failure (CHF) and sleep apnea syndrome (SAS).Fifty-one patients with stable CHF (31 males, 20 females, mean age 79.0 +/- 11.9 years; brain natriuretic peptide level of100 pg/ml) were evaluated between September 2003 and August 2004, using a Morpheus monitor. The complication rate of SAS in patients with CHF was assessed and apnea hypopnea index, oxygen desaturation index 3%, heart rate, and autonomic nerve activity under room air compared to supplemental O2 (2 l/min) over two consecutive nights.Thirty-eight (75%)of the CHF patients had SAS. Of these SAS patients, 49% suffered from central SAS and 51% had obstructive SAS. Apnea hypopnea index and oxygen desaturation index 3% improved remarkably with supplemental oxygen (p0.001), in particular, the central SAS group demonstrated prominent improvement (p0.001). Obstructive SAS patients exhibited no significant changes (p = 0.3356), but tended to exacerbate the episodes of sleep apnea. Total heart rate was decreased (p = 0.0079). Nevertheless, heart rate variability analysis showed little effect of nocturnal oxygen therapy on the autonomic nervous system during sleeping.Nocturnal oxygen therapy improved the number of sleep apnea episodes and decreased total heart rate during sleep time for the CHF patients with central SAS, despite little influence on the autonomic nervous system, based upon assessment of heart rate variability. Obstructive SAS might exacerbate the episodes of sleep apnea.

SummaryBackgroundIschemic “pre”-conditioning has been shown to have antiarrhythmic effects. The aim of this study was to investigate whether ischemic “post”-conditioning (post-CON) also has antiarrhythmic effects in ST-segment elevation myocardial infarction (STEMI) patients undergoing coronary angioplasty (PCI) as a clinical model of post-CON.Methods and resultsA total of 61 patients suffering from an acute myocardial infarction (AMI) were included. The QT dispersion (QTd) was measured before each balloon inflation (BI) and after deflation (BD) during PCI. The hemodynamic parameters and electrocardiogram were also assessed during PCI. All data were analyzed using a logistic regression analysis. A total of 36 of 61 STEMI patients could be analyzed according to the protocol. The QTd shortened significantly as the BI and BD were repeated (p

Intravenous amiodarone (AMD) induces multiple antiarrhythmic effects via blocking of Na(+), Ca(2+), and IKr channels, and beta receptors. A patient on chronic dialysis was administered AMD for nonsustained ventricular tachycardia after successful cardiopulmonary resuscitation. QT prolongation occurred 5 h after AMD administration. AMD was withdrawn at 24 h because of prolonged QTc interval (716 ms), which persisted for a further 48 h (661 ms). Ventricular premature contraction (VPC) was significantly decreased at 7h; however, VPC increased again after discontinuing AMD. Depolarization changes induced by the Na(+)-channel blocking action of AMD were analyzed. There was increasing filtered QRS-duration and duration of low-amplitude signals at voltage40 µV, and decreasing root-mean-square voltage of signals in the last 40 ms of ventricular late potentials (LPs) within 7 h. However after stopping AMD, LPs were reversed. The blood concentration of AMD reached the effective level within 10 min but decreased immediately to an ineffective level. Onset and disappearance of the VPC-inhibiting effect corresponded to the depressive effect on depolarization but not with the increase in the prolonged repolarization effect and blood concentration. Even if the QT interval is sufficiently prolonged, the Na(+)-channel blocking action is required for AMD to induce the antiarrhythmic effect.