Jun Nejima

Long-term treatment with antipsychotic drugs in conventional doses prolonged QTc dispersion, but did not increase ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease.

AbstractObjective: The aim of this study was to examine the hypothesis that long-term treatment with antipsychotic drugs in conventional doses prolongs QTc dispersion and increases ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease. Methods: We measured QTc and QTc dispersion and ventricular tachyarrhythmias in 64 patients with schizophrenia, including 59 patients who received psychiatric medications, and five patients who did not receive psychiatric medications, and 45 healthy volunteers. None of the subjects had a history of cardiac disease or showed any abnormality in chest radiograph and transthoracic echocardiographic studies. None of the subjects had electrolyte abnormality. None of the subjects were taking drugs known to influence the QT interval, other than psychiatric medications. Results: QTc and QTc dispersion were significantly (P < 0.017) increased in patients who received psychiatric medications compared with patients who did not receive psychiatric medications, or with healthy volunteers [QTc: 0.442 (0.029), 0.418 (0.029), 0.417 (0.028) s, QTc dispersion: 0.054 (0.013), 0.038 (0.017), 0.038 (0.009) s]. Daily ventricular premature beats were 183 (689), 77 (23), and 86 (149), respectively. No ventricular tachycardia was observed. There were no correlation between QTc and QTc dispersion and ventricular premature beats. Conclusion: Long-term treatment with antipsychotic drugs in conventional doses prolonged both QTc and QTc dispersion in patients with schizophrenia, but did not increase ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease. However, despite the negative findings, ventricular tachyarrhythmias may occur as a rare side-effect of antipsychotic drugs, particularly if a patient has additional risk factors.

Acute effects of intravenous nicorandil on hemodynamics in patients hospitalized with acute decompensated heart failure

BACKGROUND Nicorandil injection, a potent vasodilator with K(ATP) channel opening action and nitrate-like action, has been used for treatment of unstable angina. In the present investigation, we examined the effect of intravenous nicorandil on hemodynamics in patients with acute decompensated heart failure (ADHF). METHODS ADHF patients admitted to hospital with pulmonary artery wedge pressure (PAWP)≥18 mm Hg were enrolled. Patients received nicorandil by an intravenous bolus injection of 0.2mg/kg/5 min followed by continuous infusion at a rate of 0.05, 0.10, or 0.20mg/kg/h for 6h. RESULTS Nicorandil administration caused a significant decrease in PAWP and increase in the cardiac index (CI) that began immediately after the injection and were maintained during the continuous infusion. After 6h, nicorandil administration at 0.2mg/kg/5 min followed by 0.20mg/kg/h resulted in a decrease in PAWP (26.5%, p<0.01), an increase in CI (15.8%, p<0.05), and a decrease in total peripheral resistance (13.8%, p<0.01) in a dose-dependent manner. Nicorandil decreased blood pressure significantly, without an excessive decrease or negative impact even in patients with lower systolic blood pressure. CONCLUSION Intravenous administration of nicorandil, by bolus injection followed by continuous infusion, improves PAWP and CI in ADHF patients immediately and continuously as a potent vasodilator with combined preload and afterload reduction. These results demonstrate that nicorandil is a safe and effective new medication for the treatment of ADHF.

The combination of external high-frequency oscillation and pressure support ventilation in acute respiratory failure

Background: Effective gas exchange can be maintained in animals by using external high‐frequency oscillation (EHFO). The present study evaluates the effect of relatively long‐term duration EHFO combined with pressure support ventilation (PSV) in patients with acute respiratory failure.

Increased plasma levels of interleukin-6 and myocardial stunning after coronary reperfusion therapy

Abstract From recent studies and the present data, it is strongly suggested that interleukin-6 contributes to the development of myocardial stunning after coronary reperfusion therapy in patients with AMI.

Origin and Pathophysiological Role of Increased Plasma Endothelin-1 in Patients with Acute Myocardial Infarction:

To investigate the origin and pathophysiological role of increased plasma endothelin-1 (endothelin-1) concentration in patients with acute myocardial infarction (AMI), the authors measured plasma endothelin-1 sequentially after the onset of AMI and analyzed the origin by the simultaneously obtained blood samples from the radial artery, right atrium, and pulmonary artery in 28 patients with AMI. The data were correlated with cardiovascular hemodynamics, infarct size, and coronary arteriographic findings. Arterial endothelin-1 at twenty-four and seventy-two hours significantly correlated with mean pulmonary arterial pressure (r=0.48, r=0.46, P < 0.05, respectively), central venous pressure (r=0.42 and 0.51, P < 0.05, respectively), and pulmonary vascular resis tance (r=0.42, r=0.42, P < 0.05), and endothelin-1 at one hundred twenty hours signif icantly correlated with peak creatine kinase (r=0.53, P < 0.05) and creatine kinase isozyme MB (r=0.58, P < 0.01). Simultaneous blood samples showed no significant difference in endothelin-1 concen trations among them. However, a subgroup of patients with endothelin-1 concentration higher in the radial artery than that in the right atrium showed a significantly higher mean pulmonary arterial pressure (25.2 ±6.5 vs 17.0 ±1.6 mmHg, P < 0.05), peak creatine kinase (3594 ±1597 vs 865 ±495 IU/L, P < 0.05), and peak creatine kinase MB (214 ±91 vs 69 ±22 IU/L, P < 0.05) as compared with those in patients in whom endothelin-1 was higher in the right atrium than in the radial artery. Increased plasma endothelin-1 concentration in the early stage of AMI reflects higher pulmonary artery pressure and elevated pulmonary vascular resistance, while that in the later stage is related to the infarct size. The production of endothelin-1 in patients with severe pump failure may be accere lated in the pulmonary vascular bed, left ventricle, or systemic arterial trees, and the main origin in the later stage is possibly coronary vasculature in the infarcted area.