Chol Kim

Postoperative atrial fibrillation in patients undergoing coronary artery bypass grafting or cardiac valve surgery: intraoperative use of landiolol

BackgroundLandiolol hydrochloride is a new β-adrenergic blocker with a pharmacological profile that suggests it can be administered safely to patients who have sinus tachycardia or tachyarrhythmia and who require heart rate reduction. This study aimed to investigate whether intraoperative administration of landiolol could reduce the incidence of atrial fibrillation (AF) after cardiac surgery.MethodsOf the 200 consecutive patients whose records could be retrieved between October 2006 and September 2007, we retrospectively reviewed a total of 105 patients who met the inclusion criteria: no previous permanent/persistent AF, no permanent pacemaker, no renal insufficiency requiring dialysis, and no reactive airway disease, etc. Landiolol infusion was started after surgery had commenced, at an infusion rate of 1 μg/kg/min, titrated upward in 3–5 μg/kg/min increments. The patients were divided into 2 groups: those who received intraoperative β-blocker therapy with landiolol (landiolol group) and those who did not receive any β-blockers during surgery (control group). An unpaired t test and Fisher’s exact test were used to compare between-group differences in mean values and categorical data, respectively.ResultsSeventeen of the 105 patients (16.2%) developed postoperative atrial fibrillation: 5/57 (8.8%) in the landiolol group and 12/48 (25%) in the control group. There was a significant difference between the two groups (P=0.03). The incidence of AF after valve surgery and off-pump coronary artery bypass grafting was lower in the landiolol group, although the difference between the groups was not statistically significant.ConclusionsOur retrospective review demonstrated a marked reduction of postoperative AF in those who received landiolol intraoperatively. A prospective study of intraoperative landiolol for preventing postoperative atrial fibrillation is warranted.

Incessant non-sustained ventricular tachycardia after stimulus of electroconvulsive therapy with atropine premedication?

Abstract  Electroconvulsive therapy (ECT) is an effective and safe treatment for a variety of neuropsychiatric disorders. Premedication with atropine has been recommended in order to avoid bradycardia and transient asystole induced by ECT. In contrast, some other arrhythmias can happen such as atrial flutter and fibrillation. But ventricular tachycardia is rare. Reported herein is a case of incessant non‐sustained ventricular tachycardia, possibly triggered by atropine premedication.

Negative-balance isolated pelvic perfusion in patients with incurable symptomatic rectal cancer: results and drug dose correlation to adverse events

Background Drug leakage and lack of a drug-removal system have prevented clinical application of isolated pelvic perfusion (IPP). These barriers were overcome with negative-balance IPP (NIPP) in experimental pig models. Here, a phase 1 clinical study of NIPP was performed in patients with incurable symptomatic rectal cancer. Purpose To establish a safe regimen of high-dose regional chemotherapy with NIPP using cisplatin in patients with incurable rectal cancer. Material and Methods Between June 2004 and January 2007, NIPP therapy was performed for 23 patients (11 women, 12 men; mean age, 58 years). NIPP was routinely performed twice over a 4-week interval. Dose-limiting toxicities (DLTs) were defined using a 5 + 3 design, and cisplatin doses were escalated from 170 mg/m2, with a fixed 5-fluorouracil dose of 1000 mg/m2. The grade of adverse events (AEs) at the first and second sessions of NIPP therapy, pharmacokinetics, and antitumor response were evaluated. Results No DLTs were observed during the first session of NIPP. However, at the second session, two patients experienced the DLT of neuropathy after administration of 200 mg/m2 cisplatin. Therefore, 190 mg/m2 cisplatin was indicated as the maximum tolerated dose (MTD). The plasma pelvic-to-systemic exposure ratio was 18.4 based on the maximum concentration and 19.0 based on the concentration-time curve. Solid tumor responses included complete response in two patients, partial response in five patients, stable disease in 15 patients, and progressive disease in one patient. Conclusion NIPP may offer the safe delivery of high-dose regional chemotherapy (MTD of 190 mg/m2 cisplatin) with negligible AEs and effective control of tumor growth in patients with incurable rectal cancer.

Low-dose dexmedetomidine facilitates the carotid body response to low oxygen tension in vitro via α2-adrenergic receptor activation in rabbits.

Context Some anaesthetics exert an inhibitory effect on the response of the carotid body to low oxygen tension. However, the effect of dexmedetomidine on the carotid body response has not been reported. Objective To investigate the effect of dexmedetomidine on carotid body activity. The hypothesis is that dexmedetomidine does not have an inhibitory effect on the response of the carotid body to low oxygen tension. Design Animal experimental study in vitro. Ten carotid bodies surgically removed from male New Zealand white rabbits were tested. Setting Research laboratory of Nippon Medical School, Tokyo, Japan, from July 2008 to February 2010. Intervention The carotid body was perfused with three different concentrations of dexmedetomidine (0.1, 1.0 and 10 nmol l−1). The contribution of &agr;2-adrenergic receptors was evaluated by addition of 1.0 nmol l−1 yohimbine, an &agr;2-adrenergic receptor antagonist. Main outcome measures The differences in carotid sinus nerve activity between high oxygen tension (baseline) and low oxygen tension (peak) were analysed. Results At all three concentrations, dexmedetomidine did not depress the baseline and peak activity of the carotid body, whereas 0.1 nmol l−1 dexmedetomidine facilitated the response to low oxygen tension stimulation. The differences in carotid sinus nerve activity between baseline (pO2 80.4 ± 9.1 kPa) and peak (pO2 22.1 ± 2.6 kPa) were 140 ± 70 Hz in controls and 266 ± 116 Hz with 0.1 nM dexmedetomidine (P < 0.05). This increase was not shown in the presence of 1.0 nmol l−1 yohimbine. Conclusion Dexmedetomidine does not depress the activity of the carotid body under high oxygen tension or the response to low oxygen tension, whereas 0.1 nmol l−1 dexmedetomidine facilitates this response via &agr;2-adrenergic receptor activation.