The suppressive effects of landiolol administration on the occurrence of postoperative atrial fibrillation and tachycardia, and plasma IL-6 elevation in patients undergoing esophageal surgery: A randomized controlled clinical trial.

STUDY OBJECTIVE: To determine whether perioperative landiolol administration suppresses postoperative atrial fibrillation (AF) and the plasma cytokines elevation in patients undergoing esophageal cancer surgery. DESIGN: A prospective, randomized controlled trial. SETTING: Akita University Hospital, Akita, Japan, from April 2012 to January 2015. PATIENTS: Forty American Society of Anesthesiologists grade I-II patients undergoing elective esophagectomy. INTERVENTIONS: Patients were randomly divided into two groups, landiolol group (landiolol: 5µg/kg/min) and control group (the same volume of covered saline). Landiolol or saline was infused continuously from the induction of anesthesia until next morning. MEASUREMENTS: We examined the new onset of AF and sinus tachycardia, and measured plasma concentrations of cytokines (IL-1ß, IL-6, IL-8, IL-10, and TNF-α) just before surgery, at the end of surgery, the next day, and 2days after surgery. Data (mean±SD) were analyzed using two-way ANOVA followed by the Bonferroni"s test for post hoc comparison; a P<0.05 was considered statistically significant. MAIN RESULTS: Demographic data were similar between the landiolol and the control groups. The incidence of AF was significantly lower in the landiolol group (1/19=5.3%) compared with the control group (7/20=35%) as well as sinus tachycardia (landiolol group, 0/19=0% vs. control group, 5/20=25%). Plasma IL-6 level at the end of surgery was significantly lower in the landiolol group compared with the control group, but the other plasma cytokines levels were similar between the two groups during the entire study period. CONCLUSIONS: Perioperative landiolol administration suppressed the incidence of new-onset of AF as well as sinus tachycardia, and the plasma IL-6 elevation in patients undergoing esophageal cancer surgery.

Reducción de frecuencia en la taquicardia sinusal en pacientes con trasplante cardiaco: ¿ha llegado el momento? / Slowing sinus tachycardia in heart transplant recipients: is it time?

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Stellate ganglion block: a therapeutic alternative for patients with medically refractory inappropriate sinus tachycardia?

Inappropriate sinus tachycardia (IST) is a clinical syndrome characterized by presence of non-paroxysmal tachyarrhythmia manifesting with increased resting heart rate and exaggerated or persistent response to exercise or position. When IST is intolerable and medically refractory, invasive therapies such as sinus node modification or atrioventricular node ablation with placement of permanent pacemaker are tried to control symptoms. We present a 34 year old patient with symptomatic IST unresponsive to medical therapy who underwent anesthetic block of the right and left stellate ganglia. At four month follow up the patient demonstrated sustained improvement in heart rate and reported freedom from previous symptoms.

Ivabradine for the prevention of inappropriate shocks due to sinus tachycardia in patients with an implanted cardioverter defibrillator.

AIMS: Ivabradine is a specific blocker of the pacemaker current (I(f)) used to decrease the sinus rate. Several clinical trials have shown that it is beneficial, with or without concomitant beta-blocker therapy, in patients with stable angina or heart failure. We sought to take advantage of ivabradine's ability to decrease the maximal obtainable sinus rate in order to prevent inappropriate shocks due to sinus tachycardia in patients with an implanted cardioverter defibrillator (ICD). METHODS AND RESULTS: Prospective open-label series including all our patients with an implanted ICD who, during the course of 2010-2011, received ivabradine with the only purpose of preventing inappropriate ICD shocks for sinus tachycardia. These are patients who received one or more inappropriate shocks for sinus tachycardia or were conceived to be at very high risk for developing such complication. Our series includes five patients who received ivabradine (5-10 mg/day) in addition to their usual beta-blocker therapy. During a follow-up of 14 months no inappropriate shocks due to sinus tachycardia were recorded. CONCLUSION: It is sensible to recommend ivabradine for the prevention of inappropriate ICD shocks due to sinus tachycardia in carefully selected patients.

Alternancia eléctrica, patrón electrocardiográfico en el diagnóstico de enfermedad cardiaca grave / Electrical alternans, electrocardiogram pattern in the diagnosis of a severe heart disease

La alternancia eléctrica es un amplio concepto que describe las variaciones, latido a latido, en la dirección, amplitud y/o duración de cualquier componente del electrocardiograma. Se asocia a taponamiento cardiaco, arritmias malignas y muerte súbita. Presentamos el caso de una paciente de 77 años con alternancia eléctrica a partir de la cual se llegó al diagnóstico de taponamiento cardiaco (AU)

Electrical alternans is a broad term that describes alternate-beat variation in the direction, amplitude and duration of any component of the ECG wave-form. It is associated with cardiac tamponade, serious ventricular arrhythmias, and sudden death. We present the clinical case of a 77-year-old female with electrical alternans, from which a diagnosis of cardiac tamponade was established (AU)

Lasting reduction of heart transplant tachycardia with ivabradine is effective and well tolerated: results of 48-month study.

The safety and efficacy of ivabradine applied in heart transplant (HTx) recipients with permanent sinus tachycardia (PST) has been depicted in previous short-term follow-up studies. We sought to investigate the long-term impact of ivabradine in this patient population. From May to November 2006, 29 HTx recipients with PST, who exhibited either contraindications or intolerance of beta-blocker medication or insufficient heart rate (HR) reduction on beta-blocker treatment, first received oral ivabradine treatment (5 mg bid). Ivabradine treatment was discontinued in three patients due to adverse events within the first week. In the remaining 26 patients, resting HR was significantly lowered from 106.8 ± 9.2 at baseline to 83.2 ± 5.1 bpm after 3 months (p < 0.001). This effect remained stable in the long-term follow-up (82.1 ± 11.8 bpm after 4 years), whilst blood pressure was not affected. Apart from the corrected QT interval (QTc), there were no significant changes in ECG. The elongated QTc at baseline (469.4 ± 29.5 ms) decreased to 444.3 ± 33.1 ms after 3 months ivabradine treatment (p < 0.001). A decrease in QTc until month 9 was observed, followed by a partial increase to the upper limit of the normal value. Neither allograft rejection nor changes in left ventricular ejection fraction were observed over the follow-up period. In conclusion, ivabradine appears to be a safe and feasible long-term therapeutic option for HTx recipients with PST. It reduced the resting HR without impairment of blood pressure, myocardial contractility and cardiac conduction. The prognostic value of normalised QTc following ivabradine administration requires further observation.

A case of inappropriate sinus tachycardia after atrio-ventricular nodal reentrant tachycardia cryoablation successfully treated by ivabradine.

We illustrate a case of persistent inappropriate sinus tachycardia after slow pathway atrio-ventricular (AV) nodal reentrant tachycardia cryoablation, and inadvertent fast pathway lesion with residual first-degree AV block in a 72-year-old man with a small Koch's triangle. At the end of the cryoprocedure, the patient presented with sinus tachycardia 100 b.p.m., while PR was 300 ms. An accelerated sinus rhythm and a PR prolongation persisted over time. The patient was successfully treated with ivabradine with no effect on atrioventricular node conduction.

A case of cardiomyopathy induced by inappropriate sinus tachycardia and cured by ivabradine.

We present the case of a 67-year-old woman with cardiomyopathy induced by inappropriate sinus tachycardia (IST) and a particularly high average heart rate. The patient was resistant and/or intolerant to treatment with conventional rate-slowing medications. We used ivabradine--a specific sinus node I(f) current inhibitor--and successfully lowered the heart rate (33 beats per minute mean heart rate decrease). Symptoms, systolic function, and heart rate variability parameters recovered dramatically. No side effect was noted. We suggest that ivabradine--evaluated in trials to treat stable angina--should be considered as a second-line treatment in patients with very symptomatic and refractory IST.

Ropinirole-induced symptomatic sinus node dysfunction.

Restless legs syndrome is a neurological disorder that can be treated with ropinirole. We report the case of a patient who presented with syncope during treatment with ropinirole due to prolonged sinus pauses. The treatment was discontinued and the patient remained asymptomatic. Ropinirole may induce symptomatic sinus pauses in patients without organic sinus node dysfunction.

Phosphodiesterase-4 blunts inotropism and arrhythmias but not sinoatrial tachycardia of (-)-adrenaline mediated through mouse cardiac beta(1)-adrenoceptors.

BACKGROUND AND PURPOSE: beta(1) and beta(2)-adrenoceptors coexist in murine heart but beta(2)-adrenoceptor-mediated effects have not been detected in atrial and ventricular tissues, possibly due to marked phosphodiesterase (PDE) activity. We investigated the influence of the PDE3 inhibitor cilostamide and PDE4 inhibitor rolipram on the effects of (-)-adrenaline in three regions of murine heart. EXPERIMENTAL APPROACH: (-)-Adrenaline-evoked cardiostimulation was compared on sinoatrial beating rate, left atrial and right ventricular contractile force in isolated tissues from 129SvxC57B1/6 cross mice. Ventricular arrhythmic contractions were also assessed. KEY RESULTS: Both rolipram (1 microM) and cilostamide (300 nM) caused transient sinoatrial tachycardia but neither enhanced the chronotropic potency of (-)-adrenaline. Rolipram potentiated 19-fold (left atrium) and 7-fold (right ventricle) the inotropic effects of (-)-adrenaline. (-)-Adrenaline elicited concentration-dependent ventricular arrhythmias that were potentiated by rolipram. All effects of (-)-adrenaline were antagonized by the beta(1)-adrenoceptor-selective antagonist CGP20712A (300 nM). Cilostamide (300 nM) did not increase the chronotropic and inotropic potencies of (-)-adrenaline, but administered jointly with rolipram in the presence of CGP20712A, uncovered left atrial inotropic effects of (-)-adrenaline that were prevented by the beta(2)-adrenoceptor-selective antagonist ICI118551. CONCLUSIONS AND IMPLICATIONS: PDE4 blunts the beta(1)-adrenoceptor-mediated effects of (-)-adrenaline in left atrium and right ventricle but not in sinoatrial node. Both PDE3 and PDE4 reduce basal sinoatrial rate in a compartment distinct from the beta(1)-adrenoceptor compartment. PDE3 and PDE4, acting in concert, prevent left atrial beta(2)-adrenoceptor-mediated inotropy. PDE4 partially protects the right ventricle against (-)-adrenaline-evoked arrhythmias.

The measurement of the paced depolarization integral using the braided endocardial lead.

Previous studies have shown that the paced depolarization integral (PDI) data recorded in unipolar configuration could potentially improve the specificity of tachyarrhythmia classification in an implantable cardioverter defibrillator (ICD). However, the defibrillation protection would be compromised if the ICD case were used as an indifferent electrode. Since transvenous defibrillation leads are being investigated to be used with ICDs, this study determined if reliable PDI data could be obtained using the braided endocardial defibrillation lead (BEDL). The results demonstrated that comparable PDI values and PDI changes with epinephrine induced sinus tachycardia were obtained with all three tested sensing configurations: conventional unipolar, tip electrode to right ventricular defibrillation electrode, and tip electrode to superior vena cava defibrillation electrode. Therefore, the BEDL can be used to measure PDI data, which possibly may improve tachyarrhythmia classification in an ICD, without compromising its defibrillation protection.

Esmolol reduces autonomic hypersensitivity and length of seizures induced by electroconvulsive therapy.

We evaluated the clinical effectiveness of esmolol, an ultra-short-acting beta 1-adrenergic receptor blocking drug, to control the sinus tachycardia and increase in arterial blood pressures induced by electroconvulsive therapy (ECT). Each of 20 patients, ASA physical status I-III, participated in a double-blind, randomized study, involving four match-pair trials (placebo versus esmolol) during ECT. Each patient acted as his or her own control (total number of ECT procedures, 160). We administered a 4-min infusion of either placebo or esmolol at the rate of 500 micrograms.kg-1.min-1. We then induced anesthesia with methohexital and succinylcholine. After administration of electrical stimulation for ECT, the rate of infusion decreased to 300 micrograms.kg-1.min-1 for three additional minutes and was then discontinued. Statistically significant reductions in mean heart rate from minute 2 until minute 15 and in maximum heart rate (the mean of each patient's maximum heart rate after seizure changed from 152 +/- 23 to 115 +/- 24 beats/min) occurred in patients given esmolol. During and immediately after infusion, arterial blood pressure also decreased. Finally, the length of seizures decreased, as manifested clinically from 48 +/- 18 to 39 +/- 14 s and on electroencephalogram from 86 +/- 41 to 67 +/- 28 s. We conclude that esmolol effectively controls the hyperdynamic response to ECT and reduces the length of seizures. The significance of the latter to the overall effectiveness of ECT is not known.