• 2018-07
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  • 2019-06
  • The cardiac GP are a collection of autonomic nervous


    The cardiac GP are a collection of autonomic nervous systems comprising both afferent and efferent as well as sympathetic and parasympathetic fibers [10,11]. Radiofrequency catheter ablation eliminates the most elementary level of vagal innervation by destroying the visceral efferent limb of the parasympathetic system, thereby attenuating neural reflexes. In o6 methylguanine methyltransferase to the parasympathetic neuron, the post-ganglionic sympathetic neuron is preserved, as its neural body is located far from the heart in the paravertebral sympathetic chain and its axon usually recovers [6]. Several studies showed that a high number of parasympathetic neurons and ganglia exist in the fibrillar myocardium areas, which are targeted by endocardial radiofrequency ablation aimed at cardiac autonomic innervation [12]. Although we could not find obvious fibrillar potentials, radiofrequency delivery caused immediate autonomic reactions with an increase in heart rate. Mapping guided by HF stimulation might have allowed a vagal response to be elicited more efficiently from the GP embedded in the epicardial fat pads.
    Conflict of interest
    Introduction Several randomized trials have shown that cardiac resynchronization therapy (CRT) improves exercise capacity, quality of life, and functional class in patients with severe drug-refractory congestive heart failure (CHF) caused by left ventricular (LV) dysfunction and electrical dyssynchrony [1]. The combination of CRT and an implantable cardioverter-defibrillator (ICD) is the preferred treatment for patients with severe heart failure, dyssynchrony, and an increased risk of sudden cardiac death or for survivors of a primary ventricular arrhythmia episode. Though it produces satisfactory improvements in hemodynamic parameters, functional class, and exercise capacity, the anti-arrhythmic effect of CRT therapy is not well established. Some studies have shown that biventricular pacing (BVP) is associated with a decrease in the incidence or excitability of monomorphic ventricular tachycardia (MMVT) [2–4], while others demonstrated a pro-arrhythmic potential [5–7].
    Case report A 59-year-old woman with a previous high lateral myocardial infarction and ischemic cardiomyopathy was admitted to our institution several times owing to heart failure decompensation. Coronary angiography performed after she suffered a transmural myocardial infarction in 2008 revealed 30–40% diffuse atherosclerotic plaque after the first septal branch of the left anterior descending (LAD) artery and subtotal stenosis of the first diagonal with a small calibration. The right coronary and circumflex arteries were found to be normal. At this time, her ejection fraction was 40% with LV anterior wall hypokinesis and moderate mitral regurgitation on transthoracic echocardiography. In 2011, gated myocardial perfusion scintigraphy (TC-99m MIBI) revealed a small ischemic area near the apex and a fixed perfusion defect consistent with a transmural myocardial infarction at the anterior wall segment from the mid-ventricle to the base and at the anterior-lateral wall segment of the LV mid-ventricle with an ejection fraction of 35%. The patient׳s condition worsened over time, with her New York Heart Association (NYHA) functional class increasing from I to III. In 2013, cardiac resynchronization therapy was considered after three admissions for acute heart failure decompensation. At this time, her electrocardiogram (ECG) showed a QRS duration of 160ms with an LBBB morphology and sinus rhythm (Fig. 1). The LV ejection fraction decreased to 20% with global akinesis, and severe mitral and tricuspid regurgitation was present at the time of intervention. ICD combined with CRT was the preferred method for primary prevention as there were no prior episodes of syncope and tachycardia. Implantation of the LV lead of the CRT-D into the posterior-lateral branch of the coronary sinus was performed successfully. After the activation of the BVP mode in the operating room, an incessant electrical storm of TdP commenced. After three antitachycardia pacing (ATP) attempts, defibrillation occurred and the tachycardia started repeatedly. Each TdP episode was stopped by device defibrillation (Fig. 2). As there was no history of ventricular tachycardia (VT) since the start of heart failure, it appeared that the tachycardia was associated with the ventricular pacing mode, and the BVP mode was stopped. Owing to the patient׳s instability, we could not perform echocardiography under the BVP mode and LV pacing mode. Every pacing attempt with these modes resulted in TdP, and accordingly the device was switched off. All electrolyte levels were in the normal o6 methylguanine methyltransferase range before and after the operation. After two days without any tachycardia episode, the BVP mode was reactivated in the coronary care unit and tachycardia started again. Atrial and ventricular pacing was re-attempted, and VT started after LV pacing. No tachycardia was detected with right ventricular pacing and atrial pacing. The patient was observed in the hospital for another seven days with the device switched off and no tachycardia occurred. The patient was discharged under oral treatment with amiodarone 200mg twice daily.