• 2018-07
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  • br Conclusion br Conflict of interest


    Conflict of interest
    Case report A 65-year-old woman with permanent atrial fibrillation was admitted with diastolic neurokinin receptor failure (HF) secondary to rapid ventricular response. She had undergone single chamber pacemaker implantation (Boston Scientific Ingenio SR) two years earlier for symptomatic bradycardia (Fig. 1A). During the current admission, a chest radiograph and fluoroscopy revealed that the lead (Guidant® FINELINE™ Model 4457, passive fixation) had become dramatically twisted at 2 sites: in the pacemaker pocket and within the right atrium (Fig. 2A, B). Nevertheless, pacing/sensing and impedance parameters remained normal. In retrospect, a radiograph performed 2-months post-implant due to a respiratory tract infection already showed rotation of the impulse generator and the development of two initial loops in the lead occurring at these 2 sites simultaneously (Fig. 1B). However, this was unnoticed at that time. An echocardiogram was performed in the hospital showing a left ventricle ejection fraction of 50% with no wall motion abnormalities or significant valve disease. The patient was initially managed with optimization of HF medications. Due to rate control being unachieved and recurrent episodes of HF, atrioventricular node ablation was performed, and the patient was offered an upgrade to a biventricular pacemaker with a new right ventricular lead [1].
    Discussion Lead dislodgement is a relatively common complication of pacemaker implantation [2]. Different mechanisms of lead macro-dislodgement leading to device malfunction have been described. The twiddler syndrome is caused by the spontaneous or self-induced twisting of the generator over the axis defined by the lead, causing the typical twisted lead image [3]. In the “reel syndrome”, the generator rotates over its transverse axis resulting in a lead coiling around the generator [4]. The “ratchet syndrome” occurs due to progressive lead displacement through its fixation parts without generator rotation over any of its axes [5].
    Conflict of interest Hong is partially funded by the Dowager Countess Eleanor Peel Trust (Peel and Rothwell Jackson Travelling Fellowship), United Kingdom.
    Author contribution
    I read with great interest the article by Marino et al. entitled “Inappropriate mode switching clarified by using a chest radiograph.” . The authors have explained a case of dual-chamber pacemaker malfunction, caused by intermittent high-frequency noises. They claimed that this happened because of lead–lead interaction caused by excess slack of atrial and ventricular leads.
    Case description A 57-year-old man with no significant past medical history presented to the emergency department (ED) with complaints of dysuria, increased frequency of urination, and subjective fevers since 2 days. The patient denied any other symptoms. He did not have any chest pain, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, dizziness, or palpitations. At the time of presentation, the patient did not have a history of syncope or seizures. He worked in construction and could tolerate exercise without dyspnea. He had no family history of arrhythmias, sudden cardiac death, or coronary artery disease. He smoked 20 cigarettes daily and had no history of alcohol or illicit drug use. Vital signs on presentation were as follows: temperature, 103F (39.4°C); blood pressure, 132/80mmHg; pulse, 116/min; and respiratory rate, 17/min. Oxygen saturation was 100% on room air. Physical examination revealed mild suprapubic tenderness, without any guarding or rigidity. His cardiovascular examination revealed normal heart sounds, and regular rate and rhythm, without any murmurs, rubs, or gallops. There was no jugular venous distention, and the lungs were clear to auscultation bilaterally. He underwent electrocardiography (ECG) in the ED (Fig. 1). What would be the next most appropriate step in the management of this patient?