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PP-331: INHIBITION OF A DUAL CHAMBER PACEMAKER CAUSED BY POTENTIALS ASSOCIATED WITH DEEP INSPIRATION
S172
Posters / International Journal of Cardiology 147S2 (2011) S131–S175
of certain medications which may depress conduction system may be challenging. The purpose of this study is to evaluate medications which may cause conduction disturbances in a patient population with symptomatic bradiarrhythmia. Methods: During the last ten years, 337 patients (154 men, mean age 70, range 21–98) who were admitted with second-degree (n: 62; 18.3%), or third-degree (n: 264, 78.3%) atrioventricular block or slow atrial fibrillation (<40/min, n: 11, 3.2%) were included. Patients with acute coronary syndromes, vasovagal syncope and digitalis toxicity were excluded. Conduction defect was defined by surface ECG, and patients were followed up clinically as long as five half-lives of the drug before a decision for a permanent pacemaker were made. Study population was divided into two groups. Group 1 included patients with concomitant possible culprit medication (medication group). Group 2 included patients without concomitant culprit medication (non-medication group). Results: Group 1 consisted of 101 patients (29.9%) who had a recent medical history of a medication which may affect conduction system. Group 2 consisted of 236 patients (70.1%). The percentage of patients with second, third degree atrioventricular block and slow atrial fibrillation were similar in both groups. In medication group, 59 patients (58.4%) had to receive a permanent pacemaker during hospitalization period. In the same group 42 patients (41.6%) discharged without pacemaker implantation after resolution of conduction disturbances. These patients were followed up by surface ECG in every three months for one year. Recurrence of conduction disturbances was detected in 4 of 42 patients. Consequently these patients also received permanent pacemakers. Conclusions: According to our experience totally 37.6% of patients show resolution of severe conduction disturbances after discontinuation of culprit drug. In patients who are on drugs affecting the conduction system, it can be advised waiting until the disappearance of the effect of possible culprit drug before implanting a pacemaker. PP-330 AMIODARONE-ASSOCIATED EPIDIDYMITIS H. Acet1 , F. Ertas2 , F. Ozyurtlu1 , M.Z. Bilik1 , M.S. Ulgen3 . 1 Department of Cardiology, Diyarbakir Training and Research Hospital, Diyarbakir, Turkey; 2 Department of Cardiology, Kiziltepe State Hospital, Mardin, Turkey; 3 Department of Cardiology, Dicle University Faculty of Medicine, Diyarbakir, Turkey Objective: Amiodarone is a benzofuran derivative with predominantly class III antiarrhythmic activity that is widely used in refractory ventricular arrhythmias and atrial fibrillation in our daily clinical practice. Epididymitis may be found as a unusual but existing complication of amiodarone treatment. Epididymitis, as an unusual side-effect of amiodarone use. We present a case of non-infectious epididymitis related to amiodarone therapy. Results: 50 year- old- male was admitted to our hospital with adiagnosis paroxysmal atrial fibrillation. patient received 16 mg/kg amiodarone iv infussion for 24 hour and oral 800 mg/day amiodarone as the maintenance dose. Follow up visit was performed the fifty day of amiodarone theraphy with had a scrotal pain and right scrotal edema. He had no infectious complaints. Right epididymal oversensitivity and bilateral minimal hydrocel was found. Scrotal doppler ultrasonograph examination confirmed increased vascularization suggestive for epididymal inflamation. Urology consultation was taken for the arrangement of medication. Patient’s electrocardiography was sinus ryhthm. Scrotal pain was planned to be controlled by analgesics. Amiodarone was planned to be continuing. After 1 month of period he came to control. Cordarone theraphy was continued with at the decreased dosage. He explained scrotal pain had decreased gradually. Scrotal ultrasonography has revealed. Right epididym had no increase in vascularity and hydrocel appearance. Conclusions: Epididymitis generally related with gram negative bacterial infections and drug induced epididymitis may be
encountered in differential diagnosis. Epididymitis, as an unusual side-effect of amiodarone use. It most often concerns doses more than 400 mg per day. In adult population symptoms usually necessiate discontinuation of drug or reduction of doses. The reaction is self-limited, with or without amiodarone reduction, and does not require antimicrobial drugs, but a noninvasive urological examination may be warranted. In our case, 800 mg Amiodarone per day was enough to induce epididymalgia. Temporary discontinuation or decrease in dosage is recommended for patients who suffer noninfectious epididymitis while on amiodarone therapy. PP-331 INHIBITION OF A DUAL CHAMBER PACEMAKER CAUSED BY POTENTIALS ASSOCIATED WITH DEEP INSPIRATION S. Okutucu, H. Sunman, B. Evranos, F. Jam, S.G. Fatihoglu, L. Sahiner, E.B. Kaya, K. Aytemir, G. Kabakci, L. Tokgozoglu, H. Ozkutlu, A. Oto. Department of Cardiology, Hacettepe University, Ankara, Turkey Objective: Pacing inhibition caused by oversensing has been well documented in pacing literature. We present a case in which pacemaker inhibition occurred as a result of potentials associated with inspiration. Methods: A 67-year-old woman was implanted with a permanent DDD pacemaker due to complete AV block, severe bradycardia and syncope two years ago. She had syncope or documented bradycardia since that time. However her dizziness was not improved and she admitted to our department. Pacemaker interrogation was revealed normal atrial and right ventricular capture threshold and lead impedance. Bedside maneuvers that were performed in the patient did not show any abnormality. Twenty-four hours ambulatory electrocardiographic monitorization revealed ventricular asystole episodes. Chest x-ray and fluoroscopic studies revealed no abnormality of the leads. Results: She was evaluated again with pacemaker interrogation and ventricular sensitivity decreased and ventricular blanking period increased. However, ambulatory electrocardiographic monitorization revealed ventricular asystole episodes again. In repeated pacemaker interrogation, she was asked to perform a deep inspiration. After this maneuver, asystole episode was detected because of potentials associated with inspiration. There was no atrial electrode abnormality. There was no cross-talk between two electrodes. Right ventricular electrode was extracted. New right ventricular electrode was implanted to another site in right ventricle that was not inhibited deep inspiration. Her further clinical course was uneventful without any dizziness and syncope. Conclusions: Pacing inhibition caused by oversensing has been well known in the clinical practice. Pacemaker inhibition as a result of potentials associated with inspiration should be kept in mind in patients with asystole episodes. It can be checked easily by asking patients to take a deep breath.
Figure 1. Ambulatory electrocardiographic monitorization revealing ventricular asystole episodes.
Posters / International Journal of Cardiology 147S2 (2011) S131–S175
of certain medications which may depress conduction system may be challenging. The purpose of this study is to evaluate medications which may cause conduction disturbances in a patient population with symptomatic bradiarrhythmia. Methods: During the last ten years, 337 patients (154 men, mean age 70, range 21–98) who were admitted with second-degree (n: 62; 18.3%), or third-degree (n: 264, 78.3%) atrioventricular block or slow atrial fibrillation (<40/min, n: 11, 3.2%) were included. Patients with acute coronary syndromes, vasovagal syncope and digitalis toxicity were excluded. Conduction defect was defined by surface ECG, and patients were followed up clinically as long as five half-lives of the drug before a decision for a permanent pacemaker were made. Study population was divided into two groups. Group 1 included patients with concomitant possible culprit medication (medication group). Group 2 included patients without concomitant culprit medication (non-medication group). Results: Group 1 consisted of 101 patients (29.9%) who had a recent medical history of a medication which may affect conduction system. Group 2 consisted of 236 patients (70.1%). The percentage of patients with second, third degree atrioventricular block and slow atrial fibrillation were similar in both groups. In medication group, 59 patients (58.4%) had to receive a permanent pacemaker during hospitalization period. In the same group 42 patients (41.6%) discharged without pacemaker implantation after resolution of conduction disturbances. These patients were followed up by surface ECG in every three months for one year. Recurrence of conduction disturbances was detected in 4 of 42 patients. Consequently these patients also received permanent pacemakers. Conclusions: According to our experience totally 37.6% of patients show resolution of severe conduction disturbances after discontinuation of culprit drug. In patients who are on drugs affecting the conduction system, it can be advised waiting until the disappearance of the effect of possible culprit drug before implanting a pacemaker. PP-330 AMIODARONE-ASSOCIATED EPIDIDYMITIS H. Acet1 , F. Ertas2 , F. Ozyurtlu1 , M.Z. Bilik1 , M.S. Ulgen3 . 1 Department of Cardiology, Diyarbakir Training and Research Hospital, Diyarbakir, Turkey; 2 Department of Cardiology, Kiziltepe State Hospital, Mardin, Turkey; 3 Department of Cardiology, Dicle University Faculty of Medicine, Diyarbakir, Turkey Objective: Amiodarone is a benzofuran derivative with predominantly class III antiarrhythmic activity that is widely used in refractory ventricular arrhythmias and atrial fibrillation in our daily clinical practice. Epididymitis may be found as a unusual but existing complication of amiodarone treatment. Epididymitis, as an unusual side-effect of amiodarone use. We present a case of non-infectious epididymitis related to amiodarone therapy. Results: 50 year- old- male was admitted to our hospital with adiagnosis paroxysmal atrial fibrillation. patient received 16 mg/kg amiodarone iv infussion for 24 hour and oral 800 mg/day amiodarone as the maintenance dose. Follow up visit was performed the fifty day of amiodarone theraphy with had a scrotal pain and right scrotal edema. He had no infectious complaints. Right epididymal oversensitivity and bilateral minimal hydrocel was found. Scrotal doppler ultrasonograph examination confirmed increased vascularization suggestive for epididymal inflamation. Urology consultation was taken for the arrangement of medication. Patient’s electrocardiography was sinus ryhthm. Scrotal pain was planned to be controlled by analgesics. Amiodarone was planned to be continuing. After 1 month of period he came to control. Cordarone theraphy was continued with at the decreased dosage. He explained scrotal pain had decreased gradually. Scrotal ultrasonography has revealed. Right epididym had no increase in vascularity and hydrocel appearance. Conclusions: Epididymitis generally related with gram negative bacterial infections and drug induced epididymitis may be
encountered in differential diagnosis. Epididymitis, as an unusual side-effect of amiodarone use. It most often concerns doses more than 400 mg per day. In adult population symptoms usually necessiate discontinuation of drug or reduction of doses. The reaction is self-limited, with or without amiodarone reduction, and does not require antimicrobial drugs, but a noninvasive urological examination may be warranted. In our case, 800 mg Amiodarone per day was enough to induce epididymalgia. Temporary discontinuation or decrease in dosage is recommended for patients who suffer noninfectious epididymitis while on amiodarone therapy. PP-331 INHIBITION OF A DUAL CHAMBER PACEMAKER CAUSED BY POTENTIALS ASSOCIATED WITH DEEP INSPIRATION S. Okutucu, H. Sunman, B. Evranos, F. Jam, S.G. Fatihoglu, L. Sahiner, E.B. Kaya, K. Aytemir, G. Kabakci, L. Tokgozoglu, H. Ozkutlu, A. Oto. Department of Cardiology, Hacettepe University, Ankara, Turkey Objective: Pacing inhibition caused by oversensing has been well documented in pacing literature. We present a case in which pacemaker inhibition occurred as a result of potentials associated with inspiration. Methods: A 67-year-old woman was implanted with a permanent DDD pacemaker due to complete AV block, severe bradycardia and syncope two years ago. She had syncope or documented bradycardia since that time. However her dizziness was not improved and she admitted to our department. Pacemaker interrogation was revealed normal atrial and right ventricular capture threshold and lead impedance. Bedside maneuvers that were performed in the patient did not show any abnormality. Twenty-four hours ambulatory electrocardiographic monitorization revealed ventricular asystole episodes. Chest x-ray and fluoroscopic studies revealed no abnormality of the leads. Results: She was evaluated again with pacemaker interrogation and ventricular sensitivity decreased and ventricular blanking period increased. However, ambulatory electrocardiographic monitorization revealed ventricular asystole episodes again. In repeated pacemaker interrogation, she was asked to perform a deep inspiration. After this maneuver, asystole episode was detected because of potentials associated with inspiration. There was no atrial electrode abnormality. There was no cross-talk between two electrodes. Right ventricular electrode was extracted. New right ventricular electrode was implanted to another site in right ventricle that was not inhibited deep inspiration. Her further clinical course was uneventful without any dizziness and syncope. Conclusions: Pacing inhibition caused by oversensing has been well known in the clinical practice. Pacemaker inhibition as a result of potentials associated with inspiration should be kept in mind in patients with asystole episodes. It can be checked easily by asking patients to take a deep breath.
Figure 1. Ambulatory electrocardiographic monitorization revealing ventricular asystole episodes.