Syncope, pacemakers

Sutton R, Brignole M, Menozzi C et al. for the Vasovagal Syncope International Study (VASIS) Investigators Dual-chamber pacing in the treatment of neuraUy mediated tilt-positive cardioinbibitory syncope pacemaker versus no therapy a multicenter randomized study. Circulation 102(3), 294—299 (2000). 

Oral Severe sinus-node dysfunction, causing marked sinus bradycardia second-and third-degree AV block when episodes of bradycardia have caused syncope (except when used in conjunction with a pacemaker). 

Contraindications Bradycardia-induced syncope (except in the presence of a pacemaker), second-and third-degree AVblock, severe hepatic disease, severe sinus-node dysfunction... 

A 32-year-old woman took 800 mg of citalopram, 20 times her usual daily dose, in a suicide attempt. On admission to hospital she had a sinus bradycardia (41/ minute) but the electrocardiogram was otherwise normal, with a QT interval of 430 ms. Treatment with atropine failed to increase her heart rate and she had hypotension and syncope. A temporary pacemaker was inserted and was required for the next 6 days before it could be safely removed. 

Rothenhausler HB, Hoberl C, Ehrentrout S, Kapfhammer HP, Weber MM. Suicide attempt by pure citalopram overdose causing long-lasting severe sinus bradycardia, hypotension and syncopes successful therapy with a temporary pacemaker. Pharmacopsychiatry 2000 33(4) 150-2. 

A very uncommon adverse effect involves sinus node dysfunction (extreme bradycardia, sinus arrest, sinoatrial block), which can be associated with syncopal episodes, perhaps due to hypothyroidism (119,120). In such cases, lithium must either be withdrawn or continued in the presence of a pacemaker. At therapeutic concentrations, other cardiac conduction disturbances have been reported, sometimes in conjunction with hypercalcemia (121), but are uncommon. 

A 66-year-old woman with pre-existing first-degree AV block, developed sinus bradycardia, a junctional rhythm, a prolonged QT interval, and syncopal episodes (serum lithium concentration 1.4 mmol/1 in a 40-hours sample) about 2 weeks after beginning lithium therapy. She was treated successfully with a pacemaker and a lower dose of lithium (133). 

A 59-year-old woman with syncope and sick sinus syndrome, which remitted when lithium was withdrawn, recurred when lithium was restarted, and then persisted despite lithium withdrawal after a pacemaker was implanted she was treated successfully with lithium for 7 years (135). 

Soon after the start of donepezil treatment three patients with Alzheimer s disease developed cardiac syncope (52). In two cases, a bradydysrhythmia was documented and pacemaker implantation was considered justified rather than donepezil withdrawal. 

Historically, most pacemaker and ICD procedures have been performed on an inpatient basis. As a rule, under the circumstance, the preoperative evaluation, the actual procedure, as well as postoperative care are rendered in the hospital. In the case of both permanent pacing and ICD implantation, individuals are generally admitted with major symptoms such as syncope. The patient is formally admitted, and the procedure is scheduled after a complete workup. After the procedure, the patient is observed briefly in the hospital and subsequently discharged and referred for outpatient device follow-up. In today s cost-containment environment, such an approach is inefficient and not cost effective. Thus, there has been an attempt to abbreviate the patient s hospital stay and render care on an ambulatory basis. 

Fig. 10.13 (A) Lead II ECG in a patient with syncope intraventricular conduction block but no documented AV block at rest. (B) On exercise 2 1 AV block occurs and 1 1 AV conduction returns during the recovery period. A subsequent electrophysi-ological study revealed infranodal AV block at an atrial pacing rate of 110/min and a permanent pacemaker was implanted. No further syncope occurred.

Fig. 10.14 Very long HV interval representing severe disease of the His-Purkinje system. His bnndle recording in a patient with right bundle branch block and syncope. Left ventricular ejection fraction was normal. There was no documentation of seconder third-degree AV block before the electrophysiological study. Note the very long HV interval of 124ms measured from the His bundle potential to the earliest ventricular activation either in the surface or intracardiac leads, (normal = 35-55 ms) responsible for the first-degree AV block. Time fines = 10ms. A = low atrial depolarization, H = His bundle potential, V = Activation of high ventricular septum. Syncope disappeared after implantation of a permanent pacemaker.

Patients were enrolled if they had three or more clinically severe syncopal episodes in the last 2 years without significant electrocardiographic and cardiac abnormalities. Orthostatic hypotension and carotid sinus syncope were excluded. After ILR implantation, patients were followed until the first documented syncope (Phase 1). The ILR documentation of this episode determined the subsequent therapy and commenced Phase 11 foUow-up. Among 392 patients, the 1-year recurrence rate of syncope during Phase I was 33%. One hundred and three patients had a documented episode and entered Phase 11 53 patients received specific therapy (46) a pacemaker because of asystole of a median 11.5s duration and six anti-tachyarrhythmia therapy (catheter ablation four, implantable defibrillator one, anti-arrhythmic drug one)] and the remaining 50 patients did not receive specific therapy. The 1-year recurrence rate in 53 patients assigned to a specific therapy was 10% (burden 0.07 0.2 episodes per patient/year) compared with 41% (burden 0.83 1.57 episodes per patient/year) in the patients without specific therapy (80% relative risk reduction for patients, p = 0.002, and 92% for burden, p = 0.002). The 1-year recurrence rate in patients with pacemakers was 5% (burden 0.05 0.15 episodes per patient/year). Severe trauma secondary to syncope relapse occurred in 2% and mild trauma in 4% of the patients. 

There is perhaps no other treatment modality that is more controversial than the role of permanent cardiac pacing. Some episodes of NCS, both spontaneous and tilt-induced, are associated with profound bradycardia or asystole which led to the impetus to test pacemakers as therapy. There have been numerous trials on pacing in syncope, the results of which have been mixed. This has led to a certain degree of uncertainty regarding the role pacemakers can play in syncope if any at all. 

Finally, Peterson et al. (18) presented data on the long-term effects of permanent pacing in patients with severe recurrent syncope and reproducible tilt-induced neurocardiogenic syncope with a pronounced bradycardic component. Dual-chamber permanent pacemakers were implanted in 37 patients who were then followed for 50 24 months. Approximately 89% had a marked reduction in symptoms, while 27% had complete elimination of symptoms. There was a reduction in the overall frequency of syncopal episodes from 136 to 11 episodes/year. Interestingly, the clinical features that best predicted the usefulness of permanent pacing included a relatively younger age (56 compared to 76 years) and the absence of a prodrome (84). 

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