ABSTRACT
In an 86-year-old woman who had been treated for sick sinus syndrome, the small high-frequency current delivered by pacemaker in order to measure the minutes ventilation for utilizing the rate-response mode was transiently over-sensed on the Holter electrocardiogram. Although her pacing system was working appropriately, the numbers of the paced beats on the automatic Holter analysis were undercounted (from >60% to <5%) during the over-sensing periods because these currents were recognized as multiple pacing spikes. Physicians need to pay attention to such multiple pacing spike markers, because these can be a cause of unreliable results of the Holter analysis.
ABSTRACT
A 71-year-old woman had undergone valvular heart surgery in 1981, and implantation of a permanent ventricular pacemaker for ventricular pauses during atrial fibrillation in 2001. One year after pacemaker implantation, she complained of faintness. When pacing at 100 beats/min the pacemaker functioned properly. However, pacing and sensing failure was detected at a pacing rate of 60 beats/min. At rapid pacing rates, the lead tip was in closer contact with the endocardium, and its microdislodgment was undetectable. The symptoms have resolved since the lead was repositioned.
Subject(s)
Pacemaker, Artificial , Aged , Atrial Fibrillation/therapy , Cardiac Pacing, Artificial , Electrocardiography , Electrodes, Implanted , Equipment Failure , Female , Heart Rate , Humans , Time FactorsABSTRACT
This patient was a 50-year-old man. Oral pilsicainide unmasked a Brugada-type ECG abnormality and self-terminating polymorphic VT was repetitively induced. The polymorphic VT always developed following a specific ventricular premature complex showing a left bundle branch block pattern suggesting a limited origin in the right ventricle.
Subject(s)
Bundle-Branch Block/complications , Death, Sudden, Cardiac , Ventricular Fibrillation/etiology , Ventricular Premature Complexes/complications , Bundle-Branch Block/physiopathology , Electrocardiography , Humans , Male , Middle Aged , Syndrome , Ventricular Fibrillation/physiopathology , Ventricular Premature Complexes/physiopathologySubject(s)
Electrophysiologic Techniques, Cardiac , Long QT Syndrome/physiopathology , Adolescent , Adult , Aged , Anti-Arrhythmia Agents/pharmacology , Electrocardiography , Epinephrine/pharmacology , Female , Humans , Long QT Syndrome/congenital , Male , Mexiletine/pharmacology , Middle Aged , Sympathomimetics/pharmacologyABSTRACT
OBJECTIVES: We sought to identify the triggers of ventricular tachyarrhythmia (VTA) in experimental models of long QT type 2 (LQT2) and long QT type 3 (LQT3) syndromes. BACKGROUND: Most adverse cardiac events occurring in the long QT type 1 syndrome are related to sympathetic nerve activity. In contrast, various factors may trigger VTA in patients with LQT2 and LQT3. METHODS: The mode of onset of VTA and therapeutic effects of the potassium-adenosine triphosphate channel opener nicorandil were compared in canine models of LQT2 and LQT3, using three induction protocols: 1) bradycardia produced by atrioventricular block (BRADY); 2) programmed ventricular stimulation; and 3) electrical stimulation of the left stellate ganglion (left stellate stimulation [LSS]). Transmural unipolar electrograms were recorded, and the activation-recovery interval (ARI) was measured. RESULTS: Ventricular tachyarrhythmias developed during BRADY in all six experiments in the LQT3 model, but in none of the six experiments in LQT2. Programmed ventricular stimulation induced VTA in two experiments of the LQT2 model, but in none of the LQT3 experiments. Stimulation of the left stellate ganglion induced VTA in three experiments in LQT2 and in two experiments in LQT3. Nicorandil caused greater shortening of ARI and greater attenuation of transmural ARI dispersion in the LQT2 model than in the LQT3 model. After treatment with nicorandil, a single VTA was induced in the LQT2 model by LSS, whereas in the LQT3 model, VTA remained inducible by BRADY in four experiments and LSS in one experiment. CONCLUSIONS: An abrupt increase in sympathetic activity appeared arrhythmogenic in both models. Nicorandil attenuated the heterogeneity of ventricular repolarization and suppressed the induction of VTA in the LQT2 model, but had a limited therapeutic effect in the LQT3 model.
Subject(s)
Anti-Arrhythmia Agents/administration & dosage , Long QT Syndrome/complications , Long QT Syndrome/drug therapy , Nicorandil/administration & dosage , Tachycardia/drug therapy , Tachycardia/etiology , Animals , Blood Pressure/drug effects , Bradycardia/drug therapy , Bradycardia/etiology , Disease Models, Animal , Dogs , Electrocardiography , Heart Block/drug therapy , Heart Block/etiology , Heart Conduction System/drug effects , Infusions, Intravenous , Models, Cardiovascular , Treatment OutcomeABSTRACT
A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V1 to V3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V3 to V6 concomitant with visible QT/T alternans in leads V4 and V5, and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricular tachyarrhythmias in such patients.
