Ventricular tachycardia late after myocardial infarction is usually due to reentry in the infarct region. These reentry circuits can be large, complex and difficult to define, impeding study in the electrophysiology laboratory and making catheter ablation difficult. Pacing through the electrodes of the mapping catheter provides a new approach to mapping. When pacing stimuli capture the effects on the tachycardia depend on the location of the pacing site relative to the reentry circuit. The effects observed allow identification of various portions of the reentry circuit, without the need for locating the entire circuit. Isthmuses where relatively small lesions produced by radiofrequency catheter ablation can interrupt reentry can often be identified. A classification that divides reentry circuits into one or more functional components helps to conceptualize the reentry circuit and predicts the likelihood that heating with radiofrequency current will terminate tachycardia. These methods are helping to define human reentry circuits.
Radiofrequency catheter ablation controls VT that is sufficiently stable to allow mapping in 67% of patients despite failure of antiarrhythmic drug therapy and multiple inducible VTs. However, ablation was largely adjunctive to amiodarone and defibrillators in this referral population.
Alterations in cardiac electrophysiology that accompany myocardial infarction were studied in dogs subjected to a two-stage ligation of the anterior descending coronary artery. A multipolar transmural needle electrode was used to record electrical activity from the in situ infarcted heart 24 hours after coronary occlusion. Bipolar electrograms recorded from subendocardial regions of infarcted myocardium demonstrated the persistence of early, rapid deflections suggesting Purkinje fiber activity; evidence of ventricular muscle activity in the infarct was absent in both subendocardial and intramural electrograms. The infarcted myocardium and the adjacent non-infarcted tissue were then excised and studied with intracellular microelectrodes in vitro. Transmembrane action potentials could be recorded from one or two cell layers of subendocardial Purkinje fibers at all sites within the infarcted region, but no ventricular muscle action potentials were found. Subendocardial Purkinje fibers which survived in the infarct had reduced maximum diastolic potentials, action potential amplitudes, and maximum depolarization velocities compared with normal subendocardial Purkinje fibers; also, action potential durations in these surviving fibers were extraordinarily prolonged. Spontaneous diastolic depolarization was evident in some surviving fibers. Since subendocardial Purkinje fibers that generate abnormal action potentials survive in an infarct, these fibers may participate in the genesis of ventricular arrhythmias that accompany infarction. KEY WORDS coronary occlusion cardiac arrhythmias microelectrode bipolar electrogams transmembrane action potentials From the 597 by guest on June 9, 2015 http://circres.ahajournals.org/ Downloaded from 598 FRIEDMAN, STEWART, FENOGLIO, WIT
MethodsElectrophysiological studies were performed on both in situ infarcted myocardium and excised, superfused infarcted myocardium. In addition, isolated preparations from dogs without infarction were also studied.Surgical Production of Myocardial Infarction.-Nine mongrel dogs, (10-14 kg) were anesthetized with sodium pentobarbital (30 mg/kg, iv), intubated with a cuffed endotracheal tube, and ventilated by a positivepressure mechanical pump. A lead II electrocardiogram was continuously monitored and recorded on a switched-beam oscillographic recorder (Electronics for Medicine). Using sterile technique, the chest was opened through the fourth left intercostal space and the pericardium was reflected widely. The anterior descending branch of the left coronary artery was isolated from the accompanying vein 10-15 mm distal to its point of origin, and a two-stage ligation was performed according to the technique previously described by Harris (5). The chest was then closed in layers and an airtight seal was maintained.All dogs subjected to this surgical procedure developed extensive infarction of the anterior left ventricular wall, left anterior papillary muscle, and anterior interventricular septum, as verified by subsequent histological study. Two of the d...
RN; and the AVID InvestigatorsBackground-Implantable cardioverter defibrillator (ICD) use reduces mortality in patients with serious ventricular arrhythmias compared with antiarrhythmic drug (AAD) use. However, the relative impact of these therapies on self-perceived quality of life (QoL) is unknown. Methods and Results-Three self-administered instruments were used to measure generic and disease-specific QoL in Antiarrhythmics Versus Implantable Defibrillators trial participants. Generalized linear models were used to assess the relationships between self-perceived QoL and treatment (AAD versus ICD) and adverse symptoms and ICD shocks. To minimize the impact of missing data, only patients surviving 1 year were included in the primary analyses. Baseline characteristics among QoL participants (nϭ905) and nonparticipants (nϭ111) were similar, but participants who survived 1 year (nϭ800) were healthier at baseline than nonsurvivors (nϭ105). Of the 800 patients in the primary analysis, characteristics of those randomized to AAD (nϭ384) versus ICD (nϭ416) were similar. Overall, ICD and AAD use were associated with similar alterations in QoL. The development of sporadic shocks and adverse symptoms were each associated with reduced physical functioning and mental well-being and increased concerns among ICD recipients, whereas development of adverse symptoms was associated with reduced physical functioning and increased concerns among AAD recipients. Conclusions-ICD and AAD therapy are associated with similar alterations in self-perceived QoL over 1-year follow-up.Adverse symptoms were associated with reduced self-perceived QoL in both groups, and sporadic shocks were associated with reduced QoL in ICD recipients. (Circulation. 2002;105:589-594.)
Delivery of ICD therapy in AVID patients was common, primarily due to VT. Inappropriate ICD therapy occurred frequently. Use of ICD therapy as a surrogate endpoint for death in clinical trials should be avoided.
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