Hasan Garan

Sustained ventricular tachycardia in recent canine myocardial infarction.

To study recurrent ventricular tachycardia in the late phase of myocardial infarction (MI), transmural anteroapical infarcts were created by ligation of the left anterior descending (LAD) coronary artery in 25 dogs. Twenty dogs survived LAD ligation and underwent an open-chest electrophysiologic study an average of 20 days after MI. Programmed electrical stimulation was carried out using the extrastimulus technique and short bursts of rapid ventricular pacing via bipolar electrodes positioned at multiple left ventricular endocardial sites. Sixteen dogs had electrically induced ventricular tachycardia, and in 11, sustained ventricular tachycardia was reproducibly initiated and terminated by programmed ventricular stimulation. Short bursts of rapid left ventricular pacing from areas in periinfarct zone was the most effective technique for initiating ventricular tachycardia. The electrophysiologic phenomena in this model of sustained ventricular tachycardia in 3-week-old MI included electrically induced changes in rate and morphology and biventricular capture without termination during tachycardia.

Long-term clinical outcome of patients with prior myocardial infarction after palliative radiofrequency catheter ablation for frequent ventricular tachycardia

Patients with coronary artery disease and hemodynamically tolerated, highly frequent, sustained monomorphic ventricular tachycardia (VT) may undergo radiofrequency catheter ablation (RFCA) for elimination of > or = 1 morphologically distinct VTs. The purpose of this study was to evaluate the long-term clinical benefit following RFCA as a palliative treatment of highly frequent or incessant ischemic VT. Fifty-five patients underwent RFCA of 62 VTs. The target VT was successfully ablated in 82% of patients. Complication and perioperative mortality rates were 7.2% and 1.8%, respectively. At 5 years, total mortality was 51% and probability of freedom from all ventricular tachyarrhythmias was 28%. All patients had highly frequent or incessant drug-refractory VT before RFCA. Clinical benefit was defined as either freedom from all ventricular tachyarrhythmias, or a reduction in frequency of recurrence from > 1 episode per month before RFCA to < or = 1 episode per year of any ventricular tachyarrhythmia, including all appropriate implantable cardioverter defibrillator (ICD) therapies. By this definition, 54% of the patients continued to benefit from RFCA at 5 years. Of 19 variables analyzed with a Cox univariate model, only the presence of a left ventricular aneurysm and a previously implanted ICD were predictive of any ventricular arrhythmia recurrence. However, at 5 years over half of the surviving patients still continued to benefit from RFCA of their clinical VT. Because the overall rate of any ventricular tachyarrhythmia occurrence during follow-up is high, additional protection, such as an ICD, is required.

Repetitive responses to single ventricular extrastimuli in patients with serious ventricular arrhythmias: incidence and clinical significance.

Electrophysiologic studies were carried out in 85 patients with serious ventricular arrhythmias: 44 with recurrent sustained ventricular tachycardia (group A), 16 with recurrent nonsustained ventricular tachycardia (group B), and 25 with recent prehospital ventricular fibrillation not associated with acute myocardial infarction (group C). Programmed ventricular stimulation from the right ventricular apex included premature stimulation during normal sinus rhythm, atrial pacing, and ventricular pacing, as well as brief bursts of rapid ventricular pacing (RVP). A repetitive ventricular response (RVR) was defined as one or more nonstimulated premature ventricular depolarizations in response to a single paced premature ventricular depolarization during normal sinus rhythm or atrial pacing. RVRs were observed in seven of 44 (16%) group A patients, one of 16 (6%) group B patients, and three of 25 (12%) group C patients. In contrast, single and double premature ventricular stimuli during ventricular pacing and/or bursts of RVP resulted in the reproducible initiation of ventricular tachycardia in 40 of 44 (91%) group A patients, 10 of 16 (63%) group B patients, and 19 of 25 (76%) group C patients. We conclude that RVRs to single ventricular extrastimuli during normal sinus rhythm or atrial pacing are rare, and therefore are an insensitive index of susceptibility to serious ventricular arrhythmias in these patients.

Endocardial, intramural, and epicardial activation patterns during sustained monomorphic ventricular tachycardia in late canine myocardial infarction.

Thirteen dogs in whom at least one morphologically distinct sustained ventricular tachycardia (VT) could be reproducibly initiated by programmed cardiac stimulation 18 +/- 3 days following experimental myocardial infarction were placed on total cardiopulmonary bypass for detailed study of the endocardial and epicardial activation during VT under hemodynamically stable conditions. Thirteen morphologically distinct monomorphic VTs were investigated by simultaneous epicardial, endocardial, and intramural bipolar recordings. Local electrograms were used to generate computer-assisted isochronous-activation sequence maps. A complete reentry circuit could be mapped on the epicardial surface in 4 animals and on the endocardial surface in one other animal. In the remaining 8 animals, there was a gap period lasting 43-62 msec in the cardiac cycle during which no endocardial or epicardial activity was observed. In 6 of the 8 animals, bipolar intramural recordings from sites closely associated with regions of endocardial and epicardial conduction block showed intramural activity progressing slowly during the gap period. In these 6 animals, a reentry circuit could be completed by incorporating the local electrograms recorded from the intramural sites. VT could be reproducibly terminated by selectively rendering only these intramural sites refractory by critically timed extrastimuli that failed to result in global ventricular capture. VT could be terminated by epicardial cooling in 2 of the 4 animals with epicardial reentry. By contrast, epicardial cryoablation did not effect intramural reentry and failed to interrupt VT. In this study, intramural pathways constituted an integral part of the reentry circuit in a large proportion of the VTs.

Localized reentry. Mechanism of induced sustained ventricular tachycardia in canine model of recent myocardial infarction.

This study was undertaken to investigate the mechanism underlying sustained monomorphic ventricular tachycardia (VT) in late experimental canine myocardial infarction. The hypothesis that sustained and organized continuous electrical activity (CEA) displaying a reproducible pattern with recurrent components recorded by bipolar endocardial, intramural, or epicardial electrodes in 10 animals during electrically induced sustained monomorphic VT represented reentrant excitation in an anatomically small area of the ventricle, was evaluated in the light of the following observations: Organized CEA always preceded the first monomorphic ventricular complex (QRS) of VT as well as the discrete local electrograms from closely surrounding sites during the initiation of VT. The site of organized CEA corresponded to the site of origin of sustained VT determined by iso-chronous contour map analysis of activation sequence. Ventricular pacing at rates more rapid than that of VT failed to terminate VT despite ventricular capture unless it transformed CEA into discrete local electrograms. VT could be terminated in three animals, with a single, critically timed premature stimulus delivered at a critically located focus close to the site of CEA, which would result in local capture and interrupted CEA. In six animals, surgical ablation of the site of organized CEA effectively prevented the reinitiation of sustained VT by programmed cardiac stimulation. These data showed that organized CEA and sustained VT were closely associated phenomena and suggested that organized CEA probably represented an important component of the tachycardia circuit.

Sinus arrest during treatment with amiodarone.

began. Now that our four children are a little older and I would like to concentrate more on my work I find that reorganisation of the NHS for the second time in 10 years has left me in a backwater, and although there are pious ideas about how to train me they are very unlikely to come to anything. I will probably be replaced by a general practitioner, and whether he or she is trained in paediatrics or not does not seem to be open to discussion. This would not happen if it were not for the fact that most people in community health are women who work part-time and appear to have no influence in medical politics. I would not advise any woman to take up medicine, because unless she continues fulltime practice however hard she tries to keep up any kind of satisfying career she is doomed to failure and no support from the rest of the profession, or so it seems to me.

Late potentials on the signal-averaged electrocardiogram after canine myocardial infarction: Correlation with induced ventricular arrhythmias during the healing phase

Signal-averaged electrocardiograms (ECGs) and programmed ventricular stimulation were serially performed in 12 dogs (3 weeks of age) after experimental anteroapical myocardial infarction. At electrophysiologic study, sustained ventricular tachyarrhythmia was induced in seven dogs on at least one occasion. Of a total of 39 electrophysiologic studies, sustained monomorphic ventricular tachycardia was induced in seven studies and ventricular fibrillation in eight studies. In the remaining studies, no ventricular arrhythmia could be induced with triple ventricular extrastimuli. There was considerable day to day variability in the response to programmed stimulation and the results of the signal-averaged ECG. The signal-averaged QRS complex was significantly longer in dogs with inducible ventricular tachycardia or fibrillation (61 +/- 5 versus 57 +/- 3 ms, p = 0.02), had a lower terminal QRS amplitude (24 +/- 20 versus 46 +/- 33 microV, p = 0.04) and a longer late potential duration (19 +/- 4 versus 15 +/- 3 ms, p = 0.003) compared with that in animals with no inducible ventricular arrhythmia. Late potentials were defined as a total QRS duration greater than 58 ms, a terminal QRS amplitude less than 20 microV and a late potential duration greater than 18 ms. Using this definition, late potentials were seen in two distinct phases--immediately after coronary ligation and then beyond the first 72 h after infarction. The appearance of late potentials coincided with a change in arrhythmia inducibility from no ventricular arrhythmia to initiation of sustained monomorphic ventricular tachycardia. There is a close relation between inducibility of ventricular tachycardia in experimental canine myocardial infarction and the appearance of late potentials on the surface ECG.(ABSTRACT TRUNCATED AT 250 WORDS)

Surface electrocardiographic manifestations of tachyarrhythmias: clues to diagnosis and mechanism.

Although major developments in the analysis of arrhythmias have occurred in recent years using invasive intracardiac electrophysiologic testing, it is prudent to acknowledge the information available from the surface electrocardiograph (ECG). Many electrophysiologic concepts derived from the surface ECG were based on deductive reasoning; these have now been confirmed by programmed stimulation studies and intracardiac mapping. Further, recent advances in signal processing have enhanced the interpretative power of the surface ECG. This review will attempt to present the current status of the surface ECG in elucidating the mechanisms and site of origin of both supraventricular and ventricular tachyarrhythmias.

Role of Electrophysiologic Studies in the Treatment of Tachycardias

The treatment of recurrent ventricular tachyarrhythmias is difficult to standardize, and the effectiveness of drugs is difficult to evaluate [66A, 130L, 119S, 224S, 153W, 161W, 162W]. Serial electrophysiologic studies (EPS) have been used to improve the predictive accuracy of antiarrhythmic drug therapy. This chapter reviews the methodology, clinical results, and limitations of programmed electrical stimulation as a diagnostic and therapeutic tool for the treatment of tachycardias.

Treatment of ventricular arrhythmias.

Within the past 20 years, our knowledge concerning the epidemiology, natural history, and treatment of VT has expanded greatly. A variety of effective pharmacologic, surgical and electrical therapies for VT are now available to the clinician. Patients who present with ventricular tachyarrhythmias should undergo a comprehensive medical evaluation directed at identifying and treating such factors as ischemia, congestive heart failure, valvular heart disease, sensitivity to cardioactive drugs, and metabolic derangements. Many patients who present with asymptomatic ventricular arrhythmias do not require specific antiarrhythmic drug therapy. However, certain patients who have already suffered a life-threatening arrhythmia or who are at high risk for such arrhythmia should be vigorously treated with specific antiarrhythmic therapy guided for that individual patient. The efficacy of any antiarrhythmic treatment should be assessed by ECG monitoring, exercise testing, and/or electrophysiologic study. In the near future, potentially revolutionary new electrical therapies for ventricular tachyarrhythmias will be evaluated. It is to be hoped that these devices used in combination with pharmacologic and surgical therapies may dramatically reduce the incidence of sudden cardiac death in high-risk patients.