Identification of patients at risk of ventricular tachyarrhythmias after myocardial infarction.
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Death, Sudden↗
Biomedical subjects
A Martinez-Rubio
Publications and source records attributed to A Martinez-Rubio.
[Catheter ablation in ventricular tachycardia].
The basis for management of ventricular tachycardia (VT) is pharmacologic treatment which is effective, however, in only about 20 to 30% of the patients. With respect to this problem, alternative therapeutic modes have been developed which include, in addition to antitachycardia stimulation, electrical, palliative therapy such as the implantable automatic defibrillator, definitive measures such as map-guided antitachycardia surgery and catheter ablation. The goal of catheter ablation is the selective destruction of heart structures which are the morphologic correlate for initiation of propagation of VT. Catheter ablation was discovered by chance by Fontaine after a defibrillation during an electrophysiologic study in which a defibrillating electrode in the proximity of a catheter at the His bundle induced complete AV-block. This effect of destruction in the AV-conduction system by direct current as a therapeutic measure was further developed by Gallagher and Scheinman. The mechanism held responsible is coagulation by the electrode of neighboring tissue and barotrauma. The technique, which was initially used for ablation of the His bundle in supraventricular tachycardia, can also be used for ablation of accessory pathways or the site of origin of VT which generally lies endocardially in marginal regions of myocardial infarctions. CATHETER MAPPING: In sinus rhythm and induced VT, endocavity catheter mapping is carried out after heparinization with electrocardiograms recorded from at least six to ten sites in the right and left ventricles. At the site of early activation, detailed mapping is used for identification of the site of earliest activation, then pace-mapping is performed during sinus rhythm and VT. The morphology of the stimulated QRS complexes is compared with that of the spontaneous VT. In patients in whom VT cannot be induced, localization is carried out by pace-mapping alone. CATHETER ABLATION: After localization, in intubation narcosis and with continuously monitored arterial blood pressure, the suspected site of origin of the VT is subjected to an initial shock during sinus rhythm by means of a distal electrode of a catheter in stable contact with the endocardium. For mapping and ablation, the same catheter is used. After each subsequent shock, assessment is performed to determine if the distal electrode pair still conducts local ventricular signals and if ventricular stimulation is possible. The shock energy delivered is 100, 200 or 400 Joules. At the time of shock discharge, the remaining electrodes or catheters are disconnected. In the case of bradycardia or tachycardia after the shock, immediate connection to an external stimulation generator is established. At the time of the shocks, relaxation is provided by succinylcholine. All shocks are delivered from the anode. The integrity of the catheter is tested after each shock, no catheter is used more than three or four times. At the earliest, ten minutes after shock delivery, induction of clinical VT is attempted with programmed stimulation and if induction is possible, at the same site a maximum of two more shocks are delivered or, after renewed mapping, another shock is delivered to a different site. Induced non-clinical VT is not subjected to ablation.(ABSTRACT TRUNCATED AT 400 WORDS)
Atrioventricular Node↗
Pathophysiological mechanisms of ventricular tachyarrhythmias.
The pathophysiological background for ventricular tachyarrhythmias based on experimental and clinical evidence is presented. Sudden cardiac death may occur as the first manifestation of coronary artery disease without antecedent complaints or it may occur in patients with a previous myocardial infarction. In the latter situation, a circumscribed area of cardiac tissue may be responsible for the genesis and maintenance of a ventricular tachyarrhythmia which may be called the 'arrhythmogenic substrate'. This zone of electrically abnormal ventricular myocardium is usually located at the border of a previous myocardial infarction, and is characterized by islands of relatively viable muscle alternating with areas of necrosis and, later, fibrosis. The consequent fragmentation of the propagating electromotive forces leads to the development of high-frequency components that can be recorded directly or non-invasively using signal-averaging techniques. These signals have been called ventricular late potentials. The 'arrhythmogenic substrate' may be present permanently or may rise acutely and be present only transiently in the case of extensive ischaemia or acute myocardial infarction. In the setting of a chronic 'arrhythmogenic substrate', this electrically abnormal tissue may be triggered by spontaneously occurring ventricular ectopic beats or salvoes or by programmed ventricular stimulation, as well as by transient episodes of ischaemic causing spontaneous arrhythmias. These trigger factors modify the 'arrhythmogenic substrate' in such a way that ventricular tachyarrhythmias are sustained. It is apparent that sudden cardiac death is due to a wide spectrum of pathophysiological mechanisms which may be interrelated. There is obviously no single parameter that helps the clinician to predict the propensity for sudden cardiac death in the individual patient.
Coronary Disease↗
Catheter ablation of ventricular tachycardia using defibrillator pulses: electrophysiological findings and long-term results.
Catheter ablation of ventricular tachycardia (VT) was attempted in 24 patients (mean age 49 +/- 15.1 years) with a history of recurrent sustained VT resistant to previous antiarrhythmic drug therapy. 14 patients (58.3%) had also failed to respond to long-term administration of amiodarone alone and in combination with class I antiarrhythmic drugs. Endocardial catheter mapping during induced or spontaneous VT and/or pacemapping were performed to identify the site of origin of VT. Direct-current high-energy anodal shocks were delivered from a conventional cardioverter with stored energies of 100, 200 or 400 J via the distal electrode of conventional catheters. A total of 139 shocks was delivered during the ablation procedure. One patient died from wall perforation. Within 1 week of ablation, nine patients developed spontaneous recurrences of monomorphic sustained VT, identical to the clinical VT, and one patient developed a VT with a new morphology. In addition, four patients had a recurrence of their clinical VT after several weeks. In seven of 14 patients with spontaneous recurrences after the first ablation procedure and in three patients in whom VT was again inducible at the end of the first week, a second ablation procedure was performed. One patient with inducible VT after the first and second ablation sessions was given a third ablation procedure, and was discharged from hospital on anti-arrhythmic drugs which were successful despite being previously ineffective. After a mean follow-up period of 14.1 +/- 9.1 months, there were no spontaneous recurrences of sustained VT in 17 patients (71%) (nine without antiarrhythmic drugs and eight on antiarrhythmic drugs). In the remaining patients, incessant non-sustained VT (n = 2) or recurrent sustained VT (n = 2) occurred, and two patients died suddenly (at 2 and 21 months). There was no correlation between catheter mapping data or the results of pre-discharge electrophysiological study and clinical outcome during long-term follow-up. Complications related to catheter ablation included pulmonary oedema, cardiac tamponade, femoral artery occlusion, multiple episodes of ventricular tachycardia/fibrillation and thrombus formation, each in one patient (major complications; n = 7,29.1%), as well as transient third degree AV block, transient right or left bundle branch block, transient marked ST elevation or transient atrial tachycardia (minor complications; n = 8, 33.3%). The results suggest that catheter ablation might become an effective procedure for the non-pharmacological treatment of sustained VT.(ABSTRACT TRUNCATED AT 400 WORDS)
Adolescent↗
[Behavior of ventricular late potentials following catheter ablation of ventricular tachycardia].
In 10 patients non-invasively recorded signal-averaged electrocardiograms were obtained before and after direct-current ablation of ventricular tachycardia (right ventricular origin n = 5; left ventricular origin n = 5). The algorithms proposed by Simson and Karbenn et al. were used (modified Frank leads, high-pass filter cut-off frequency 25 Hz). No differences were observed between the mean values of the duration of the QRS-complex, the mean voltage during the last 40 ms of the QRS-complex, the duration of the late potentials and the number of patients having late potentials before and after ablation, respectively. The success of ablation could not be predicted by the signal-averaged ECG. There was no difference between the averaging parameters of those patients without recurrences of ventricular tachycardia during the follow-up period and those with (n = 3). Thus, the signal-averaged ECG did not prove helpful in predicting a successful outcome of direct-current catheter ablation of ventricular tachycardia.
Adult↗
Termination of re-entrant ventricular tachycardia by subthreshold stimulus applied to the zone of slow conduction.
A 52-year-old female patient developed recurrent sustained ventricular tachycardia during the first week after left ventricular aneurysmectomy. The patient had no history of ventricular tachycardia preoperatively. As her tachycardias proved to be resistant to several antiarrhythmic drugs, catheter ablation was considered. To define the site of origin of ventricular tachycardia, endocardial catheter mapping and pace-mapping were performed. In addition, the response to single premature stimuli applied during ventricular tachycardia was assessed. At a site in the basal portion of the antero-septal area of the left ventricle, early presystolic endocardial activity during ventricular tachycardia was found. Continuous pacing as well as premature stimulation from that site showed a marked delay between the stimulus artefacts and the induced QRS complexes. The stimulus-induced QRS complexes were identical to QRS complexes of spontaneous and induced ventricular tachycardia. At very short critical coupling intervals of single premature stimuli that did not capture the ventricles (non-propagated stimuli), ventricular tachycardia was reproducibly terminated. These findings are explained by assuming that the catheter was located within the zone of slow conduction of the re-entrant circuit, possibly in its proximal portion.
Atrioventricular Node↗
Prognostic significance of ventricular late potentials in the postmyocardial infarction period.
Ventricular late potentials in patients after myocardial infarction can be assumed to herald an increased risk of future sudden cardiac death or symptomatic sustained ventricular tachycardia. This holds particularly true for patients studied early after recent myocardial infarction whereas patients assessed later in the subsequent course have a substantially lesser incidence of arrhythmic events, probably due to intercurrent death of those at high risk. Of prognostic importance appears not only the presence but also the duration of late potentials. A meaningful role is also assumed by the extent of left ventricular functional impairment (EF less than 40%). However, in consideration of the complex mechanisms that can lead to sudden cardiac death, no single method predicts with high sensitivity the occurrence of a ventricular tachyarrhythmic event. Sudden cardiac death can be incurred on the basis of chronic electrophysiological abnormalities as a consequence of regional slow conduction in the border zone of a previous myocardial infarction precipitated by trigger factors such as spontaneous ventricular arrhythmias. Sudden cardiac death or symptomatic sustained ventricular tachycardia can also occur due to sudden and transient changes in the electrophysiological properties of the myocardium due to ischemia. Whether the combination of late potentials with clinical parameters such as ventricular arrhythmias detected in the ambulatory ECG and those induced with programmed electrical stimulation will lead to more accurate identification of patients at risk prerequisites further elucidation. Currently available literature indicates that in patients with late potentials, ventricular tachycardias can be induced more frequently by programmed electrical stimulation and that the combination of both phenomena confers a particularly high risk.
Atrioventricular Node↗
Effects of non-pharmacological interventions on ventricular late potentials.
The purpose of the paper is to review the presently available information of the effects of non-pharmacological interventions for the control of drug-refractory ventricular tachyarrhythmias on non-invasively recorded ventricular late potentials. During recent years, non-pharmacological interventions have evolved as an alternative form of treatment to control drug-refractory ventricular tachyarrhythmias. The effects of these non-pharmacological measures on ventricular late potentials are poorly understood. Successful surgical control of ventricular tachycardia often normalizes the signal averaged ECG and may eliminate delayed potentials. Thus, this non-invasive test may be useful in assessing surgical efficacy in subgroups of patients with ventricular tachycardia. However, the clinical value of late potentials in assessing surgical efficacy in the individual case may be limited as the sensitivity and specificity of the loss of late potentials after antitachycardia surgery are low. In addition, the effects of transvenous catheter ablation on ventricular late potentials will be reviewed. The available information suggests that this intervention has little effects on the presence or absence of late potentials. Thus, non-invasive recording of late potentials seems not to be helpful in predicting the acute and long-term efficacy of catheter ablation. In conclusion, changing of the parameters in the signal-averaged QRS complex after antitachycardia surgery may be useful in predicting the efficacy of surgical interventions for drug-refractory ventricular tachycardias in subgroups of patients. However, the sensitivity and predictive accuracy of this test are low, thus limiting its clinical usefulness.
Cardiac Pacing, Artificial↗
Reduced beat-to-beat changes of heart rate: an important risk factor after acute myocardial infarction.
The prognostic significance of heart rate variability derived from 24-hour electrocardiographic recordings was investigated in 250 patients with acute myocardial infarction. During a follow-up of 6 months 15 patients experienced a serious arrhythmic event. These patients showed a significantly reduced beat to beat variability (p = 0.006), a slightly reduced 5-min variability (p = 0.04) and no significant differences in the 24-hour variability compared to the patients free of arrhythmic events. Based on Cox proportional hazard analysis, beat to beat variability remained an independent risk factor (p = 0.0036) in addition to the presence or absence of ventricular late potentials (p = 0.0004) and history of previous infarction (p = 0.04).
Aged↗