Sustained Ventricular Tachycardia In Patients Research Articles

Antagonism of quinidine's electrophysiologic effects by epinephrine in patients with ventricular tachycardia

The purpose of this study was to determine whether pharmacologically induced elevations in the plasma epinephrine concentration within reported physiologic limits alter the response to quinidine during electropharmacologic testing. Twenty-one patients with coronary artery disease and a history of unimorphic ventricular tachycardia were found to have inducible sustained unimorphic ventricular tachycardia that was suppressed by treatment with oral quinidine gluconate. Epinephrine was then infused at a rate of either 25 or 50 ng/kg per min and testing was repeated. These infusion rates of epinephrine were previously demonstrated to result in elevations of the plasma epinephrine concentration in the range of concentrations that occur during a variety of stresses.Quinidine significantly lengthened the ventricular refractory periods and the QRS duration at a ventricular pacing cycle length of 350 ms, which was used as an index of intraventricular conduction. Epinephrine partially or completely reversed the effects of quinidine on ventricular refractory periods, but had no effect on QRS duration. During electropharmacologic testing of quinidine, no ventricular tachycardia was inducible in 12 patients, and only nonsustained ventricular tachycardia, 8 to 48 beats in duration, was inducible in 9 patients. Retesting during infusion of epinephrine demonstrated inducible sustained unimorphic ventricular tachycardia in 2 of the 12 patients in whom quinidine had completely suppressed the induction of ventricular tachycardia and in 8 of the 9 patients in whom only nonsustained ventricular tachycardia had been inducible during testing of quinidine.In conclusion, physiologic elevations in the plasma epinephrine concentration may reverse quinidine-induced prolongation of ventricular refractoriness but not intraventricular conduction. Epinephrine may facilitate the induction of sustained ventricular tachycardia in patients in whom quinidine has suppressed this arrhythmia. Patients in whom nonsustained ventricular tachycardia is inducible during electropharmacologic testing may be particularly susceptible to antagonism by epinephrine of quinidine's therapeutic effects.

Value of the signal-averaged electrocardiogram as a predictor of the results of programmed stimulation in nonsustained ventricular tachycardia

A prospective assessment of several clinical variables, left ventricular function indexes, Holter recording characteristics and signal-averaged electrocardiogram (ECG) for their value in predicting the inducibility of sustained ventricular tachyarrhythmias was carried out in a consecutive series of 105 patients with nonsustained ventricular tachycardia (VT). The patients were divided into 3 groups based on the results of programmed electrical stimulation: group 1, 22 patients with induced sustained monomorphic VT; group 2, 14 patients with induced ventricular fibrillation (VF) and group 3, 69 patients with no induced sustained VT/VF. Left ventricular ejection fraction < 0.40, history of syncope/presyncope and abnormal signal-averaged ECG were significantly more common in group 1 than in group 3. No significant difference was found between groups 2 and 3. The sensitivity, specificity and predictive accuracy of the signal-averaged ECG for the induction of sustained monomorphic VT were 64, 89 and 84%, respectively. Using stepwise discriminant function analysis, the signal-averaged ECG was found to be the single most accurate screening test to predict the inducibility of sustained VT in patients with nonsustained VT and Its value was independent of the etiology of heart disease and the length of spontaneous runs. Because of the very high specificity and negative predictive accuracy, patients with normal signal-averaged ECGs may not require invasive evaluation.

Short- and long-term reproducibility of the signal-averaged electrocardiogram in coronary artery disease

In recent years, there has been a marked increase in the number of studies involving the signal-averaged electrocardiogram (SAECG). 1–3 This renewed interest in SAECGs is related to the finding that late potentials (LP) detected on SAECG are specific noninvasive markers for spontaneous or inducible sustained ventricular tachycardia in patients with coronary artery disease (CAD). 1–6 However, data on reproducibility and stability of these signals are available only in normal subjects. 5 The purpose of our study was to examine the short- and long-term reproducibility of the quantitative indexes of SAECGs in patients with CAD.

Correlation between signal-averaged electrocardiogram and programmed stimulation in patients with and without spontaneous ventricular tachyarrhythmias

This study examined the incidence of delayed ventricular activation on signal-averaged electrocardiograms and the incidence of inducible sustained ventricular tachycardia (VT) at programmed stimulation (1 or 2 extrastimuli) in patients with and patients without spontaneous ventricular tachyarrhythmias. The correlation between delayed ventricular activation and inducible VT was investigated in 371 patients with acute myocardial infarction (AMI). In 32 patients with no ventricular disease and no spontaneous arrhythmias (group 1), ventricular activation time averaged 115 ± 2 ms, compared with 166 ± 3 ms (p <0.001) for 65 patients with spontaneous ventricular tachyarrhythmias late after AMI (group II). In AMI patients with no spontaneous arrhythmias, ventricular activation time averaged 133 ± 2 ms for 306 patients studied 1 to 4 weeks after AMI (group III) and 130 ± 2 ms for 67 patients studied 3 to 12 months after AMI (group IV). The values for group III and group IV patients were each significantly higher than for group I (p <0.001), but lower than that for group 11 (p <0.001). The incidence of delayed ventricular activation was 89% for group 11, 26% for group III and 18% for group IV. Sustained VT was not Inducible in group I patients, but was inducible in 78% of group 11 (p <0.001 vs group I) and 20% of group III (p <0.05 vs group 1; p <0.001 vs group II) (group IV was not studied). In the 371 group 11 and group III patients, there was a strong correlation (p <0.001) between the presence of delayed ventricular activation and the ability to induce VT. Thus, delayed ventricular activation detected on the signal-averaged electrocardiogram may be a noninvasive predictor of the ability to induce sustained VT in patients with and without spontaneous ventricular tachyarrhythmias.

Sustained ventricular tachycardia in patients with dilated cardiomyopathy: electrophysiological testing

Sustained ventricular tachycardia in patients with dilated cardiomyopathy: electrophysiological testing

Alterations in norepinephrine content and beta adrenoceptor regulation in myocardium bordering aneurysm in human heart: their possible role in the genesis of ventricular tachycardia.

On the assumption that alterations in the adrenergic system may play a role in generating ventricular tachycardia in patients with myocardial post-infarction apical aneurysm, we evaluated norepinephrine concentration, number and affinity of both beta 1 and beta 2 adrenoceptors in perianeurysmatic tissue in twelve patients operated upon for congestive heart failure and recurrent sustained ventricular tachycardia. Concentration of norepinephrine in perianeurysmatic tissue was 0.1 +/- 0.05 micrograms g-1 tissue (n = 8), this value being much lower than that found in papillary muscle (n = 10) from patients with mitral valve stenosis (0.8 +/- 0.02 micrograms g-1 tissue) (P less than 0.01). The total number of beta adrenoceptors (71.4 +/- 7.8 v. 48.0 +/- 5.1 fmol mg-1 protein; P less than 0.01) and the percentage of beta 1 subtype were found to be higher in perianeurysmatic tissue (approximately 90%) than in papillary muscle (approximately 68%). Out of twelve patients with aneurysm, beta 2 adrenoceptors had considerably decreased in three patients and were absent in the remaining nine. Decrease in the neuronally released norepinephrine associated with contrasting behaviours of beta 1 and beta 2 adrenoceptors suggests the presence of a profound alteration in the sympathetic innervation of the perianeurysmatic myocardial tissue that may contribute to the genesis of sustained ventricular tachycardia in patients with postinfarction apical aneurysm.

Electrophysiologic characteristics of ventricular tachycardia or fibrillation in relation to age of myocardial infarction

Evaluation of ventricular myocardium after the onset of acute myocardial infarction (AMI) suggests that the substrate for ventricular arrhythmias changes as the AMI heals. To determine if the ability of programmed stimulation to initiate ventricular tachycardia (VT) varies according to the interval between AMI and electrophysiologic testing, the clinical and electrophysiologic data of 42 patients with spontaneous sustained VT and 12 patients with ventricular fibrillation (VF) more than 3 days after a single AMI were analyzed. For patients with VT, there were no significant differences in the incidence of initiation of sustained monomorphic VT among those evaluated 1 to 3 weeks (100%), 3 to 8 weeks (75%), 2 to 6 months (100%), 6 to 18 months (80%) or more than 18 months (81%) after AMI, and the mean number of extrastimuli required for initiation did not differ among the groups. Patients evaluated more than 4 weeks after the initial episode of VT had a lower incidence of inducible VT than those studied earlier (14 of 21 [71%] vs 21 of 21 [100%], p < 0.05), although this appeared to be a result of earlier termination of the stimulation protocol owing to initiation of polymorphic arrhythmias in those studied later. The 14 patients evaluated within 8 weeks of AMI had significantly faster VT rates (mean cycle length 269 ± 45 ms) than the 28 patients studied later (320 ± 75 ms, p < 0.01), possibly because of more out-of-hospital presentations of VT in patients studied later. More patients studied within 3 weeks of AMI had anterior infarcts (100%), but otherwise there were no differences in age, AMI location or ejection fraction. Among patients with VF, 5 of 7 (71%) studied less than 8 weeks and 3 of 5 patients (60%) studied more than 8 weeks after AMI had inducible VT (difference not significant). Thus, the ability to induce sustained VT in patients with spontaneous episodes of sustained VT or VF after AMI appears to be independent of the interval between AMI and programmed stimulation.

Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: electrophysiologic testing and lack of response to antiarrhythmic drug therapy.

Eleven consecutive patients with idiopathic dilated cardiomyopathy and spontaneous, sustained ventricular tachycardia (VT) of uniform morphology underwent programmed ventricular stimulation and serial antiarrhythmic drug testing. The mean ejection fraction was 30 +/- 6.4%. Sustained VT was induced by programmed electrical stimulation in all 11 patients. A mean of 3.7 +/- 2.4 antiarrhythmic drugs were evaluated by programmed stimulation, including at least one experimental agent in eight patients. In nine of 11 patients VT remained inducible on all drug therapy. During a mean follow-up period of 21 +/- 14 months there were four sudden deaths and two patients with recurrences of VT. In all six patients with sudden death or recurrence of VT, the arrhythmia remained inducible on drug therapy. Three patients who died suddenly had a hemodynamically stable, induced tachycardia on antiarrhythmic therapy. Of eight patients treated with amiodarone, only two were successfully treated. We conclude that in patients with sustained VT and idiopathic dilated cardiomyopathy, VT can be induced by programmed electrical stimulation. VT will usually remain inducible on antiarrhythmic therapy, and sudden death can occur despite slowing and improved tolerance of the induced arrhythmia. Amiodarone may have limited efficacy, and more aggressive therapy, such as surgery or implantation of an automatic internal defibrillator, should be considered in this patient population.

Facilitation of ventricular tachycardia induction with abrupt changes in ventricular cycle length

The effect of abrupt short-to-long changes in cycle length (CL) on the postulated reentrant circuit of ventricular tachycardia (VT) was evaluated. This was performed using single and double ventricular extrastimuli in a group of 21 patients clinically suspected of having VT in whom VT could not be induced at comparable or shorter constant CLs. A second group of 10 patients without suspected VT was similarly studied. Compared with constant CLs of equal or shorter duration preceding the single or double ventricular extrastimuli, abrupt short-to-long CL changes resulted in (1) initiation of sustained VT in 13 of 21 patients in whom VT could not be induced at constant CLs despite the use of shorter S 1S 3 by 66 ± 17 ms; (2) increased incidence of initiation of sustained VT after the V 3 phenomenon resulting from macroreentry within the His-Purkinje system (ReHPS); (3) a small but higher incidence of sustained VT due to sustained Re-HPS; and (4) no induction of sustained or nonsustained VT with either method in the second group of patients. These results provide additional support for reentry as the basis for sustained ventricular tachyarrhythmias. Abrupt short-to-long CL changes may be effective for initiating sustained VT in patients at risk for these arrhythmias.

Recurrent sustained ventricular tachycardia: structure and ultrastructure of subendocardial regions in which tachycardia originates.

Surgical resection of the endocardium and subendocardium often abolishes chronic recurrent sustained ventricular tachycardia in patients with healed myocardial infarcts or ventricular aneurysms, presumably by interrupting the reentrant pathway. To define the morphologic characteristics of cells in the reentrant pathway, we studied the histology and ultrastructure of the endocardial resections of 23 patients who underwent this procedure. Bundles of apparently viable myocardial fibers embedded in dense fibrous tissue were identified throughout the endocardial resections from all patients. These bundles of cells were separated from one another by fibrous tissue but extended uninterrupted to the margins of the surgical resection. In 14 patients Purkinje fibers were identified beneath the thickened endocardium whereas the remaining bundles were composed of ventricular muscle. The Purkinje fibers appeared to have normal ultrastructure and ventricular cells with both normal and abnormal ultrastructures were present. The abnormal muscle cells were characterized by loss of contractile elements, aggregates of dilated sarcoplasmic reticulum, and osmiophilic dense bodies. The sarcolemma was intact and the nuclear chromatin was evenly dispersed suggesting that these cells were still viable. The abnormal structure and arrangement of the surviving cardiac fibers in the endocardium may cause the abnormal electrophysiologic function that results in ventricular tachycardia.