Incidence Of Inducible Ventricular Tachycardia Research Articles

Influence of standard modifiable risk factors on ventricular tachycardia after myocardial infarction

Abstract Background Sudden cardiac death due to ventricular tachyarrhythmia is the single greatest cause of death within two years after myocardial infarction (MI), especially early in the first 30 days. Purpose We aimed to assess the incidence of inducible ventricular tachycardia (VT) early after MI in those with standard modifiable risk factors (SMuRFs) versus those without. Methods Consecutive patients with LVEF ≤40% on day 3–5 after ST elevation myocardial infarction (STEMI) who underwent electrophysiology study were prospectively recruited. Positive EPS was defined as sustained monomorphic VT cycle length ≥200ms for > 10 seconds, or shorter duration if hemodynamic compromise occurred. The primary outcomes were inducibility of VT and all-cause mortality. Results A total of 410 patients, of which 126 had inducible VT on EPS, early after myocardial infarction were included. In our multiple regressions model, when smoking history was considered, ex-smokers were identified at increased risk of VT at EPS (adjusted OR 2.0, p=0.033) whilst those who never smoked or were current smokers had comparable risk. It also showed that the presence of any SMuRF apart from current smoker also conferred an increased risk of inducible VT (adjusted OR 1.9, p=0.043). For every 10 years increase in age the risk of death increased by a multiplicative factor of 1.3, for every 10% decrease in LVEF (%) the risk of death increased by a multiplicative factor of 1.9 and in patients with previous IHD, the risk of death was doubled. Neither the number of SMuRFs nor the presence of any SMuRF were associated with mortality. Conclusion In our cohort of patients with LVEF<40% early after STEMI who had an EPS to assess for inducible VT, either the presence of any of the three SMuRFs (hypertension, hypercholesterolemia or diabetes mellitus) or previous smoking doubled the chance of having VT induced. These data provide valuable information that could be integrated into clinical care protocols after myocardial infarction to improve long-term patient outcomes and further reinforces the need to modify SMuRFs in patients with ischemic heart disease.

Induction of ventricular tachycardia with the fourth extrastimulus and its relationship to risk of arrhythmic events in patients with post-myocardial infarct left ventricular dysfunction

The prognostic significance of ventricular tachycardia (VT) induced by three extrastimuli (ES) is similar to that of VT induced by one or two ES in patients with coronary disease and abnormal left ventricular (LV) function. The significance of VT inducible with four ES is unclear. To examine the prognostic significance of VT inducible with the fourth ES in patients with post-myocardial infarct (MI) LV dysfunction. Consecutive patients (n= 432) with post-MI LV ejection fraction ≤40% underwent electrophysiological (EP) studies for risk stratification. Inducible VT ≥ 200 ms cycle length (CL) with one to four ES was considered inducible. The primary endpoint of arrhythmia (sudden death or spontaneous VT/ventricular fibrillation) was compared among patients with VT inducible with less than or equal to two, three, and four ES. The incidence of inducible VT was 37.9% (n= 164). In patients with inducible VT, inducibility was with less than or equal to two, three, and four ES in 24% (n= 39), 46% (n= 75), and 30% (n= 50). Compared to VT induced with less than or equal to three ES, VT induced with the fourth ES was of shorter CL (218 vs. 256 ms, P = 0.01) and more likely to be haemodynamically unstable requiring cardioversion (77 vs. 55%, P = 0.05). After 3 years the primary endpoint occurred in 28 ± 8, 28 ± 6, and 18 ± 6% in patients with VT induced with less than or equal to two, three, and four ES, respectively (P= 0.31) and in 5 ± 2% of EP-negative patients (P< 0.01). In patients with post-MI LV dysfunction, VT can be induced in a significant proportion of patients with the fourth ES. These patients are at comparable risk of arrhythmia to patients with inducible VT with less than or equal to three ES.

Resveratrol Attenuates Ventricular Arrhythmias and Improves the Long-Term Survival in Rats with Myocardial Infarction

The effects of resveratrol treatment on ventricular arrhythmia, survival, and late cardiac remodeling were evaluated in rats with myocardial infarction (MI). Three groups of rats (S: ham-operated, MI, and MI pre-treated with resveratrol) were treated in an in vivo MI model by ligation of left anterior descending coronary artery. The electrocardiogram signals were monitored and recorded for 24 h using an implanted telemetry transmitter. The incidence of ventricular arrhythmias during the first 24-h after MI was also evaluated. Meanwhile, invasive in vivo electrophysiology with pacing in the right ventricle was performed in each group to assess the inducibility of ventricular arrhythmias. Administration of resveratrol significantly suppressed the MI-induced ventricular tachycardia and ventricular fibrillation (0.4 +/- 0.2 in Resv group vs. 7.1 +/- 2.2 in MI group episodes per hour per rat, P < 0.01). Data also showed that the incidence of inducible ventricular tachycardia was lower in the Resv group than the MI group (46% vs. 81%, P < 0.01). The infarct size and mortality in the Resv group at 14 weeks were reduced by 20% and 33%, respectively, compared with the MI groups. Results from patch clamp recording revealed that resveratrol inhibited L-type calcium current (I (Ca-L)), and selectively enhanced ATP-sensitive K(+) current (I (K,ATP)) in a concentration-dependent manner. These results suggested that the emerging anti-arrhythmic character induced by resveratrol treatment in rat hearts could be mainly accounted for by inhibition of I (Ca-L) and enhancement of I (K,ATP). Administration of resveratrol also improved the long-term survival by suppressing left ventricular remodeling.

Streptokinase therapy during infarct evolution reduces the incidence of inducible ventricular tachycardia in infarct survivors

Streptokinase therapy during infarct evolution reduces the incidence of inducible ventricular tachycardia in infarct survivors

Reduction in incidence of inducible ventricular tachycardia after myocardial infarction by treatment with streptokinase during infarct evolution

The aim of this study was to determine whether intravenous streptokinase administered with or without oral aspirin to patients with evolving myocardial infarction reduces the inducibility of ventricular tachycardia at electrophysiologic study and thus the risk of sudden death in infarct survivors. Of 159 patients randomized at Westmead Hospital to the multicenter Second International Study of Infarct Survival (ISIS-2) after streptokinase and aspirin in acute myocardial infarction, 87 underwent electrophysiologic testing 6 to 28 days after infarction to determine their risk of subsequent ventricular arrhythmias (streptokinase 20 patients; aspirin 25 patients; streptokinase and aspirin 21 patients; both placebos 21 patients). Patients who underwent electrophysiologic testing had similar clinical characteristics to those of patients who did not. The stimulation protocol comprised up to and including four extrastimuli applied to the right ventricular apex at twice diastolic threshold. An abnormal result was defined as ventricular tachycardia with a cycle length ≥ 230 ms lasting ≥ 10 s.Ventricular tachycardia was inducible at electrophysiologic study in 8 patients who received placebo streptokinase, but in no patient who received active streptokinase (8 of 46 versus 0 of 41; p = 0.005, Fisher's exact test). Ventricular tachycardia was inducible in 4 patients who received aspirin therapy and 4 who did not (4 of 41 versus 4 of 46; p = NS). During a mean follow-up period of 39 ± 9 months, there were no spontaneous episodes of ventricular tachycardia, ventricular fibrillation or witnessed sudden death in the streptokinase-treated group compared with three such events in the placebo-treated group (p = 0.13).When compared with placebo therapy, intravenous streptokinase substantially reduced the incidence of inducible ventricular tachycardia in infarct survivors. No similar benefit was attributable to aspirin therapy.

Effect of isoproterenol on induction of ventricular tachyarrhythmias in the normal and infarcted canine heart

The influence of isoproterenol on induction of ventricular arrhythmias was evaluated in 10 normal dogs and 17 dogs with experimentally induced myocardial infarction. Programmed stimulation (using up to 6 extrastimuli) was performed before and then during infusion of isoproterenol (2 μg/minute followed by 4 μg/minute). Isoproterenol facilitated induction of sustained monomorphic ventricular tachycardia (cycle length 163 ± 26 msec) in 5 of the 10 animals with no inducible baseline arrhythmia ( P < 0.05). Isoproterenol did not affect cycle length or the number of extrastimuli required in animals with baseline ventricular tachycardia (cycle length 158 ± 15 msec before versus 163 ± 17 msec during isoproterenol, P = 0.3; extrastimuli 3.8 ± 0.6 before versus 3.8 ± 0.4 during isoproterenol infusion, P = 0.3). Isoproterenol did not significantly facilitate induction of ventricular fibrillation in either normal dogs or those studied after production of myocardial infarction. We conclude that infusion of isoproterenol increases the incidence of inducible ventricular tachycardia in the infarcted heart, but does not facilitate the induction of ventricular fibrillation in infarcted or normal hearts, despite the use of an aggressive protocol for programmed stimulation. Isoproterenol is, therefore, a safe and useful adjunct to programmed stimulation in this setting.

Evaluation of Patients with Bundle Branch Block and “Unexplained” Syncope: A Study Based on Comprehensive Electrophysiologic Testing and Ajmaline Stress

Thirty-five patients with bundle branch block (BBB) and unexplained syncope underwent electrophysiologic study (EPS) including programmed ventricular stimulation and ajmaline administration (1 mg/kg, IV) to induce infra-His block. A prolonged HV interval (greater than 55 ms) was present in 16 of the 35 patients. Ajmaline-induced HV block occurred in 12 patients (complete HV block in 10, and 2:1 HV block in two). Monomorphic ventricular tachycardia (VT) was inducible in nine (25.7%) and polymorphic VT in two patients (5.7%). Left ventricular ejection fraction (LVEF) was less than 40% in five patients (45.5%) with inducible VT. Two patients had an unexpected co-existence of inducible HV block and VT. The remaining 14 patients (40%) had no detectable abnormality. The incidence of inducible VT was higher (45% vs 13.3%), and the presence of negative studies was lower (30% vs 53.3%) in patients with structural heart disease (n = 20), when compared to those with no significant heart disease (n = 15) (differences not significant [NS]). During a mean follow-up period of 16.5 +/- 9.2 months, all the patients with inducible HV block have been asymptomatic after having received permanent pacemakers. Patients with inducible monomorphic VT (except one with poor left ventricular function who died suddenly) have also been asymptomatic on antiarrhythmic drugs. Of the remaining patients, seven with normal EPS, two with prolonged HV intervals but no inducible HV block (despite being given permanent pacemakers) and one patient with polymorphic VT on antiarrhythmic drugs continue to have recurrent syncope. Approximately 60% of patients with BBB and unexplained syncope have clinically significant electrophysiologic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)