Antitachycardia burst pacing for pleomorphic reentrant ventricular tachycardias associated with non-coronary artery diseases: a morphology specific programming for ventricular tachycardias. (1/8)

To study the role of antitachycardia burst pacing in patients with reentrant pleomorphic ventricular tachycardia (VT) associated with non-coronary artery diseases, the efficacy of antitachycardia pacing and appropriate antitachycardia pacing cycle length were evaluated in each pleomorphic VT morphology of seven patients. Seven patients were included in this study. Clinically documented pleomorphic VTs were reproduced in an electrophysiologic study. For each VT, rapid ventricular pacing was attempted from the apex of the right ventricle at a cycle length which was 20 ms shorter than that of VT and repeated after a decrement of the cycle length in steps of 10 ms until the VT was terminated or accelerated. All 16 VTs could be entrained by the rapid pacing, and 13 of the 16 VTs (81%) were terminated, whereas pacing-induced acceleration was observed in the other 3 VTs of the 3 patients. VT cycle length (VTCL), block cycle length (BCL) which was defined as the longest VT interrupting paced cycle length, %BCL/VTCL and entrainment zone which was defined as VTCL minus BCL, varied in each VT morphology of each patient. In two patients, antitachycardia pacing was effective in all VT morphologies and the maximum difference of the %BCL/VTCL among the pleomorphic VTs was less than 10%. Thus, antitachycardia pacing seemed to be beneficial for these patients. In the other 5 patients, a difference of more than 10% in %BCL/VTCL was observed among the pleomorphic VT morphologies and/or at least one VT morphology showed pacing-induced acceleration. Compared to the 13 terminated VTs, three accelerated VTs had a wide entrainment zone [160 +/- 44 vs 90 +/- 48 ms, p < 0.04] and small %BCL/VTCL [61 +/- 6 vs 77 +/- 11%,p<0.03]. In pleomorphic VTs associated with non-coronary artery diseases, responses to rapid pacing was not uniform; VT might be terminable or accelerated even in the same patient. We need to pay close attention when programming antitachycardia pacing in patients with pleomorphic VT.  (+info)

The D allele of the angiotensin-converting enzyme gene and reperfusion-induced ventricular arrhythmias in patients with acute myocardial infarction. (2/8)

The renin-angiotensin system may play a pivotal role in reperfusion ventricular arrhythmias (RVA). The purpose of this study was to investigate the association between angiotensin-converting enzyme (ACE) gene polymorphism and RVA in patients with acute myocardial infarction (AMI) in a case-control study. Patients who had undergone successful coronary intervention for AMI were enrolled (n= 127, male/female: 97/30, mean age, 62.6 years). The incidence of RVA was continuously monitored by ECG at a coronary care unit. The severity of ventricular arrhythmias was evaluated in terms of the Lown's grade and patients with a high risk of ventricular arrhythmias that may cause sudden cardiac death (Lown's grade > or =2) within 5 h of coronary intervention were defined as cases (n=59), and otherwise as controls (n=68). A receiver operating characteristic curve was used to determine the discriminatory ability of continuous variables and to produce dummy variables for use in a logistic regression analysis. Cases had a significantly higher body mass index, higher maximal levels of serum creatine kinase, and a shorter time preceding coronary intervention than controls. The severity of coronary atherosclerosis was similar between the 2 groups. The frequency distribution of ACE genotypes in cases differed from that in controls (II/ID/DD: 22.0%/52.6%/25.4% vs 44.1%/41.4%/14.7%, p<0.05, by the Mantel-Haenzel chi-square test). The ACE-D allele had additive and dominant effects with regard to the occurrence of significant ventricular arrhythmias after adjusting for other risk factors. The ACE-D allele may play a pivotal role in sudden cardiac death in patients with AMI.  (+info)

Five cases of aconite poisoning: toxicokinetics of aconitines. (3/8)

Aconite poisoning was examined in five patients (four males and one female) aged 49 to 78 years old. The electrocardiogram findings were as follows: ventricular tachycardia and ventricular fibrillation in case 1, premature ventricular contraction and accelerated idioventricular rhythm in case 2, AIVR in case 3, and nonsustained ventricular tachycardia in cases 4 and 5. The patient in case 1 was given percutaneous cardiopulmonary support because of unstable hemodynamics, whereas the other patients were treated with fluid replacement and antiarrhythmic agents. The main aconitine alkaloid in each patient had a half-life that ranged from 5.8 to 15.4 h over the five cases, and other detected alkaloids had half-lives similar to the half-life of the main alkaloid in each case. The half-life of the main alkaloid in case 1 was about twice as long as the half-lives in the other cases, and high values for the area under the blood concentration-time curve and the mean residence time were only observed in case 1. These results suggest that alkaloid toxicokinetics parameters may reflect the severity of toxic symptoms in aconite poisoning.  (+info)

Electrophysiological study and 'slow' ventricular tachycardia predict appropriate therapy: results from a single-centre implantable cardiac defibrillator follow-up. (4/8)

AIMS: To account for appropriate and inappropriate therapies and cardiac death (CD) in a cohort of consecutive implantable cardiac defibrillator (ICD) eligible patients and to identify baseline predictors of these outcomes. METHODS AND RESULTS: During follow-up of 288 consecutive ICD-treated patients, clinical, biochemical, echocardiographic, arteriographic, and electrophysiological (EP) data at baseline were individually matched with survival data and electrograms retrieved during device interrogation. Predictors of therapy and CD were identified by multivariate analyses. Eighty-eight per cent of cases were secondary prevention and 12% were primary prevention. About 770 patient-years of ICD follow-up were analysed. Median follow-up was 22.7 months. Forty-eight per cent of patients had appropriate therapy for at least one ventricular tachyarrhythmia. Seventy per cent of tachycardias were successfully treated with anti-tachy pacing alone. Overall risk of therapy was higher for patients with ischaemic heart disease (IHD) than with non-IHD (51 vs. 37%; P = 0.049). Low left ventricular ejection fraction (LVEF), positive EP study, and 'slow' ventricular tachycardia predicted appropriate therapy. Cardiac death was predicted by nephropathy, low LVEF, amiodarone use, and supraventricular tachycardia (SVT). Inappropriate therapy affected 12.2% of patients and was predicted by known SVT and IHD. CONCLUSION: Electrophysiological study and slow VT predicted appropriate therapy. Amiodarone use predicted CD. Inappropriate therapy remains an important issue largely predictable by SVT.  (+info)

Reentrant ventricular tachycardia originating in the right ventricular outflow tract: slow conduction identified by right coronary artery ostium pacing. (5/8)

A case of reentrant ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) is described. An electrophysiological study revealed that programmed stimulation from the right ventricle apex induced 2 types of VT with similar left bundle branch block configuration and inferior axis. Yet, VT cycle length (CL) was different; one was stable, sustained VT with a CL of 360 ms and the other was hemodynamically intolerable VT with a CL of 330 ms. Similarly for both VTs, perfect pace mapping was obtained at the anterior septum beneath the pulmonary valve in the RVOT, and exits of both VTs were very close. Entrainment mapping during stable VT was performed and the anterior septum RVOT was designated as the exit for the stable VT. Intriguingly, entrainment pacing from the ostium of the right coronary artery showed that the post-pacing interval was identical to VTCL. The stimulus to QRS interval was very long (340 ms) during entrainment with concealed fusion, and the right coronary artery ostium was therefore consistent with the VT reentry circuit inner loop or the upper portion of the VT reentry circuit exit. These findings suggest that the stable VT reentry circuit had a slow conduction zone from the ostium of the right coronary artery to the exit in the anterior septum RVOT. When radiofrequency catheter ablation was performed at the 2 exits of the anterior septum RVOT, both VTs then could not be induced.  (+info)

More pronounced diastolic left ventricular dysfunction in patients with accelerated idioventricular rhythm after reperfusion by primary percutaneous coronary intervention. (6/8)

OBJECTIVE: Reperfusion-induced accelerated idioventricular rhythm (AIVR) during primary percutaneous coronary intervention (pPCI) may be a sign of left ventricular (LV) dysfunction. We compared LV dynamic effects of reperfusion between patients with and without reperfusion-induced AIVR during pPCI for ST-elevation myocardial infarction (STEMI). METHODS: We studied 15 consecutive patients, who presented with their first acute anterior STEMI within 6 hours after onset of symptoms, and in whom LV pressure-volume (PV) loops were directly obtained during pPCI. Immediate effects of pPCI on LV function were compared between patients with (n = 5) and without (n = 10) occurrence of AIVR after reperfusion, as well as the direct effects of AIVR on LV function compared to sinus rhythm. RESULTS: Patients with reperfusion-induced AIVR showed more pronounced diastolic LV dysfunction before the onset of the arrhythmia, i.e., a delayed active relaxation expressed by Tau (53 +/- 15 vs. 39 +/- 6 ms; p = 0.03), a worse compliance curve (p = 0.01), and a higher end-diastolic stiffness (p = 0.07). At the end of the procedure, AIVR patients showed less improvement in diastolic LV function, indicated by a downward shift of the compliance curve (-3.1 +/- 2.3 vs. -7.5 +/- 1.4 mmHg; p = 0.001), a decrease in end-diastolic stiffness (13 +/- 18 vs. 34 +/- 15%; p = 0.03) and end-diastolic pressure (12 +/- 8 vs. 29 +/- 19%; p = 0.07). CONCLUSION: STEMI patients with reperfusion-induced AIVR after pPCI showed more pronounced diastolic LV dysfunction before and after AIVR than patients without AIVR, which suggests that diastolic LV dysfunction contributes to the occurrence of AIVR and that AIVR is a sign of diastolic LV dysfunction.  (+info)

Acute haemodynamic effects of accelerated idioventricular rhythm in primary percutaneous coronary intervention. (7/8)

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Accelerated idioventricular rhythm associated with propranolol treatment in a child. (8/8)

Accelerated idioventricular rhythm (AIVR) is a ventricular arrhythmia most commonly seen in adults with underlying cardiac disease. It is important to establish the diagnosis when it occurs to differentiate this benign phenomenon from dangerous ventricular tachycardia. We present the case of a healthy child who developed episodes of AIVR associated with propranolol treatment. Her 24-hour electrocardiography recording showed AIVR with difference between sinus and ventricular beats. The arrhythmia resolved with the discontinuation of propranolol, and eventually the case was in sinus rhythm. This patient is the first case of AIVR associated with propranolol treatment in the literature.  (+info)