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PubMed1975

Double ectopic accelerated ventricular and nonaccelerated ventricular or supraventricular rhythms.

Three patients with acute inferior wall myocardial infarction has accelerated idioventricular rhythms alternating and (or) coexisting with: (a) AV junctional (or low atrial) rhythm (Case 2); (b) paroxysmal ventricular tachycardia and another accelerated idioventricular rhythm (Case 3); and (c) AV junctional rhythm, paroxysmal ventricular tachycardia and accelerated idioventricular rhythm from another center (Case 4). The tracings from a fourth patient (Case 1) served to focus attention on one of the most pertinent features of accelerated idioventricular rhythms, namely the gradual decrease in rate to values below that of the preexisting basic rhythm. Cardioacceleration with atropine and cardiosuppression with lidocaine failed to abolish the arrhythmias or relieve the symptoms in cases 3 and 4. Atrial stimulation proved the most effective mode of therapy in these two patients.

Arrhythmias, Cardiac↗
PubMed1991

Predictive value of ventricular arrhythmias for patency of the infarct-related coronary artery after thrombolytic therapy.

In animal studies reperfusion of coronary arteries is commonly accompanied by ventricular arrhythmias. It is not certain, however, whether ventricular arrhythmias can be used as a reliable non-invasive marker of reperfusion in humans. Two-channel Holter recordings were obtained from the start of an intravenous infusion of streptokinase until coronary angiography (2.8 (2.7) hours (mean SD)) afterwards) in 57 patients with acute myocardial infarction of less than four hours who were generally not treated with antiarrhythmic drugs. Ventricular arrhythmias occurred in 21 (37%) of the 57 patients: accelerated idioventricular rhythm in 13 patients and non-sustained ventricular tachycardia in 15 patients. Seven patients had both accelerated idioventricular rhythm and non-sustained ventricular tachycardia. Coronary angiography showed a patent infarct-related vessel in 12 (92%) of the 13 patients with accelerated idioventricular rhythm (95% confidence interval 66 to 99%), in 22 (50%) of the 44 patients without accelerated idioventricular rhythm (95% CI 34 to 66%), in 11 (73%) of the 15 patients with non-sustained ventricular tachycardia (95% CI 45 to 92%), and in 23 (55%) (95% CI 39 to 71%) of the 42 patients who did not have non-sustained ventricular tachycardia. Seventeen (81%) of the 21 patients with accelerated idioventricular rhythm, or non-sustained ventricular tachycardia, or both, had a patent infarct-related vessel (95% CI 58 to 94%) as did 17 (47%) of the 36 patients with no ventricular arrhythmia (95% CI 29 to 65%). In patients with accelerated idioventricular rhythm after thrombolysis the infarct-related vessel is almost certain to be patent; but the infarct-related coronary artery can still be patent when no arrhythmia is seen.

Acute Disease↗
PubMed1986

Ventricular arrhythmias during reperfusion.

Accelerated idioventricular rhythm has been used as a marker for coronary reperfusion. The incidence of accelerated idioventricular rhythm and ventricular tachycardia was evaluated in 52 consecutive patients undergoing thrombolysis with intracoronary streptokinase during acute myocardial infarction. Complete 12-hour Holter recordings during and after intracoronary streptokinase were obtained in 39 patients. Reperfusion was documented in 17 patients (44%), no reperfusion in 14 (36%), and subtotal occlusion in eight (20%). Accelerated idioventricular rhythm occurred in 83%, 57%, and 63% of patients by group, respectively (p greater than 0.05). Ventricular tachycardia occurred in 100%, 71%, and 100% of patients by group, respectively (p less than 0.05). These data demonstrate that accelerated idioventricular rhythm is not specific for reperfusion and cannot be used as a marker for this event, and that ventricular tachycardia is more common with reperfusion and subtotal occlusion.

Cardiac Catheterization↗
PubMed2005

[Complications of transcatheter interventional occlusion of ventricular septal defects].

OBJECTIVE: To investigate the complications and their prevention in patients with perimembranous ventricular septal defect (VSD) experiencing transcatheter interventional occlusion. METHODS: From July, 2002 to May, 2004, totally 262 (138 males, 124 females) perimembranous VSD patients underwent transcatheter interventional occlusion in the department. The age ranged from 2 to 18 years (mean 9.3 +/- 5.8 years), and the body weight ranged from 11.0 to 65.0 kg (mean 30.5 kg). The implanted occluder with imported Amplatzer eccentric perimembranous VSD occluder, domestic double-disk, domestic eccentric perimembranous VSD and PDA occluder were attempted in 12, 212, 28 and 6 cases, respectively. Among them, 3 cases were complicated with ductus arteriosus, 4 with atrial septal defects and 1 with patent ductus arteriosus plus atrial septal defect. The associated defects were treated with other occluders at the same time. RESULTS: The diameters of VSD measured by transthoracic echocardiography before occlusion and by ventriculography during the procedure ranged from 2.7 to 13 mm (mean 6.5 mm) and from 1.3 to 14.0 mm (mean 6.8 mm), respectively. The defects in 256 cases (97.7%) were successfully occluded. The implant occluder was from 4 to 16 mm in size. Serious complications occurred in 8 cases (3.1%), including 5 cases of high degree atrioventricular block (AVB) (2.0%), 2 cases of hemolysis (0.8%) and 1 case of displacement of the occluder (0.4%). Amongst 5 cases of high degree AVB, permanent pacemaker was implanted only in 1 case due to high degree AVB 50 days after treatment, whereas the others all recovered. Two cases of hemolysis were completely recovered. One case of occluder displacement was emergently transferred to cardiac surgery. Other complications included residual shunt during 6 month follow-up in 1 case (0.4%), minor aortic regurgitation in 5 cases (2.0%), minor tricuspid regurgitation during 6 month follow-up in 4 cases (1.6%), and accelerated idioventricular rhythm or accelerated atrio-ventricular junctional tachycardia combined with atrioventricular interference-dissociation by ECG in 75 cases (29%) but they recovered after 3 - 5 days of corticosteroid treatment. Forty-one cases (16%) complicated with complete or incomplete right bundle branch block, of whom 50% recovered during follow-up. Still, there were 4 cases (1.6%) who were complicated with complete left bundle branch block but were all recovered during follow-up and 26 cases (10%) who were complicated with intraventricular block. There were no Significant difference in complications between cases who accepted imported Amplatzer occluders and domestic occluders. CONCLUSION: Transcatheter interventional occlusion is a safe, effective and ideal method with low incidence of serious complications for perimembranous VSD. Long term follow-up and clinical research should be carried out to improve the level of VSD interventional therapy.

Adolescent↗
PubMed1991

Prevalence, characteristics and significance of ventricular premature complexes and ventricular tachycardia detected by 24-hour continuous electrocardiographic recording in the Cardiac Arrhythmia Suppression Trial. CAST Investigators.

The prevalence, characteristics and significance of ventricular arrhythmias detected by ambulatory electrocardiography were evaluated in 1,498 patients who were randomized to encainide, flecainide or placebo in the Cardiac Arrhythmia Suppression Trial. The mean ventricular premature complex (VPC) frequency at baseline was 133 +/- 257 VPCs/hour. Nonsustained ventricular tachycardia (VT) (rate greater than or equal to 120 beats/min) was present in 22% of patients. Accelerated idioventricular rhythm (rate less than 120 beats/min) occurred in 22% of subjects. There were 63 deaths/resuscitated cardiac arrests in the active treatment (encainide/flecainide) group and 26 in the placebo group. In the treatment group mortality increased with increasing VPC frequency, (p = 0.006), whereas in the placebo group such a relation was not present. Mortality/resuscitated cardiac arrest increased in patients with greater than or equal to 2 VT episodes than in those with less than or equal to 1 episode in the active treatment group (p = 0.04). There was no significant association between VT and mortality/resuscitated cardiac arrest in the placebo group. The presence of accelerated idioventricular rhythm was not associated with increased mortality/resuscitated cardiac arrest in either the active treatment or placebo groups. However, mortality was lower in patients with accelerated idioventricular rhythm rates less than 100 beats/min than in those with rates greater than or equal to 100 beats/min (p = 0.05). Thus, in the Cardiac Arrhythmia Suppression Trial the previously described association between mortality/resuscitated cardiac arrest and ventricular arrhythmias (VPC and VT) were only observed in the active treatment group. In addition, based on the results obtained in this highly selected population, it is suggested that the definition of accelerated idioventricular rhythm should be a rate less than 100 beats/min, and at a rate greater than or equal to 100 beats/min it should be categorized as VT.

Anti-Arrhythmia Agents↗
PubMed1983

Limitation of infarct size with thrombolytic agents--electrocardiographic indexes.

Forty-four patients with acute transmural myocardial infarction underwent cardiac catheterization 4.7 +/- 1.3 hours (+/- SD) after the onset of persistent chest discomfort. Thirty-nine patients had total occlusion of infarct-related vessels; 27 of these 39 had successful intracoronary thrombolysis. Twenty of these 27 patients (74%) had reperfusion arrhythmia. Accelerated idioventricular rhythm was most often observed with reperfusion of all myocardial zones, while sinus bradycardia and hypotension accompanied reperfusion of the inferoposterior left ventricle. Three patients with spontaneous accelerated idioventricular rhythm had patient, stenosed, infarct-related vessels on the initial coronary angiogram. Patients with unsuccessful intracoronary thrombolysis did not demonstrate these specific arrhythmias. While there is rapid control of injury current with successful intracoronary thrombolysis, Q waves develop rapidly after reperfusion; however, in the days after intracoronary thrombolysis, there is a decline in Q wave with partial regrowth in R wave amplitude in some patients. Thus, specific arrhythmias, most notably accelerated idioventricular rhythm, are useful markers for the occurrence and timing of successful coronary arterial recanalization. In addition, rapid control of injury current and partial regrowth of R waves are electrocardiographic markers of myocardial salvage.

Aged↗
PubMed1980

Heart rate and ectopic prematurity in relation to sustained ventricular arrhythmias.

Forty-four patients with acute myocardial infarction were studied using 24-hour electrocardiographic monitoring. A linear correlation has been shown to exist between heart rate preceding accelerated idioventricular rhythm and ventricular tachycardia and the rates of these. The prematurity index was found to be inversely related to the preceding heart rate and also to the rate of accelerated idioventricular rhythm or ventricular tachycardia. Faster heart rates preceded extrasystoles with shorter prematurity indices and a significant inverse correlation was observed between preceding heart rate and prematurity index. Patients developing ventricular tachycardia had more frequent isolated ventricular extrasystoles and faster heart rates preceding the episode as compared with patients not showing ventricular tachycardia. No association was observed between ventricular tachycardia and accelerated idioventricular rhythm. All four patients developing ventricular fibrillation showed preceding ventricular tachycardia, with three of these patients demonstrating faster rates of ventricular tachycardia (greater than 170/min) and shorter prematurity indices (less than 0.80) than patients without ventricular fibrillation. Heart rate may influence the severity of ventricular arrbythmia; the prematurity of an extrasystole is of importance in patients developing accelered idioventricular rhythm or ventricular tachycardia.

Arrhythmias, Cardiac↗
PubMed1993

[Is sudden reperfusion more arrhythmogenic during thrombolysis for myocardial infarction?].

The object of this study was to analyse ventricular arrhythmias occurring during intravenous thrombolysis for acute myocardial infarction with respect to ST segment changes on 24 hour Holter ECG monitoring initiated at the same time as thrombolytic therapy and on repeated 12 lead electrocardiogrammes. Forty-one patients in whom the infarct-related artery was patent at coronary angiography carried out 30.5 +/- 3.1 hours (< or = 24 hours in 59% of cases) after the onset of chest pain were included. The time to normalisation of the ST segment was defined as the interval between maximum ST elevation to a steady state and helped identify rapid (< or = 60 minutes, n = 13) from intermediate (60-180 minutes, n = 15) and slow (> 180 minutes, n = 13) reperfusion. The incidence of ventricular arrhythmias was the same in all three groups, except for prolonged ventricular tachycardias (> 15 complexes): 69%, 13% and 15% respectively (p = 0.002). The number of arrhythmias was greater when the ST segment changes were rapid than when they were intermediate or slow. This was true for ventricular extrasystoles (p < 0.05), accelerated idioventricular rhythms (p < 0.05), early (< or = 6 hours from onset of thrombolysis) accelerated idioventricular rhythms (p < 0.01) and ventricular tachycardias (p < 0.05). Therefore, the number of ventricular arrhythmias seems to be related to the speed of ST segment change, suggesting that more sudden reperfusion is more arrhythmogenic.

Arrhythmias, Cardiac↗
PubMed1992

Holter recording of ventricular arrhythmias during intravenous thrombolysis for acute myocardial infarction.

Ventricular arrhythmias during thrombolysis for acute myocardial infarction and their relation to coronary artery patency were examined. Twenty-four-hour Holter monitoring was begun 3.1 +/- 0.2 hours after onset of pain in 40 patients (age 54 +/- 1.6 years; anterior infarction 42.5%) treated with streptokinase (42.5%) or recombinant tissue-type plasminogen activator (57.5%) (delay from pain 3.3 +/- 0.2 hours). A Marquette 8000 computer was used for Holter analysis. The infarct-related artery was considered as patent (72.5%) or non-patent (27.5%) according to coronary angiography (delay from pain 26.7 +/- 2.5 hours; 60% less than 24 hours). Ventricular arrhythmias were present in all patients. Tolerance was good (1 cardioversion for ventricular fibrillation). The incidence of accelerated idioventricular rhythm was not different between patients with a patent and nonpatent artery (90 vs 82%), nor for ventricular tachycardia (VT) (83 vs 73%). Coronary artery patency was associated with a 14-, 13- and 32-fold increase of ventricular premature complexes, VT and accelerated idioventricular rhythms, respectively. The increased incidence of sustained VT (patent 38%; nonpatent 0%; p less than 0.05) and early (before the first 6 hours) accelerated idioventricular rhythm (patent 76%; nonpatent 18%; p less than 0.01) associated with artery patency suggests that these arrhythmias may be noninvasive diagnostic criteria for reperfusion (sensitivity 38 vs 76%, and specificity 100 vs 82%). A positive correlation was found between the frequency of ventricular premature complexes and VT, and peak creatine kinase.

Arrhythmias, Cardiac↗
PubMed1992

[Holter monitoring of ventricular arrhythmia during the 24 first hours of myocardial infarction treated with intravenous thrombolysis].

The aim of this study was to assess ventricular arrhythmias after intravenous thrombolysis for acute myocardial infarction and to determine their relationship with coronary artery patency. A 24 hour Holter recording was started 3.1 +/- 0.2 hours after the onset of pain in 40 patients (age 54 +/- 1.6 years, 42.5% anterior infarcts) treated by streptokinase (42.5%) or tissue plasminogen activator (57.5%) within 3.3 +/- 0.2 hours of the beginning of symptoms. The arrhythmias were analysed on a Marquette 8000 computer. Coronary angiography was systematic and was performed 26.7 +/- 2.5 hours (within 4 hours in 60% of patients) after the onset of pain to define coronary artery patency (TIMI 2 and 3: 72.5%) or occlusion (TIMI 0 or 1: 27.5%). Ventricular arrhythmias were common and generally well tolerated (one defibrillation for ventricular fibrillation). Accelerated idioventricular rhythms and ventricular tachycardias were equally prevalent in patients with patent arteries (90% and 83%) as with occluded arteries (82% and 73%). The prevalence of sustained ventricular tachycardias (> 15 complexes) and of early accelerated idioventricular rhythms (< or = 6 hours) was significantly higher in patients with patent coronary arteries: 38% versus 0% (p < 0.05) and 76% versus 18% (p < 0.01). These arrhythmias may be considered to be non-invasive markers of early coronary reperfusion, with a sensitivity of 38 and 76% and a specificity of 100 and 82%. Coronary patency was associated with higher numbers of ventricular extrasystoles, ventricular tachycardias and accelerated idioventricular rhythms by a factor of 14, 13 and 32 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Acceleration of idioventricular rhythms by histamine in guinea pig heart: mediation by H2 receptors.

To evaluate the ability of histamine to induce ventricular arrhythmias, we studied the effects of histamine on ventricular rhythmicity in the isolated guinea pig heart with complete atrioventricular conduction block. As a function of dose (0.1-30 microgram), histamine enhanced the idioventricular rate by increasing the rate of firing of the original pacemaker and also by causing the sudden appearance of faster idioventricular rhythms that coincided with changes in pacemaker site. Anaphylaxis in the isolated guinea pig heart with complete atrioventricular conduction block caused histamine release and acceleration of idioventricular rate. The effects of histamine on idioventricular rhythmicity were not attenuated by the histamine H1 receptor antagonist chlorpheniramine, but were antagonized by the H2 receptor antagonist cimetidine. Moreover, the selective H2 agonist 4-methylhistamine (4MeH) accelerated the idioventricular rate, whereas 2-(2-thiazolyl) ethylamine (ThEA), at doses selective for H1 receptor activation, did not. The effects of histamine on idioventricular rhythmicity were not modified by the beta-adrenergic blocker pindolol. The mechanism by which histamine increases idioventricular rate probably involves two components: (1) an enhancement in automaticity of the original pacemaker, and (2) the induction of faster rhythms via reentry and/or afterdepolarizations. Whatever the mechanism, both components of the ventricular chronotropic action of histamine appear to involve exclusively histamine receptors of the H2 type. Thus, our results suggest that H2 receptor antagonists may have a role as specific antiarrhythmic agents in the treatment of cardiac dysfunctions caused by histamine release.

Anaphylaxis↗