Idioventricular Rhythm Research Articles

Protective effects of captopril against ischemia/reperfusion-induced ventricular arrhythmias in vitro and in vivo

The effects of the converting enzyme inhibitor captopril on the susceptibility of the heart to ventricular arrhythmias following ischemia, both in vitro and in vivo, were studied. In isolated rat hearts, captopril, administered either before or at the end of ischemia, reduced ventricular fibrillation upon reperfusion after 15 minutes of local ischemia. Reduction of purine overflow, improvement in contractility, and increase in coronary blood flow occurred concomitantly. In vivo, a closed-chest pig model was used to determine the effects of captopril, administered at the end of ischemia and continued orally, on the susceptibility to ventricular arrhythmias during the chronic phase of myocardial infarction. Myocardial ischemia was induced by 60-minute inflation of a balloon catheter in the left anterior descending coronary artery. Upon reperfusion, an accelerated idioventricular rhythm occurred, both in 10 untreated and in 10 captopril-treated animals. Creatine kinase levels during the reperfusion period were significantly lower after captopril treatment. Two weeks after the short-term experiments, monomorphic ventricular tachycardia could be induced with programmed electrical stimulation in six of eight surviving untreated pigs. In contrast, in none of the six surviving captopril-treated animals was ventricular tachycardia inducible. Thus, early intervention with captopril during the development phase of myocardial infarction may have beneficial effects on the subsequent development of ventricular arrhythmias. Salvage of ischemic myocardium, improvement in ventricular function, beneficial effects on coronary flow, and decreased activity of the sympathetic nervous system may all contribute.

Usefulness of the accelerated idioventricular rhythm as a marker for myocardial necrosis and reperfusion during thrombolytic therapy in acute myocardial infarction

The value of the accelerated Idioventricular rhythm (AIVR) as a marker for myocardial necrosis and/or reperfusion was prospectively studied in 87 patients admitted with persistent ischemic chest pain. All patients received streptokinase. Necrosis was diagnosed by new Q waves and an increase in plasma enzymes. Reperfusion was documented angiographically. Myocardial necrosis occurred in 72 patients and reperfusion in 70 patients, 58 of whom had myocardial necrosis. Of 27 patients with AIVR, 26 had both necrosis and reperfusion (p < 0.001). AIVR started after a long coupling interval to the preceding sinus rhythm and was regular. Configuration depended on the reperfused infarct vessel. Reperfusion of the left anterior descending branch showed most configurations of AIVR and with the least QRS width. Reperfusion of the circumflex branch never had a left bundle branch block-like configuration. AIVR from reperfusion of the right coronary artery never had an inferior axis. AIVR occurring during persistent ischemic chest pain is a marker for both myocardial necrosis and reperfusion of the infarct vessel. AIVR starts with a long coupling interval and is regular. The QRS configuration may be useful for the noninvasive identification of the infarct vessel.

Mechanisms of clinical tachycardias

Animal data suggest that cardiac arrhythmias can result from a variety of mechanisms. In clinical settings, arrhythmias that are easily initiated and terminated with programmed electrical stimulation are often designated as reentry tachycardias. However, proof of reentry is contingent upon demonstration of the entire circuit; this relation has been proposed for arrhythmias associated with large circuits, such as those seen in the Wolff-Parkinson-White syndrome. Reentry has also been proposed as the mechanism responsible for a variety of other tachycardias, including bundle branch and atrioventricular nodal reentry tachycardia, permanent junctional reentrant tachycardia, reentry tachycardia associated with nodoventricular Mahaim fibers and inducible atrial and ventricular tachycardia. Documentation of triggered rhythms as the mechanism responsible for clinical arrhythmias has been even more difficult. Examples of arrhythmias resulting from triggered activity may include those associated with digitalis toxicity arising from the atria, the atrioventricular junction or the ventricles. Clinical arrhythmias due to triggered activity in the absence of digitalis have also been described. Cardiac arrhythmias that cannot be induced by electrical stimulation are presumably due to normal or abnormal automaticity. Examples of normal automaticity in the human heart are sinus rhythm and junctional and idioventricular escape rhythms. Tachycardias by abnormal automaticity have seldom been investigated for the purpose of documenting the mechanism and therefore the limited data available make it difficult to draw any final conclusions.

The paradox of sudden slowing of idioventricular rhythm during exercise in complete heart block: Modulation of automatic focus, concealed reentry, or wedensky inhibition?

As a rule, exercise enhances the rate of discharge of idioventricular rhythms in complete atrioventricular (AV) block. The opposite effect, a sudden drop in the rate of discharge with subsequent resetting of the firing rate, was observed in an 18-year-old boy with chronic complete AV block. Two mechanisms for this paradoxical response to exercise are proposed: (1) delay in discharge of the automatic pacemaker focus by successful penetration of electrotonic potentials from nonconducted P waves across the area of block in the AV conduction system and into the pacemaker focus; and (2) discharge of the pacemaker focus by concealed reentrant extrasystoles. Wedensky inhibition is ruled out because of the resetting of the firing rate.

A school boy case associated with transient myocardial thickening and various patterns of conducting disturbance, especially multifocal accelerated idioventricular rhythm (AIVR)

A school boy case associated with transient myocardial thickening and various patterns of conducting disturbance, especially multifocal accelerated idioventricular rhythm (AIVR)

症例 Accelerated idioventricular rhythmの心拍数がi数年の経過にて徐々に増加し,ventricular tachycardiaの状態に移行した1女児例

症例 Accelerated idioventricular rhythmの心拍数がi数年の経過にて徐々に増加し,ventricular tachycardiaの状態に移行した1女児例

Effect of Betablockade on Ventricular Escape Rhythms: Comparison of Effects of Propranolol and Pindolol

Effect of Betablockade on Ventricular Escape Rhythms: Comparison of Effects of Propranolol and Pindolol

Effect of metaraminol during acute inferior wall myocardial infarction accompanied by hypotension: Preliminary study

This study was designed to evaluate the effects of metaraminol (Aramine) in six patients with evolving acute inferior wall myocardial infarction accompanied by hypotension and warm limbs. There were 16 episodes of acute inferior wall ischemia, and the response to therapy was judged by evaluating blood pressure and ST segment and T wave abnormalities. Three patients received intravenous isosorbide dinitrate and two received streptokinase as the initial therapy. The mean ST segment elevation was significantly reduced (from 4.94 +/- 1 to 0.5 +/- 0.7 [p less than 0.0001]) after metaraminol infusion was initiated. The average T wave height also decreased (from 6.8 +/- 2 to -1.3 +/- 2.5 mm [p less than 0.0005]). The average heart rate decreased from 82 +/- 11 to 69 +/- 9 beats/min (p less than 0.05) and the mean arterial blood pressure increased from 81 +/- 12 mm Hg before metaraminol treatment to 126 +/- 8 mm Hg after treatment. All these changes occurred within a few minutes after metaraminol therapy was instituted. In 12 episodes, accelerated idioventricular rhythm appeared concomitantly with the resolution of ST segment elevation. Coronary angiography performed between 4 and 10 days after admission demonstrated significant obstruction in all infarct-related arteries, but none was totally occluded. Left ventricular function was normal in three patients and slightly hypokinetic in the inferior wall in two. These results indicate that in a selected group of patients with acute inferior myocardial infarction, metaraminol administration (in certain hemodynamic circumstances) can alleviate acute ischemia within a few minutes and thereby reduce ischemic injury.

Time course and characteristics of ventricular arrhythmias after reperfusion in acute myocardial infarction

The time course and characteristics of ventricular arrhythmias were studied in 45 consecutive patients with acute myocardial infarction who received intravenous streptokinase and underwent 24-hour Holter monitoring both after admission and before discharge 8 ± 3 days later. In 41 of the 45 patients, thrombolytic treatment resulted in reperfusion as determined by characteristic clinical signs, i.e., rapid relief of pain associated with rapid resolution of ST-segment elevation and simultaneous abrupt increase in serum creatine kinase-MB activity. During the first 24 hours after reperfusion, the prevalence of ventricular premature complexes (VPCs) and couplets was nearly 100%, with an average frequency of 67 VPCs (range 1 to 1,336, median 44) and 6 couplets per hour per patient (range 1 to 97, median 4). Ninety percent of patients had an average of 8 runs of accelerated idioventricular rhythm per hour per patient (range 1 to 226, median 5) and 23% of the patients had an average of 2 runs of ventricular tachycardia per hour per patient (range 1 to 22, median 2) during the first 24 hours after reperfusion. The frequency of arrhythmias began to decrease 8 to 12 hours after reperfusion. Except for VPCs, ventricular arrhythmias were rare during the predischarge Holter study. Arrhythmias after reperfusion did not produce clinical symptoms and did not degenerate into ventricular fibrillation even though the patients were not receiving antiarrhythmic therapy. In the 4 patients without signs of reperfusion, the prevalence and frequency of all ventricular arrhythmias during the 24 hours after treatment was lower than in patients with reperfusion, and none had an accelerated idioventricular rhythm. Before discharge, there were only rare VPCs in 2 of these 4 patients. Our findings indicate that in patients with AMI, ventricular arrhythmias occur more often during the first 8 to 12 hours after reperfusion, are infrequent at the time of hospital discharge, and rarely produce clinical compromise, even in the absence of therapy.

Diffuse Triple-vessel Coronary Artery Spasm Complicated by Idioventricular Rhythm and Syncope

A 70-year-old man presented with diffuse triple-vessel coronary arterial spasm accompanied by ST segment elevation in the inferior and anterior leads when the severity of pain moderated. At the beginning, he noted throat and chest pain followed by syncope. Atropine, norepinephrine, and lidocaine were administered therapeutically. The initial electrocardiogram showed an idioventricular rhythm without ST segment deviations, which made the prompt diagnosis of coronary arterial spasm difficult.

Effects of propafenone on sinus nodal and ventricular automaticity: In vitro and in vivo correlation

The electrophysiologic effects of the new antiarrhythmic drug, propafenone, were evaluated in anesthetized closed-chest dogs and on isolated cardiac tissues with the microelectrode technique. Propafenone (2 to 4 mg/kg intravenously) had no effect on sinus rate or on sinus nodal recovery time, but caused a dose-dependent significant decrease in the rate of idioventricular rhythm and increased the duration of ventricular overdrive suppression in dogs (n = 8) with complete atrioventricular block. On isolated canine Purkinje fibers (n = 8) manifesting automaticity with resting membrane potential less negative than −70 mV, propafenone reduced the slope of phase 4 depolarization and reduced the rate of automatic impulse initiation in a concentration-dependent manner (10 −6M–4.10 −5M). At these concentrations, propafenone had no effect on rabbit sinus nodal automaticity (n = 8) or on sinoatrial conduction. However, significant depression of sinus nodal automaticity occurred with propafenone concentrations above 5.10 −6M in the presence of cholinergic or complete autonomic blockade with atropine (10 −6M) and propranolol (5.10 −5M). Propafenone caused a concentration-dependent decrease in the disparity of Purkinje fiber-ventricular muscle action potential duration (APD), mainly by shortening Purkinje fiber APD. We conclude: (1) that propafenone suppresses idioventricular rhythm in the intact dog, most likely by depressing Purkinje fiber automaticity; (2) the depressant effect of propafenone on sinus nodal automaticity is evident only during cholinergic receptor blockade; and (3) the antiarrhythmic properties of propafenone may include removal of APD disparity by selective shortening of Purkinje fiber and not of ventricular muscle APD.

Clinical types of proarrhythmic response to antiarrhythmic drugs

The problem of drug-induced or drug-aggravated cardiac arrhythmias has been recognized for many years. Digitalis glycosides and class I, II, III or IV antiarrhythmic drugs can cause severe sinus node dysfunction or atrioventricular block. Digitalis can cause a variety of supraventricular arrhythmias; atrial tachycardia with block and nonparoxysmal atrioventricular junctional tachycardia are the most characteristic. Recognition that class IA and class III antiarrhythmic drugs can aggravate arrhythmias or cause new arrhythmias in patients being treated for potentially malignant or malignant ventricular arrhythmias has intensified the interest in proarrhythmia in recent years. Several characteristic types of proarrhythmic response have been described. Torsades de pointes (multiform) ventricular tachycardia (VT) accompanied by prolongation of the QT interval can be caused by class IA and class III antiarrhythmic drugs as well as other drugs that bind to the membrane sodium channels of ventricular cells, for example, tricyclic antidepressants. Uniform VT in patients with malignant ventricular arrhythmias and poor left ventricular function is a characteristic proarrhythmic response to class IC antiarrhythmic drugs. Bidirectional VT or accelerated idioventricular rhythm are characteristic of digitalis toxicity. More difficult to establish as proarrhythmic responses are increased frequency of ventricular premature depolarizations and increased ease of inducing VT with programmed ventricular stimulation.

Holter detection of cardiac arrhythmias in intracranial subarachnoid hemorrhage

To determine the frequency and severity of cardiac arrhythmias in intracranial Subarachnoid hemorrhage, 120 nonselected patients were prospectively studied by 24-hour Holter monitoring. Arrhythmias were found In 96 of 107 patients (90%) with adequate Holter recording: ventricular premature complexes in 49, nonsustained ventricular tachycardia in 5, supraventricular premature complexes in 29, paroxysmal supraventricular tachycardia or atrial fibrillation in 9, sinoatrial block and arrest in 29, second-degree atrioventricular block in 1, atrioventricular dissociation in 4 and idioventricular rhythm in 2. Life-threatening ventricular arrhythmias (torsades de pointes-type ventricular tachycardia) occurred in 4 patients, degenerating into either ventricular flutter or fibrillation in 2. ST-segment changes suggestive of acute transitory myocardial ischemia were found in 8 patients (1.5 mm or more of ST depression in 7 patients and 1.5 mm or more of ST elevation in 1 patient). The frequency and severity of arrhythmias were significantly higher in patients studied within 48 hours of Subarachnoid hemorrhage; serious ventricular arrhythmias were associated with QTc prolongation more than 550 ms and with hypokalemia less than 3.5 mEq/liter. No correlation was found between age, clinical condition, site and extent of subarachnoid hemorrhage and either the occurrence or severity of arrhythmias. The results of our study indicate an extremely high incidence of arrhythmias, sometimes serious, in subarachnold hemorrhage, especially in the first 48 hours after hemorrhage. Continuous electrocardiographic monitoring is therefore mandatory.

Accelerated idioventricular rhythm during flexible fiberoptic bronchoscopy

We report the case of a patient who developed severe hypoxemia and an unusual arrhythmia, accelerated idioventricular rhythm, during flexible fiberoptic bronchoscopy. Coronary artery disease was subsequently suspected despite an unremarkable history and physical examination, and confirmed by a thallium 201 imaging. The appearance of accelerated idioventricular rhythm during fiberoptic bronchoscopy should raise the possibility of underlying coronary artery disease.

Ventricular Tachycardia, or Accelerated Junctional Rhythm?

To the Editor. —The article Ventricular Tachycardia in Acute Rheumatic Fever by Freed et al 1 discusses the fact that malignant ventricular arrhythmias have not been described in association with acute rheumatic fever. The authors describe a patient who is thought to have paroxysmal ventricular tachycardia. The figures published are much more consistent with an accelerated junctional rhythm with abberation, sometimes called an accelerated idioventricular rhythm or nonparoxysmal junctional tachycardia. This arrhythmia has an entirely different mechanism (enhanced atrioventricular junctional automaticity) as well as a much more benign prognosis, and it is common in acute rheumatic fever. 2 The accelerated junctional rhythm is characterized by moderate acceleration of the rate above the sinus rate and onset and termination with intermediate or fusion beats, and it is frequently found in abnormalities where the pathologic process involves the atrioventricular node. This abnormality is characteristic of acute rheumatic carditis. The benign course in

Cardiac effects of carbamazepine (CBZ)

Carbamazepine (CBZ) has documented effects on all levels of the cardiac conduction system, with bradycardia as a result. In cases of AV-block of high degree, CBZ may suppress the ventricular escape rhythm and is therefore contraindicated. Due to its antiarrhythmic properties CBZ has been classified according to Vaughan-Williams classification of antiarrhythmic drugs to group I. In older patients (>60 years) an ECG should be measured before CBZ is started. In younger patients an ECG is not necessary unless the pulse is less than fifty or clinical history reveals anything suspectedly for cardiac conduction disorder.

Electrocardiographic alterations induced by AGEPC in Wistar rats in relation to its hypotensive and hematologic effects

1. AGEPC administration into Wistar rats caused no remarkable thrombocytopenia, slight decrease of the percent count of PMNs in whole blood accompanied by anequal leukocytopenia and a transient increase in hematocrit, due to fluid extraversion. 2. Apart from the dramatic fall in blood pressure caused by AGEPC, relatively sinus bradyeardia was recorded at doses over 6 μg/kg b.w. 3. S-T segment elevation, mainly evident in II, III and AVF leads, was also recorded within the first minutes after AGEPC administration, at doses over 1 μg/kg b.w. 4. At lethal doses, various degrees of A-V block resulting in complete A-V block with idioventricular rhythm, or injury pattern resulting in ventricular fibrillation or ventricular flutter, were recorded. 5. At sublethal doses no arrhythic manifestations were recorded, while S-T segment elevation upward inversion became gradually normal.

Concentration-Dependent Protection by Captopril Against Myocardial Damage During Ischemia and Reperfusion in a Closed Chest Pig Model

We previously reported concentration-dependent protection of captopril against ischemia-reperfusion injury in the isolated rat heart. In order to study these effects in vivo, we developed a closed-chest pig model. Reversible occlusion of the left coronary artery was achieved with a PTCA catheter during one hour. Captopril (C) i.v. was given in two different concentrations (0.6 mg/kg/10 min + 0.3 mg/kg/2 hr and 6 mg/kg/10 min + 3.0 mg/kg/2 hr) during the experiments to 11 and 10 pigs, respectively, versus 12 controls, who received only saline. Due to malignant ventricular arrhythmias, nine pigs died during ischemia. At the end of the reperfusion period of two hours, eight pigs were alive in each group. In the C-treated pigs, maximum creatine kinase after two hours of reperfusion was significantly lowered to 6,337 +/- 709 U/L in the high dose group versus 8,285 +/- 851 U/L in the low dose group and 9,635 +/- 1,115 U/L in the saline group. A reduction of local inosine overflow in the coronary sinus was seen. Maximum noradrenaline overflow after 5 min reperfusion diminished dose-dependently to 695 +/- 284 and 3,129 +/- 1,728 pg/ml in the C treated groups versus 4,693 +/- 2,277 pg/ml in the saline group. Mean arterial blood pressure and cardiac output decreased significantly during ischemia and reperfusion, but no significant differences occurred between the treated and untreated groups. Reperfusion arrhythmias, mainly accelerated idioventricular rhythm disturbances, were comparable among the three groups. We conclude that in vivo administration of C reduces myocardial damage upon reperfusion after one hour of ischemia in a dose-dependent way.(ABSTRACT TRUNCATED AT 250 WORDS)

TACH-MAN: Tachyarrhythmia Management

TACH-MAN is an interactive program that simulates medical emergencies in a hypothetical patient suffering from a variety of common tachycardias, including ventricular tachycardia complicating myocardial infarction or drug treatment, supraventricular tachycardia, atrial fibrillation, atrial flutter, idioventricular rhythm, and rate-dependent bundle-branch block. If treatment is appropriate, the patient is cured; if improper, the player suffers a funeral dirge and tombstone exhibition. The intended audience consists of physicians, coronary care nurses, and rescue squad and other medical professionals caring for patients with tachycardia. One begins by selecting either a random or a specific scenario played on either of two levels: an introductory level that emphasizes the fundamentals of arrhythmia recognition and management, and an advanced level that stresses the fine points of management and the importance of speed in decision making. The program begins with a display of an electrocardiogram, the digital heart rate, respiratory rate, and blood pressure. The electrocardiogram and

Effects of diltiazem on reperfusion-induced arrhythmias in vitro and in vivo

The effects of the calcium antagonist, diltiazem, on myocardial injury during ischemia and reperfusion were studied both in vitro, in the isolated rat heart, and in vivo, in a closed-chest pig model. In the isolated rat heart, administration of diltiazem before or at the onset of ischemia resulted in a dose-dependent reduction of the incidence and duration of ventricular fibrillation. This reduction was associated with a dose-dependent reduction in overflow of ATP catabolites (adenosine, inosine, hypoxanthine and xanthine). Both changes were significant at concentrations of 3 X 10(-7) M diltiazem and higher. When 3 X 10(-7) M diltiazem was administered upon reperfusion no effect on the incidence of ventricular fibrillation and on ischemia induced total purine overflow was observed. However, the duration of ventricular fibrillation and purine overflow at 5 min after reperfusion were significantly reduced. In the pig experiments all untreated animals (n = 8) showed accelerated idioventricular rhythm (AIVR) upon reperfusion which lasted for 22 +/- 5 min after which sinus rhythm returned. Only two out of five treated animals (450 micrograms/kg/2 h) had an AIVR. Upon reperfusion both groups showed a substantial rise in noradrenaline concentration in the coronary sinus blood, but after 5 min this was significantly less in the treated group. Creatine kinase-kinetics were not altered by diltiazem, but the maximum creatine kinase level was significantly reduced. Within 4 days after the acute experiment 50% of the untreated animals died suddenly, whereas no sudden deaths occurred in the diltiazem group (P less than 0.05). Seven days after the acute experiment, sustained ventricular tachycardia could be induced with programmed electrical stimulation in three out of four surviving untreated pigs. In none of the diltiazem treated pigs was ventricular tachycardia inducible. The results of this study show that the calcium antagonist diltiazem can beneficially influence the events during ischemia and during reperfusion, both in vitro and in vivo; this benefit is associated with a reduction of ATP catabolism, creatine kinase release and noradrenaline overflow. Furthermore, diltiazem reduces electrical instability in the chronic phase of myocardial infarction.