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At least 163 records · Page 9Linked to original sources
PubMed1985

[Idiopathic ventricular arrhythmia in children. Apropos of 24 cases].

The severity and prognosis of idiopathic ventricular arrhythmias in childhood were studied in 24 patients (12 boys, 12 girls) with an average age of 8 years at the time of diagnosis of the arrhythmia. Investigations included clinical assessment and analysis of basal ECG (morphology of the arrhythmias) and dynamic recordings (Holter and exercise stress testing). The clinical course was followed for an average of 3.8 years. The patients were classified in two groups: monomorphic arrhythmias (Group I) and polymorphic arrhythmias (Group II). Group I was divided into 4 subgroups: isolated ventricular extrasystoles (IA), 11 patients; ventricular extrasystoles with bursts of ventricular tachycardia (IB), 6 patients; sustained ventricular tachycardia without intercritical extrasystoles (IC), 1 patient; accelerated idioventricular rhythm (ID), 2 patients. Subgroups IA, IB and ID were characterised by the absence of symptoms, the disappearance of the arrhythmia on exercise, the decreased efficacy of antiarrhythmic drugs and an excellent prognosis. Therapeutic abstention was the rule in these patients. Patients in Group IC were characterised by the variability of their symptoms, the absence of exercise induced arrhythmias, the need for treatment in most cases and a good long-term prognosis. Group II was divided into 2 subgroups: adrenergic polymorphic ventricular tachycardia (IIA), 2 patients, and non-adrenergic polymorphic ventricular tachycardia (IIB), 2 patients. Patients in Subgroup IIA were characterised by syncope on exercise or emotion, the need for betablocker therapy which considerably improved the patients symptoms but which did not usually prevent sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

[Dynamics of ventricular arrhythmia in the acute period of myocardial infarction].

Patients with acute myocardial infarction exhibited during the first three days of the disease pronounced intra- and interindividual variability in the amount of ventricular ectopic complexes and significant differences in the dynamics of the number of single premature beats and complexes in the so-called "complex" arrhythmias--paired premature beats, periods of ventricular tachycardia and accelerated idioventricular rhythm. The regularities revealed may be used for the additional evaluation of antiarrhythmic drugs efficacy in myocardial infarction.

Aged↗
PubMed1988

[The incidence of ventricular arrhythmia following direct current ablation, high-frequency current ablation and laser photo-ablation].

Incidence and severity of ventricular arrhythmias (VA) following transvenous catheter ablation have so far not been fully elucidated. In the present study we evaluated the comparative incidence of postablation ventricular arrhythmias following high voltage-direct current electrical ablation (DCA), radiofrequency-ablation (RFA), and laser-photoablation (LPA). Experiments were performed on a total of 26 anesthetized mongrel dogs (BW: 20-30 kg). DCA (n = 14; 150-200 J) and RFA (n = 7; 38.5-72.5 J) were performed unipolarly via a 6F USCI catheter, LPA (n = 5; 40-80 J) was delivered through a quarz core fiber (diameter 0.4 mm) housed within a special designed catheter. Energies were delivered to various sites of free wall and apical endocardium of the left ventricle. Immediately after DCA fast runs of ventricular tachycardia (VT) developed in 13 out of 14 dogs degenerating into ventricular fibrillation in two animals. Mean cycle length of induced VT was 298 +/- 86 ms. Persistent VA, morphologically mainly characterized by an accelerated idioventricular rhythm interrupted by runs of ventricular salvoes, occurred in 12 animals (mean rate: 78 +/- 13 VPB/min 3 h after ablation). During VT early endocardial activations were recorded from the ablation site. No significant correlation between total applied energy (150-550 J) and incidence of arrhythmogenic effects was observed. RFA and LPA induced ventricular salvoes and runs of non-sustained ventricular tachycardia, in one animal ventricular fibrillation occurred during RFA; however, no persistent arrhythmic activity developed after RFA and LPA, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

[Syncope with a rare etiology, cardiac hydatidosis].

A case of left ventricular hydatid disease causing mitral insufficiency and revealed by accelerated idioventricular rhythm (AIVR) is reported. The traditional and more recent diagnostic procedures including echocardiography and immunology are reviewed. The persistence of AIVR and mitral insufficiency after excision of the cyst are discussed with respect to the surgical treatment.

Adult↗
PubMed1995

A life-threatening complication of extreme hyperkalemia in a patient on maintenance hemodialysis.

A 68-year-old female on two-year chronic hemodialysis for chronic renal failure due to chronic pyelonephritis, was admitted to hospital for weakness, dulled sensorium and dizziness. On examination the patient was in a state of circulatory collapse, the electrocardiogram showed an accelerated idioventricular rhythm and laboratory analysis revealed extreme hyperkalemia (K+ 10.1 mmol/l). There were no common causes of shock, such as hypovolemia, sepsis, heart failure and presence of vasodilator drugs. The patient was treated with calcium gluconate, sodium bicarbonate and sodium chloride (to oppose the effects of hyperkalemia on the cell membrane to minimize cardiac and neuromuscular toxicity), insulin and dextrose (to increase the transport of K+ from the extracellular to the intracellular compartment), and hemodialysis (to remove K+ from the body). At the end of the hemodialysis session, the patient was in a clinically good condition, blood pressure was 160/90 mm Hg and the serum K+ concentration was normal. The case appeared to suggest that extreme hyperkalemia may have direct effects on vascular resistance, causing hypotension and shock.

Aged↗
PubMed1993

Reperfusion arrhythmias in acute myocardial infarction.

In 27 patients with acute myocardial infarction (MI) and their infarct-related coronary artery being completely occluded who received thrombolytic therapy or percutaneous transluminal coronary angioplasty, reperfusion was confirmed by immediate coronary angiography in 24. Reperfusion arrhythmias (RA) occurred in 19 (79.2%) of the patients, including ventricular arrhythmias in 13 (54.2%). Ventricular fibrillation and sustained ventricular tachycardia developed in 2 (8.4%) and accelerated idioventricular rhythm in 5 (20.8%), the latter was a reliable indicator of coronary recanalization. Transient sinus bradycardia or AV block occurred in 10 (66.7%) of the 15 patients with inferoposterior MI. The occurrence of RA was not related to the duration of ischemia; ventricular RA was also not related to the location of MI and the occurrence and severity of ischemic arrhythmias before reperfusion.

Aged↗
PubMed1995

[Evaluation of a standard electrocardiogram in acute myocardial infarct and therapy with thrombolysis].

Electrocardiography the cheapest, quickest and most readily available supportive examination method in patients with acute coronary events is irreplaceable also in the era of thrombolysis. The authors present a review of data from the literature on evaluation of the success of thrombolysis based on the electrocardiogram. They emphasize in the first place the importance of a rapid drop or normalization of the ST segment and/or the presence of so-called reperfusion arrhythmias (in particular an early, frequent, repetitive accelerated idioventricular rhythm). The authors mention also changes of the QRS complex, the T wave and Q-T interval during thrombolytic treatment.

Electrocardiography↗
PubMed1996

[The electrocardiogram in acute myocardial infarct in the "thrombolytic era"].

Authors presented the basic criteria for indicating thrombolytic therapy in patients with acute myocardial infarction according to literature data and their own experience regarding the judgment of changes in initial standard electrocardiogram (without any changes after administration of nitroglycerine and/or chest pain resolution). They are: 1. ST segment elevation > or = 0.1 mV, in at least two contiguous leads, 2. new or a presumably new bundle branch block, 3. ST segment depression in thoracic leads V1-V3 in the presumptive presence of acute posterior myocardial infarction. It is appropriate to repeat the recording, to perform echocardiography (or coronary angiography) and to evaluate in complexity the general clinical status in case of nonspecific changes on the electrocardiogram. Authors include a review of literature data on evaluation of cases with successful thrombolysis based on standard electrocardiogram. They emphasized strongly the meaning of a fast and sustained decrease/normalisation of ST segment and/or presence of so called reperfusion arrhythmias (namely early, frequent, repetitive accelerated idioventricular rhythm). The authors presented also the changes of QRS complex, T wave and Q-T interval with thrombolytic therapy. The evaluation of ST segment re-elevation during and after thrombolytic therapy still requires to be studied into greater detail. (Tab. 5, Ref. 65.)

Electrocardiography↗
PubMed1998

[In Process Citation]

Reperfusion arrhythmias originate as a consequence of the complex of cellular and humoral reactions accompanying the opening of coronary artery. As the primary cause of their generation are considered the chemically defined substances that are produced and accumulated in myocardium during reperfusion. The key role id ascribed to free oxygen radicals but of importance are also other substances such as calcium, thrombin, platelet activating factor, inositol triphosphate, angiotensin II and others. These chemical mediators of reperfusion arrhythmias operate as modulators of cellular electrophysiology causing the complex changes at the level of ion channels. It is supposed that in the genesis of reperfusion arrhythmias unlike ischemic arrhythmias operate nonreentrant mechanisms such as abnormal or enhanced automacy and triggered activity due to afterdepolarizations. As a typical reperfusion arrhythmia is considered an early (within 6 hours after start of thrombolysis), frequent (> 30 episodes/hour) and repetitive (occurring during > 3 consecutive hours) accelerated idioventricular rhythm (AIVR). AIVR with such characteristics has a high specificity and positive predictive accuracy but relative low sensitivity as a predictor of reperfusion. Thus, in occurrence of AIVR, recanalization of infarction-related coronary artery is very probable, but in absence of AIVR, reperfusion is still not excluded. The following arrhythmias are regarded also as markers of reperfusion: frequent premature ventricular complexes (> twofold increase in frequency within 90 minutes after the start of thrombolysis), a significant increase of episodes in nonsustained ventricular tachycardia, sinus bradycardia and probably also high degree atrioventricular blocks. At present, there is no definite evidence, as to whether sustained ventricular tachycardia and especially ventricular fibrillation can be caused by reperfusion. Reperfusion arrhythmias are an important noninvasive marker of successful recanalization of infarction-related coronary artery. However, they are also a sign of reperfusion injury and a finding which may limit the favourable effect of reperfusion. In account of that, there is a very intensive search for pharmacologic interventions which could protect or attenuate the reperfusion injury and thereby also the genesis of reperfusion arrhythmias. Although promising results were obtained with many substances antagonizing the effects of mediators of reperfusion injury, there is no definite recomendation for their use under clinical conditions. However, the results from the latest clinical trials with ACE inhibitors are very promising. These trials render relative conclusive evidence, that ACE inhibitors could have a protective effect against reperfusion arrhythmias. (Ref. 89, Tab. 1.)

Journal Article↗
PubMedDate not supplied

[Reperfusion arrhythmias].

Reperfusion arrhythmias originate as a consequence of the complex of cellular and humoral reactions accompanying the opening of coronary artery. As the primary cause of their generation are considered the chemically defined substances that are produced and accumulated in myocardium during reperfusion. The key role is ascribed to free oxygen radicals but of importance are also other substances such as calcium, thrombin, platelet activating factor, inositol triphosphate, angiotensin II and others. These chemical mediators of reperfusion arrhythmias operate as modulators of cellular electrophysiology causing the complex changes at the level of ion channels. It is supposed that in the genesis of reperfusion arrhythmias unlike ischemic arrhytmias operate nonreentrant mechanisms such as abnormal or enhanced automacy and triggered activity due to afterdepolarizations. As a typical reperfusion arrhythmia is considered an early (within 6 hours after start of thrombolysis), frequent (> 30 episodes/hour) and repetitive (occurring during > 3 consecutive hours) accelerated idioventricular rhythm (AIVR). AIVR with such characteristics has a high specificity and positive predictive accuracy but relative low sensitivity as a predictor of reperfusion. Thus, in occurrence of AIVR, recanalization of infarction-related coronary artery is very probable, but in absence of AIVR, reperfusion is still not excluded. The following arrhythmias are regarded also as markers of reperfusion: frequent premature ventricular complexes (> twofold increase in frequency within 90 minutes after the start of thrombolysis), a significant increase of episodes in nonsustained ventricular tachycardia, sinus bradycardia and probably also high-degree atrioventricular blocks. At present, there is no definite evidence, as to whether sustained ventricular tachycardia and especially ventricular fibrillation can be caused by reperfusion. Reperfusion arrhythmias are an important noninvasive marker of successful recanalization of infarction-related coronary artery. However, they are also a sign of reperfusion injury and a finding which may limit the favourable effect of reperfusion. In account of that, there is a very intensive search for pharmacologic interventions which could protect or attenuate the reperfusion injury and thereby also the genesis of reperfusion arrthythmias. Although promising results were obtained with many substances antagonizing the effects of mediators of reperfusion injury, there is no definite recommendation for their use under clinical conditions. However, the results from the latest clinical trials with ACE inhibitors are very promising. These trials render relative conclusive evidence, that ACE inhibitors could have a protective effect against reperfusion arrhythmias. (Ref. 89, Tab. 1.)

Arrhythmias, Cardiac↗
PubMed1976

Association of ventricular extrasystoles and ventricular tachycardia with idioventricular rhythm.

Patients with acute myocardial infarction were monitored for ventricular arrhythmias in the first 48 hours. Idioventricular rhythm (rate less than 100/minute) occurred in 35 out of 224 patients (15.6%) during the first day and in 13 out of 192 patients not receiving treatment on the second day (6.8%). This arrhythmia was frequently preceded by late ventricular extrasystoles, which often showed variation of their coupling intervals to the preceding QRS. Double ventricular extrasystoles separated by larger than or equal to 600 ms were also precursors of idioventricular rhythm. Idioventricular rhythm at times could be described as an escape rhythm, but on other occasions it was undoubtedly an accelerated rhythm. Spontaneous changes in the idioventricular cycle length were frequent on single one-minute electrocardiographic recordings. The rate of the dominant rhythm in patients with episodes of idioventricular rhythm was significantly slower than the heart rate of patients without this arrhythmia. Idioventricular rhythm was more frequent in patients with inferior infarction. Idioventricular rhythm sometimes preceded ventricular tachycardia but there was only a significant association between ventricular tachycardia and idioventricular rhythms with rates of over 75/minute. Irregular idioventricular rhythm frequently accelerated to ventricular tachycardia. It is suggested that the term benign idioventricular rhythm be reserved for those rhythms below 75/minute, and that the term rapid idioventricular rhythm should be used for rhythms between 75 and 120/minute. The rate of idioventricular rhythm is related to the probability of development of life-threatening ventricular arrhythmias during the first 48 hours after myocardial infarction.

Cardiac Complexes, Premature↗
PubMedDate not supplied

[Idioventricular rhythm in childhood].

Idioventricular or accelerated ventricular rhythm has been reported frequently in adults--usually in association with acute myocardial infarction, sometimes in other heart diseases, but also in healthy individuals. Until today the origin of this rhythm disturbance is unknown, its nature benign and doesn't influence the prognosis adversely. The ectopic idioventricular rhythm was present intermittently, competed with the similar frequency of sinus rhythm and subdued by increasing the basic sinus rate was subdued. Such patients needs no therapy! The onset of idioventricular rhythm was observed in infancy and childhood too, but only a few reports exists. One case of idioventricular rhythm occurring in a 9-year-old girl is presented. In our opinion, cardiologic basic diagnostic methods (including echocardiography), Holter monitoring and possibly ergometry are sufficient to characterize this benign rhythm anomaly and to avoid unnecessary and perhaps dangerous treatment with antiarrhythmic drugs.

Atrioventricular Node↗
PubMed1993

Cardiac arrest presenting with rhythms other than ventricular fibrillation: contribution of resuscitative efforts toward total survivorship.

OBJECTIVE: The medical literature portrays a bleak prognosis for out-of-hospital cardiac arrest cases presenting with asystole, idioventricular rhythms with pulselessness, or primary electromechanical dissociation. In view of evolving philosophies to waive resuscitation attempts in such cases, we sought to delineate the actual contribution toward overall survivorship that is provided by resuscitation efforts for patients who have these electrocardiographic presentations. DESIGN: A prospective outcome study which analyzed all out-of-hospital cardiac arrest cases in a large city for a 2-yr period in terms of presenting electrocardiogram, age, sex, presence and status of witnesses, performance of bystander cardiopulmonary resuscitation, and survival to successful hospital discharge. SETTING: A large urban municipality (population, two million) served by a single, centralized emergency medical services program. PATIENTS: Excluding cases associated with trauma, drugs, airway obstruction, submersion or primary respiratory illness, 2,404 consecutive adult out-of-hospital cardiac arrest patients were studied. INTERVENTIONS: Standard advanced cardiac life support. MEASUREMENTS AND MAIN RESULTS: Although survival "rates" of patients with asystole, idioventricular rhythms with pulselessness, and electromechanical dissociation were low (1.6%, 4.7% and 6.9%, respectively), 22.2% of the 193 total survivors (confidence interval: +5.9%) initially presented with one of these electrocardiographic rhythms (14 asystole, 18 idioventricular rhythms with pulselessness, 10 electromechanical dissociation, plus one other). CONCLUSIONS: Despite poor survival "rates," resuscitative efforts for patients presenting with asystole, electromechanical dissociation, and idioventricular rhythms with pulselessness all contribute significantly toward a community's total survivorship from out-of-hospital cardiac arrest. Initial, aggressive attempts at resuscitation still should be emphasized in such patients.

Accelerated Idioventricular Rhythm↗
PubMed2004

Accelerated ventricular rhythm in the neonatal period: a review and two new cases in asymptomatic infants with an apparently normal heart.

UNLABELLED: Accelerated ventricular rhythm (AVR) was observed in two newborn infants. In the first case, arrhythmia was noted during the foetal period. Both neonates were asymptomatic and had no evidence of cardiac disease. The arrhythmia eventually disappeared when the infants were 4 mo and 24 d old, respectively. AVR in the neonatal period is reviewed in this report and recent information regarding appropriate diagnostic evaluation, differentiation from ventricular tachycardia and treatment is outlined. CONCLUSION: Accelerated ventricular rhythm is a benign and self-limited arrhythmia in the neonatal period. However, it is important to differentiate it from other serious rhythm disorders, mainly ventricular tachycardia, in order to avoid unnecessary and potentially harmful treatment and to relieve parental anxiety.

Accelerated Idioventricular Rhythm↗