Presumed primary cardiac mast cell tumor, pericardial effusion, and arrhythmia in a dog.

A 13-year-old female spayed border collie cross presented for pericardial effusion, arrhythmia, and a suspected cardiac mass. Echocardiogram revealed severe thickening and hypokinesis of the interventricular septum with a heterogenous, cavitated myocardium, concerning for neoplasia. Electrocardiogram revealed predominantly accelerated idioventricular rhythm with frequent periods of nonsustained ventricular tachycardia. Occasional prolonged PR intervals terminating in an aberrantly conducted QRS complex were present. These beats were postulated to represent either first-degree atrioventricular block with aberrant QRS conduction or atrioventricular dissociation. Cytology of the pericardial effusion revealed atypical, suspected neoplastic, mast cells. The patient was euthanized, and postmortem examination confirmed full-thickness infiltration of the interventricular septum by a mast cell tumor, with metastasis to the tracheobronchial lymph node and spleen. Given the anatomic location of the mass, the observed atrioventricular nodal conduction delay may represent neoplastic infiltration of the atrioventricular node. Neoplastic infiltration of the ventricle was suspected to cause the accelerated idioventricular rhythm and ventricular tachycardia. To the authors' knowledge, this is the first reported case of a primary cardiac mast cell tumor causing arrhythmia and pericardial effusion in a dog.

Ritme idioventricular accelerat transitori en un nounat afectat d’acidèmia metilmalònica / Ritmo idioventricular acelerado en un neonato afecto de acidemia metilmalónica / Transient accelerated idioventricular rhythm in a newborn with methylmalonic academia

Introducció: el ritme accelerat idioventricular (RIVA) és una disrítmia originada a nivell dels feixos de His, de les fibres de Purkinje o dels miòcits ventriculars, molt rara en infants i nadons. Cas clínic: es presenta el cas d'un nounat a terme amb la presència de RIVA els primers dies de vida, sense repercus-sió hemodinàmica, i que s'autolimita als dos mesos d'edat. Posteriorment es va diagnosticar d'acidèmia metilmalònica tipus mut0, i es va iniciar el tractament amb dieta específica, carnitina i vitamina B12, amb bon control metabòlic. En el seguiment presenta extrasístoles ventriculars aïllades i un desenvolupament físic i psicomotor correctes. Comentaris: la identificació d'aquesta disrítmia pot ser difícil i és de gran transcendència, ja que planteja el diagnòstic diferencial principalment amb la taquicàrdia ventricular. El seu pronòstic generalment és benigne i tendeix a la resolució espontània; per tant, els fàrmacs antiarítmics no estan indicats. La coexistència de RIVA i acidèmia metilmalònica en un mateix pacient no ha estat descrita fins al moment

Introducción. El ritmo acelerado idioventricular (RIVA) es una disritmia originada a nivel de los haces de His, de las fibras de Purkinje o de los miocitos ventriculares, muy rara en niños y neonatos. Caso clínico. Se presenta el caso de un recién nacido a término con la presencia de RIVA los primeros días de vida, sin repercusión hemodinámica, y que se autolimita a los dos meses de edad. Posteriormente se diagnosticó de acidemia metilmalónica tipo mut0, y se inició el tratamiento con dieta específica, carnitina y vitamina B12, con buen control metabólico. En el seguimiento presenta extrasístoles ventriculares aisladas y un desarrollo físico y psicomotor correctos. Comentarios. La identificación de esta disritmia puede ser difícil y es de gran trascendencia, puesto que plantea el diagnóstico diferencial principalmente con la taquicardia ventricular. Su pronostico es, generalmente, benigno y tiende a la resolución espontánea; por tanto, los fármacos antiarrítmicos no están indicados. La coexistencia de RIVA y acidemia metilmalónica no ha sido descrita hasta el momento en un mismo paciente (AU)

Introduction. The accelerated idioventricular rhythm (AIVR) is a very rare pediatric dysrhythmia originated in the bundles of His, Purkinje fibers, or ventricular myocytes. Case report. A term newborn presented with AIVR in the first days of life; he was hemodynamically stable, and the arrhythmia resolved by two months of age. The infant was subsequently diagnosed with mut0 methylmalonic acidemia, and was started on specific diet, carnitine, and vitamin B12, with good response. On follow-up, the infant was found to have isolated ventricular extrasystoles and normal physical and psychomotor development. Comments. The identification of this dysrhythmia can be difficult; its prompt recognition is critical due to its differential diagnosis with ventricular tachycardia. The prognosis is usually benign, with spontaneous resolution in most cases; thus, antiarrhythmic agents are not indicated. The coexistence of AIVR and methylmalonic academia has not been previously described (AU)

Ventricular arrhythmias in children with attention deficit disorder--a symptom of autonomic imbalance?

OBJECTIVES: Potential side effects of stimulants for attention deficit disorder are in the focus of scientific discussions, intensified by the higher number of prescriptions. Children with known arrhythmias or other severe cardiac problems should not receive stimulants because of their sympathomimetic effects. METHODS: This is a retrospective analysis of 24-hour Holter electrocardiograms from 100 consecutive children with attention deficit disorder from January, 2006 to April, 2012. RESULTS: In all, nine children had significant ventricular arrhythmia (mean age 11.4 ± 3.1 years, 77% male, 77% received methylphenidate). All these children had ventricular parasystole - four of them with an accelerated idioventricular rhythm. A significant circadian rhythm of premature ventricular contractions in seven children and the effect of standing and exercise clearly indicate the influence of the autonomic nervous system. In these children, hourly analysis of circadian rhythm within a 24-hour period showed a highly significant correlation between premature ventricular contractions and the vagal tone indicated by the heart rate variability parameter RMSSD (r = -0.83; p < 0.001). Ventricular arrhythmia was unaffected in seven children who received methylphenidate before diagnosis and decreased during metoprolol treatment in two children. CONCLUSION: By Holter electrocardiogram analysis, we observed a remarkably high incidence of ventricular parasystole and accelerated idioventricular rhythm in nine of 100 children with attention deficit disorder, which depends on autonomic imbalance and not on stimulant treatment.

Rapidly fatal community-acquired pneumonia due to Klebsiella pneumoniae complicated with acute myocarditis and accelerated idioventricular rhythm.

We describe a previously healthy 52-year-old man with rapidly fatal community-acquired pneumonia caused by Klebsiella pneumoniae. The patient developed acute renal dysfunction, accelerated idioventricular rhythm (acute myocarditis), lactic acidosis and septic shock. He died within 15 hours after admission despite intravenous levofloxacin (750 mg daily) and aggressive medical treatment.

Autonomic patterns preceding and following accelerated idioventricular rhythm in acute myocardial infarction.

INTRODUCTION: We have investigated the potential relationship between cardiac autonomic activity and accelerated idioventricular rhythm (AIVR) in response to reperfusion in the setting of an acute myocardial infarction (AMI) through spectral analysis of heart rate variability (HRV). METHODS AND RESULTS: We studied 16 patients with AMI who developed spontaneous sustained AIVR after initiation of intravenous thrombolysis. Sympathovagal interactions were evaluated by analysis of the low- (LF) and high-frequency (HF) spectral components of HRV for each 5-min interval over the 30-min periods preceding and following AIVR. The occurrence of AIVR was related to the ST-segment elevation resolution and the angiographic evidence of restored coronary flow to assess timely reperfusion and sustained coronary artery patency. The analysis of spectral components over time revealed combined responses of both autonomic limbs preceding and following AIVR, which were not followed by corresponding changes in heart rate. Ten minutes before AIVR, there was a characteristic continuous increase in LF, in the setting of a concomitant withdrawal of HF, suggestive of a progressive sympathetic predominance. After the end of AIVR, the opposite pattern was found with an increased HF and decreased LF, indicative of parasympathetic rebound overactivity. All patients showed signs of fast reperfusion and complete restoration of coronary flow. CONCLUSION: Our results indicate that reperfusion-induced AIVR is modulated by sympathetic stimulatory effects, whereas a counterregulatory vagal response seems to exert a profound effect upon its suppression. Clinically, the occurrence of early sustained AIVR appears to offer reliable information about both timely reperfusion and sustained and effective coronary artery patency.

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.

[Repeated blackout in a patient with accelerated idioventricular rhythm].

There has been no report that Accelerated Idioventricular rhythm (AIVR) causes a syncope attack. The patient described in this report is very rare because AIVR chronic without any heart diseases has been observed for 13 years, and because it is considered that AIVR is closely associated with his repeated blackouts. A 62-year-old male was admitted to our hospital because of repeated syncopal attacks. He reported that he occasionally felt lightheaded after strenuous lifting and pushing or pulling against resistance. We found that AIVR could produce a remarkable arterial pressure drop partly because of ventricular asynergy and loss of timed atrial contribution. Furthermore, we observed syncopal attacks during Valsalva maneuver and found abnormalities of baroreceptor reflex (Lack of reflex tachycardia and weakened evershoot phenomenon). It is concluded that AIVR is not a benign arrhythmia in this patient because it has been a possible cause of syncope attack due to systemic arterial pressure drop and baroreceptor abnormalities.