Disease relevance of Arrhythmia

• In the Cardiac Arrhythmia Suppression Trial, designed to test the hypothesis that suppression of ventricular ectopy after a myocardial infarction reduces the incidence of sudden death, patients in whom ventricular ectopy could be suppressed with encainide, flecainide, or moricizine were randomly assigned to receive either active drug or placebo [1].
• The increase in mortality with vesnarinone was attributed to an increase in sudden death, presumed to be due to arrhythmia [2].
• Mutations in RyR2 linked to exercise-induced arrhythmias (in patients with catecholaminergic polymorphic ventricular tachycardia [CPVT]) reduced the affinity of FKBP12.6 for RyR2 and increased single-channel activity under conditions that simulate exercise [3].
• We conclude that amiodarone is effective for long-term therapy of recurrent ventricular tachyarrhythmias, that induction of arrhythmia during therapy does not always predict efficacy, and that side effects are frequent but do not usually limit therapy [4].
• A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome [5].

Psychiatry related information on Arrhythmia

• Emotional stress, isoproterenol infusion and exercise all elicited similar arrhythmias [6].
• Cardiac arrhythmias during wakefulness and sleep in 15 patients with sleep-induced obstructive apnea, and the effect of atropine and tracheostomy on these arrhythmias were studied by continuous overnight Holter electrocardiographic, respiratory and electroencephalographic recordings [7].
• The discharges may also be associated with cardiac arrhythmias, changes in free amino acids, and changes in prolactin level, and the discharges also may serve as a stimulus for a conditioned reflex [8].
• The most common form is the late-onset pseudo-Pompe disease, which is characterized by severe cardiomyopathy and mild myopathy appearing in the second or third decade, prominent arrhythmia with Wolf-Parkinson-White syndrome, and sometimes mental retardation [9].
• The effect of esmolol on ST-segment depression and arrhythmias after electroconvulsive therapy [10].

High impact information on Arrhythmia

• At the tissue level, arrhythmia could be due to slowing of electrical spread after both Na(+) current decrease and cell-to-cell uncoupling as well as cell depolarization and Ca(2+) current increase [11].
• Thus, an Irx5 repressor gradient negatively regulates potassium-channel-gene expression in the heart, forming an inverse I(to,f) gradient that ensures coordinated cardiac repolarization while also preventing arrhythmias [12].
• These data suggest that reduced PDE4D activity causes defective RyR2-channel function associated with heart failure and arrhythmias [13].
• Phosphodiesterase 4D deficiency in the ryanodine-receptor complex promotes heart failure and arrhythmias [13].
• We show that, in mice lacking the homeodomain transcription factor Irx5, the cardiac repolarization gradient is abolished due to increased Kv4.2 potassium-channel expression in endocardial myocardium, resulting in a selective increase of the major cardiac repolarization current, I(to,f), and increased susceptibility to arrhythmias [12].

Chemical compound and disease context of Arrhythmia

• In one case the available Fab fragment supply was inadequate to reverse a massive suicidal ingestion of digoxin, and the patient died after recurrent ventricular arrhythmias [14].
• Titration of the dose of a calcium-entry-blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested [15].
• Oral flecainide acetate for the treatment of ventricular arrhythmias [16].
• The risk of a recurrence of arrhythmia was significantly lower in patients who received sotalol than in those who received other antiarrhythmic drugs, and the risk was lower in those who had not previously failed to respond to antiarrhythmic drugs than in those who had [17].
• Cardiac arrhythmias associated with disopyramide [18].

Biological context of Arrhythmia

• There were no significant differences in the characteristics of sleep, the frequency of ventricular arrhythmias, daytime arterial-blood gas values, or the left ventricular ejection fraction during the base-line, placebo, and theophylline phases of the study [19].
• A reduction in Kir2.1 prolonged the terminal phase of the cardiac action potential, and in the setting of reduced extracellular K(+), induced Na(+)/Ca(2+) exchanger-dependent delayed afterdepolarizations and spontaneous arrhythmias [20].
• The mechanosensitive cation channel (MscCa) transduces membrane stretch into cation (Na(+), K(+), Ca(2+) and Mg(2+)) flux across the cell membrane, and is implicated in cell-volume regulation, cell locomotion, muscle dystrophy and cardiac arrhythmias [21].
• Our understanding of the genetic basis of disease has expanded with the identification of rare DNA sequence variations ("mutations") that evoke inherited syndromes such as cystic fibrosis, congenital epilepsy, and cardiac arrhythmias [22].
• Destructive counterparts include familial heart block ending in fatal arrhythmias, similar results in the long QT syndrome, and the pathogenesis of both Uhl's anomaly and arrhythmogenic right ventricular dysplasia; in each apoptosis is an important factor [23].

Anatomical context of Arrhythmia

• Hence, tyrosine, presumably acting in the central nervous system, can protect against certain ventricular arrhythmias [24].
• CONTEXT: Cisapride, a gastrointestinal tract promotility agent, can cause life-threatening cardiac arrhythmias in patients susceptible either because of concurrent use of medications that interfere with cisapride metabolism or prolong the QT interval or because of the presence of other diseases that predispose to such arrhythmias [25].
• To gain insight into the mechanism of arrhythmia susceptibility, we simulated the effect of reduced Kir2.1 using a ventricular myocyte model [20].
• Since both propranolol therapy and saphenous-vein bypass surgery have become accepted treatments for patients with symptomatic coronary-artery disease, it is important to determine if either influences the prevalence of ventricular arrhythmias in these patients [26].
• Dromotropic effects of adenosine and adenosine antagonists in the treatment of cardiac arrhythmias involving the atrioventricular node [27].

Gene context of Arrhythmia

• MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia [28].
• SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome [29].
• Mutations in the three known genes of the KCNQ branch of the K+ channel gene family underlie inherited cardiac arrhythmias (in some cases associated with deafness) and neonatal epilepsy [30].
• LQT was the primary cardiac manifestation, present in 71% of KCNJ2 mutation carriers, with ventricular arrhythmias present in 64% [20].
• With the exception of KCNE3, mutations in all these partner subunits have been found to lead to an increased propensity for cardiac arrhythmias [31].

Analytical, diagnostic and therapeutic context of Arrhythmia

• Patients whose arrhythmia was inducible by programmed electrical stimulation were assigned to treatment with electrophysiologically guided drug therapy based on serial testing (61 patients) or with metoprolol (54 patients) [32].
• During preoperative hospitalization, one patient in each group A and the control group suffered an increase in anginal symptoms compared with 15 patients in group B, three of whom also had new ventricular arrhythmias [33].
• A series of models were constructed to predict mortality achieved by different arrhythmia management strategies that reduced sudden death by 50 percent and 75 percent--reductions estimated to be within the range for amiodarone and implantable defibrillators [34].
• In addition, intravenous gentamicin suppressed the onset of arrhythmias under ischemic and reperfusion conditions in vivo [35].
• We assessed whether signal-averaged electrocardiography could identify patients with sustained ventricular arrhythmias in 41 patients with non-ischemic cardiomyopathy [36].

References