Disease relevance of Cardiac Complexes, Premature

• Ankyrin-B mutation also leads to altered Ca2+ signalling in adult cardiomyocytes that results in extrasystoles, and provides a rationale for the arrhythmia [1].
• Immediately after intravenous (IV) injections of epinephrine chloride, ventricular premature beats and apparent accelerated idioventricular rhythm occurred in one patient and possible ventricular tachycardia occurred in the other [2].
• Couplets were noted in 56% versus 60% and ventricular tachycardia (VT) (three or more consecutive ventricular premature beats) in 27% versus 29% of patients randomized to enalapril versus hydralazine-isosorbide dinitrate, respectively [3].
• In the ouabain and postinfarction preparations, right ventricular epicardial pacing induced ventricular premature beats or tachycardias whose recovery intervals after cessation of pacing shortened and showed overdrive acceleration as pacing rate increased [4].
• Lidocaine eliminated His bundle extrasystoles that blocked entirely (concealed) or conducted with functional left bundle-branch block by improving His-Purkinje conduction and by lengthening the coupling interval of the premature His bundle extrasystole [5].

Psychiatry related information on Cardiac Complexes, Premature

• The patient had serious psychiatric problems; the ventricular premature beats were provoked by psychophysiologic stress, increased during REM sleep, were reduced by meditation, and were controlled by beta-adrenergic blockade, phenytoin and digitalization [6].

High impact information on Cardiac Complexes, Premature

• To determine the efficacy of digitalis drugs in suppressing ventricular ectopic activity, 142 patients with frequent (greater than 1 per minute) ventricular premature beats underwent acetyl strophanthidin tolerance testing [7].
• The number of ventricular premature beats after reperfusion in knockout mice, however, was much less than in wild-type mice [8].
• 4) Combinations of lidocaine and quinidine have a superadditive effect on the Vmax of early extrasystoles [9].
• In the present investigation, cholinergic stimulation was produced by administering the selective muscarinic agent methacholine (MCh) and ventricular vulnerability was assessed by measuring the repetitive extrasystole (RE) threshold [10].
• OBJECTIVES: The purpose of this study was to verify in a long-term follow-up whether frequent monomorphic right ventricle extrasystoles may progress to arrhythmogenic right ventricular dysplasia (ARVD) [11].

Chemical compound and disease context of Cardiac Complexes, Premature

• There was 100% suppression of runs of premature beats in 11 patients after lorcainide and 99% suppression in 10 patients after lidocaine.(ABSTRACT TRUNCATED AT 250 WORDS)[12]
• When examined on premature beats, AT was delayed, depending on the coupling interval and the fiber direction when saline, flecainide or lidocaine was infused [13].
• The acute electrophysiologic effects of clinical doses of procainamide, lidocaine, metoprolol, digoxin and atropine upon the conduction of ventricular premature beats, were studied in 48 healthy volunteers [14].
• Patients treated with diltiazem had lower numbers of ventricular premature beats/hour (8.1 +/- 7.8 vs 20.5 +/- 11.2; P < 0.05) [15].
• Evaluation of pentisomide on stable ventricular premature beats. Comparison with placebo [16].

Biological context of Cardiac Complexes, Premature

• The faster HERG deactivation could be involved in reperfusion-induced arrhythmias by reducing K+ conductance in the early diastole, thus increasing the risks of premature beats [17].
• Iopromide and ioversol induced transient changes in blood pressure (decrease followed by an increase), left ventricular end-diastolic pressure (increase), heart rate (decrease), contractility (increase followed by decrease), and electrocardiogram (extrasystoles, ST depression) [18].
• This protocol could not detect abnormalities in atrial function in early affected patients with heritable cardiomyopathy and atrial premature beats [19].

Anatomical context of Cardiac Complexes, Premature

• In the rat coronary artery ligation model, disopyramide (class I), amefalone and melperone significantly (P less than 0.05) reduced the number of extrasystoles [20].
• The accelerated inactivation time course of HERG/MiRP1(V65M) channels may decrease I(Kr) current density of myocardial cells, thereby impairing the ability of myocytes to repolarize in response to sudden membrane depolarizations such as extrasystoles [21].
• Accuracy of the value <0 msec (obtained by subtracting the time interval between high right atrium and His-bundle atrial activation during atrial premature beats from that obtained during sinus rhythm) for discriminating the superior vena cava or upper portion of the crista terminalis from the pulmonary vein (PV) foci was 100% [22].
• On the other hand, low doses of lidocaine caused speeding of early extrasystoles, i.e., coupling intervals (less than 250 ms) in the Purkinje system but not in the myocardium [23].
• Lithium and KBR effects particularly for the extrasystole can be explained through the inhibition of Ca entry via Na-Ca exchange giving support to the participation of the Na-Ca exchanger in the Ca influx from the extracellular space [24].

Gene context of Cardiac Complexes, Premature

• The plasma ANP level was significantly higher in patients with rather than without PAF attacks (75 +/- 41 vs. 54 +/- 60 pg/ml, p = 0.01), although there were no significant differences in age, left atrial dimension or high grade atrial premature beats between the groups [25].
• Prognostic significance of heart rate turbulence following ventricular premature beats in patients with idiopathic dilated cardiomyopathy [26].
• Patients with COPD had higher rate of ventricular premature beats (VPBs) as compared to control subjects (924 +/- 493 beats vs 35 +/- 23 beats, p = 0.009) [27].
• Isolated ventricular premature beats and runs of slow ventricular rhythm with H(2)O(2) more frequently occurred in HF compared to SHAM despite an increased antioxidant capacity including Cu/Zn and Mn superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase [28].
• However, with the addition of each successive premature beat, the HPS-RRP of the postextrasystolic beat alternated between lower and higher values, in a manner dependent on whether there was an odd or even number of premature beats [29].

Analytical, diagnostic and therapeutic context of Cardiac Complexes, Premature

• In a multicentre study efficacy and safety of propafenone 450 mg day-1 and 750 mg day-1 was studied in 97 patients with frequent ventricular premature beats (VPB greater than 30 h-1) [30].
• During the first 30 min of myocardial ischaemia the number of extrasystoles in the timolol-treated dogs (327 +/- 179) was less than in the control group (888 +/- 168) and none of the dogs that received timolol fibrillated [31].
• RESULTS: Holter monitoring showed a heart rate higher after formoterol, 24 microg, than after formoterol, 12 microg, and salmeterol, 50 microg, and supraventricular or ventricular premature beats more often after formoterol, 24 microg [32].
• RESULTS: Fetal arrhythmia persisted into the neonatal period in three cocaine-exposed infants; two were delivered via emergency cesarean sections for presumed fetal bradycardia and were subsequently found to have asymptomatic frequent and blocked atrial premature beats [33].
• Signal-averaged ECG in prediction of the short-term suppression of ventricular premature beats by Mexiletine [34].

References