Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q96S42 (nodal)
 22,877 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty dogs were studied 3 to 9 days after myocardial infarction. None had ventricular arrhythmias during sinus rhythm, and ventricular automaticity (as revealed by sinus nodal crush procedure or vagal stimulation, or both) was within the normal range. With regular atrial pacing or pacing with long-short cycle sequences it was possible to induce ventricular arrhythmias in all animals. Quadrigeminal and pentageminal rhythms (19 of 20 dogs) and trigeminal (17 of 20) and bigeminal ventricular rhythms (8 of 20) were observed. These rhythms which were manifest or partially or entirely concealed were always associated with delayed and fractionated electrical activity within the "infarcted" subepicardium. Continuous electrical activity (electrical activity that bridged the interval between two or more successive beats) was recorded from the infarct zone. Such activity either was manifest as ventricular arrhythmia during atrial pacing or remained concealed until atrial pacing was stopped and then was manifest as ventricular tachycardia.
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PMID:Continuous concealed ventricular arrhythmias. 7 99

The authors previously showed that cyclopropane-epinephrine-induced bigeminal arrhythmias can best be explained by a re-entrant mechanism. They have now obtained evidence for reentry in bigeminal arrhythmias during infusions of epinephrine (.5-3 mug/kg/min) in dogs anesthetized with .8 per cent halothane. Both a critical level of blood pressure and a critical increase in heart rate were necessary for arrhythmias to be induced in any given animal. Artificial elevation of the blood pressure during infusion of a subthreshold dose of epinephrine could induce bigeminy, and the arrhythmia could be aborted by a sudden reduction of blood pressure. The heart rate accelerated approximately 40 beats/min prior to the onset of bigeminy, and atrial pacing at similarly increased rates during subthreshold infusion of epinephrine could induce bigeminy. Stimulation of the peripheral end of the cut right cervical vagus reduced heart rate and converted bigeminy to sinus rhythm. Bradycardia was not the sole mechanism of the vagal effect since conversion to sinus rhythm could also be achieved with more rapid stimulation of the vagus when the heart rate was maintained constant by atrial pacing. Under these conditions further acceleration of the heart rate could reinstate a bigeminal arrhythmia that was again sensitive to further increases in the frequency of vagal stimulation, and it is concluded that the vagus acts on the spread of the re-entrant impulse. This is best shown with cyclopropane anesthesia, because AV-nodal block occurs more easily with halothane. In addition, very brief periods of increased heart rate caused prolonged periods of bigeminy, which indicates that changes in heart rate may alter the electrophysiology of the halothane-sensitized myocardium to promote bigeminal arrhythmias by a re-entry mechanism.
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PMID:Halothane-epinephrine-induced cardiac arrhythmias and the role of heart rate. 119 May 23

The effects of alternating cycle lengths (bigeminal rhythm) on His-Purkinje system refractoriness were studied in 14 patients using His bundle and right bundle recordings. Programmed atrial stimulation at constant cycle length (method I) was scanned using the atrial extrastimulus technique (A2) and compared with an atrial cycle length of identical duration coupled to A2 on alternate beats (method II). The results showed that (a) despite shorter cycle length of the His-Purkinje system with method II due to effect of A2 on atrioventricular nodal conduction (699 +/- 90 vs. 743 +/- 87 ms, P less than 0.001), the relative refractory period of the His-Purkinje system was always longer with method II (463 +/- 52 vs. 440 +/- 43 ms, P less than 0.001). A similar increase also occurred in effective refractory period of the His-Purkinje system; (b) while functional right bundle branch block occurred in eight patients and functional left bundle branch block in two patients with method I, functional right bundle branch block occurred in all 14 patients and left bundle branch block in seven patients with method II; (c) in two patients where both functional right and left bundle branch block occurred with method I this never was manifest at identical degree of abbreviation of His-Purkinje system cycle length but was manifest at identical abbreviation in each of seven patients with method II; (d) site of conduction delay and/or block during functional right bundle branch block was always proximal, i.e., between the His bundle and right bundle recordings with both methods. During method II this resulted in shortening of the subsequent right bundle cycle length relative to the subsequent His bundle (and of necessity left bundle) cycle length. The finding of increased His-Purkinje system refractoriness despite shorter preceding cycle length of the His-Purkinje system during atrial bigeminy has never been previously described and suggests that classical concepts of His-Purkinje system behavior may require revision in this setting. Secondly, during atrial bigeminy the occurrence of alternating functional bundle branch block cannot be accounted for solely by the degree of abbreviation of His-Purkinje system cycle length, but may be explained by a relative shortening of the next ipsilateral bundle branch cycle length in the bundle manifesting block.
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PMID:Effects of alternating cycle lengths on refractoriness of the His-Purkinje system. 674 7

Escape-capture bigeminy is a bigeminal rhythm in which each escape beat is followed by a captured beat. This dysrhythmia is very rare, because its manifestation requires the sinus interval to be longer than the escape interval. This is possible only with severe sinus nodal disease, where the intrinsic sinus rate is extremely low, or with a sinus rhythm associated with an accelerated junctional rhythm. The authors review the case of a 75-year-old man who presented with occasional dizziness and near-syncopal episodes. He was diagnosed with escape-capture bigeminy and subsequently underwent pacemaker placement.
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PMID:The great escape: junctional escape-capture bigeminy. 1708 32

A Holter recording obtained from a patient with atrial fibrillation showed ventricular extrasystoles often in bigeminal rhythm. Most extrasystoles were followed by a long return cycle, and only in a few instances the postextrasystolic interval was short. The latter phenomenon was interpreted as a manifestation of poor retrograde concealed penetration of the ventricular impulse into the atrioventricular (A-V) junction: accordingly, an ensuing relatively early fibrillation impulse reached the ventricular chamber, since it did not find the A-V node refractory. These events are similar to what happens in interpolated ventricular extrasystoles occurring during sinus rhythm, the absent or minimal concealed retrograde penetration of the ectopic impulse into the A-V node being necessary to permit anterograde conduction of the ensuing sinus impulse. Analysis of the recording also revealed that a very long (>2 second) interval between two consecutive narrow beats only occurred after an "interpolated" extrasystole. This was interpreted with the same mechanism underlying the "postponed compensatory pause" observed at times after interpolated ventricular extrasystoles during sinus rhythm: the minimal or nil penetration of the ventricular ectopic impulse into the A-V junction, followed by conduction of an ensuing early atrial impulse, "shifts to the right" the A-V nodal refractory period, preventing conduction of several further supraventricular impulses and generating a pause. Both interpolated ventricular extrasystoles and the phenomenon of "postponed compensatory pause" are, thus, conceivable during atrial fibrillation, although no definite demonstration is possible.
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PMID:Ventricular extrasystoles with interpolation or postponed compensatory pause during atrial fibrillation: fact or fiction? 2334 32

The electrocardiogram of a 72-year-old woman showed episodes of nonsustained narrow QRS complex tachycardia. Tracing analysis suggested that the arrhythmia was due to interpolated atrial extrasystoles occurring in bigeminal rhythm. Interpolation of atrial extrasystoles is a rare phenomenon. In this condition, a premature atrial beat is "sandwiched" between 2 normal sinus beats, and sinus PP interval containing the extrasystole is often longer than unaffected sinus cycles. Alternative mechanisms for the arrhythmia are discussed, such as: (1) sinus node reentry; (2) 1:2 response to atrial ectopy over the fast and the slow atrioventricular nodal pathways; and (3) couplets of atrial extrasystoles.
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PMID:An unusual narrow QRS complex tachycardia: what is the mechanism? 2503 60