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MEDICINA DELLO SPORT
A Journal on Sports Medicine
Official Journal of the Italian Sports Medicine Federation
Indexed/Abstracted in: BIOSIS Previews, EMBASE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,163
Medicina dello Sport 1999 September;52(3):191-200
Electrophysiologic mechanisms and clinical significance of the supraventricular tachyarrhythmias in the normal heart
D'Este D., Bertaglia E., Zerbo F., Pascotto P.
Unità Operativa di Cardiologia, Ospedale Civile di Mirano (Venezia)
The authors describe the clinical significance and the electrophysiologic mechanism of supraventricular arrhythmias in normal subjects. Atrial ectopic tachycardia is caused nearly always by an abnormal impulse formation. Most of these arrhythmias are benign, but in the incessant form some subjects develop ventricular dysfunction (tachycardiomyopathy). In about 20% of cases these arrhythmias desappeare with age. Atrial flutter is due to a reentrant mechanism involving large areas of the right atrium in which, during the arrhythmia, the lateral wall is activated craneocaudally and the septum is activated caudocranially. Generally is a well tolerated, paroxysmal arrhythmia, even though in some cases it can induce a sudden increase of the heart rate with a significant reduction of cardiac output. Idiopatic (“lone”) atrial fibrillation is a paroxysmal arrhythmia probably caused by a random reentry of multiple wandering wavelets. Sometimes it is caused by ectopic beats originating from the pulmonary veins. The tolerability depends on the heart rate during the attacks. The thromboembolic risk is thought to be negligible. The underlying mechanism of atrioventricualr junctional reciprocating tachycardia is a reentry confined to the junctional area in which antegrade conduction of the impulse occurs over a slowly conducting pathway and the retrograde conduction occurs over a rapidly conducting pathway. It is a paroxysmal tachycardia generally well tolerated except for those subjects in whom the heart rate during tachycardia is extremely high or in those with neurally mediated syncope induced by tachycardia. Wolff-Parkinson-White syndrome is characterized by the presence of an atrioventricular anomalous pathway through which the impulse is conducted retrogradely to the atria causing a circus movement tachycardia. In some cases the tachycardia degenerate in an atrial fibrillation that can be conducted rapidly to the ventricles through the anomalous pathway causing a ventricular fibrillation. The subjects at risk to develop a lifethreathing arrhythmia can be identified only by an electrophysiologic study. In some cases the conduction over the anomalous pathway occurs retrogradely only (concealed anomalous pathway) causing a circus movement tachycardia identical to that described for the Wolff-Parkinson-White syndrome but without the risk of degeneration in ventricular fibrillation. The permanent junctional reciprocating tachycardia is a reentry tachycardia in which the antegrade limb of the reentry is the atrioventricular node and the retrograde limb is an anomalous pathway with decremental conducting properties. This arrhythmia is typically permanent, being induced by sinus rhythm. Some subject can develop a tachycardiomyopathy. The “nodoventricular” tachycardia is a reentry arrhythmia due to the presence of an anomalous pathway (Mahaim fiber) with atrioventricular node-like properties connecting the right atrium with the right bundle branch. In some cases this tachycardia, paroxysmal and generally well tolerated, is due to a fiber connecting the atrioventricular node and the right ventricular myocardium.