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Titolo:
UNEQUAL ATRIAL STRETCH IN DOGS INCREASES DISPERSION OF REFRACTORINESSCONDUCIVE TO DEVELOPING ATRIAL-FIBRILLATION
Autore:
SATOH T; ZIPES DP;
Indirizzi:
INDIANA UNIV,SCH MED,KRANNERT INST CARDIOL,1111 W 10TH ST INDIANAPOLIS IN 46202 INDIANA UNIV,SCH MED,KRANNERT INST CARDIOL INDIANAPOLIS IN 46202 RICHARD L ROUDEBUSH VET AFFAIRS MED CTR INDIANAPOLIS IN 46202
Titolo Testata:
Journal of cardiovascular electrophysiology
fascicolo: 9, volume: 7, anno: 1996,
pagine: 833 - 842
SICI:
1045-3873(1996)7:9<833:UASIDI>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONTRACTION-EXCITATION FEEDBACK; MECHANOELECTRICAL FEEDBACK; DILATED CARDIOMYOPATHY; INDUCED ARRHYTHMIAS; CANINE HEARTS; VOLUME LOAD; REPOLARIZATION; ELECTROPHYSIOLOGY; ENLARGEMENT; POTENTIALS;
Keywords:
ATRIAL REFRACTORINESS; THICK REGION; THIN REGION; REGIONAL ATRIAL STRETCH; CONTRACTION-EXCITATION FEEDBACK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
T. Satoh e D.P. Zipes, "UNEQUAL ATRIAL STRETCH IN DOGS INCREASES DISPERSION OF REFRACTORINESSCONDUCIVE TO DEVELOPING ATRIAL-FIBRILLATION", Journal of cardiovascular electrophysiology, 7(9), 1996, pp. 833-842

Abstract

Introduction: We have shown previously that acute atrial dilation prolonged atrial refractoriness. We hypothesized that this increase in refractoriness might be heterogeneous and could create an electrophysiologic substrate leading to atrial fibrillation, The purpose of the present study was to test that hypothesis. Methods and Results: We studied23 anesthetized open chest dogs, Bipolar plunge electrodes were placed in the medial free wall of the right atrium (thin region) and in thelower crista terminalis of the right atrium (thick region), Two bipolar plunge electrodes were also placed in the left ventricular apex to stimulate and record, Atrial effective refractory period (ERP) was measured in a group of nine dogs using the atrial extrastimulus method (A1A2) in two ways: during atrial pacing (AP) and during simultaneous atrioventricular (AV) pacing that achieved an AV interval of 0 msec (AV = 0). One liter/hour of normal saline was infused intravenously to elevate right atrial pressure and produce right atrial stretch. Atrial ERPs were measured before and after the normal saline infusion, To compare the extent of atrial stretch produced by volume overload, two pairsof sonomicrometer transducers were implanted in the thick and thin regions in a separate group of six dogs. The area encompassed by sonomicrometers was measured before and after saline infusion. The inducibility of atrial fibrillation was compared before and after saline infusion using rapid AP in another group of five dogs. Atrial pressure duringsinus rhythm increased from 5.1 +/- 0.96 mmHg to 6.3 +/- 0.93 mmHg after normal saline infusion (P < 0.01), ERP increased ire the thin freewall from 151 +/- 14.3 to 172 +/- 14.7 msec (AV = 0), and from 149 +/- 12.0 to 170 +/- 14.3 msec (AP), ERP increased in the thick crista terminalis from 134 +/- 9.9 to 147 +/- 10.2 msec (AV = 0), and from 133 /- 7.9 to 146 +/- 9.8 msec (AP) (P < 0.01), The increase in ERP in the thin free wall exceeded that in the thick crista terminalis (P < 0.01), increasing the dispersion of atrial ERP, After 500-mL saline infusion for 30 minutes, the increase of area in the thin region was 12.8% /- 3.7%, and that in the thick was 3.5% +/- 3.2%, The increase of thearea in the thin region after 1000 mt for 1 hour was 18.8% +/- 6.2%, and that in the thick region was 6.3% +/- 5.1% (P < 0.01), Atrial fibrillation was not induced in any dog before saline infusion, but induced in all five dogs after saline infusion. Conclusions: Atrial ERP in the thin right atrial free wall exceeds the ERP of the thick crista terminalis, and an increase in atrial pressure produced by saline infusion exaggerates this difference by stretching thin segments of the atrial myocardium more than it stretches thick regions. Thus, atrial stretch, by increasing the dispersion of atrial ERP, may be conducive to thedevelopment of atrial fibrillation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 10:01:11