Hyperdynamic circulation of arteriovenous fistula preconditions the heart and limits infarct size

Citation
Ma. Mahgoub et al., Hyperdynamic circulation of arteriovenous fistula preconditions the heart and limits infarct size, ANN THORAC, 68(1), 1999, pp. 22-28
Citations number
20
Categorie Soggetti
Cardiovascular & Respiratory Systems","Medical Research Diagnosis & Treatment
Journal title
ANNALS OF THORACIC SURGERY
ISSN journal
00034975 → ACNP
Volume
68
Issue
1
Year of publication
1999
Pages
22 - 28
Database
ISI
SICI code
0003-4975(199907)68:1<22:HCOAFP>2.0.ZU;2-A
Abstract
Background. Chronic arteriovenous fistulae (AVF) create sustained hyperdyna mic circulation. It is not known whether hyperdynamic circulation alters my ocardial sensitivity to ischemia and reperfusion injury. We tested the hypo thesis that AVF activate molecular responses that increase tolerance to inf arction in dogs. Methods. Twelve dogs were divided into two groups: 1) AVF group, where an A VF in the femoral region was done; and 2) sham-operated group teach n = 6). After 8 weeks, left ventricular performance was determined from stroke wor k/end-diastolic length relationship. Myocardial biopsy was obtained to dete rmine heat-shock protein 70 and adenosine triphosphate (ATP) pool. Left ant erior descending coronary artery was occluded for 90 minutes at 37 degrees C, followed by 4 hours of reperfusion. Coronary blood flow was determined u sing different colored microspheres. Results. The fistula group showed improvement of left ventricular performan ce (p = 0.03). The infarct size was significantly lower in the fistula grou p; it was 9.2 +/- 2.0% in the fistula group versus 28.4 +/- 5.2% in the sha m group (p < 0.05). ATP depletion during ischemia was less in the fistula g roup (p = 0.02). Regional myocardial blood now was significantly higher in the fistula group (p = 0.03). Conclusions. Peripheral AVF improve the left ventricular performance, and d ecrease infarct size and ATP depletion. This protective effect is caused by the development of collaterals in the coronary circulation without express ion of heat-shock protein 70. (C) 1999 by The Society of Thoracic Surgeons.