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Am J Physiol Heart Circ Physiol (August 8, 2002). doi:10.1152/ajpheart.00402.2002
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Articles in PresS, published online ahead of print August 8, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00402.2002
Submitted on May 17, 2002
Accepted on August 5, 2002

The Trauma Induced by Non-Traumatic Coronary Devices and its impact on vascular reactivity and morphology

Jorg M Strotmann1*, Johann Bauersachs1, Daniela Fraccarollo1, Michael Kirchengast2, Philipp A Schnabel3, Jaromir Sykora3, Georg Ertl1, and Wolfram Voelker1

1 Medical University Clinic, University of Wuerzburg, Wuerzburg, Germany
2 Institute of Pharmacology and Toxicology, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Mannheim, Germany
3 Institute of Pathology, University of Heidelberg, Heidelberg, Germany

* To whom correspondence should be addressed. E-mail: J.Strotmann{at}medizin.uni-wuerzburg.de.

Objective: This study evaluated the impact of low-pressure balloon devices on coronary morphology and function. Methods: An active coronary perfusion catheter (2.5 mm balloon diameter, inflation with 1 bar for 30 minutes) was placed in the left anterior descending coronary artery of 12 German landrace pigs under general anaesthesia. After three months coronary segments with balloon contact were compared with control segments taken from the right coronary artery regarding to histology, vascular reactivity and the expression of endothelial NO-synthase (eNOS). Results: 33 balloon treated segments were analyzed. Twenty of these segments (61%) showed neointima formation. In these segments endothelium-independent relaxation induced by sodium nitroprusside was preserved. However, endothelium-dependent bradykinin-induced relaxation was significantly attenuated compared with both, the control segments and the balloon-treated segments without neointima formation. Conclusion: In over 60% of the ballooned arterial segments low-pressure balloon devices induced neointima formation accompanied by reduced endothelium-dependent relaxation. Thus, interventions with so-called non-traumatic coronary devices can induce relevant vascular injury with potential adverse clinical consequences.




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