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J Thorac Cardiovasc Surg 2007;133:1581-1587
© 2007 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Beck and back: A paradigm change in coronary sinus interventions—pulsatile stretch on intact coronary venous endothelium

^a Department of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria
^d Department of Internal Medicine 2, Division of Cardiology, Medical University of Vienna, Vienna, Austria
^c Institute of Biomedical Research, Medical University of Vienna, Vienna, Austria
^e Core Unit for Medical Statistics and Informatics, Section of Clinical Biometrics, Medical University of Vienna, Vienna, Austria
^b TU BioMed, University of Technology, Vienna, Austria
^f Carinthia University of Applied Sciences, Medical Information Technology, Klagenfurt, Austria.

Received for publication July 22, 2006; revisions received November 20, 2006; accepted for publication December 28, 2006.

^_* Address for reprints: Werner Mohl, MD, PhD, Medical University of Vienna, Department of Cardiothoracic Surgery, Waehringer Guertel 18-20, 1090 Vienna, Austria. (Email: werner.mohl{at}meduniwien.ac.at).

Objectives: Strategies to recover myocardium in therapeutically unresponsive patients are again under scrutiny, including techniques developed in the pioneering days of cardiothoracic surgery such as retroperfusion via the coronary sinus—the Beck procedure. An underestimated aspect of retroperfusion is the formation of new vessels. This early observation of neoangiogenesis may be an important mechanism in observed benefits. We hypothesized that periodic pressure elevation in coronary veins induces an analogy to shear stress angiogenic pulses by activating venous endothelium. Pulsatile stretch on venous endothelium can be achieved easily by a pressure-controlled intermittent balloon blockade of the coronary sinus outflow.

Methods: Three hours of myocardial ischemia was induced in 12 pigs. Pressure-controlled intermittent coronary sinus occlusion was applied in 6 animals 15 minutes after occlusion of the left anterior descending coronary artery. Postmortem myocardial specimens were taken, and heme oxygenase-1, vascular endothelial growth factor gene expression, and hypoxia-induced factor activity were measured.

Results: As compared with controls, treated animals released an angiogenic pulse by a 4-fold increase of heme oxygenase-1 gene expression in the infarct area (P < .001), together with a 2.5-fold enhanced transcription of vascular endothelial growth factor in the infarct (P < .006), border (P < .002), and remote (P < .02) areas, whereas hypoxia-induced factor activity was similar in both groups. A significant correlation (P < .01) of the achieved coronary sinus pressure elevation and gene expression was found.

Conclusions: Mechanotransduction of pulsatile stretch on coronary venous endothelium by pressure-controlled intermittent coronary sinus occlusion induces heme oxygenase-1 and vascular endothelial growth factor gene expression, leaving the ischemic pathway of the hypoxia-induced factor activity unchanged. This cascade of molecular events closes the argument gap to historical reports of the Beck procedure on revascularization and myocardial salvage.