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Eur J Cardiothorac Surg 2009;35:229-234. doi:10.1016/j.ejcts.2008.09.010
Copyright © 2009, European Association for Cardio-thoracic Surgery. Published by Elsevier. All rights reserved.

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Hilmar Doerge
Marlon Coulibaly
Friedrich A. Schoendube
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Right arrow Cardiac - physiology

Progressive right ventricular failure is not explained by myocardial ischemia in a pig model of right ventricular pressure overload

Jan D. Schmittoa,*, Hilmar Doergea, Heiner Postb, Marlon Coulibalya, Christian Sellina, Aron F. Popova, Samuel Sossallaa, Friedrich A. Schoendubea

a Department of Thoracic-, Cardiac- and Vascular Surgery, Universitätsmedizin Goettingen, Georg-August-Universität Goettingen, Germany
b Department of Cardiology, University of Graz, Austria

Received 5 March 2008; received in revised form 1 September 2008; accepted 8 September 2008.

* Corresponding author. Address: Department of Thoracic-, Cardiac- and Vascular Surgery, University Hospital of Goettingen, Robert-Koch Straße 40, 37099 Goettingen, Germany. Tel.: +49 551 39 6001; fax: +49 551 39 6002. (Email: schmitto{at}med.uni-goettingen.de).

Background: Current concepts of acute pulmonary embolism suggest that right ventricular (RV) dilatation and failure are the consequence of pressure overload-induced RV hypoperfusion and ischemia. Methods: Sixteen human-sized hybrid pigs were instrumented for the measurement of RV and aortic pressure, aortic and right coronary artery blood flow (RCA BF), RV oxygen consumption (RV MVO2) and RV free wall segment length. The pulmonary artery was constricted (PAC) to increase RV peak pressure acutely 2.5-fold (from 27 ± 2 to 64 ± 3 mmHg, n = 9), and the constriction was maintained for 6 h. Results: At 10 min after PAC, a RV work index (RVWI, RV pressure-segment length loops) was increased 2.3-fold, indicating an initial RV adaptation to increased afterload. At 1 h, 3 h and 6 h after PAC, however, RVWI decreased progressively towards control levels, while RCA BF and RV MVO2 continued to increase. The arterial-coronary venous pH difference did not increase throughout the protocol. Arterial troponin T concentration increased from 0.08 ± 0.03 to 0.80 ± 0.20 ng/ml at 6 h after PAC. None of the parameters changed in control animals (n = 7). Conclusion: We conclude that in our model RV failure during PAC develops in spite of increased coronary blood flow and MVO2. Thus, mechanisms different from ischemia may contribute to progressive RV failure after pulmonary embolism.

Abbreviations: AOPmean = mean aortic pressure • BG = banding group • CG = control group • CVP = central venous pressure • HR = heart rate • LV = left ventricle • n.a. = not assessed • PAC = constricted pulmonary artery • pH art = arterial pH • pH ven = RV coronary venous pH • RCA BF = right coronary artery blood flow • RV = right ventricle • RV dP/dt max = maximum first derivative of RV pressure • RV dP/dt min = minimum first derivative of RV pressure • RV edP = end-diastolic RV pressure • RV MVO2 = right ventricular oxygen consumption • RV pP = RV peak pressure • RVWI = RV work index • SLed = end-diastolic RV segment length • SLes = end-systolic RV segment length • {Delta}SL = percent segment shortening • Trop T = serum troponin T concentration

Key Words: Right ventricular function • Pressure overload • Ischemia • Pulmonary embolism







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Copyright © 2009 European Association for Cardio-Thoracic Surgery. Published by Elsevier. All rights reserved.