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J Thorac Cardiovasc Surg 2004;128:793-794
© 2004 The American Association for Thoracic Surgery
Brief communication |
a Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University School of Medicine, Sendai, Japan
b Department of Intensive Care Medicine, Tohoku University School of Medicine, Sendai, Japan
c Department of Cardiovascular Medicine, Tohoku University School of Medicine, Sendai, Japan
Received for publication March 4, 2004; accepted for publication March 10, 2004.
* Address for reprints: Yoshinori Okada, MD, Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryomachi, Aoba-ku, Sendai 980-8575, Japan
yokada@idac.tohoku.ac.jp
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Pulmonary hypertension (PH) caused by transient left ventricular failure (LVF) is a known complication after double or bilateral lung transplantation (BLTX) for patients with end-stage PH.1,2 In these patients the right ventricle (RV) becomes large and hypertrophic because of increased pulmonary vascular resistance, whereas the left ventricle (LV) becomes small and slight because of chronic preload reduction.3 Normalization of pulmonary vascular resistance by means of BLTX suddenly increases left ventricular preload, which sometimes leads to a hemodynamic situation susceptible to LVF. Prevention and treatment for this complication primarily consist of inotropic support and vasodilator therapy to reduce left ventricular afterload.2 We present here a patient with primary PH who had repeated PH episodes after BLTX, for which preventative therapy composed of catecholamines and vasodilators was not effective. However, the episodes were paradoxically prevented with a ß-blocker, propranolol. The clinical course and a possible mechanism responsible for the effect of the ß-blocker are presented.
Clinical summary
A 39-year-old man complained of dyspnea on exertion in 1996,
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