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Cardiovascular Research 2003 58(3):621-631; doi:10.1016/S0008-6363(03)00290-6
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Lung structural remodeling and pulmonary hypertension after myocardial infarction: complete reversal with irbesartan

Jean-François Jasmin, Angelino Calderone, Tack-Ki Leung, Louis Villeneuve and Jocelyn Dupuis*

Research Center, Montreal Heart Institute and University of Montreal, Montreal, Quebec, Canada

dupuisj{at}icm.umontreal.ca

* Corresponding author. Research Center, Montreal Heart Institute, 5000 Belanger Street East, Montreal, Quebec, Canada, H1T 1C8. Tel./fax: +1-514-376-1355.

Objectives: The severity of pulmonary hypertension associated with heart failure carries a poor prognosis. The lungs are very sensitive to the constrictive and proliferative effects of angiotensin-II and could represent a preferential target for this peptide. Methods: Rats with large myocardial infarcts or sham surgery received the angiotensin-II receptor antagonist irbesartan (40 mg/kg/day) or vehicle for 2 or 8 weeks (n = 5 to 8 for each group). Hemodynamic and morphometric measurements were obtained followed by immunohistochemistry, immunofluorescence analysis and electron microscopic characterization of lung sections. Results: The infarct groups developed progressive pulmonary hypertension and right ventricular hypertrophy with elevated left ventricular filling pressures (all P<0.01). Despite similar infarct size, filling pressures were lower (P<0.01) while pulmonary hypertension and right ventricular hypertrophy were completely normalized by irbesartan. Isolated lungs pressure–flow relationships were identical at 2 weeks. At 8 weeks it was steepest and shifted upward in the infarct group (P<0.001), and completely normalized by irbesartan. Lung weight doubled after infarct with no evidence of pulmonary edema and was also normalized by irbesartan. Important lungs structural remodeling evidenced by collagen and reticulin deposition, thickening of the alveolar septa and proliferation of cells with ultrastructural characteristics of myofibroblasts (pericytes) were identified after infarct. Conclusions: After large myocardial infarct there is important pulmonary structural remodeling in which myofibroblasts (pericytes) proliferation may play an important role. This initially protective mechanism against high filling pressures could eventually contribute to the development of pulmonary hypertension and right ventricular hypertrophy. Future studies are needed to determine if angiotensin-II directly modulates pulmonary remodeling after myocardial infarct.

KEYWORDS Angiotensin; Heart failure; Pulmonary circulation; Hypertension; Remodeling


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