Role of aldosterone on lung structural remodelling and right ventricular function in congestive heart failure

Rats with moderate to large myocardial infarcts (MI) and CHF were studied. Two weeks after MI, spironolactone 100 mg/kg/day (n = 21) or no treatment (n = 24) were given for 3 weeks and compared to sham (n = 8).Infarct size was similar by ultrasound and pathologic measures in both MI groups.The MI-untreated group developed important lung remodelling with nearly doubling of dry lung weight (p < 0.01), reduced left ventricular (LV) fractional shortening (16 ± 2% vs. 53 ± 1%; mean ± SEM, p < 0.0001), pulmonary hypertension (RV systolic pressure: 40 ± 3 mmHg vs. 27 ± 1 mmHg, p < 0.01) and RV hypertrophy (RV/(LV + septum): 38 ± 3% vs. 24 ± 1%, p < 0.05). Spironolactone had no effect on these parameters and did not improve LV or RV performance (tricuspid annular plane systolic excursion and RV myocardial performance index) measured by echocardiography. CHF induced a restrictive respiratory syndrome with histological lung fibrosis: this was also unaffected by spironolactone. Finally, isolated lung MYFs did not proliferate after exposure to aldosterone.Aldosterone does not significantly contribute to pulmonary remodelling and RV dysfunction associated with CHF. Other mechanisms are responsible for the beneficial effects of spironolactone in CHF.Pulmonary hypertension (PH) is a frequent complication of congestive heart failure (CHF). Conversely, left heart disease represents the single most prevalent causative factor for PH. PH, especially when associated with right ventricular (RV) dysfunction, reduces exercise capacity and represents an important independent prognostic factor in CHF [1]. At the core of pulmonary adaptations to CHF lies pulmonary structural remodelling with abundant proliferation of alveolar wall myofibroblasts (MYFs) [2-5]. MYFs are star-shaped cells that have a physiological role in growth, development and repair of tissue, and express morphological characteristics of both fibroblasts and smooth muscle cells [3]. The proliferation of MYFs is also associate