Structural remodelling of lungs in chronic heart failure.

In order to determine whether morphological changes could account for a previously reported reduction in pulmonary capillary ltration in heart failure, we studied pulmonary morphology in lungs from a guineapig chronic heart failure model. Heart failure was induced by banding the ascending aorta with sham operated animals serving as controls; all animals were studied at 158 ± 6 days post-operation. Following banding, a reduction in aortic ow, increased peripheral vascular resistance and raised left ventricular end diastolic, left atrial and right ventricular pressures together with increased right ventricle to body weight ratio (all p < 0.05) are indicative of established pulmonary hypertension and heart failure. This was associated with an increase in pulmonary septal volume fraction (38.1 ± 3.1% vs 24.6 ± 2.3 %, p < 0.01) and reticulin fibre density. There was also evidence of siderophage infiltration and examination of pulmonary ultra structure revealed a signicantly thicker alveolar-capillary barrier in heart failure (1278 ±76 vs 638 ± 32 nm, p < 0.001), thickening of both the alveolar (89%, p < 0.01) and capillary (69%, p < 0.05) basal laminae with pericyte and collagen inltration of the alveolar-capillary barrier. We hypothesise that these pulmonary adaptations provide protection from oedema formation, but whilst initially protective, are also likely to confer major long-term disadvantages in chronic heart failure