Interstitial lung edema and bronchial hyperreactivity

More than half among cardiac patients with interstitial lung edema exhibit bronchial hyperresponsiveness to pharmacological stimuli (methacholine, histamine). On the contrary, bronchial hyperresponsiveness to ultrasound nebulized distilled water is particularly rare in these patients. Patients with mitral value disease and bronchial hyperresponsiveness show PEF oscillations larger than normals, but even smaller than asthmatics. Wheeze, higher coefficient of variation of PEF, lower baseline FEV1 have been shown to be significant associated with an increased probability of methacholine bronchial response in patients with mitral valve disease. Increased bronchial wall thickness, bronchial vein engorgement, vagal hyperactivity have been suggested to play a pathogenetic role in bronchial hyperreactivity of cardiac patients. Vagal hyperactivity received support by the reported fair bronchodilating effect of ipratropium bromide in patients with exacerbation of heart failure. Some patients, even complaining of cardiac asthma, do not have bronchial hyperreactivity. Some broncho-protective factors have been suggested to be produced in these patients. Atrial natriuretic peptide (ANP), which may reach high serum levels in patients with cardiac failure, may be such a factor, due to its relaxant effect on bronchial smooth muscle. A significant relationship between serum ANP and methacholine PD20FEV1 has been reported in patients with mitral stenosis. So, it is quite possible that ANP counteracts the increase in bronchial reactivity due to interstitial lung edema.