Bronchial Hyperresponsiveness in Patients with Chronic Congestive Heart Failure: DISCUSSION
In the present study, we measured bronchial responsiveness to acetylcholine in patients with left heart disorders and noticed that the median value for PC20-FEV1 in patients with a history of congestive heart failure was lower than that in patients without such history. Makino et al have reported with the same protocols as our bronchial provocation test that the PC20-FEV1 value of asthmatic subjects was lower than 1 mg/ml and that of normal control subjects was higher than 10 mg/ml. In our study, because all patients without a clinical history of congestive heart failure (group 1) have a PC20-FEV1 above 1 mg/ml, their bronchial responsiveness was considered to be within normal limits. In contrast, the PC20-FEV! in patients with a history of congestive heart failure (group 2) was lower than 1 mg/ml in 23 (70 percent) of 33. Their bronchial responsiveness seems to have increased considerably.
There have been many reports of pulmonary mechanical abnormalities in patients with congestive heart failure; ie, pulmonary congestion has produced both restrictive and obstructive changes, and rapid saline solution infusion into normal men has led to derangement of small airway function. Pathophysiological, decreased lung compliance due to increased lung water and blood volume may explain the restrictive changes in acute pulmonary congestion. Fibrosis and respiratory muscle fatigue may also contribute to later changes. Obstructive changes have been attributed to increased airway resistance due to airway edema resulting from the pulmonary edema. Since we excluded the patients whose FEV/FVC was less than 70 percent in the present study, all subjects were considered to have no obstructive change. In addition, because the mean values for FVC or FEVt in all groups were above 80 percent, the restrictive changes, if any, seem to be modest. Moreover, the AFEV, in group 2 was higher than that in group 1 (Table 1). Therefore, the increase in bronchial responsiveness that we observed could not be explained by narrowing of bronchial caliber alone. How a patients bronchial responsiveness was increased remains a matter of speculation, but neural reflex is a possibility to be taken into consideration. Kikuchi et al reported an increase of bronchial reponsiveness to histamine in dogs by inflating a balloon in the left atrium. These investigators concluded that pulmonary vascular congestion made the bronchial hyper- reaction through vagal reflexes by narrowing of peripheral airways.
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Jones et al and Chung et al also showed that pulmonary vascular congestion reduced small airway caliber by vagal reflexes. Rolla et al documented that rapid saline solution infusion produced an increase of bronchial responsiveness to methacholine in normal men. These investigators concluded that acute minimal interstitial pulmonary edema increased bronchial responsiveness. Other researchers have suggested that excess pericapillary interstitial fluid may increase airway tone by stimulating the type-J receptors and the lung irritant receptors reflex. Nevertheless, all of these studies were on acute pulmonary congestion. Therefore, the previously mentioned explanations could not be simply extrapolated into our chronic congestive cases. Our data show that the cardiac function and the grade of pulmonary congestion obtained by cardiac catheterization does not correlate with bronchial hyperresponsiveness. These results indicate that bronchial hyperresponsiveness is caused not only by reflex but also by some organic bronchial changes. Recently, airway edema has been considered to relate to bronchial hyperresponsiveness in bronchial asthma. Therefore, airway edema is the most reasonable cause of bronchial hyperresponsiveness in patients with congestive heart failure. The clinical implication of bronchial hyperresponsiveness in patients with congestive heart failure remains unclear. Generally, the cause of wheezing in congestive heart failure has been recognized as a narrowing of bronchial caliber due to bronchial wall edema; however, functional bronchoconstriction similar to bronchial asthma may also contribute to wheezing. In conclusion, our observation of the increase of bronchial hyperresponsiveness to acetylcholine in patients with congestive heart failure suggests that bronchial hyperresponsiveness may be the product of sustained airway edema accompanying long-term pulmonary congestion. Whether or not this bronchial hyperresponsiveness is reversible by reducing pulmonary congestion remains to be clarified.
