Bronchial Hyperresponsiveness in Patients with Chronic Congestive Heart Failure
“O ronchial hyperresponsiveness to nonspecific stimuli is an almost universal finding in patients with bronchial asthma. On the other hand, paroxysmal dyspnea similar to an asthma attack frequently occurs in patients with congestive heart failure; however, no data are available in the literature on bronchial hyperresponsiveness in these patients. Therefore, to investigate the relationship between pulmonary congestion due to congestive heart failure and bronchial responsiveness, we measured bronchial responsiveness to acetylcholine in 51 patients with left heart disorders.
Materials and Methods
Subjects
Fifty-one patients (27 women and 24 men; age range, 37 to 77 years) participated in the study. We excluded atopic patients, current smokers, and patients whose FEV, was less than 70 percent of their FVC in order to exclude patients with chronic obstructive pulmonary disease or bronchial asthma. We could not detect other reasons for these patients to have reactive airways, eg, a history of exposure to toluene diisocyanates or sensitivity to sodium metabisulfite. All of the patients had been proven by several cardiologists to have left heart disorders (idiopathic cardiomyopathy, valvular disease, old myocardial infarction, or hypertensive heart disease). The onset of congestive heart failure was identified according to the New York Heart Associations criteria on the basis of the patients’ clinical symptoms, eg, dyspnea on effort, orthopnea, and paroxysmal nocturnal dyspnea; however, all of the patients did not have the symptoms of typical cardiac asthma attack. We divided the subjects into two groups on the basis of their history of congestive heart failure. Croup 1 included 18 patients without a history of congestive heart failure. In addition, we divided the patients with a history of congestive heart failure (group 2) into two subgroups on the basis of clinical symptoms at the time of study. Croup 2a consisted of 18 patients with clinical evidence of congestive heart failure in the past that had cleared by the time of study. Croup 2b consisted of 15 patients who had mild clinical symptoms of congestive heart failure at the time of study. None of the subjects had ever used B-adrenergic blockers, B-adrenergic agonists, methylxanthines, or corticosteroids; however, they were given either diuretics, calcium antagonists, or nitrates (or some combination). levitra plus
Bronchial Provocation Tests
The tests were performed while the patients symptoms were mild and stable. All medication was stopped at 9 pm on the previous day to allow a washout time of 18 hours before the measurement of bronchial responsiveness at 3:30 pm on the test day. Bronchial responsiveness was evaluated with acetylcholine. Acetylcholine chloride was dissolved in physiologic saline solution to make solutions of 0.08, 0.16, 0.31, 0.63, 1.25, 2.5, 5, 10, and 20 mg/ml Saline and acetylcholine solutions were inhaled from a nebulizer (DeVilbiss 646) operated by compressed air at 5 L/min. Saline solution was inhaled first for two minutes, and the FEV, was measured (Autospiror HI-498). Respiratory system impedance at 3 Hz was also measured (Nihon Kohden MZR-4000) at the same time. If the change in FEV, from the baseline after inhalation of saline solution was 10 percent or less, inhalation of acetylcholine was started. Acetylcholine solution was inhaled for two minutes under tidal breathing with a nose clip, and this was followed immediately by spirometry. Increasing concentrations were given until a fall of 20 percent or more in FEV, was noted. The PC20-FEV, was calculated and used as a parameter of bronchial responsiveness.
Cardiac Catheterization and Chest Roentgenograms
Catheterization of the left side of the heart was performed on 32 of the 51 subjects. Swan-Ganz catheterization was also performed on each of them. Six of the other 17 subjects received Swan-Ganz catheterization alone. The interval between the bronchial provocation test and cardiac catheterization was less than 30 days. The CO, mPAP, mPCWP, LVEF, and LVEDP were measured, and the CI was calculated as follows: CI = СО/body surface area. Within a week after the bronchial provocation test, all subjects underwent standard postero-anterior chest roentgenograms, and the CTRs of these roentgenograms were collected.
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Statistics
The variables of baseline pulmonary (unction tests and cardiac catheterization were analyzed using a one-way AN OVA and a modified Students f-test. Since in our protocol, values of PC20- FEV, of more than 20 mg/ml cannot be measured, they were combined and treated as a group. We compared PC20-FEV, between the groups by using their median value, and these were analyzed by a nonparametric procedure (Mann-Whitney U-test). Correlation coefficients between (PC20-FEV,) and each hemodynamic variable were calculated by using Spearman’s rank correlation coefficient. A p value of less that 0.05 was taken as significant.
