PURPOSE: A variety of abnormalities in pulmonary function have been attributed to, or are believed to be, exacerbated by congestive heart failure. Separating out specific contributions from cardiac versus pulmonary disease is difficult. In order to investigate the impact of cardiac disease on pulmonary function, we performed spirometry on patients immediately before and after cardiac transplantation. PATIENTS AND METHODS: Seventeen patients (13 men, 4 women) with a mean age of 44 years (range: 20 to 62 years) were studied before and 15 +/- 10 (mean +/- SD) months after cardiac transplantation. Eleven patients had a significant smoking history. RESULTS: In comparing pre- and post-transplant spirometric results, forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) increased substantially after transplant (3.34 +/- 0.96 L versus 3.89 +/- 1.00 L, p = 0.0054, and 2.63 +/- 0.80 L versus 2.95 +/- 0.83 L, p = 0.042, respectively). FEV1/FVC was not significantly different between study states in the entire group (0.78 +/- 0.10 versus 0.76 +/- 0.10, p = NS), nor was it different in those patients with and without a smoking history (0.76 +/- 0.11 versus 0.72 +/- 0.10, p = NS, and 0.87 +/- 0.06 versus 0.84 +/- 0.02, p = NS, respectively). Furthermore, normal lung volumes were obtained after transplant in those patients without a smoking history in contrast to those with a smoking history. Finally, the increase in FVC after cardiac transplantation directly correlated with the decrease in cardiac volume with cardiac replacement (r = 0.83, p less than 0.0001). CONCLUSION: We conclude that in patients selected as cardiac transplant candidates (those without severe obstructive lung disease), restrictive but not obstructive pulmonary physiology can be attributed in part to congestive heart failure, and a major part of the reduction in lung volumes is secondary to the space occupied by a large heart. Other factors, such as accompanying pleural effusions and interstitial edema, likely contribute to the reduction in lung volumes. Abnormal pulmonary function secondary to chronic congestive heart failure in this selected population is completely reversible with normalization of cardiovascular physiology and anatomy.
PURPOSE: A variety of abnormalities in pulmonary function have been attributed to, or are believed to be, exacerbated by congestive heart failure. Separating out specific contributions from cardiac versus pulmonary disease is difficult. In order to investigate the impact of cardiac disease on pulmonary function, we performed spirometry on patients immediately before and after cardiac transplantation. PATIENTS AND METHODS: Seventeen patients (13 men, 4 women) with a mean age of 44 years (range: 20 to 62 years) were studied before and 15 +/- 10 (mean +/- SD) months after cardiac transplantation. Eleven patients had a significant smoking history. RESULTS: In comparing pre- and post-transplant spirometric results, forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) increased substantially after transplant (3.34 +/- 0.96 L versus 3.89 +/- 1.00 L, p = 0.0054, and 2.63 +/- 0.80 L versus 2.95 +/- 0.83 L, p = 0.042, respectively). FEV1/FVC was not significantly different between study states in the entire group (0.78 +/- 0.10 versus 0.76 +/- 0.10, p = NS), nor was it different in those patients with and without a smoking history (0.76 +/- 0.11 versus 0.72 +/- 0.10, p = NS, and 0.87 +/- 0.06 versus 0.84 +/- 0.02, p = NS, respectively). Furthermore, normal lung volumes were obtained after transplant in those patients without a smoking history in contrast to those with a smoking history. Finally, the increase in FVC after cardiac transplantation directly correlated with the decrease in cardiac volume with cardiac replacement (r = 0.83, p less than 0.0001). CONCLUSION: We conclude that in patients selected as cardiac transplant candidates (those without severe obstructive lung disease), restrictive but not obstructive pulmonary physiology can be attributed in part to congestive heart failure, and a major part of the reduction in lung volumes is secondary to the space occupied by a large heart. Other factors, such as accompanying pleural effusions and interstitial edema, likely contribute to the reduction in lung volumes. Abnormal pulmonary function secondary to chronic congestive heart failure in this selected population is completely reversible with normalization of cardiovascular physiology and anatomy.