Abnormal Spirometry in Congenital Heart Disease: Where Do We Go From Here?
"But the gods, foreknowing that the palpitation of the heart in the expectation of danger and the swelling... of passion was caused by fire, formed... as a supporter to the heart the lung... as a soft spring, that, when passion was rife within, the heart, beating against a yielding body, might be cooled and suffer less, and might... join with passion in the service of reason." Timaeus, Plato1
The close relationship between the heart and lungs has been appreciated for over 2,000 years, though the functions of each organ and their connection were misunderstood. While Plato's assertion that the lungs' purpose is to support the heart may be considered an early case of cardiac chauvinism, his description of their close interaction aligns with our current understanding. Not only is efficient cardiopulmonary coupling critical to support tissue metabolic demands at rest and with effort, but cardiac and pulmonary development are also intertwined. Cardiac dysfunction produces readily appreciated and dynamic effects on measured pulmonary function; the converse is equally true. As the electrocardiogram is affected by pulmonary disease, spirometry provides a window on cardiac function. Hutchinson's description of spirometry and the divisions of thoracic volume in the mid-19th century had been applied to patients with heart disease by the early-20th century and it was quickly clear that heart disease was associated with abnormal vital capacity.2, 3, 4 These relationships have been explored extensively in acquired heart and lung disease, but investigation in congenital heart disease has generally been limited to small series. In this issue of Circulation Alonso-Gonzalez, Borgia and colleagues present data on spirometry from a large cohort of adults with congenital heart disease. 5 The authors report two major findings. First, there is a high prevalence of markedly abnormal forced vital capacity (FVC) in this population. Second, reduced FVC is associated with increased mortality.
- forced vital capacity
- adult congenital heart disease
- Received January 22, 2013.
- Accepted January 23, 2013.
- Copyright © 2013, Circulation