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Hackensack University Medical Center, Hackensack, NJ New Jersey Medical School, Newark, NJ
Correspondence to: Albert D. Carilli, MD, FCCP, 75 Summit Ave, Hackensack, NJ 07601; URM2{at}hotmail.com
To the Editor:
We read with great interest the article by Asad et al in CHEST (August 2003)1 on acute right atrial strain, and P-wave amplitude and axis in the treatment of obstructive airways disease in patients experiencing exacerbation. Their key message was the rapid reversal of characteristic ECG changes with treatment from the emergency department presentation to hospital ward admission. Similarly, in 1973, Carilli et al2 demonstrated in a retrospective study the predictive value of P-wave amplitude and axis in estimating the severity of nonasthmatic airway obstructive disease in the quiescent state. A good correlation of P-wave amplitude and axis with FEV1/FVC and residual volume/total lung capacity was seen, also demonstrating a continuum in regression equations. We agree with Yue et al,3 in their accompanying editorial, that the study was well-designed but lacking in clinical and functional data. Patients with clinical phenotypes of diffuse obstructive airways disease (ie, chronic bronchitis/bronchiolitis, emphysema and bronchial asthma) are a clinically and pathophysiologically heterogeneous population. These various phenotypes most often coexist, and the proportion of each is difficult to quantitate clinically by pulmonary function testing and chest-imaging techniques.
The variability of airways obstruction is a defining criteria for the asthmatic type. Although these data are lacking in the study by Asad et al, the point is well-made that P-wave changes reflect the natural history of pulmonary arterial hypertension (PAH) in patients with diffuse obstructive airways disease. Transient elevations in pulmonary artery pressures occur with slowly progressing chronic PAH resulting from alveolar hypoxia during exacerbations with vascular reactivity and remodeling of the pulmonary artery vasculature.4 Although the common denominator for diffuse obstructive airways disease is PAH, only 10 to 15% will have P pulmonale.2 With coexistent heart disease, the P-wave changes are obscured.23 Other factors, such as the type of inflammation or the predominance of a specific phenotype associated with parenchymal destructive changes and fibrosis, have a major role in morbidity and mortality. Asthmatic obstructive airways disease differs significantly in the type of airways inflammation and the response to therapy. It is believed that both types may coexist in an individual.5 We make a plea to define the term COPD with greater specificity on presentation or in clinical studies. Distinguishing phenotypes will result in optimizing the diagnosis and prognosis, and in targeted management choices.
References
University of Massachusetts Medical School, Worcester, MA
Correspondence to: David H. Spodick, MD, FCCP, Division of Cardiovascular Medicine, University Campus, 55 Lake Ave North, Worchester, MA 01655; e-mail: spodickd{at}ummhc.org
To the Editor:
Drs. Carilli and Seiden present work that amplifies our findings. The results were based on pulmonary considerations (eg, severity of nonasthmatic airway obstruction), whereas ours were from a cardiac perspective, that is, P waves under changing COPD severity respond dynamically, and the "P pulmonale" is the extreme of the response occurring, as is the case in their data in about 15% of cases. Hitherto (ie, since 1935), P pulmonale has been considered to be a dichotomous variable, whereas our results demonstrate that the P wave in such patients is a continuous variable. The further discussion by Carilli and Seiden is very much on point and contributes to our understanding.
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