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Sif Hansdottir, MD
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From the University of Iowa Carver College of Medicine.

Correspondence to: Sif Hansdottir, MD, University of Iowa Hospitals and Clinics, 200 Hawkins Dr, C33GH, Iowa City, IA 52242; e-mail: sif-hansdottir@uiowa.edu


Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

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Chest. 2014;145(2):413-414. doi:10.1378/chest.13-2157
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To the Editor:

I thank Drs Arrigo and Huber for their comments on our review in CHEST.1 As Drs Arrigo and Huber point out, comparative epidemiologic studies looking at the prevalence of different World Health Organization groups of pulmonary hypertension (PH) are not available. A community-based, retrospective echocardiographic study2 out of Australia found that the minimum “indicative” prevalence of all groups of PH was 326 in 100,000. In this study, 68% of patients had PH due to left-side heart disease (LHD), and 9% had PH due to respiratory disease or sleep-disordered breathing.2 Patients with PH due to LHD may have been overrepresented in this study, however, as they may be more likely than patients with lung disease to undergo echocardiography. Therefore, we agree with Drs Arrigo and Huber that the prevalence of PH in lung disease may be underestimated. It is also worth noting that many common heart and lung diseases have mutual risk factors, and it may not always be clear whether the cause of PH is one or the other or both.

We also agree with Drs Arrigo and Huber that the pathophysiology of PH due to LHD is much more complicated than simple hydrostatics. Indeed, there is not a linear relationship between the severity of LHD and the development and severity of PH. Similarly, it has been shown that the correlation between pulmonary arterial pressure and lung function is weak.3 Why some patients with heart and/or lung disease develop PH while others do not is still unknown. It is likely that there are genetic determinants of disease susceptibility that are yet to be elucidated. Whether these mechanisms involve vascular reflexes like the Hermo-Weiler reflex in patients with heart disease, hypoxic pulmonary vasoconstriction in patients with lung disease, or other diverse mechanisms involved in the pathogenesis of PH is unknown.

References

Hansdottir S, Groskreutz DJ, Gehlbach BK. WHO’s in second? A practical review of World Health Organization group 2 pulmonary hypertension. Chest. 2013;144(2):638-650. [CrossRef] [PubMed]
 
Strange G, Playford D, Stewart S, et al. Pulmonary hypertension: prevalence and mortality in the Armadale echocardiography cohort. Heart. 2012;98(24):1805-1811. [CrossRef] [PubMed]
 
Scharf SM, Iqbal M, Keller C, Criner G, Lee S, Fessler HE; National Emphysema Treatment Trial (NETT) Group. Hemodynamic characterization of patients with severe emphysema. Am J Respir Crit Care Med. 2002;166(3):314-322. [CrossRef] [PubMed]
 

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References

Hansdottir S, Groskreutz DJ, Gehlbach BK. WHO’s in second? A practical review of World Health Organization group 2 pulmonary hypertension. Chest. 2013;144(2):638-650. [CrossRef] [PubMed]
 
Strange G, Playford D, Stewart S, et al. Pulmonary hypertension: prevalence and mortality in the Armadale echocardiography cohort. Heart. 2012;98(24):1805-1811. [CrossRef] [PubMed]
 
Scharf SM, Iqbal M, Keller C, Criner G, Lee S, Fessler HE; National Emphysema Treatment Trial (NETT) Group. Hemodynamic characterization of patients with severe emphysema. Am J Respir Crit Care Med. 2002;166(3):314-322. [CrossRef] [PubMed]
 
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