From the Division of Cardiology (Dr Arrigo) and Division of Pulmonology (Dr Huber), University Hospital Zurich.
Correspondence to: Mattia Arrigo, MD, Division of Cardiology, University Hospital Zurich, Raemistrasse 100, Switzerland; e-mail: email@example.com
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Pulmonary hypertension is increasingly recognized as an important clinical condition, and the review article by Hansdottir et al1 in CHEST (August 2013) on pulmonary hypertension caused by cardiac disease is very timely. We agree with the statement of the authors that pulmonary hypertension due to left-side heart disease is probably the most common cause for elevated pulmonary pressure; however, comparative epidemiologic studies between the different clinical groups are lacking, and we guess that the prevalence of pulmonary hypertension in group 3 (pulmonary hypertension due to lung diseases or hypoxic conditions) is commonly underestimated. In addition to the remarks of the authors, we would like to emphasize one point that is commonly encountered as a misconception: While up to two-thirds of patients with aortic stenosis show increased pulmonary pressures, the prevalence and severity of pulmonary hypertension due to aortic stenosis is unrelated to the severity of the valve disease as shown in an echocardiographic study in 388 patients by Faggiano and coworkers.2
Of note, this conclusion is also true for patients with systolic heart failure,3 in which the extent of reduced left ventricular ejection fraction is unrelated to the severity of pulmonary pressure and is also at least partially true for diastolic heart failure,4 where the postcapillary hypertension related to diastolic dysfunction is only one component of the global severity of pulmonary hypertension.
Passive backpressure in the pulmonary circulation was found to result in active vasoconstriction of the pulmonary arterioles to protect the low-pressure pulmonary vascular bed against the potentially damaging increase of the capillary pressure. This phenomenon is known as Kitaev reflex or Hermo-Weiler reflex (reviewed in Arrigo and Huber5). Whether individual differences in the activity of this reflex are responsible for the severity of pulmonary hypertension secondary, but unrelated, to severity of the heart disease is unknown but might provide a probable explanation.
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