Customize your JAMA Network experience by selecting one or more topics from the list below.
In Reply We appreciate the kind words by Mehmood and echo many of his concerns about how to integrate this knowledge into clinical practice. In our recent publication,1 we demonstrated that there was increased mortality risk with mild echocardiographic pulmonary hypertension (PH) and that these mild elevations in were associated with reduced right ventricular (RV) function and RV–pulmonary artery (PA) coupling. The US expert consensus recommends a threshold RV systolic pressure (RVSP) of 40 mm Hg for further investigation of pulmonary pressures, which our data suggest inadequately captures risk in a patient population being assessed for cardiopulmonary symptoms.2 This idea is further supported by recent reconsideration of the hemodynamic definition of PH at the sixth World Symposium on Pulmonary Hypertension. The diagnostic threshold for PH was lowered to a mean PA pressure of 20 mm Hg, which corresponds approximately to a systolic pressure of 33 mm Hg. We thought it was important to examine risk using echocardiographic data because most patients with PH, particularly with heart failure or chronic obstructive pulmonary disease, never undergo invasive hemodynamic assessment. Although our data derived from an electronic health record cohort, data from the Prospective Comparison of ARNI With ARB Global Outcomes in HF With Preserved Ejection Fraction (PARAGON-HF) randomized clinical trial,3 which were collected according to a standardized protocol and interpreted in a central core laboratory, also found an increased risk of clinical events beginning at an estimated RVSP of approximately 33 mm Hg.
Uniform measurement of RV function is important to perform in all patients undergoing echocardiography to adequately frame clinical interpretation of the RVSP. We also agree that reporting of quantitative measures of RV function should be standard in all patients undergoing echocardiography, as recommended by the American Society of Echocardiography.4
Although a large proportion of patients with mildly elevated pressure by echocardiography do not require invasive measurements, in many cases, such information should prompt further assessment of potential etiologies, such as sleep studies, pulmonary function testing, or exercise echocardiography. We recognize that clinical trials in this population will be challenging because of the lower event rates in comparison with patients with more advanced disease. We support careful application of Mehmood’s suggestions to address this challenge: use of echocardiography to monitor therapeutic response in select patients and use of RV-PA coupling as a surrogate end point. A mountain of epidemiologic evidence demonstrates risk among patients with mild PH. We now have to turn our attention to developing strategies for identifying effective interventions for the pulmonary vasculature and the RV in patients with evidence of mild PH.
Corresponding Author: Evan L. Brittain, MD, MSc, Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 1215 21st Ave S, Medical Center East, Ste 5027, Nashville, TN 37232-8802 (email@example.com).
Published Online: March 25, 2020. doi:10.1001/jamacardio.2020.0325
Conflict of Interest Disclosures: None reported.
Huston JH, Brittain EL. Echocardiographic Pulmonary Hypertension and Right Heart Function—The Big Picture—Reply. JAMA Cardiol. Published online March 25, 2020. doi:10.1001/jamacardio.2020.0325
Coronavirus Resource Center
Create a personal account or sign in to: