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Original Research: PULMONARY HYPERTENSION |

ECG Monitoring of Treatment Response in Pulmonary Arterial Hypertension Patients

Ivo R. Henkens, MD; C. Tji-Joong Gan, MSc; Serge A. van Wolferen, MD; Miki Hew, MSc; Anco Boonstra, MD, PhD; Jos W. R. Twisk, PhD; Otto Kamp, MD, PhD; Ernst E. van der Wall, MD, PhD; Martin J. Schalij, MD, PhD; Anton Vonk Noordegraaf, MD, PhD, FCCP; Hubert W. Vliegen, MD, PhD
Author and Funding Information

*From the Department of Cardiology (Drs. Henkens, van der Wall, Schalij, and Vliegen, and Ms. Hew), Leiden University Medical Center, Leiden, the Netherlands; and the Departments of Pulmonology (Mr. Gan and Drs. van Wolferen, Boonstra, and Vonk Noordegraaf), Clinical Epidemiology and Biostatistics (Dr. Twisk), and Cardiology (Dr. Kamp), VU University Medical Center, Amsterdam, the Netherlands.

Correspondence to: Anton Vonk Noordegraaf, MD, PhD, FCCP, Department of Pulmonology, VU University Medical Center, De Boelelaan 1117, PO Box 7057, 1007 MB Amsterdam, the Netherlands; e-mail: a.vonk@vumc.nl


This study was supported by an unrestricted research grant to the Leiden University Medical Center, Department of Cardiology, from Actelion Pharmaceuticals Nederland bv (Woerden, the Netherlands). Mr. Gan was financially supported by the Netherlands Organization for Scientific Research, “Mozaïek grant,” project No. 017.001.154.

The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(6):1250-1257. doi:10.1378/chest.08-0461
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Background:  The potential use of the ECG for monitoring treatment effects in patients with pulmonary arterial hypertension (PAH) has not been investigated. We evaluated whether the ECG is useful for monitoring treatment response based on changes in pulmonary vascular resistance (PVR).

Methods:  An ECG was recorded in 81 PAH patients at the time of diagnostic right heart catheterization and after 1 year of treatment. Patients were treated according to the guidelines. Patients were divided into two groups based on PVR (ie, < 500 or > 500 dyne · s · cm–5). A positive treatment response was defined as a > 25% decrease in PVR to an absolute PVR of < 500 dyne · s · cm–5.

Results:  At baseline, the 19 patients with a PVR of < 500 dyne · s · cm–5 had a significantly lower P amplitude in lead II, a less rightward oriented QRS axis, and a more rightward T axis than the 62 patients with a PVR of > 500 dyne · s · cm–5. Overall (n = 81), the mean (± SD) change in PVR was −143 ± 360 dyne · s · cm–5 after 1 year of treatment (p < 0.001). Twelve patients (19%) with a baseline PVR of > 500 dyne · s · cm–5 were classified as responders. Receiver operating characteristic analysis determined that the P amplitude in lead II (area under the curve [AUC], 0.80; 95% confidence interval [CI], 0.67 to 0.94; p < 0.01), QRS axis (AUC, 0.70; 95% CI, 0.52 to 0.89; p = 0.03), and T axis (AUC, 0.90; 95% CI, 0.82 to 0.97; p < 0.001) were important determinants of treatment response. The presence of a P amplitude in lead II of < 0.175 mV and a T axis of ≥ 25° combined had a positive and negative predictive value for treatment response of 0.81 (95% CI, 0.37 to 0.96) and 0.94 (95% CI, 0.86 to 0.99), respectively.

Conclusions:  Routine ECG evaluation can be an important contribution in the assessment of treatment response in PAH patients.

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