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Heart rate (HR) at rest is an important marker of prognosis in heart failure, but has not been addressed in pulmonary arterial hypertension (PAH). To determine the prognostic value of HR at rest in patients with PAH, we retrospectively analyzed 140 consecutive patients with idiopathic PAH. Electrocardiogram (ECG)-derived HR at rest was evaluated as a potential predictor of adverse prognosis (death or lung transplantation), in addition to World Health Organization functional class, 6-minute walk distance, and hemodynamics before and approximately 1 year and 2 years after initiation of PAH treatment. During follow-up, 49 patients (35%) died, and 5 patients (4%) underwent lung transplantation. Before treatment initiation and after 1 year and 2 years of treatment, respectively, a higher HR at rest was an independent predictor of adverse prognosis (hazard ratios per 10-beats/min increase 1.76, 95% confidence interval 1.42 to 2.18, 2.31, 95% confidence interval 1.58 to 3.38, 2.1, 95% confidence interval 1.39 to 3.19, respectively, p <0.001 for all). Change in HR between the first and last ECG also independently predicted prognosis (hazard ratio per 1-beat/min increase 1.03, 95% confidence interval 1.01 to 1.06). In conclusion, a higher HR at rest and an important increase in HR at rest during follow-up signify a considerable risk of death in patients with PAH. ECG-derived HR at rest is an important marker of prognosis and should be assessed before and at frequent intervals after initiation of treatment for PAH. [Copyright &y& Elsevier]

The article assesses whether the electrocardiogram (ECG) is useful for monitoring treatment response based on changes in pulmonary vascular resistance (PVR) in patients with pulmomary arterial hypertension (PAH). An ECG was recorded in 81 PAH patients at the time of diagnostic right heart catheterization and a year after treatment. Results conclude that routine ECG evaluation can be a vital contribution to assess the treatment response in PAH patients.

The study aim was to assess three-dimensional electrocardiogram (ECG) changes during development of pulmonary arterial hypertension (PAH). PAH was induced in male Wistar rats (n = 23) using monocrotaline (MCT; 40 mg/kg sc). Untreated healthy rats served as controls (n = 5). ECGs were recorded with an orthogonal three-lead system on days 0, 14, and 25 and analyzed with dedicated computer software. In addition, left ventricular (LV)-to-right ventricular (RV) fractional shortening ratio was determined using echocardiography. Invasively measured RV systolic pressure was 49 (SD 10) mmHg on day 14 and 64 (SD 10) mmHg on day 25 vs. 25 (SD 2) mmHg in controls (both P < 0.001). Baseline ECGs of controls and MCT rats were similar, and ECGs of controls did not change over time. In MCT rats, ECG changes were already present on day 14 but more explicit on day 25: increased RV electromotive forces decreased mean QRS-vector magnitude and changed QRS-axis orientation. Important changes in action potential duration distribution and repolarization sequence were reflected by a decreased spatial ventricular gradient magnitude and increased QRS-T spatial angle. On day 25, LV-to-RV fractional shortening ratio was increased, and RV hypertrophy was found, but not on day 14. In conclusion, developing PAH is characterized by early ECG changes preceding RV hypertrophy, whereas severe PAH is marked by profound ECG changes associated with anatomical and functional changes in the RV. Three-dimensional ECG analysis appears to be very sensitive to early changes in RV afterload. [ABSTRACT FROM AUTHOR]