title: Strong linear relationship between heart rate and mean pulmonary artery pressure in exercising patients with severe precapillary pulmonary hypertension.
abstract: The contribution of heart rate (HR) to pulmonary artery hemodynamics has been suggested in pulmonary hypertension (PH). Our high-fidelity pressure, retrospective study tested the hypothesis that HR explained the majority of mean pulmonary artery pressure (mPAP) and pulse pressure (PApp) variation in 12 severe precapillary PH patients who performed incremental-load cycling while in the supine position. Seven idiopathic pulmonary arterial hypertension patients and five chronic thromboembolic PH patients were studied. Four to five PAP-thermodilution cardiac output (CO) points (mean: 4.4) were obtained. At rest, mPAP was 57 ± 9 mmHg, PApp was 51 ± 11 mmHg, HR was 90 ± 12 beats/min, and stroke volume (SV) was 50 ± 22 ml. At peak exercise, mPAP was 76 ± 10 mmHg, PApp was 67 ± 11 mmHg, and HR was 123 ± 18 beats/min (i.e., 71 ± 10% of maximum HR, each P < 0.05), whereas SV was 51 ± 20 ml (P = not significant). The input resistance did not change (mPAP/CO = 14.1 ± 4.1 vs. 13.5 ± 4.4 mmHg·min·l(-1)). The relative increase in mPAP was related to the relative increase in HR (n = 12, r(2) = 0.74) but not in CO. mPAP was linearly related to CO in 8 of 12 patients (median r(2) = 0.83) and to HR in 12 of 12 patients (median r(2) = 0.985). The parsimony principle favored the latter fit. PApp was linearly related to mPAP in 12 of 12 patients (median r(2) = 0.985), HR in 10 of 12 patients (median r(2) = 0.97), CO in 7 of 12 patients (median r(2) = 0.87), and SV in 1 of 12 patients. A strong linear relationship between HR and mPAP was consistently documented in severe precapillary PH patients who performed supine exercise. The limited value of thermodilution CO to predict mPAP could be explained by unavoidable precision errors in CO measurements, unchanged/decreased SV on exercise, curvilinearity of the mPAP-CO relationship at high flow, or flow-independent additional mechanisms increasing mPAP on exercise.
authors.affiliation: Physiology Department, Université Paris Sud-Faculté de Médecine-EA4533-APHP, Le Kremlin Bicêtre, France;
authors.forename: Denis
authors.initials: D
authors.lastname: Chemla
authors.forename: Vincent
authors.initials: V
authors.lastname: Castelain
authors.forename: Susana
authors.initials: S
authors.lastname: Hoette
authors.forename: Nicolas
authors.initials: N
authors.lastname: Creuzé
authors.forename: Steeve
authors.initials: S
authors.lastname: Provencher
authors.forename: Kaixian
authors.initials: K
authors.lastname: Zhu
authors.forename: Marc
authors.initials: M
authors.lastname: Humbert
authors.forename: Philippe
authors.initials: P
authors.lastname: Herve
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery / Q000502:physiology*; D012146:Rest / Q000502:physiology; D012189:Retrospective Studies; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology; D016683:Supine Position / Q000502:physiology
keywords: cardiac output; exercise; heart rate; pulmonary artery pressure; pulmonary hypertension; pulse pressure; right ventricle