Strong linear relationship between heart rate and mean pulmonary artery pressure in exercising patients with severe precapillary pulmonary hypertension

Author:

Chemla Denis1,Castelain Vincent2,Hoette Susana3,Creuzé Nicolas1,Provencher Steeve4,Zhu Kaixian1,Humbert Marc56,Herve Philippe67

Affiliation:

1. Physiology Department, Université Paris Sud-Faculté de Médecine-EA4533-APHP, Le Kremlin Bicêtre, France;

2. Hôpitaux Universitaires de Strasbourg, Service de Réanimation Médicale, Strasbourg, France;

3. Pulmonary Division, University of Sao Paulo, Sao Paulo, Brazil;

4. Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec, Université Laval, Québec City, Québec, Canada;

5. Service de Pneumologie-APHP, Hôpital Bicêtre, Le Kremlin Bicêtre, France;

6. Institut National de la Santé et de la Recherche Médicale UMR-S999, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France; and

7. Physiology Department, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France

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, r2 = 0.74) but not in CO. mPAP was linearly related to CO in 8 of 12 patients (median r2 = 0.83) and to HR in 12 of 12 patients (median r2 = 0.985). The parsimony principle favored the latter fit. PApp was linearly related to mPAP in 12 of 12 patients (median r2 = 0.985), HR in 10 of 12 patients (median r2 = 0.97), CO in 7 of 12 patients (median r2 = 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.

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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