Relationship between Pulmonary Artery Stiffness and Functional Capacity in Patients with Heart Failure with Reduced Ejection Fraction

• Published in: Korean circulation journal Vol. 47; no. 6; pp. 929 - 938
• Main Authors: Yildirim, Erkan, Celik, Murat, Yuksel, Uygar Cagdas, Gungor, Mutlu, Bugan, Baris, Dogan, Deniz, Gokoglan, Yalcin, Kabul, Hasan Kutsi, Gormel, Suat, Yasar, Salim, Koklu, Mustafa, Barcin, Cem
• Format: Journal Article
• Language: English
• Published: Korea (South) The Korean Society of Cardiology 01-11-2017; 대한심장학회
• Subjects: Original; 내과학; Heart failure; Pulmonary artery; Vascular stiffness; Ejection fraction; Stroke volume
• ISSN: 1738-5520; 1738-5555
• DOI: 10.4070/kcj.2017.0081

Functional capacity varies significantly among patients with heart failure with reduced ejection fraction (HFrEF), and it remains unclear why functional capacity is severely compromised in some patients with HFrEF while it is preserved in others. In this study, we aimed to evaluate the role of pulmonary artery stiffness (PAS) in the functional status of patients with HFrEF.
A total of 46 heart failure (HF) patients without overt pulmonary hypertension or right HF and 52 controls were enrolled in the study. PAS was assessed on parasternal short-axis view using pulsed-wave Doppler recording of pulmonary flow one centimeter distal to the pulmonic valve annulus at a speed of 100 mm/sec. PAS was calculated according to the following formula: the ratio of maximum flow velocity shift of pulmonary flow to pulmonary acceleration time.
PAS was significantly increased in the HFrEF group compared to the control group (10.53±2.40 vs. 7.41±1.32, p<0.001). In sub-group analysis of patients with HFrEF, PAS was significantly associated with the functional class of the patients. HFrEF patients with poor New York Heart Association (NYHA) functional capacity had higher PAS compared those with good functional capacity. In multivariate regression analysis, NYHA class was independently correlated with PAS.
PAS is associated with functional status and should be taken into consideration as an underlying pathophysiological mechanism of dyspnea in patients with HFrEF.