Pulmonary vascular remodelling in athletes: an anti-concept to be proved

Abstract

Studies of highly trained athletes using ultrasound and gold standard right heart catheter techniques have consistently demonstrated at rest and during exercise that pulmonary vascular resistances (PVRs) are similar (or slightly lower) in athletes and non-athlete healthy subjects (Table 1), and are markedly different to patients with pulmonary hypertension (PH). 1,2 Although right heart catheterisation is required to establish the diagnosis and select appropriate treatment strategies in PH, cardiopulmonary and echo Doppler exercise testing along with strain imaging analysis may detect early signs of right heart pulmonary circulation unit dysfunction and provide additional prognostic information. [1][2][3][4] In this edition of the European Journal of Preventive Cardiology, Domenech-Ximenos et al. compared 93 highly trained endurance athletes (53% men) with 72 healthy controls (58% men), who were younger and performed less than 3 hours moderate exercise per week. They underwent resting cardiovascular magnetic resonance (CMR) imaging to assess cardiac dimensions and function, as well as pulmonary artery dimensions and flow. 5 As would be expected based on current understanding of athletic cardiac remodelling, cardiac chamber volumes, left ventricular (LV) mass and stroke volume (SV) were significantly greater in the athletes while both LV and right ventricular (RV) ejection fractions were slightly lower. 6,7 A novel finding in this study was that the indexed pulmonary artery area was significantly greater in the athletes. It is perhaps not surprising that the pulmonary arteries were slightly larger in athletes. In fact, the cardiovascular adaptations to greater exercise flows would incorporate larger vascular conduits to reduce resistance to flow. Furthermore, they reported that seven of 93 (9.3%) asymptomatic endurance athletes had markedly elevated PVR suggestive of PH. Thus, they suggested that athletes have a 10,000-fold increase in the risk of PH as compared with the general population. They proposed that athletes can maintain superior exercise capacities despite grossly abnormal increases in PVR. The departure from normal physiology comes in the form of a formula in which an estimate of PVR was derived from CMR data of 100 PH patients. 8 PVR was found to be inversely related to pulmonary artery average velocity and RV ejection fraction. 8 A regression formula was derived from 80 PH patients and validated in the remaining 20 PH patients. Crucially, however, the formula has not been validated in healthy individuals nor in athletes.Can we extrapolate a formula derived from patients with PH for use in ostensibly healthy athletes? Extreme caution would seem warranted. In PH, the low mean pulmonary artery flow velocities reflect reduced RV SV and cardiac output. This is not true of the athletes in the study; RV SV was greater than in the non-athlete controls. The lower mean velocities need to be considered with the larger pulmonary arteries given that SV can be calculated as the product of time-integral of the velo...

Reply from the authors: Moving forward to identify those highly-trained athletes with potentially worse adaptation to intense exercise

“…Rodriguez-Palomares 2 and La Gerche et al. 3 have commented on our work, both in invited editorials. We appreciate their time and effort to carefully read and comment on our article and to raise a scientific discussion in this regard.…”

“…Thus, La Gerche et al. 3 are not being fully accurate when stating in their editorial the following: ‘they suggested that athletes have a 10,000-fold increase in the risk of pulmonary hypertension as compared to the general population’, since we never inferred an estimated risk, but only presented observational data in our specific population.…”