Background Residence at high altitudes (HAs) may increase cardiovascular risk due to hypobaric hypoxia, but its synergy with pulmonary hypertension cause is unclear. This study compared clinical profile and biventricular remodeling in patients with pulmonary hypertension at HA and low altitude, and explored associate risk factors. Methods A total of 137 patients with pulmonary hypertension who underwent cardiovascular magnetic resonance imaging were categorized into the HA (altitude ≥2500 m) and low altitude groups based on their zip code. Multiple linear regression was used to identify risk factors for ventricular remodeling. Results The HA group showed higher hemoglobin, liver enzyme, and γ‐glutamyl transpeptidase levels. Accordingly, the left ventricular ejection fraction in the HA group was reduced (50.91±10.13% versus 58.10±7.84%, P =0.001), whereas the left ventricular volume was enlarged (all P <0.05). The HA group exhibited a higher right ventricular remodeling index, lower right ventricular cardiac output (all P< 0.05), and reduced biventricular longitudinal peak strain (right ventricle: −11.48±4.25% versus −13.26±2.75%, P= 0.001; left ventricle: −11.24±3.65% versus −13.42±2.83%, P= 0.018). Multiple linear regression analyses revealed that the γ‐glutamyl transpeptidase level was associated with deteriorated biventricular function (left ventricular ejection fraction, B=−0.06; right ventricular ejection fraction, B=−0.110; all P< 0.05), whereas the hemoglobin level was associated with the left ventricular longitudinal peak strain (B=0.599; P< 0.05), particularly among HA residents. Conclusions HA residence was linked to more severe biventricular remodeling in patients with pulmonary hypertension, particularly in the left ventricle. Higher γ‐glutamyl transpeptidase levels were independently associated with biventricular remodeling parameters.
Wanlin et al. (Wed,) studied this question.