Key result
Pulmonary hypertension is linked to ~54% lower endothelium-dependent vasodilatation compared to healthy controls.
Why the study?
The authors sought to assess endothelium-dependent and endothelium-independent flow-mediated vasodilatation across different pulmonary hypertension groups and determine their relationship with disease severity and targeted treatment status.
Is systemic arterial vasodilatory reserve impaired in patients with pulmonary hypertension compared to healthy controls?
Case-Control (n=58)
Is systemic arterial vasodilatory reserve impaired in patients with pulmonary hypertension compared to healthy controls?
Patients with pulmonary hypertension have impaired systemic vasodilatory reserve regardless of clinical subgroup, suggesting generalized vascular dysfunction beyond the pulmonary arteries.
Impaired vasodilatation signals endothelial dysfunction in pulmonary hypertension; leaves open its causal role and therapeutic targeting.
OBJECTIVE: Endothelium-dependent (ED) and endothelium-independent (EI) flow-mediated vasodilatation (FMD) have been used as measures of systemic arterial vasodilatory reserve. In this study, we aimed to assess both ED-FMD and EI-FMD in different groups with pulmonary hypertension (PH), and to investigate the relationship of these measures with clinical, echocardiographic, and invasive parameters of diseases severity and targeted treatment status. METHODS: Our study population comprised 41 patients with PH [28 (68.2%) women, age 46.3±19.6 years] including idiopathic pulmonary arterial hypertension, Eisenmenger syndrome, and chronic thromboembolic PH in whom diagnosis were confirmed in accordance with current guidelines and 17 age and sex-matched healthy controls. The brachial artery (BA) was used for assessment of FMD with Duplex ultrasound, and serial changes in diameter were recorded at baseline, 1, and 3 minutes after termination of 2-minute external occlusive compression for ED-FMD, and after sublingual intake of glycerol trinitrate for EI-FMD, respectively. RESULTS: Compared with controls, overall the PH group showed significantly lower ED-FMD (0.65±0.21 vs. 0.30±0.23 and 0.65±0.18 vs. 0.24±0.21) and EI-FMD (0.67±0.15 vs. 0.37±0.25 and 0.75±0.20 vs. 0.32±0.24) responses at 1st and 3rd min (p<0.001 for all). All these changes in the values of ED-FMD and EI-FMD were comparable among the PH subgroups. Neither ED-FMD nor EI-FMD were correlated with measures of PH severity and targeted therapy (TT) status (p>0.05). CONCLUSION: Our results suggest an impaired BA vasodilatory reserve in patients with PH regardless of the clinical subgroup. Although these findings seem to be consistent with systemic dysfunction, acute FMD may not reflect the severity of PH and cannot be used as a potential surrogate for outcome in this setting.
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Demirel et al. (2021) conducted a case-control in Pulmonary hypertension (n=58). Pulmonary hypertension vs. Healthy controls was evaluated on Endothelium-dependent (ED) and endothelium-independent (EI) flow-mediated vasodilatation (FMD) at 1 and 3 minutes (p=<0.001). Pulmonary hypertension was associated with significantly lower endothelium-dependent (0.30 vs 0.65) and endothelium-independent (0.37 vs 0.67) vasodilatation at 1 minute compared to controls (p<0.001).
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