Tissue Oxygenation Measure Predicts PH Outcomes: Study
A lower PvO2 was associated with poor outcomes in PAH, CTEPH patients, regardless of vasodilator treatment
Mixed venous oxygen tension (PvO2) — a measure for tissue oxygenation — is a significant predictor of outcomes in pulmonary hypertension (PH), a study suggested.
Specifically, lower PvO2 was significantly associated with poor outcomes in people with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH), regardless of treatment with vasodilators.
PvO2 may be a therapeutic target in PH, but further investigation is needed, the researchers noted.
The study, “Mixed venous oxygen tension is a crucial prognostic factor in pulmonary hypertension: a retrospective cohort study,” was published in BMC Pulmonary Medicine.
PH is a progressive disease marked by abnormal changes in the small blood vessels that supply the lungs, increased resistance to blood flow, and elevated blood pressure.
The established prognostic (outcome) risk factors for PH include high right atrial blood pressure (the blood pressure in the upper-right chamber of the heart), an abnormal cardiac index — a measure of the volume of blood pumped by the heart — and reduced mixed venous oxygen saturation (SvO2), which indicates that the output of the heart is not high enough to meet the oxygen needs of tissues.
Like SvO2, mixed venous oxygen tension (PvO2) — the balance between oxygen consumption and oxygen delivery — is related to tissue oxygenation. But, unlike SvO2, PvO2 reflects actual tissue hypoxia, or a lack of oxygen.
However, the relevance of tissue hypoxia measured by PvO2 in people with PAH and CTEPH has not been reported. PAH is caused by a narrowing of the pulmonary arteries, while CTEPH is due to blood clots in the lungs.
This study, by researchers at Chiba University, Japan, looked into the association of PvO2 with long-term prognosis in PAH and CTEPH, and compared PvO2 to other prognostic factors.
The team examined the medical records of 138 patients with PAH, mostly women (81.9%) with a mean age of 50.2 years. Among them, 44.2% had heritable (HPAH) or idiopathic (IPAH) PAH. Those treated with therapies that dilate the blood vessels (vasodilators) were significantly older and had significantly lower oxygen pressure in arterial blood.
The study also included 268 CTEPH patients, primarily women (72.8%), with a mean age of 57.4 years. Some received vasodilators alone, while others underwent pulmonary endarterectomy (PEA) to relieve a pulmonary artery blockage, or balloon pulmonary angioplasty (BPA), to dilate pulmonary arteries. A third “supportive” group was treated solely with anticoagulants (blood thinners) and oxygen supplementation therapy.
Those in the PEA/BPA group were significantly younger and had a higher mean pulmonary artery pressure (mPAP) than those receiving vasodilators alone, and many had residual PH and were treated with vasodilators.
PAH patients with tissue hypoxia at diagnosis, defined as a PvO2 of less than 35 mmHg, had significantly poorer survival rates than those without tissue hypoxia, regardless of vasodilator treatment. Similar results were seen in both HPAH and IPAH.
In CTEPH patients who had undergone PEA or BPA, there was no difference in survival between those with and without tissue hypoxia. In contrast, survival was significantly poorer in vasodilator-treated and supportive group patients with hypoxia than in those without hypoxia.
Without tissue hypoxia at diagnosis, there was a significant difference in survival among the three groups, with poor prognosis in the supportive group, whereas there were no differences between the PEA/BPA and vasodilator-treated groups. In comparison, with hypoxia at diagnosis, survival was significantly different among the three groups, including PEA/BPA and medication groups.
Outcome analysis showed age, cardiac index, PvO2, and medication use were significant PAH prognostic factors. In particular, in the group treated with vasodilators, PvO2, cardiac index, and age were prognostic factors. In the untreated group, PvO2 was the only significant prognostic factor.
In all CTEPH patients, low PvO2 and PEA/BPA treatment were significant prognostic factors. In the PEA/BPA group, no significant prognostic factors other than age remained, whereas in the medication group, low PvO2 was the significant outcome indicator.
In the PAH group, PvO2 significantly correlated with the cardiac index and the alveolar-arterial oxygen gradient (A-aDO2) — the difference between the oxygen concentration in the arteries and the alveoli, the tiny air sacs in the lungs. Correlation analysis suggested that cardiac index was more influential on PvO2 than A-aDO2.
Likewise, PvO2 correlated with cardiac index and A-aDO2 in the CTEPH group, but in contrast, A-aDO2 was a more important determinant of PvO2 than the cardiac index.
Treatment significantly improved mean pulmonary artery pressure and pulmonary vascular resistance — or resistance to blood flow in the pulmonary arteries — in PAH patients and the CTEPH medication group. However, no improvements were observed in oxygenation measures, including PvO2. Similar trends were observed in IPAH and HPAH.
In the PEA/BPA group with CTEPH individuals, all blood-related and oxygenation parameters, including PvO2, were significantly improved with treatment.
“The present study revealed PvO2 as a crucial prognostic factor in PH,” the researchers concluded. “The prognostic impact of tissue hypoxia affects different aspects of PAH and CTEPH, reflecting their distinct [development].”
“Therefore, PvO2 can be considered a therapeutic target in patients with PH, warranting further investigation,” they said.