To the Editor:
Dimopoulos et al1 likened the microcirculation of stable patients with pulmonary arterial hypertension (PAH) and congestive heart failure (CHF) and matched normal subjects. They found an effect on the microcirculation, measured by near-infrared spectroscopy with vascular occlusion test (NIRS-VOT), in patients with PAH and CHF and a deleterious action of hyperoxia (performed in the PAH group). Despite a very meticulous work and a conclusion that seems fair and pragmatic, their results should be interpreted carefully. I would like to raise several issues.
First, the authors did not comment on the role of hypoxemia in patients with PAH in their study. A partial means of moderating this would have been to assess the extraction of tissue oxygen (O2) as a surrogate of microcirculatory function.2 Elevation of the extraction before VOT would indicate microcirculatory dysfunction with decreased O2 supply to tissue in local demand-supply dependence. This value can be obtained noninvasively and calculated as follows: microvascular oxygen extraction rate (μOER) = (SpO2 − StO2)/0.5 × SpO2 (where StO2 is muscle tissue oxygenation). When fit for SpO2, μOER values were 33.6, 31, 28, and 20.3 for PAH in the basal state and hyperoxia, CHF, and normal subjects, respectively. A discussion of these results (yet more abnormally high values in PAH) and the role of chronic tissue hypoxia would have been interesting. Accordingly, a decrease in O2 consumption is seen in tissue with chronic hypoxia, termed conformance.3 Are we confronted with a paradoxical response to hypoxia (greed for O2, opposite what is expected with conformance) or microvascular dysfunction? Nevertheless, the paucity of data on cardiac output and the role of chronic hypoxia make this derived value questionable. One can also imagine a different behavior of cells in chronic hypoxia, further amending the dynamic curves (ie, O2 consumption rate, reactive hyperhemia time, and time interval) compared with the princeps work during sepsis.4
Accordingly, elevated venous pressure has been related to impaired microvascular tissue perfusion.5 Thus, a possible modification of post-capillary venous vessel capacitance would obscure NIRS-VOT-derived values. In PAH patients, the role of such a right-sided outflow obstruction has been overlooked in this study. Moreover, from several intrinsic technological limiting factors, NIRS-VOT explores a derivative of the values of tissue oxygenation and may be dependent on the diffusion of O2 in the context of hyperoxia.
I think that it may be reasonable to conclude that those patients with PAH likely had a microcirculatory dysfunction, potentially exacerbated by hyperoxia. However, a validation of NIRS-VOT to explore the microcirculation is required in this context of chronic hypoxemia and right-sided overpressure before more formal conclusions can be made. A joint (or with replacement of NIRS) assessment by sidestream dark field imaging would be interesting.
Footnotes
The author has disclosed no conflicts of interest.
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