Cerebral microvascular blood flow and CO 2 reactivity in pulmonary arterial hypertension

Treptow, Erika; Oliveira, Mayron F.; Soares, Aline Alves; Ramos, Roberta Pulcheri; Medina, Luiz Antonio Rodrigues; Lima, Rita C.; Alencar, Maria Clara; Ferreira, Eloara Vieira Machado; Ota-­Arakaki, Jaquelina Sonoe; Tufik, Sérgio; Nery, Luíz Eduardo; Bittencourt, Lia Rita Azeredo; Neder, J. Alberto

doi:10.1016/j.resp.2016.08.001

Cited by 16 publications

(9 citation statements)

References 40 publications

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“…Indeed, the low values for %TLC in the study patients were associated with an elevation in mean PtcCO 2 , which suggests relationships between impairment of pulmonary function due to the respiratory muscle dysfunction in IPAH patients and nocturnal hypercapnia. In addition to the impairment in pulmonary function, previous studies suggested that in PAH patients the cerebral microvascular blood flow response against PaCO 2 elevation is suppressed, thereby ameliorating the stimuli to breathe [30]. The integration of these factors may contribute to the high prevalence of nocturnal hypercapnia among IPAH patients.…”

Section: Plos Onementioning

confidence: 99%

Nocturnal hypercapnia with daytime normocapnia in patients with advanced pulmonary arterial hypertension awaiting lung transplantation

et al. 2020

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Background Pulmonary arterial hypertension (PAH) is frequently complicated by sleep disordered breathing (SDB), and previous studies have largely focused on hypoxemic SDB. Even though nocturnal hypercapnia was shown to exacerbate pulmonary hypertension, the clinical significance of nocturnal hypercapnia among PAH patients has been scarcely investigated. Method Seventeen patients with PAH were identified from 246 consecutive patients referred to Kyoto University Hospital for the evaluation of lung transplant registration from January 2010 to December 2017. Included in this study were 13 patients whose nocturnal transcutaneous carbon dioxide partial pressure (PtcCO 2) monitoring data were available. Nocturnal hypercapnia was diagnosed according to the guidelines of the American Academy of Sleep Medicine. Associations of nocturnal PtcCO 2 measurements with clinical features, the findings of right heart catheterization and pulmonary function parameters were evaluated. Results Nocturnal hypercapnia was diagnosed in six patients (46.2%), while no patient had daytime hypercapnia. Of note, nocturnal hypercapnia was found for 5 out of 6 patients with idiopathic PAH (83.3%). Mean nocturnal PtcCO 2 levels correlated negatively with the percentage of predicted total lung capacity (TLC), and positively with cardiac output and cardiac index.

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Section: Plos Onementioning

confidence: 99%

Nocturnal hypercapnia with daytime normocapnia in patients with advanced pulmonary arterial hypertension awaiting lung transplantation

et al. 2020

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“…In addition, impaired CBF regulatory mechanisms are impaired as well in HF and as a possible consequence, blood pressure modulations is buffered less efficiently and may fail to meet increased metabolic demands with exercise [102][103][104]. Recently, we [5] and others [105,106] demonstrated that patients with PAH also have lower CBF and impaired regulatory mechanisms, altering the buffering of blood pressure changes and potentially explaining why patients with PAH are more prone to syncope after Valsalva-induced decreases in blood pressure [107]. At exercise, cerebral oxygenation was also markedly impaired during incremental [5,106] and endurance exercise [108], tightly correlating with the exercise capacity of patients with PAH [5].…”

Section: Impaired Cerebrovascular Function and Oxygenationmentioning

confidence: 99%

Exercise intolerance in pulmonary arterial hypertension: insight into central and peripheral pathophysiological mechanisms

et al. 2021

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Exercise intolerance is a cardinal symptom of pulmonary arterial hypertension (PAH) and strongly impacts patients' quality of life (QoL). Although central cardiopulmonary impairments limit peak oxygen consumption (V′O2peak) in patients with PAH, several peripheral abnormalities have been described over the recent decade as key determinants in exercise intolerance, including impaired skeletal muscle (SKM) morphology, convective O2 transport, capillarity and metabolism indicating that peripheral abnormalities play a greater role in limiting exercise capacity than previously thought. More recently, cerebrovascular alterations potentially contributing to exercise intolerance in patients with PAH were also documented. Currently, only cardiopulmonary rehabilitation has been shown to efficiently improve the peripheral components of exercise intolerance in patients with PAH. However, more extensive studies are needed to identify targeted interventions that would ultimately improve patients' exercise tolerance and QoL. The present review offers a broad and comprehensive analysis of the present literature about the complex mechanisms and their interactions limiting exercise in patients and suggests several gaps in knowledge that need to be addressed in the future for a better understanding of exercise intolerance in patients with PAH.

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“…Hence, alterations in two key CBF regulation mechanisms in PAH, for example, an attenuated dynamic cerebral autoregulation and a lower cerebrovascular reactivity to CO 2 , might result in the inability of exercise‐induced hypocapnia to dampen changes in MCAv. As such, CBF becomes more reliant on MAP (Malenfant et al, 2017; Treptow et al, 2016), and may eventually lead to a progressive breakdown of the blood–brain barrier resulting in extravascular edema and cerebral vessel frailty (Ogoh & Ainslie, 2009). Whether these abnormal CBF regulation mechanisms contribute to a 1.5 times higher odds of developing a stroke for PAH patients remains to be addressed (Shah, Sutaria, & Vyas, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…However, we acknowledge limitations of this interpretation. First, the aforementioned studies were conducted only in healthy subjects and secondly, other factors might influence the MCA diameter in PAH patients such as a lower cerebrovascular reactivity to CO 2 (Malenfant et al, 2017; Treptow et al, 2016), attenuating the influence of hypocapnia on MCA diameter during exercise. Therefore, we recognize that care must be taken when interpreting the present data about MCAv as a surrogate of CBF in the present study.…”

Section: Discussionmentioning

confidence: 99%

Continuous reduction in cerebral oxygenation during endurance exercise in patients with pulmonary arterial hypertension

et al. 2020

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Background Patients with pulmonary arterial hypertension (PAH) have lower cerebral blood flow (CBF) and oxygenation compared to healthy sedentary subjects, the latter negatively correlating with exercise capacity during incremental cycling exercise. We hypothesized that patients would also exhibit altered CBF and oxygenation during endurance exercise, which would correlate with endurance time. Methods Resting and exercise cardiorespiratory parameters, blood velocity in the middle cerebral artery (MCAv; transcranial doppler) and cerebral oxygenation (relative changes in cerebral tissue oxygenation index (ΔcTOI) and cerebral deoxyhemoglobin (ΔcHHb); near‐infrared spectroscopy) were continuously monitored in nine PAH patients and 10 healthy‐matched controls throughout endurance exercise. Cardiac output (CO), systemic blood pressure (BP) and oxygen saturation (SpO2), ventilatory metrics and end‐tidal CO2 pressure (PETCO2) were also assessed noninvasively. Results Despite a lower workload and endurance oxygen consumption, similar CO and systemic BP, ΔcTOI was lower in PAH patients compared to controls (p < .01 for interaction). As expected during exercise, patients were characterized by an altered MCAv response to exercise, a lower PETCO2 and SpO2, as wells as a higher minute‐ventilation/CO2 production ratio (trueV˙normalE/V˙CO2 ratio). An uncoupling between changes in MCAv and PETCO2 during the cycling endurance exercise was also progressively apparent in PAH patients, but absent in healthy controls. Both cHHb and ΔcTOI correlated with trueV˙normalE/V˙CO2 ratio (r = 0.50 and r = −0.52; both p < .05 respectively), but not with endurance time. Conclusion PAH patients present an abnormal cerebrovascular profile during endurance exercise with a lower cerebral oxygenation that correlate with hyperventilation but not endurance exercise time. These findings complement the physiological characterization of the cerebral vascular responses to exercise in PAH patients.

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Cerebral microvascular blood flow and CO 2 reactivity in pulmonary arterial hypertension

Cited by 16 publications

References 40 publications

Nocturnal hypercapnia with daytime normocapnia in patients with advanced pulmonary arterial hypertension awaiting lung transplantation

Nocturnal hypercapnia with daytime normocapnia in patients with advanced pulmonary arterial hypertension awaiting lung transplantation

Exercise intolerance in pulmonary arterial hypertension: insight into central and peripheral pathophysiological mechanisms

Continuous reduction in cerebral oxygenation during endurance exercise in patients with pulmonary arterial hypertension

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