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abstracts & posters

Decreased microvascular perfusion is a physiological biomarker of vaso-occlusive crisis due to mental stress and pain anticipation in sickle cell disease

key information

source: American Society of Pediatric Hematology/Oncology

year: 2017

authors: Saranya Veluswamy, Payal Shah, Maha Khaleel, Wanwara Thuptimdang, John Sunwoo, Patjanaporn Chalacheva, Roberta Kato, Jon Detterich, John Wood, Jennie Tsao, Lonnie K. Zeltzer, Richard Sposto, Michael Khoo, Thomas D. Coates


Background: Sickle cell disease (SCD) is an inherited blood disorder characterized by vaso-occlusive crises (VOC). Abnormal hemoglobin-S polymerizes after releasing oxygen to tissue which leads to the formation of sickled red blood cells (RBC) that obstruct the blood flow in the capillary circuit. Any trigger that decreases microvascular perfusion can further promote vaso-occlusion with increased risk of VOC. We used a novel methodology to quantify the regional microvascular blood flow (MBF) as a physiological biomarker of neural response to thermal pain and showed that there was a greater change in MBF due to thermal pain in patients with SCD. Interestingly, we noticed that there was decrease in MBF when subjects were told they were about to experience pain, suggesting that neural induced vasoconstriction might be a physiologic link between common VOC triggers like stress and vaso-occlusion. Objectives: To determine if pain anticipation and mental stress causes decrease in MBF in SCD.

Results: When subjects were told that they were about to experience severe pain from heat applied to their arm in the pain anticipation task, there was a significant decrease in MBF compared to baseline(p<0.0001). However, there was no significant difference in MBF compared to baseline when heat pain was applied without verbal instructions. There was a significant decrease in MBF during N-back and Stroop compared to baseline(p<0.01).

Conclusion: There was a profound vasoconstriction response (VCR) to anxiety induced by pain anticipation and stress tasks which is congruent with clinical observations that social and mental stress can trigger VOC. Unlike our previous studies, the VCR response during thermal pain was not significant, in the absence of induced anxiety. This could explain objectively how stress may play a role in the initiation of VOC in SCD by enhancing neural mediated vasoconstriction and increasing the likelihood of vaso-occlusion. Importantly, the methodology presented here offers a way to quantify physiological response to mental stress.

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