Effect of Heat Exposure on Inflammation and Platelet Activity in Adults with Heart Disease

INTRODUCTION: Extreme heat events are associated with a greater risk of cardiovascular mortality, especially in adults with pre-existing heart disease. The pathophysiological mechanisms mediating these relationships remain unknown. One proposed mechanism, supported by pre-clinical studies employing heat stroke models of severe body hyperthermia, is that heat exposure causes an inflammatory response leading to platelet activation and clot formation. It remains unknown if milder body hyperthermia, such as the one experienced during exposure to a hot environment, elicits an inflammatory response and/or increases platelet activity in adults living with heart disease.OBJECTIVES & HYPTOHESES: To assess whether exposure to a hot and humid environment (1) increases circulating concentrations of inflammatory cytokines and (2) induces platelet activation in adults with heart disease.METHODOLOGY: Adults living with coronary artery disease (67±8 years; 13M/2F) sat within a climate chamber maintained at 38°C and 50% humidity for 3h. Core (rectal) and skin temperatures were measured continuously. Blood samples were drawn before and 2.5h into heat exposure. The blood samples were analyzed for IL-6, IL-8, IL-18, TNFα and IL-1β (multiplexed bead-based immunoassay). Platelet aggregation was measured by impedance (Multiplate assay) induced with ADP (6.5 μM), TRAP (15 μM) and collagen (1.5 μg/ml). The total-thrombus analysis system (T-TAS, PL-CHIP) was used to measure thrombus onset time and total thrombogenicity.RESULTS: Core and skin temperatures increased by 0.35 ± 0.24°C and 4.85 ± 0.84°C, respectively (p<0.05). There were no changes (Δpost-pre) in IL-6 (0.31 ± 1.91 pg/ml, p=0.60), IL-18 (-10.29 ± 21.01 pg/ml, p=0.16), IL-8 (1.10 ± 2.39 pg/ml, p=0.18), TNFα (-1.12 ± 4.10 pg/ml, p =0.39), or IL-1β (0.53 ± 2.36 pg/ml, p=0.48) during heat exposure. Moreover, heat exposure did not increase platelet activation in response to ADP (-8.31 ± 33.70 U, p=0.34), TRAP (16.19 ± 36.54 U, p=0.10), or collagen (-9.19 ± 30.31 U, p=0.24). Lastly, there was no change in thrombus onset time (2.18 ± 37.31 s, p=0.850) or total thrombogenicity (2.8 ± 168.7 PL-AUC, p=0.90).CONCLUSION: These results suggest that inflammation predisposing to thrombus formation may not contribute to the greater cardiac risk associated with short-term exposure to humid heat. Canadian Institutes for Health Research. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.