The effects of heatwaves and cold spells on patients admitted with acute ischemic stroke

This study aimed to explore the effects of heatwaves and cold spells on blood pressure, thrombus formation, and systemic inflammation at admission in patients with ischemic stroke.

Data of patients with ischemic stroke who were admitted to the Second Hospital of Tianjin Medical University between May 2014 and March 2019 were reviewed, along with meteorological data from the same time period. A total of 806 clinically confirmed patients with ischemic stroke (34-97 years old) were included in the final analysis. Heatwaves and cold spells were defined as ≥2 consecutive days with average temperature >95^th percentile (May-August) and <5^th percentile (November-March), respectively. Coagulation parameters, inflammation indices, blood pressure, and neurological impairment were evaluated within 24 hours of admission. General linear and logistic regression models were created to investigate the relationships of heatwaves and cold spells with the examination results of patients with ischemic stroke at admission.

After adjustment for potential environmental confounders, heatwaves were positively associated with high systolic blood pressure (SBP) (β=8.693, P=0.019), diastolic blood pressure (DBP) (β=3.665, P=0.040), reduced thrombin time (TT) (β=-0.642, P=0.027), and activated partial thromboplastin time (APTT) (β=-1.572, P=0.027) in ischemic stroke patients at admission. Cold spells were positively associated with high SBP (β=5.277, P=0.028), DBP (β=4.672, P=0.012), fibrinogen (β=0.315, P=0.011), globulin (β=1.523, P=0.011), and reduced TT (β=-0.784, P<0.001) and APTT (β=-1.062, P=0.024). Cold spells were also associated with a higher risk of respiratory infection [odds ratio (OR) =2.677, P=0.001].

Exposure to heatwaves or cold spells was associated with blood pressure and coagulation at admission in patients with ischemic stroke. Cold spells also resulted in higher levels of inflammation. These findings suggest that changes in coagulation, blood pressure, and inflammation may be the potential biological mechanisms underlying the cerebrovascular effects of exposure to extreme temperatures.