5. VASCULAR THERMOSTAT: THERMAL STRESS ON HEART AND BRAIN HEALTH

VASCULAR THERMOSTAT:
THERMAL STRESS ON HEART AND BRAIN HEALTH

A. Alymidin Kyzy, G.Ravi
Asian International University named after Satkynbai Tentishev
Department of Therapeutic and Specialized Disciplines

Abstract
Background. Extreme environmental temperatures, encompassing both heat and cold
waves, are increasingly recognized as primary triggers for acute cardiovascular and
cerebrovascular events. According to the World Health Organization, approximately 37% of
heat-related deaths are attributable to human-induced climate change.
Objective. To explore the divergent physiological pathways through which thermal stress
precipitates life-threatening conditions such as myocardial infarction, heart failure, and stroke.
Methods. This review conducted a comprehensive search of peer-reviewed literature
indexed in PubMed, Google Scholar, and Nature Portfolio for studies published between
January 2015 and March 2026. Physiological reports detailing autonomic responses
(vasodilation vs. vasoconstriction) to thermal triggers, as well as research assessing the impact
of rapid temperature fluctuations on vascular stability, were included in the analysis.
Results. The analysis revealed two distinct pathological pathways. Heat-related stress
triggers systemic vasodilation, requiring a 50–70% increase in cardiac output. Profuse
sweating leads to fluid loss and hemoconcentration, promoting the release of inflammatory
factors, atherosclerotic plaque instability, and ischemic stroke. Additionally, heat stress
reduces cognitive processing speed by 10–15%. Cold-related stress activates the sympathetic
nervous system, causing peripheral vasoconstriction and acute hypertension: systolic blood
pressure rises by 10–20 mmHg upon sudden cold exposure. Elevated fibrinogen levels,
combined with hypertension, significantly increase the risk of hemorrhagic stroke and
myocardial infarction. Sudden daily temperature fluctuations exceeding 5–6°C more than
double the risk of ischemic stroke. Cold-related mortality contributes more to global
cardiovascular mortality than heat-related mortality.
Conclusion. Both heat and cold pose significant yet mechanistically distinct threats to heart
and brain health: heat causes rapid-onset ischemic events through fluid loss and inflammation,
while cold waves induce prolonged risk through sustained hypertensive pressure.
Understanding these mechanisms is essential for clinical preparedness and the development
of targeted public health interventions.
Keywords: cardiovascular disease, heat stress, cold-stress hypertension, climate medicine,
thermoregulation.