PubMed21 Apr 2026Circulation● 6/10i Nonoptimal Temperature and Cardiovascular Health: A Scientific Statement From the American Heart Association.
Hanneman K, Alahmad B, Ghosh A, Khatana SAM, Huang M et al.
Extreme heat and cold increase cardiovascular events including myocardial infarction, stroke, heart failure decompensation, arrhythmias, and sudden cardiac death through mechanisms including autonomic activation, endothelial dysfunction, and inflammation. American Heart Association scientific statement synthesizing current evidence on temperature-related cardiovascular risks. This establishes the scientific foundation linking climate change to cardiovascular disease burden, providing new rationale for prevention strategies and potentially expanding the addressable patient population for cardiometabolic therapies. Healthcare systems contribute significantly to greenhouse gas emissions, creating a paradox where cardiovascular treatments may worsen climate-driven health risks.
Strategic Signal
This AHA statement legitimizes climate-cardiovascular health as a clinical priority, potentially expanding addressable populations for preventive cardiometabolic therapies. Payers may begin incorporating climate vulnerability into risk stratification models, favoring therapies with proven cardiovascular protection like GLP-1s and SGLT2 inhibitors. The healthcare emissions paradox could accelerate adoption of lower-carbon treatment delivery models, including digital monitoring and oral formulations over injectables.
CardiovascularReal-world evidence
Original Abstract
Ambient temperature is a key environmental driver of cardiovascular health. With rising global temperatures and increasing frequency, intensity, and duration of extreme temperature events, understanding the cardiovascular impacts of nonoptimal temperature is more urgent than ever. Short-term exposures to both heat and cold increase the risk of cardiovascular events, including myocardial infarction, stroke, heart failure decompensation, arrhythmias, and sudden cardiac death. Climate, built environment, socioeconomic variables, physiological vulnerability, and systemic inequities exacerbate these risks. There is also a growing appreciation of the importance of contextual factors such as geographic location, housing, occupation, and individual-level exposure. A range of biological mechanisms, including autonomic and neurohormonal activation, endothelial dysfunction, inflammation, hemoconcentration, and impaired thermoregulation, mediate temperature-related cardiovascular risk. Nonoptimal temperatures affect not only the incidence of cardiovascular disease but also health care access and delivery. They can increase demand for emergency care, disrupt operations, and pose challenges to the resilience and sustainability of health systems. Meanwhile, cardiovascular care contributes significantly to health care-related greenhouse gas emissions, highlighting a paradox in which efforts to protect cardiovascular health can indirectly contribute to climate-driven risks. This scientific statement synthesizes current knowledge of the relationship between nonoptimal temperature and cardiovascular health, highlights inequalities in exposure and outcomes, and identifies actionable strategies at the individual, community, health system, and public policy levels. Last, this scientific statement outlines significant research gaps and future priorities, including the need for improved exposure assessment, better understanding and measurement of the impact of long-term exposures, interactions with medications and coexposures, and identification of risk modifiers. Coordinated action is needed in research, clinical practice, and policy to mitigate the rising risks of nonoptimal temperatures on cardiovascular health in a changing climate.