Climate change is not only transforming natural ecosystems and accelerating biodiversity loss, it is increasingly threatening human health. Among its most direct and deadly manifestations are extreme temperatures. Heatwaves have grown markedly in frequency, intensity, and duration since the 1950s, a trend strongly driven by anthropogenic climate change and projected to accelerate throughout the 21st century. Global assessments underscore the magnitude of this threat: the Global Burden of Disease 2023 study estimated 17.5 million healthy life-years lost worldwide as a consequence of high temperatures.1 Nowhere is this problem more acute than in Europe, the world’s fastest-warming continent, where more than 60 000 heat-related deaths occurred in the summer of 2022,2 despite nearly two decades of heat-health action plans implemented after the catastrophic 2003 events. A substantial share of this heat-related burden is cardiovascular in nature. While respiratory mortality often dominates the early peak of extreme heat events, cardiovascular disease (CVD) contributes heavily to both mortality and morbidity across all world regions. A comprehensive meta-analysis of 266 studies3 showed that each 1°C increase above local heat thresholds raised all-cause cardiovascular mortality by 2.1%, with extreme increases for stroke (3.8%) and acute coronary syndrome (3.5%). Heat exposure also elevates the risk of arrhythmias, out-of-hospital cardiac arrest, and non-fatal ACS, underscoring that the cardiovascular system is among the organ systems most sensitive to thermal stress. Yet the distribution of this burden is far from equal. Extreme heat does not strike populations uniformly; instead, it interacts with pre-existing social vulnerabilities. Disadvantaged groups, those with lower socioeconomic status, limited healthcare access, racial or ethnic marginalization, or poor housing conditions, are both more exposed and less able to adapt. Their neighbourhoods often have fewer green spaces, higher traffic volumes, more air pollution, and more intense urban heat islands. These overlapping exposures illustrate that climate change rarely acts alone: it amplifies other environmental risks such as air pollution, noise, and poor housing quality, creating cumulative stressors that increase cardiovascular susceptibility. The interplay between air temperature and air pollution has emerged as a focal point in recent epidemiology. An analysis of 482 cities across 24 countries4 demonstrated that heat-related cardiovascular and respiratory mortality is strongly modified by concentrations of fine particulate matter (PM2.5), nitrogen dioxide, and ozone. Physiologically, this is unsurprising: both heat and air pollution disrupt vascular regulation, induce oxidative stress, and activate systemic inflammation. Heat can enhance pollutant toxicity, for example, by increasing ozone formation, and pollutants can impair thermoregulation, creating a dangerous feedback loop for cardiovascular stability. European country-level studies further confirm the cardiovascular relevance of heat. Night-time temperatures, in particular, have gained attention: insufficient cooling during the night places sustained cardiovascular stress on vulnerable individuals (Figure 1).5 Beyond extreme heat, temperature variability—rapid increases or drops—also carries risk. One recent analysis found that sudden upward temperature shifts were linked to same-day increases in myocardial infarction admissions, while sudden downward shifts increased risk 2–3 days later.6 That heat-related increases in mortality often exceed increases in hospital admissions suggests that many cardiovascular events occur out of hospital, fatal before medical care can be provided. Conceptual illustration highlighting how extreme heat interacts with multiple cardiovascular risk factors. The graphic depicts pollution, vascular and cardiac vulnerability, medication use, and urban heat exposure surrounding a central thermometer—emphasizing that rising temperatures amplify cardiovascular stress, worsen underlying disease, and increase the risk of acute events The physiological mechanisms underlying these risks are well understood and centred around the body’s two major pathways of heat adaptation.7 Peripheral vasodilation: Heat exposure causes blood vessels in the skin to dilate, diverting circulation towards the periphery to facilitate heat loss. This reduces cardiac preload and lowers stroke volume. The heart compensates by increasing both heart rate and contractility, raising myocardial oxygen demand. In individuals with underlying CVD, this mismatch between oxygen supply and demand can precipitate myocardial ischaemia, type 2 myocardial infarction, or even cardiogenic shock. Sweating and dehydration: Sweating is essential for thermoregulation, but without adequate fluid replacement, intravascular volume decreases. This further reduces stroke volume and triggers additional compensatory tachycardia. Severe dehydration may lead to acute kidney injury due to renal hypoperfusion, splanchnic hypoperfusion with endotoxemia, and increased risk of multi-organ failure. Additional mechanisms include heat-induced systemic inflammation, increased blood viscosity, and a prothrombotic state. Thermal stress can also alter drug pharmacodynamics. A recent study found significantly higher risks of non-fatal myocardial infarction on hot days among users of antiplatelet agents or beta-blockers, with combined use associated with a 75% higher risk.8 Strikingly, the effect was more pronounced in younger individuals (25–59 years), underscoring that thermal vulnerability extends beyond the elderly. Looking ahead, projections for Europe are deeply concerning. Modelling studies integrating age-specific exposure–response relationships predict 700 000 to 2 million climate-related deaths this century under different climate and population scenarios.9 Crucially, increases in heat-related mortality consistently outweigh decreases in cold-related mortality across all models. These findings reinforce a clear message: Europe’s future cardiovascular burden will be increasingly shaped by heat unless aggressive mitigation and adaptation measures are undertaken. Fortunately, effective strategies exist. Urban planning interventions, such as expanding green and blue spaces, redesigning cities with reflective materials, and reducing urban heat islands, can substantially decrease temperatures and protect vulnerable communities. Comprehensive heat-health action plans, when implemented according to WHO core components, have demonstrably reduced heat-related deaths. Their success depends on strong governance, early-warning systems, communication strategies, targeted protection for vulnerable groups, and resilient health and social care systems. Crucially, cardiologists have a central role to play. Climate change must become part of routine clinical conversations, particularly with patients at elevated cardiovascular risk. Counselling on hydration, medication management during heatwaves, avoidance of peak heat exposure, and recognition of early symptoms can save lives. Beyond clinical practice, cardiologists carry significant societal influence. Nurses and physicians consistently rank among the most trusted professions in Europe. Their voices in public discourse, calling for climate action, resilient healthcare systems, and environmental protection, can accelerate policy change. This is especially necessary because environmental determinants of CVD remain profoundly underrepresented in professional discourse. Although 18% of the EU’s CVD burden is attributable to environmental factors,10 the ESC Congress 2025 devoted only 0.2% of its sessions to environmental risks. Closing this gap will require leadership from cardiovascular professionals who recognize climate change not as an abstract global issue but as an immediate, modifiable driver of cardiovascular morbidity and mortality. Climate change is already reshaping the epidemiology of CVD. The scientific evidence is unequivocal. The tools for prevention and adaptation are available. What remains is the commitment, clinical, societal, and political, to act decisively. Nothing to declare.
Schneider et al. (Mon,) studied this question.