IPM Take
Cardiology has become extraordinarily precise about the risks inside the patient and comparatively imprecise about the risks outside the window.
Blood pressure can be measured to the millimetre. LDL cholesterol can guide treatment thresholds. Diabetes, kidney disease and smoking are embedded in prevention pathways. Yet the temperature outside, the air a patient breathes, whether they have air conditioning, whether they work outdoors and whether a heatwave disrupts access to medication rarely enter cardiovascular risk assessment with anything close to the same formality.
The evidence is making that separation increasingly difficult to defend.
Extreme heat and cold are associated with myocardial infarction, stroke, heart-failure decompensation, arrhythmias and sudden cardiac death. Air pollution interacts with vascular inflammation and thrombosis, while heat can amplify dehydration, haemoconcentration and cardiovascular workload. These exposures can occur simultaneously, and the same meteorological event can be manageable for one patient but dangerous for another depending on age, cardiovascular disease, kidney function, occupation, housing and access to cooling.
This does not mean clinicians should add a “climate score” to every cardiovascular risk calculator tomorrow. The evidence for short-term temperature-related cardiovascular events is considerably stronger than the evidence linking climate change directly to long-term obesity, insulin resistance or incident diabetes, and prospective evidence that climate-informed clinical interventions prevent cardiovascular events remains limited.
But waiting for a perfect risk algorithm would miss the policy point.
Climate is already altering the environment in which cardiovascular prevention operates. Health systems now need to decide whether environmental risk remains something public-health agencies monitor separately or becomes part of cardiovascular preparedness itself.
Executive Summary
A review published in EMJ Cardiology on 23 October 2026 argues that climate change should increasingly be viewed as a cardiometabolic risk multiplier because it modifies several exposures already linked to cardiovascular disease, including temperature, air pollution, wildfire smoke, physical-activity environments, food systems and disruption of healthcare delivery.
The strongest evidence concerns temperature.
A global analysis using mortality and temperature data from 32 countries estimated that approximately 1.8 million cardiovascular deaths per year between 2000 and 2019 were associated with non-optimal temperatures, equivalent to approximately 8.9% of cardiovascular mortality in the analysis. Cold accounted for the larger historical burden, although heat-related cardiovascular mortality increased over time.
A 2026 American Heart Association scientific statement concluded that short-term exposure to both heat and cold is associated with increased risk of myocardial infarction, stroke, heart-failure decompensation, arrhythmias and sudden cardiac death.
Climate-related cardiovascular risk is not limited to temperature. Heat interacts with ozone and particulate pollution, wildfire conditions can expand smoke exposure across large populations, and multiple environmental stressors may act together rather than independently.
One US study involving more than 270,000 adults aged 18 to 64 with acute myocardial infarction found that simultaneous exposure to high ozone and high temperature was associated with greater acute myocardial infarction risk than the low-exposure reference condition.
Evidence around metabolic disease requires greater caution. Heat, pollution, physical inactivity, food-system disruption, sleep disturbance and socioeconomic stress may contribute to metabolic vulnerability, but evidence that climate change itself directly causes obesity, insulin resistance or type 2 diabetes remains considerably less mature than evidence for acute cardiovascular effects.
The policy implications are therefore primarily about adaptation, exposure reduction and health-system resilience rather than creating a new climate-specific clinical diagnosis.
Why it matters
- HTA bodies: Environmental interventions rarely resemble conventional medical technologies, yet heat-warning systems, cooling interventions, air-filtration strategies, resilient healthcare infrastructure and exposure-monitoring tools may all affect cardiovascular outcomes. HTA frameworks may increasingly need methods for evaluating preventive interventions whose benefits emerge across populations and sectors rather than through a single drug or device.
- Payers: Climate-related cardiovascular events can increase emergency demand, destabilise chronic disease and interrupt access to medications and routine care. Payers may increasingly need to consider whether prevention programmes identify patients who are particularly vulnerable during heatwaves, poor-air-quality events and infrastructure disruption, especially among people with heart failure, kidney disease and diabetes.
- Industry / innovation partners: Environmental data could become a new layer in personalised cardiovascular care. Digital platforms combining weather, air quality, medication information and patient characteristics could potentially identify periods of elevated vulnerability, but the field needs prospective evidence showing that such alerts actually change behaviour and reduce events before environmental risk becomes another stream of data without demonstrated clinical value.
Modern cardiovascular prevention is built around the idea that risk lives largely within the individual. Clinicians measure cholesterol, blood pressure, glucose and kidney function, ask about smoking and family history, calculate risk and then try to change the biological trajectory before myocardial infarction, stroke or heart failure occurs.
That model has saved lives, but it rests on an increasingly incomplete assumption: that the environment in which those risk factors operate is relatively stable.
Climate change is challenging that assumption.
A review published in EMJ Cardiology connects the physics of a warming planet with the biology of cardiovascular disease, arguing that climate change is better understood as an exposure amplifier than as one isolated risk factor. Increasing greenhouse-gas concentrations alter the Earth’s energy balance, but the health consequences appear through much more immediate channels: extreme heat, altered air quality, wildfire smoke, flooding, disruption of food systems, reduced opportunities for safe physical activity and pressure on healthcare infrastructure.
None of those pathways requires a carbon dioxide molecule to interact directly with a coronary artery.
The chain is environmental.
A heatwave changes fluid balance, cardiovascular workload and the ability of patients with heart failure, coronary disease or kidney disease to maintain physiological stability. Wildfire conditions increase exposure to fine particulate pollution. High temperatures can increase ground-level ozone formation. Flooding or power failure can disrupt medication storage, dialysis, transport and access to care.
Cardiovascular risk therefore emerges from the interaction between a vulnerable patient and a changing environment.
Temperature offers the clearest example because the evidence is already substantial. Both high and low temperatures are associated with cardiovascular morbidity and mortality, with risk generally increasing as conditions move away from the locally optimal range.
A global study using daily mortality and temperature data from 32 countries estimated that around 1.8 million cardiovascular deaths each year between 2000 and 2019 were associated with non-optimal temperatures, representing approximately 8.9% of cardiovascular mortality in the analysis.
Most of that historical burden was associated with cold rather than heat, which is an important corrective to the tendency to treat climate-related cardiovascular disease as synonymous with heatwaves.
But the direction of change matters too.
Cold-related excess cardiovascular mortality declined over the study period, while the heat-related proportion increased. A warmer climate therefore does not simply replace cold deaths with heat deaths in a straightforward way, because adaptation, housing, geography, ageing and underlying population health all modify the relationship.
That complexity is reflected in the American Heart Association’s 2026 scientific statement on non-optimal temperature and cardiovascular health. The statement concludes that short-term heat and cold exposures are associated with myocardial infarction, stroke, heart-failure decompensation, arrhythmias and sudden cardiac death, while emphasising that vulnerability depends heavily on geography, housing, occupation, socioeconomic conditions and underlying disease.
The biological mechanisms are plausible and increasingly well characterised.
During extreme heat, the cardiovascular system must redirect blood toward the skin to dissipate heat while sweating reduces circulating fluid volume. Heart rate can rise, dehydration can increase blood viscosity and neurohormonal responses can place additional pressure on already vulnerable cardiovascular systems.
For a healthy person, those adjustments may remain manageable.
For someone with heart failure, coronary disease, kidney dysfunction or impaired thermoregulation, the margin for compensation can be far narrower.
That difference is why ambient temperature alone cannot define risk.
A 38°C day has a different clinical meaning for an older adult with heart failure living alone in poorly insulated housing than for a healthy younger adult with access to air conditioning. The hazard is environmental, but vulnerability is biological and social.
The same principle applies to air quality.
Fine particulate pollution can promote oxidative stress, endothelial dysfunction, inflammation, autonomic imbalance and thrombosis, intersecting directly with pathways already central to cardiovascular disease.
Climate change can modify those exposures through wildfire activity, drought, atmospheric chemistry and meteorological conditions affecting the formation and dispersion of pollutants.
More importantly, environmental stressors rarely arrive one at a time.
Heat can coincide with elevated ozone. Wildfire smoke can occur during extreme temperature events. A power outage can remove access to cooling at precisely the moment that the cardiovascular stress from heat is highest.
Research is beginning to examine those compound exposures rather than studying each hazard independently.
One US analysis followed more than 270,000 adults aged 18 to 64 who experienced an acute myocardial infarction and compared their temperature and ozone exposure on the day of the event with nearby control days. The combination of ozone at 60 parts per billion and temperature at the 95th percentile was associated with a 33% higher odds of acute myocardial infarction relative to the study’s low-exposure reference.
That estimate should not be translated into a universal individual risk because it came from an observational case-crossover study and depended on a specific reference exposure and modelling strategy.
Its broader implication is nevertheless important.
Environmental risk may be interactive.
A cardiovascular prevention model that asks whether temperature is dangerous and then separately asks whether pollution is dangerous may therefore miss what happens when the two arrive together.
That problem is encouraging a move toward the concept of the exposome, in which health is understood as the cumulative consequence of multiple environmental exposures over time rather than a collection of isolated variables.
For cardiovascular medicine, that could eventually include temperature, particulate pollution, noise, chemical exposures, neighbourhood design and social vulnerability alongside conventional clinical risk factors.
The metabolic side of the argument needs more restraint.
Climate-health discussions can easily move from plausible pathways to claims stronger than the evidence supports. Extreme heat can reduce opportunities for outdoor physical activity, food-system disruptions can affect diet and socioeconomic shocks can interfere with chronic-disease care, while pollution and environmental stress may interact with metabolic physiology.
But that does not establish that climate change itself directly causes obesity or type 2 diabetes.
The EMJ review explicitly makes this distinction, noting that evidence for long-term causal effects on obesity, insulin resistance and incident diabetes is less mature than the evidence connecting temperature extremes with acute cardiovascular outcomes.
That distinction is important because climate and health policy will lose credibility if every chronic disease trend is attributed to climate change regardless of evidentiary strength.
The stronger claim is also the more useful one.
Climate change modifies the conditions under which cardiometabolic risk develops and under which established disease becomes harder to manage.
That brings the issue directly into health-system policy.
In January 2026, the European Society of Cardiology, American College of Cardiology, American Heart Association and World Heart Federation issued their first joint statement calling for environmental stressors to be treated as important contributors to cardiovascular disease.
The significance of that statement is less about adding another entry to the list of risk factors and more about changing where responsibility sits.
If cardiovascular risk is partly determined by air quality, heat exposure, housing, transport and urban design, then prevention cannot be delivered entirely inside the consultation room.
A clinician can advise a patient with heart failure to remain hydrated during heat, but cannot install air conditioning in unsafe housing.
A cardiologist can tell a patient to exercise, but cannot make outdoor activity safe during extreme heat or severe air pollution.
A physician can optimise medication, but cannot prevent a flood from closing a pharmacy or a power failure from disrupting refrigeration.
Environmental cardiovascular prevention therefore crosses institutional boundaries in a way conventional prevention often does not.
Health departments, urban planners, housing authorities, employers, transport systems and energy policy all become part of the cardiovascular prevention architecture.
That is also why climate vulnerability is an equity issue.
People do not experience environmental hazards equally, and they do not have equal capacity to adapt.
Older adults, people with established cardiovascular disease, outdoor workers and under-resourced communities may face greater exposure or have less access to cooling, safe housing and healthcare. A well-insulated home, reliable electricity and flexible employment can turn a heatwave into an inconvenience. Their absence can turn the same event into a medical risk.
Geography further complicates the evidence.
Much of the epidemiological literature on climate and cardiovascular disease comes from high- and middle-income countries, while low-income settings remain substantially underrepresented despite often having lower adaptive capacity.
That creates a policy danger: risk estimates generated in places with widespread air conditioning, reliable electricity and functioning emergency systems may not transfer cleanly to communities without those protections.
In climate-health policy, exposure is only half the equation.
Adaptive capacity determines what exposure becomes.
This is where cardiovascular medicine may need to distinguish between adaptation and mitigation.
Adaptation means protecting patients from hazards already occurring through measures such as heat-health warning systems, cooling access, climate-resilient hospitals, air-quality alerts and contingency plans for medication and chronic-disease care.
Mitigation addresses the upstream processes driving climate change.
The two can overlap in ways that make cardiovascular policy particularly interesting.
Cleaner energy can reduce combustion-related air pollution. Walking and cycling infrastructure can lower transport emissions while increasing physical activity. Green urban design can reduce heat exposure while creating environments more conducive to exercise. Dietary shifts may influence both environmental impact and cardiovascular risk.
A systematic review of climate-mitigation strategies identified renewable energy, active transport, green space and dietary change among interventions with potential cardiovascular co-benefits.
That language matters.
Climate mitigation does not need to be sold to cardiovascular medicine solely as environmental altruism. Some interventions may deliver nearer-term health benefits through cleaner air, greater physical activity and healthier urban environments even before their long-term climate effects are realised.
The next question is how much of this belongs in clinical care.
There is currently little justification for asking cardiologists to become meteorologists or for adding environmental exposures indiscriminately to every cardiovascular algorithm.
Prospective evidence showing that climate-informed clinical interventions reduce cardiovascular events remains limited.
But there is an important middle ground between ignoring environmental risk and building an entirely new clinical specialty around it.
Health systems could identify patients particularly vulnerable during extreme heat. Electronic records could support targeted warnings during severe temperature or air-quality events. Cardiac rehabilitation programmes could adjust outdoor activity advice. Hospitals could plan medication access and continuity of care around extreme weather. Public-health alerts could be tailored to people with heart failure, kidney disease or other high-risk conditions rather than addressed only to the population as a whole.
The technology for much of that already exists.
What is missing is evidence about which interventions actually prevent events, how they should be integrated into workflows and who should pay for them.
That makes climate and cardiovascular health an implementation problem as much as an epidemiological one.
The traditional cardiovascular model asks what risk factors the patient carries.
A climate-informed model adds another question: what risk environment is the patient entering?
The distinction will matter increasingly as heat extremes, wildfire smoke and other environmental hazards become more frequent or severe in parts of the world.
Cardiovascular prevention does not need to abandon cholesterol, blood pressure, glucose or smoking.
It needs to recognise that those risks do not operate in a vacuum.
The next era of cardiovascular prevention may depend not only on treating the vulnerable patient, but on understanding the increasingly unstable environment in which that patient has to live.
