Editorials

Temperature changes and the risk of cardiac events

BMJ 2010; 341 doi: http://dx.doi.org/10.1136/bmj.c3720 (Published 10 August 2010) Cite this as: BMJ 2010;341:c3720
  1. Paola Michelozzi, head of environmental epidemiology unit,
  2. Manuela De Sario, epidemiologist
  1. 1Lazio Region Department of Epidemiology, Via di Santa Costanza 53, 00198 Rome, Italy
  1. michelozzi{at}asplazio.it

    Prevention strategies should target subgroups who are vulnerable to heat and cold

    Climate change is a concern in many regions of the world where extreme hot and cold temperatures may affect people with cardiovascular diseases and increase the incidence of coronary events. The impact may be greater in areas with inequalities in the access to medical services.1

    In the linked study (doi:10.1136/bmj.c3823), Bhaskaran and colleagues assessed the effect of temperature on the risk of myocardial infarction and other acute coronary syndromes2; they performed a time series analysis across 15 conurbations in England and Wales using clinically confirmed hospital admissions data. They found that each 1°C reduction in daily mean temperature was associated with a 2.0% (95% CI 1.1% to 2.9%) cumulative increase in the risk of myocardial infarction for 28 days; the highest risk was within two weeks of exposure. They found no association at higher temperatures.

    The results for cold temperatures are consistent with several other studies,3 although others have found that myocardial infarction is associated with higher temperatures. The absence of an effect of heat on myocardial infarction agrees with results from a previous study in Paris during the 2003 heat wave, which found an increased risk of sudden cardiac death but no increase in myocardial infarction.4 Moreover, results from a large European multi-city study reported contrasting patterns, with heat affecting mortality from cardiovascular disease but having no effect on hospital admissions for cardiovascular diseases. This suggests that deaths from cardiac disease occur before patients receive medical treatment or are admitted to hospital.5

    The main strength of the present study is that myocardial infarction was confirmed by clinical data.2 To date, few studies have investigated the effect of temperature on specific cardiac outcomes. Most evidence is on cardiovascular causes as a whole and does not distinguish between differences in the course of the disease or the underlying mechanisms through which temperature may worsen conditions and increase the risk of death. Future studies should assess the effect of temperature on specific causes and improve the accuracy of disease definition by collecting information from disease registers integrated with administrative data.

    Underlying physiological mechanisms are better known for cold than for heat. Cold exposure may trigger coronary disease in susceptible people through inflammatory and coagulation responses.6 Previous work on the protective effect of aspirin suggests that part of the effect of cold may be mediated by changes in platelet function.2 Heat exposure is associated with physiological changes such as increases in heart rate, blood viscosity, and coagulability,7 but data supporting a specific link to myocardial infarction are lacking. The association between heat exposure and sudden death from cardiac disease may be explained by the occurrence of conditions other than myocardial infarction, such as heart failure, conduction disorders, and arrhythmias. It may also be caused by the impairment of one or more thermoregulatory response and a limited ability to increase myocardial workload after peripheral vasodilation.4 8

    From a public health perspective the identification of population subgroups vulnerable to heat and cold is important for effective prevention. Individual susceptibility may be exacerbated by underlying chronic medical conditions and drug treatments that affect the body’s capacity to adapt to temperature changes.9 Bhaskaran and colleagues found that people aged 75-84 years with previous coronary heart disease who were not taking aspirin were at higher risk on cold days.2 Moreover, socioeconomic factors such as social isolation could increase the risk of fatal cardiac events as a result of delay in reaching emergency care.

    Clinicians should be aware that exposure to environmental heat and cold is a risk factor for cardiovascular disease and should consider this in risk prevention and management. Bhaskaran and colleagues’ observation on the protective effect of aspirin supports the clinical recommendation of monitoring disease and treatment to improve compliance with evidence based treatments in myocardial infarction because a low use of drugs (β blockers, angiotensin modifying agents, and statins) has been documented in these patients.2 10

    Improving prevention and management strategies will be even more important in the future because climate change predictions indicate that the burden of cardiovascular disease will increase, mostly because of an increase in climate extremes.1 Rising global temperature will bring some health benefits such as lower cold related mortality, but these will be outweighed by cardiovascular mortality and morbidity associated with increased frequency and intensity of heat waves, most especially in elderly and socially isolated people living in urban areas.1

    Climate change and human disease are related in several ways. Actions to reduce greenhouse gases based on lifestyle changes at the population and individual level may have substantial benefits for health and climate protection. For example, lowering saturated fat intake by reducing consumption of animal products is a healthy food choice recommended in prevention guidelines for coronary heart disease and a recognised strategy to reduce greenhouse gas emissions.11 12

    Notes

    Cite this as: BMJ 2010;341:c3720

    Footnotes

    • Research, doi:10.1136/bmj.c3823
    • Competing interests: All authors have completed the Unified Competing Interest form at http://www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: PM and MDS have support from Lazio Region Department of Epidemiology for the submitted work; no relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.

    • Provenance and peer review: Commissioned; not externally peer reviewed.

    References