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<p>Temperature changes affect cardiovascular health through multiple physiological and environmental pathways. Cold exposure activates the sympathetic nervous system and the renin-angiotensin-aldosterone system, increases blood pressure, cardiac afterload and myocardial oxygen demand and can thereby promote ischemia, angina pectoris and myocardial infarction. In contrast, exposure to heat causes vasodilation, fluid loss through sweating, tachycardia and a&#xa0;rise in myocardial oxygen demand; dehydration, inflammation and prothrombotic changes can further increase the risk of acute cardiovascular events and renal dysfunction. Epidemiological data consistently show a&#xa0;U-shaped association between ambient temperature and cardiovascular mortality, with older adults and patients with pre-existing cardiovascular disease being particularly vulnerable. Air pollution, especially fine particulate matter, ozone and nitrogen dioxide can amplify heat-related risks. Beyond the immediate effects of temperature extremes, long-term adaptation leads to a&#xa0;shift in the minimum mortality temperature toward warmer conditions, while climate change increases exposure to heat waves and warm nights. We summarize the underlying pathophysiological mechanisms, clinical consequences and the growing relevance of temperature-related cardiovascular risks for public health. Effective climate adaptation, reduction of urban heat islands, promotion of low-emission transport and health-oriented urban planning are essential components in the prevention of temperature-associated morbidity and mortality.</p>

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Herz und Klima

  • 期刊论文

  • 发表日期：

    2026年6月30日

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  • Christoph Maack,
  • Andreas Daiber,
  • Alexandra Schneider,
  • Jos Lelieveld,
  • Omar Hahad

摘要

Temperature changes affect cardiovascular health through multiple physiological and environmental pathways. Cold exposure activates the sympathetic nervous system and the renin-angiotensin-aldosterone system, increases blood pressure, cardiac afterload and myocardial oxygen demand and can thereby promote ischemia, angina pectoris and myocardial infarction. In contrast, exposure to heat causes vasodilation, fluid loss through sweating, tachycardia and a rise in myocardial oxygen demand; dehydration, inflammation and prothrombotic changes can further increase the risk of acute cardiovascular events and renal dysfunction. Epidemiological data consistently show a U-shaped association between ambient temperature and cardiovascular mortality, with older adults and patients with pre-existing cardiovascular disease being particularly vulnerable. Air pollution, especially fine particulate matter, ozone and nitrogen dioxide can amplify heat-related risks. Beyond the immediate effects of temperature extremes, long-term adaptation leads to a shift in the minimum mortality temperature toward warmer conditions, while climate change increases exposure to heat waves and warm nights. We summarize the underlying pathophysiological mechanisms, clinical consequences and the growing relevance of temperature-related cardiovascular risks for public health. Effective climate adaptation, reduction of urban heat islands, promotion of low-emission transport and health-oriented urban planning are essential components in the prevention of temperature-associated morbidity and mortality.