Climate change is no longer a distant environmental abstraction for cardiologists — it is actively reshaping the epidemiological profile of cardiovascular disease. As heat waves intensify and cold snaps persist, understanding how ambient temperature drives cardiac events has become clinically urgent, particularly for the growing population of older adults managing pre-existing heart conditions.
This review published in Herz synthesizes the dual physiological mechanisms through which temperature extremes stress the cardiovascular system. Cold exposure triggers sympathetic nervous system activation and engages the renin-angiotensin-aldosterone system, elevating blood pressure, increasing afterload, and raising myocardial oxygen demand — a cascade that heightens ischemic risk. Heat exposure follows a different but equally dangerous trajectory: peripheral vasodilation, sweat-induced fluid loss, compensatory tachycardia, and a prothrombotic inflammatory milieu together elevate the risk of acute cardiovascular events and renal impairment. Epidemiological data across multiple populations consistently describe a U-shaped relationship between ambient temperature and cardiovascular mortality, with the minimum-mortality temperature varying by region and shifting upward as populations acclimatize over time. Air pollutants — particularly fine particulate matter (PM2.5), ozone, and nitrogen dioxide — act as co-exposures that amplify heat-related cardiovascular risk beyond temperature effects alone.
This synthesis is timely but not wholly novel — the U-shaped temperature-mortality curve has been documented for over two decades. What elevates the current review is its integration of long-term acclimatization dynamics and the air pollution co-exposure dimension, which is often underappreciated in clinical cardiology settings. A meaningful limitation is that much of the underlying epidemiology is observational and population-level, making it difficult to isolate temperature effects from socioeconomic confounders like housing quality or healthcare access. The practical implication for health-conscious adults is that temperature extremes are cardiovascular stressors comparable in mechanism — if not magnitude — to conventional risk factors, and environmental conditions warrant consideration alongside lipid panels and blood pressure readings.
