Heart Failure as a Climate–sensitive Syndrome: Environmental Stressors, Vulnerable Phenotypes, and Clinical Implications

Background Climate change and environmental degradation are increasingly recognized as major determinants of cardiovascular health. Heart failure (HF), characterized by limited hemodynamic and autonomic reserve, appears particularly sensitive to ambient environmental stressors, yet remains underrepresented in climate–cardiology research. Objective To synthesize current epidemiological and mechanistic evidence linking climate–related environmental exposures with HF outcomes, and to frame HF as a climate–sensitive clinical syndrome with distinct vulnerability patterns. Methods We performed a narrative synthesis of epidemiological and mechanistic studies published between 2005 and 2025, including large population–based cohorts, multinational registries, and meta–analyses involving millions of individuals across North America, Europe, and Asia. Evidence addressing ambient temperature extremes, air pollution (PM₂.₅, PM₁₀, NO₂, O₃), and wildfire smoke was integrated with established cardiovascular and cardiopulmonary pathophysiological mechanisms. Results Population–level studies consistently demonstrate a U– or J–shaped association between ambient temperature and HF outcomes, with extreme cold and heat associated with 12–37% increases in HF mortality and marked seasonal peaks in HF hospitalizations. Long–term exposure to PM₂.₅ is associated with approximately 20% higher HF incidence and ∼9% higher HF mortality per 10 μg/m³ increase, while short–term pollution peaks trigger acute HF admissions within days. Wildfire–related PM₂.₅ and compound exposures (heat plus pollution) produce supradditive increases in cardiovascular and respiratory hospitalizations, particularly among older adults. Mechanistically, environmental stressors converge on hemodynamic overload, autonomic imbalance, lung–heart interactions, systemic inflammation, endothelial dysfunction, and microvascular injury, disproportionately affecting patients with HFpEF, right–sided HF, chronic kidney disease, multimorbidity, and socioeconomic disadvantage. Conclusions Heart failure emerges as a climate–sensitive cardiovascular syndrome, with environmental exposures acting as predictable and potentially modifiable triggers of decompensation. Integrating climate and pollution variables into HF risk assessment, patient counseling, and preventive strategies may reduce avoidable hospitalizations, while targeted research is needed to define effective mitigation and equity–focused interventions.