Background/Objectives: Heart failure (HF) is a leading cause of morbidity and mortality worldwide, with a higher prevalence among older adults. Iron deficiency (ID), affecting up to 50% of HF patients, is closely linked to chronic inflammation, exacerbating HF outcomes. This review aims to explore the interplay between inflammation, ID, and HF, focusing on older patients, and to identify therapeutic gaps and emerging treatment strategies. Methods: A comprehensive review of the literature was conducted, emphasizing the pathophysiological mechanisms of inflammation and ID in HF, the challenges of current diagnostic criteria, and the limitations of available treatments. Emerging pharmacological and diagnostic approaches were analyzed. Results: Chronic inflammation in HF, particularly in older adults, promotes functional ID through elevated hepcidin levels, impairing iron availability and worsening anemia. Current diagnostic criteria, relying heavily on ferritin, often misclassify ID due to inflammation. Intravenous (IV) iron therapy shows clinical benefits in patients with <50% left ventricular ejection fraction (LVEF), but the evidence is limited in heart failure with preserved ejection fraction (HFpEF). Emerging therapies, such as Sodium-Glucose Cotransporter-2 inhibitors (SGLT2is) and prolyl hydroxylase inhibitors like Roxadustat, offer promising avenues to improve iron metabolism and outcomes. Conclusions: ID and inflammation significantly impact HF progression, particularly inolder adults. Refining diagnostic criteria and exploring innovative therapies are critical to addressing these challenges. Future research should prioritize personalized approaches targeting inflammation and ID, especially in underrepresented populations, such as HFpEF and elderly patients.

Cardiovascular (CV) diseases remain a global health challenge, with ischemic heart disease (IHD) being the primary cause of both morbidity and mortality. Despite optimal pharmacological therapy, older patients with IHD exhibit an increased susceptibility to recurrent ischemic events, significantly impacting their prognosis. Inflammation is intricately linked with the aging process and plays a pivotal role in the evolution of atherosclerosis. Emerging anti-inflammatory therapies have shown promise in reducing ischemic events among high-risk populations. This review aims to explore the potential of targeted anti-inflammatory interventions in improving clinical outcomes and the quality of life for older patients with IHD.

Background/Objectives: Heart failure (HF) is a leading cause of morbidity and mortality worldwide, with a higher prevalence among older adults. Iron deficiency (ID), affecting up to 50% of HF patients, is closely linked to chronic inflammation, exacerbating HF outcomes. This review aims to explore the interplay between inflammation, ID, and HF, focusing on older patients, and to identify therapeutic gaps and emerging treatment strategies. Methods: A comprehensive review of the literature was conducted, empha-sizing the pathophysiological mechanisms of inflammation and ID in HF, the challenges of current diagnostic criteria, and the limitations of available treatments. Emerging pharmacological and diagnostic approaches were analyzed. Results: Chronic inflamma-tion in HF, particularly in older adults, promotes functional ID through elevated hepcidin levels, impairing iron availability and worsening anemia. Current diagnostic criteria, relying heavily on ferritin, often misclassify ID due to inflammation. Intravenous (IV) iron therapy shows clinical benefits in patients with <50% left ventricular ejection fraction, but evidence is limited in HF with preserved ejection fraction (HFpEF). Emerging therapies, such as sodium-glucose cotransporter-2 inhibitors and prolyl hydroxylase inhibitors like Roxadustat, offer promising avenues to improve iron metabolism and outcomes. Conclusions: ID and inflammation significantly impact HF progression, particularly in older adults. Refining diagnostic criteria and exploring innovative therapies are critical to addressing these challenges. Future research should prioritize personalized approaches targeting inflammation and ID, especially in underrepresented populations, such as HFpEF and elderly patients.

Seasonal influenza is not only a respiratory infection but also a clinically relevant trigger of acute cardiovascular events. In adults with established cardiovascular disease, particularly older adults and patients with recent acute coronary syndrome or heart failure, influenza vaccination should be considered a low-risk, evidence-supported component of cardiovascular prevention rather than solely protection against respiratory disease. The evidence addresses three related but distinct questions: influenza infection as a cardiovascular trigger; influenza vaccination versus placebo or no vaccination; and enhanced or high-dose vaccination versus standard-dose vaccination. Randomized trials and meta-analyses support reductions in major adverse cardiovascular events, cardiovascular mortality, and all-cause mortality in higher-risk secondary-prevention populations, with particularly persuasive evidence after myocardial infarction. Recent pragmatic active-comparator trials of high-dose inactivated influenza vaccine, including DANFLU-2 and GALFLU, and the individual-level pooled FLUNITY-HD analysis provide incremental evidence in adults aged 65 years or older, strongest for hospitalization for influenza or pneumonia, cardiorespiratory hospitalization, and heart failure hospitalization. The current priority is implementation: screening, offering, documenting, and communicating vaccination across hospitalization, outpatient cardiology, cardiac rehabilitation, heart failure pathways, primary care, pharmacies, and long-term care. Influenza vaccination should complement, not replace, established guideline-directed cardiovascular therapies.

Background/Objectives: Respiratory syncytial virus (RSV) causes morbidity in older adults with cardiovascular disease, in whom infection may precipitate severe lower respiratory tract disease, hospitalization, functional decline, and cardiovascular destabilization. We evaluate the evidence for RSV vaccination in cardiovascular disease and propose a jurisdiction-adaptable framework for integrating vaccination into cardiovascular care. Methods: Observational studies, randomized trials, pragmatic and test-negative studies, prespecified cardiovascular analyses of DAN-RSV, and eligibility recommendations were narratively synthesized and translated into a pathway encompassing patient identification, eligibility and risk assessment, vaccine delivery and co-administration, documentation, and follow-up. Results: Acute cardiac events are frequent during RSV hospitalization, and cardiovascular risk may persist after infection. Randomized trials establish protection against RSV-associated lower respiratory tract disease and respiratory illness, while real-world studies support effectiveness against RSV-related hospitalization. DAN-RSV reduced all-cause cardiorespiratory hospitalization but did not demonstrate significant reductions in cardiovascular hospitalization, myocardial infarction, heart failure (HF) hospitalization, atrial fibrillation, stroke, cardiovascular death, or major adverse cardiovascular events; observational associations with lower post-vaccination cardiovascular-event rates remain hypothesis-generating. The framework prioritizes adults aged ≥75 years and those aged 50–74 years with high-risk cardiovascular conditions where consistent with national recommendations, embeds vaccination assessment across cardiology, HF, primary care, pharmacy, and long-term care, and incorporates co-administration, documentation, and outcome surveillance. Conclusions: The principal contribution is a pathway for moving RSV vaccination from recommendation to routine preventive care for adults with cardiovascular disease. It anchors implementation in established RSV and cardiorespiratory benefits while treating cardiovascular-event reduction as a research priority rather than a demonstrated indication.