Clara Bonanad

Herpes zoster (HZ), commonly known as shingles, results from reactivation of latent varicella-zoster virus (VZV). Beyond pain and postherpetic neuralgia, HZ is associated with a transient increase in vascular events. This narrative review examines HZ as a vascular trigger, the mechanisms of VZV-associated vascular injury, and the evidence for recombinant zoster vaccine (RZV). Self-controlled studies show that ischemic stroke and myocardial infarction rates peak during the first days to weeks after HZ and decline over subsequent months. Direct arterial infection provides the strongest mechanistic evidence; inflammatory, thrombotic, and autonomic pathways offer additional, less directly established explanations. Randomized trials demonstrate that RZV prevents HZ and postherpetic neuralgia, with sustained protection in long-term follow-up. Associations between vaccination and fewer cardiovascular events derive mainly from observational studies and vary by vaccine platform and endpoint. We use transient post-zoster cardiovascular vulnerability as a clinical framework, not a validated syndrome. Eligible adults should receive RZV for its established prevention benefits, while clinicians should remain alert to new vascular symptoms after HZ. Whether RZV causally reduces cardiovascular events requires dedicated prospective studies and randomized trials.

Background: Polypharmacy is highly prevalent in patients with heart failure (HF), but the prognostic significance of severe polypharmacy remains uncertain. This systematic review and meta-analysis evaluated its association with all-cause mortality in adults with HF. Methods: PubMed, MEDLINE, Embase, Scopus and the Cochrane Library were searched from inception through August 2026. Observational studies assessing severe polypharmacy (the highest medication-burden category in each study; ≥9 to ≥15 medications) and all-cause mortality in adults with HF were eligible. Adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) were pooled using a random-effects model. Leave-one-out sensitivity analyses and post hoc threshold-specific analyses were performed. Risk of bias and certainty of evidence were assessed using the Newcastle–Ottawa Scale (NOS) and GRADE, respectively. The protocol was registered in PROSPERO (CRD420261507517). Results: Nine studies included 44,213 patients. Severe polypharmacy was not significantly associated with all-cause mortality (HR 1.04, 95% CI 0.86–1.26; p = 0.67; I² = 79%). NOS scores ranged from 6 to 9. Leave-one-out HRs ranged from 0.996 to 1.097, with all 95% CIs including 1. In six studies defining severe polypharmacy as ≥10 medications, the pooled HR was 1.15 (95% CI 1.00–1.32; p = 0.054; I² = 37.8%). Certainty of evidence was very low because of serious inconsistency and imprecision. Conclusions: No statistically significant association was identified, but very low certainty of evidence precludes firm conclusions, and clinically important associations cannot be excluded. Medication count should be interpreted alongside treatment appropriateness and clinical complexity.

Background/Objectives: Streptococcus pneumoniae is a major cause of community-acquired pneumonia and invasive pneumococcal disease, particularly in older adults and people with cardiovascular disease. Pneumococcal infection may precipitate heart failure, arrhythmias, myocardial infarction, stroke, functional decline, hospitalization, and death. This review examines pneumococcal disease as a cardiovascular stressor, the effectiveness of adult pneumococcal vaccination, and the comparative clinical relevance of higher-valency conjugate vaccines. Methods: We conducted a narrative review of randomized trials, phase 3 immunogenicity and safety studies, real-world effectiveness analyses, observational cardiovascular cohorts, meta-analyses, epidemiological surveillance reports, regulatory documents, and current European, U.S., and Spanish recommendations. Results: Clinical evidence supports protection against vaccine-type invasive pneumococcal disease and pneumococcal pneumonia. Associations between pneumococcal vaccination and lower myocardial infarction risk derive predominantly from observational studies and do not establish causality; a reduction in cardiovascular events remains unproven. The 23-valent polysaccharide vaccine is an older, unconjugated platform that induces a T-cell-independent response without the immunological memory produced by conjugate vaccines; therefore, a higher nominal valency does not necessarily imply greater or more durable clinical effectiveness. PCV20 and PCV21 are higher-valency conjugate vaccines with partially overlapping non-nested serotype compositions. Both have adult regulatory indications in Spain, but their evidence bases differ: PCV20 has phase 3 immunogenicity and safety evidence plus emerging real-world effectiveness data, whereas PCV21 currently has a broad phase 3 immunogenicity and safety program. No head-to-head clinical-outcome study has established superior effectiveness of either vaccine. Differences in estimated serotype coverage reflect epidemiological overlap and do not directly quantify clinical protection. Spanish serotype epidemiology is highly dynamic, with persistent adult disease caused by serotypes included in each formulation and recent increases in selected legacy serotypes retained in PCV20. A serotype-specific association between serotypes 3 and 9N and cardiovascular events has been reported in one invasive-disease cohort but was not reproduced in a larger pneumococcal pneumonia cohort. Conclusions: Pneumococcal vaccination should be integrated into cardiovascular care for eligible adults to prevent pneumococcal disease. Any additional benefit in preventing myocardial infarction or other cardiovascular events, including long-term complications, remains uncertain. Vaccine selection should follow official recommendations and consider age, previous vaccination, regional epidemiology, serotype-associated disease burden and severity, antimicrobial resistance, and availability rather than valency or immunogenicity alone.

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.

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.

Population aging has shifted the burden of cardiovascular disease toward older adults living with multimorbidity, frailty, cognitive vulnerability, functional impairment, and treatment burden. Yet much of the contemporary cardiovascular evidence still derives from randomized clinical trials (RCTs) designed around biologically homogeneous participants, limiting applicability to real-world geriatric cardiology. Our objective was to perform a comparative methodological analysis of two contemporary European cardiovascular RCTs, HI-COR-65 and SENEKA, as illustrative cases and to propose a geriatric-oriented framework for improving trial design in older adults with cardiovascular multimorbidity. We qualitatively compared both trials across five domains: population representativeness, clinical objectives and outcome hierarchy, exclusion criteria, multidisciplinarity, and patient perspective, including participation burden and patient-reported outcomes. Both trials represent important progress by explicitly enrolling older adults with clinically relevant cardiovascular multimorbidity. However, the analysis identified recurring limitations: geriatric complexity is acknowledged but not operationalized through comprehensive geriatric assessment or vulnerability-based stratification; safety and participation requirements may preferentially select robust older adults; outcome hierarchies remain variably aligned with patient priorities; and intervention models are predominantly pharmacological and monodisciplinary. Future cardiovascular trials in older adults should move from chronological inclusion toward pragmatic, complexity-sensitive design. We propose the Comprehensive Geriatric Cardiology (COMGERCARDIO) framework, which integrates baseline geriatric assessment, vulnerability-adaptive interventions, hierarchical patient-centered outcomes, stratified analysis, and implementation evaluation to generate evidence that is scientifically robust, clinically usable, and equitable for aging populations.

Objectives: This study aims to describe real-world clinical profiles, treatment patterns and one-year outcomes of older adults hospitalized for acute heart failure (HF) across different admission services, and to examine whether sex influences these characteristics and outcomes. Methods: We performed a retrospective study including 1226 patients aged ≥80 years hospitalized for acute HF between 2018 and 2021. Patients were categorized by admitting service (cardiology [CAR] or internal medicine [IM]) and sex. The primary endpoint was all-cause mortality at 12 months, with secondary endpoints including HF readmission and a composite of death or HF readmission. Results: The mean age was 87.4 ± 4.4 years, 65.8% were women, and 80% presented HF with preserved ejection fraction (HFpEF). Admission services reflected differing patient profiles: individuals admitted under IM were older, predominantly female, and more frequently presented with HFpEF and worse functional class, while CAR admissions included a higher proportion of patients with ischemic disease. Use of guideline-directed medical therapy varied according to clinical characteristics and admitting service. At 12 months, mortality and the composite endpoint differed across admission services, whereas HF readmission rates were similar. Sex-stratified analyses showed no difference in all-cause mortality or in the composite endpoint, but women experienced more frequent HF readmissions. Conclusions: Among very old adults hospitalized for acute HF, clinical profiles, therapeutic patterns, and outcomes differ according to patient characteristics and hospital admission pathways. Sex also shapes clinical presentation and readmission patterns. These findings highlight the importance of harmonized, multidisciplinary, and sex-sensitive HF care pathways to address the diverse needs of an aging HF population.