Frailty and cardiovascular events: chicken or egg?

This editorial refers to ‘Frailty trajectories after a cardiovascular event among community-dwelling older people’, by A. Z. Z. Phyo, et al., https://doi:10.1093/eurjpc/zwaf095. Frailty and cardiovascular disease (CVD) are closely linked, particularly in older adults, influencing each other in ways that require careful attention in clinical practice. Which comes first? Does frailty accelerate cardiovascular decline, or do cardiovascular events (CVEs) trigger frailty progression? More than just coexisting conditions, frailty and CVD appear to reinforce each other, shaping long-term health trajectories. Defined by reduced physiological reserve and increased vulnerability to stressors, frailty is no longer a concept confined to geriatric medicine—it is now recognized as a key factor across all domains of cardiology.1 Frailty is now well established as a prognostic marker in CVD, particularly heart failure. Notably, recent major therapeutic trials are increasingly factoring in frailty status, acknowledging its role in refining clinical decision-making.2 However, important questions remain: Can cardiovascular interventions slow frailty progression? Could targeting frailty improve cardiac outcomes? Longitudinal studies like that of Phyo et al. provide valuable insights into these issues.3 The study, ‘Frailty trajectories after a cardiovascular event among community-dwelling older people,’ by Phyo et al. provides crucial insights into how CVEs shape frailty trajectories.3 This landmark study followed 19 111 community-dwelling older adults over a median of 8.3 years, all initially free of CVD. Frailty was assessed annually using two complementary tools: the Frailty Index (FI), measuring 64 deficits across physical, cognitive, and social domains, and the Fried phenotype, which evaluates physical frailty through metrics like grip strength and walking speed. Their findings reveal a clear pattern: frailty increases significantly following CVEs, particularly stroke, myocardial infarction (MI), and hospitalization for heart failure (HHF). Stroke and HHF had the most pronounced short-term impact, which may reflect their higher inflammatory burden, prolonged recovery times, and effects on mobility. While the Fried phenotype captured short-term physical declines, the FI revealed sustained frailty progression, increasing by an average of 3.65 points immediately after a CVE and continuing to worsen over time. These results suggest that CVEs do more than temporarily weaken patients—they may accelerate a broader, long-term accumulation of deficits. By focusing on a community-dwelling population, this study expands our understanding beyond hospital-based research. It highlights that frailty is also a concern for individuals living independently. Certain subgroups appeared particularly vulnerable, including women, individuals over 80 years, those living alone, and patients with polypharmacy. These findings reinforce the need to consider frailty in a broader socio-medical context, where biological, social, and environmental determinants all play a role. The relationship between frailty and CVD runs both ways: while CVEs accelerate frailty, frailty itself is a strong predictor of future cardiovascular events.1 Studies show that frail individuals are at higher risk of developing CVD. Frailty has been associated with a nearly threefold increased risk of stroke, coronary heart disease, and peripheral vascular disease, and an almost ninefold risk of heart failure compared to robust individuals.4 These findings suggest that frailty is not just a marker of biological aging but an active contributor to cardiovascular vulnerability. One possible explanation lies in inflammaging(definition)—the chronic, low-grade inflammation that accompanies aging. Growing evidence suggests that shared inflammatory pathways between frailty and CVD, particularly in heart failure, may underpin their strong and interdependent association.5 Phyo et al.’s findings highlight the value of assessing frailty alongside cardiac function after CVEs, offering crucial insights into patient vulnerability and shaping long-term recovery strategies. However, standardizing frailty assessment in cardiology remains a challenge. The FI is highly sensitive for tracking long-term frailty progression but may not be practical for routine clinical use. Simpler tools, such as the FRAIL Scale or Clinical Frailty Scale (CFS), offer quick, practical alternatives, feasible for non-specialists and paramedics.1 FRAIL Scale offers a concise, five-item questionnaire evaluating fatigue, resistance, ambulation, illnesses, and weight loss. Similarly, the Clinical Frailty Scale (CFS) uses a visual scoring system ranging from 1 (very fit) to 9 (terminally ill), enabling quick and reliable evaluations in acute care settings Haut du formulaireBas du formulaire. In heart failure patients, a multi-domain frailty assessment model has recently been proposed by the Heart Failure Association of the European Society of Cardiology (HFA-ESC), integrating clinical, functional, psycho-cognitive, and social domains.6 These tools effortlessly integrate into clinical workflows, making comprehensive frailty assessment more accessible. When frailty is not identified and managed early, its impact extends beyond an individual patient’s prognosis. At the patient level, frailty is associated with higher morbidity and mortality, increased hospitalizations, prolonged recovery times, and greater dependence on caregivers. Without timely intervention, frailty can accelerate functional decline, limiting treatment options and leading to poorer cardiovascular outcomes.1,7 For clinicians, frailty presents a different challenge. Frail patients are often excluded from clinical trials, which means that many therapeutic decisions are based on extrapolated data rather than robust evidence. This gap in research contributes to uncertainty in treatment strategies, making it difficult to establish clear, evidence-based guidelin