Preventing cardiovascular disease in older adults: One size does not fit all

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Release date: January 1, 2018
Expiration date: December 31, 2018
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Frailty and cardiovascular disease are highly interconnected and increase in prevalence with age. Identifying frailty allows for a personalized cardiovascular risk prescription and individualized management of hypertension, hyperlipidemia, diabetes, and lifestyle in the aging population.


  • With the aging of the population, individualized prevention strategies must incorporate geriatric syndromes such as frailty.
  • However, current guidelines and available evidence for cardiovascular disease prevention strategies have not incorporated frailty or make no recommendation at all for those over age 75.
  • Four-meter gait speed, a simple measure of physical function and a proxy for frailty, can be used clinically to diagnose frailty.



When assessing and attempting to modify the risk of cardiovascular disease in older patients, physicians should consider incorporating the concept of frailty. The balance of risk and benefit may differ considerably for 2 patients of the same age if one is fit and the other is frail. Because the aging population is a diverse group, a one-size-fits-all approach to cardiovascular disease prevention and risk-factor management is not appropriate.

See related editorial

Our recommendations for cardiovascular disease prevention in older adults, considering frailty
Much research remains to be done regarding cardiovascular risk in the frail elderly. In this article, we review the complex interaction between frailty and cardiovascular disease and what the limited data can tell us about how to incorporate frailty into the optimization of high blood pressure, dyslipidemia, and other modifiable risk factors in this vulnerable group (Table 1).


The number of older adults with multiple cardiovascular risk factors is increasing as life expectancy improves. US residents who are age 65 today can expect to live to an average age of 84 (men) or 87 (women).1

However, the range of life expectancy for people reaching these advanced ages is wide, and chronologic age is no longer sufficient to determine a patient’s risk profile. Furthermore, the prevalence of cardiovascular disease rises with age, and age itself is the strongest predictor of cardiovascular risk.2

Current risk calculators have not been validated in people over age 80,2 making them inadequate for use in older patients. Age alone cannot identify who will benefit from preventive strategies, except in situations when a dominant disease such as metastatic cancer, end-stage renal disease, end-stage dementia, or end-stage heart failure is expected to lead to mortality within a year. Guidelines for treating common risk factors such as elevated cholesterol3 in the general population have generally not focused on adults over 75 or recognized their diversity in health status.4 In order to generate an individualized prescription for cardiovascular disease prevention for older adults, issues such as frailty, cognitive and functional status, disability, and comorbidity must be considered.


Clinicians have recognized frailty for decades, but to date there remains a debate on how to define it.

Clegg et al5 described frailty as “a state of increased vulnerability to poor resolution of homeostasis after a stressor event,”5 a definition generally agreed upon, as frailty predicts both poor health outcomes and death.

Indeed, in a prospective study of 5,317 men and women ranging in age from 65 to 101, those identified as frail at baseline were 6 times more likely to have died 3 years later (mortality rates 18% vs 3%), and the difference persisted at 7 years.6 After adjusting for comorbidities, those identified as frail were also more likely to fall, develop limitations in mobility or activities of daily living, or be hospitalized.

The two current leading theories of frailty were defined by Fried et al6 and by Rockwood and Mitnitski.7

Fried et al6 have operationalized frailty as a “physical phenotype,” defined as 3 or more of the following:

  • Unintentional weight loss of 10 pounds in the past year
  • Self-reported exhaustion
  • Weakness as measured by grip strength
  • Slow walking speed
  • Decreased physical activity.6

Rockwood and Mitnitski7 define frailty as an accumulation of health-related deficits over time. They recommend that 30 to 40 possible deficits that cover a variety of health systems be included such as cognition, mood, function, and comorbidity. These are added and divided by the total possible number of variables to generate a score between 0 and 1.8

The difficulty in defining frailty has led to varying estimates of its prevalence, ranging from 25% to 50% in adults over 65 who have cardiovascular disease.9


Studies have highlighted the bidirectional connection between frailty and cardiovascular disease.10 Frailty may predict cardiovascular disease, while cardiovascular disease is associated with an increased risk of incident frailty.9,11

Frail adults with cardiovascular disease have a higher risk of poor outcomes, even after correcting for age, comorbidities, disability, and disease severity. For example, frailty is associated with a twofold higher mortality rate in individuals with cardiovascular disease.9

A prospective cohort study12 of 3,895 middle-aged men and women demonstrated that those with an elevated cardiovascular risk score were at increased risk of frailty over 10 years (odds ratio [OR] 1.35, 95% confidence interval [CI] 1.21–1.51) and incident cardiovascular events (OR 1.36, 95% CI 1.15–1.61). This suggests that modification of cardiovascular risk factors earlier in life may reduce the risk of subsequently becoming frail.

Biologic mechanisms that may explain the connection between frailty and cardiovascular disease include derangements in inflammatory, hematologic, and endocrine pathways. People who are found to be clinically frail are more likely to have insulin resistance and elevated biomarkers such as C-reactive protein, D-dimer, and factor VIII.13 The inflammatory cytokine interleukin 6 is suggested as a common link between inflammation and thrombosis, perhaps contributing to the connection between cardiovascular disease and frailty. Many of these biomarkers have been linked to the pathophysiologic changes of aging, so-called “inflamm-aging” or immunosenescence, including sarcopenia, osteoporosis, and cardiovascular disease.14


Next Article:

Frailty and cardiovascular disease: A two-way street?

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