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FP
Family Medicine

Heart Failure In Older Adults

April 28, 2021.
Michael W. Rich, MD, Professor of Medicine, Cardiovascular Division, Associate Program Director for Research, Washington University School of Medicine in St. Louis; Director, Cardiac Rapid Evaluation Unit, Barnes-Jewish Hospital, St. Louis, MO

Educational Objectives


The goal of this program is to improve the diagnosis and treatment of heart failure in older adults. After hearing and assimilating this program, the clinician will be better able to:

1. Diagnose heart failure with reduced ejection fraction.

2. Diagnose heart failure with preserved ejection fraction.

3. Choose an appropriate pharmacologic agent to treat heart failure in an older adult.

4. Identify the devices used as therapy in patients with heart failure.

5. Recognize the contributions of multimorbidity and frailty to the management of older adults with heart failure.

Summary


Background: older adults are those ≥75 yr of age; the ages of 65 to 75 yr represents a transition from middle to older age; in adults ≥75 yr of age, the heart and blood vessels undergo structural and physiological changes that affect risk for and response to cardiovascular disease; heart failure in older adults represents the convergence of age-related changes in the cardiovascular system and the rising prevalence of common medical conditions that predispose to the development of heart failure, eg, hypertension, diabetes, coronary artery disease, valvular heart disease

Prevalence: heart failure increases with age in men and women; in younger individuals 20 to 40 yr of age, the prevalence is <0.5%; prevalence increases to 1.5% in adults 40 to 60 yr of age and to 5% to 7% in those 60 to 79 yr of age; in adults ≥80 yr of age, prevalence is >12% (roughly comparable by sex); hospitalizations for heart failure in adults 70 to 90 yr of age account for 33% of all hospitalizations for heart failure; the rates of hospitalization related to heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF) are almost equal; HFpEF indicates an ejection fraction of ≥45%, whereas HFrEF indicates an ejection fraction of <45%

Risk factors: hypertension and coronary artery disease — are the 2 most important medical conditions that predispose to the development of heart failure; both increase progressively with age; because of the improved survival of middle-aged adults with cardiovascular disease, the number of older adults who have or are at risk of developing heart failure is increased; normal aging — the aging of cardiovascular structure and function leads to or predisposes to the development of heart failure

Effects of normal aging: vascular stiffness — the large arteries become stiffer as a result of the deposition of collagen, collagen cross-linking, and a decline in the number of elastin fibers; systolic blood pressure increases gradually with increasing age; vascular stiffness also leads to increased resistance to left ventricular ejection; as a result, when the heart contracts, it needs to work harder to pump blood; increased myocardial stiffness — leads to impaired diastolic filling or diastolic dysfunction; predisposes older adults to the development of HFpEF (which is also referred to as diastolic heart failure)

Decreased responsiveness to beta-adrenergic stimulation: is most obvious in the association between maximum heart rate and age; the formula 220 minus age is used to predict maximum heart rate; because cardiac output is equal to heart rate multiplied by stroke volume, maximum cardiac output decreases as a function of increasing age; this contributes to the decline in maximum cardiac output as a function of age

Impaired mitochondrial production of adenosine triphosphate (ATP): the mitochondria can produce a sufficient amount of ATP at rest in older adults; therefore, ejection fraction is not affected by normal aging (ie, a normal ejection fraction in an older adult is the same as in a younger healthy individual); during exercise or other stress, however, the mitochondria cannot upregulate ATP production and therefore cannot maintain the ejection fraction as well as in a younger individual in response to stress

Other age-related changes in the cardiovascular system: decreased baroreceptor responsiveness — the baroreceptors in the neck do not respond to mild changes in stroke volume or blood pressure; predisposes older adults to syncope, dizziness when standing, and falls; impaired sinus node function — the sinus node has 5000 functioning pacemaker cells at birth; by 75 yr of age, ≈90% have degenerated; sick sinus syndrome is an age-related condition of sinus node dysfunction and is the most common reason for pacemaker implantation in older adults; impaired endothelial function — the coronary arteries dilate less in older adults than in younger adults; vasodilation is the main mechanism by which the heart improves coronary blood flow in response to increased myocardial oxygen demand; an imbalance exists between oxygen supply and demand in the face of increased stress in older adults (ie, demand ischemia); under extreme stress such as severe hypertension, cardiac troponins may be elevated even in an individual without fixed coronary artery diseases (partially related to impaired endothelial function)

Consequences of an aging cardiovascular system: cardiovascular reserve capacity is markedly reduced; older adults are less able to compensate in response to any kind of stress, eg, vigorous exercise (physiological stress), pneumonia (pathologic stress); explains why illness is more likely to be complicated by acute heart failure in older hospitalized adults

Age-related changes in other organ systems: kidneys — glomerular filtration rate declines at a rate of ≈8 mL/min per decade; the decrease in renal function affects the ability of the kidneys to excrete salt and water load, which contributes to cardiorenal syndrome; lungs — elastic recoil is lost, vital capacity in minute ventilation is reduced, and ventilation/perfusion (V/Q) mismatching is increased; leads to worsening symptoms of shortness of breath in older adults with heart failure; hemostatic system — risk for thrombosis increases; risk for venous thromboembolic disease (ie, deep vein thrombosis and pulmonary embolism) increases; risk for arterial thrombosis (including stroke) increases, especially the development of left atrial appendage thrombus in the context of atrial fibrillation; musculoskeletal system — changes include sarcopenia (loss of muscle mass and strength) and osteopenia (loss of bone mass, especially in women); these changes contribute to the age-related decline in function that is exacerbated by heart failure

Guideline-directed medical therapy (GDMT) of HFrEF: includes angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers and β-blockers; β-blockers that have shown beneficial effects and are approved for the treatment of heart failure in the United States are carvedilol, metoprolol succinate, and bisoprolol; the cornerstone of GDMT are mineralocorticoid antagonists, eg, spironolactone, eplerenone; hydralazine nitrates in combination are efficacious in Black adults; diuretics are also used for symptom control and to reduce peripheral edema; digoxin is used to control symptoms and to decrease the risk for hospitalizations; there are limitations to these medications in older adults because most randomized clinical trials enrolled adults <75 yr of age and patients with multimorbidity were not included

Sacubitril-valsartan: (eg, Entresto) is a newer agent approved for the treatment of HFrEF; speaker suggests it should be first-line therapy; the PARADIGM-HF trial studied >8000 patients with ejection fraction of ≤40% and New York Heart Association (NYHA) class II to IV heart failure; sacubitril-valsartan therapy led to a reduction in all-cause mortality of 16%, a reduction in cardiovascular mortality of 20%, and a reduction in hospitalizations for heart failure of 21%; the trial found no significant differences in primary or secondary outcomes in subgroups of patients >65 or >75 yr of age, ie, the therapy was proven effective in all patients with HFrEF; speaker notes improvements in functional capacity, shortness of breath, quality of life, and sexual function with sacubitril-valsartan therapy

Sodium-glucose cotransporter-2 (SGLT2) inhibitors: are another newer agent; the DAPA-HF trial studied the addition of the SGLT2 inhibitor dapagliflozin to standard GDMT in ≈4700 patients with ejection fraction ≤40% and NYHA class II to IV heart failure; although SGLT2 inhibitors were originally designed for the treatment of diabetes, they are beneficial in patients with heart failure regardless of whether the patient also has diabetes; in the DAPA-HF trial, only 42% of patients had diabetes; patients were randomly assigned to 10 mg dapagliflozin once daily or placebo; the trial reported no significant adverse effects; dapagliflozin was beneficial in reducing the primary outcomes of worsening heart failure by ≈30% and cardiovascular death by ≈18%; all-cause mortality was reduced by 17%; the trial also reported a decrease in recurrent heart failure events; efficacy was not reduced in older adults >65 yr of age; 2 additional studies of SGLT2 inhibitors reported similar results

Updates to guidelines: although SGLT2 inhibitors are not yet incorporated into the guidelines an update is under way; in the updated guidelines, angiotensin receptor neprilysin inhibitors are the preferred medications above ACE inhibitors or angiotensin receptor blockers, which are recommended as second-line therapies in individuals who cannot tolerate or cannot afford sacubitril/valsartan; guideline medical therapies include β-blockers (eg, carvedilol, metoprolol succinate, bisoprolol), mineralocorticoid antagonists (primarily spironolactone), SGLT2 inhibitors (eg, dapagliflozin, empagliflozin), hydralazine nitrates in Black patients, diuretics to maintain normal volume status, and digoxin (may be used in certain cases)

Heart failure with preserved ejection fraction: accounts for 10% to 20% of hospitalizations for heart failure in adults <65 yr of age; represents >50% of heart failure in patients >75 yr of age; is more prevalent in women than in men; the predisposing conditions are hypertension, coronary artery disease, valvular heart disease, and diabetes; symptoms include shortness of breath with exertion, exercise intolerance, and swelling of extremities; is associated with better short-term prognosis than HFrEF; proven therapies for HFpEF are lacking; no single agent has been shown to reduce mortality in patients with HFpEF; sacubitril-valsartan — was examined as a therapy in the PARAGON-HF trial; the trial included 4800 patients with NYHA class II to IV heart failure and ejection fraction ≥45%; mean age of the population was 73 yr and ≈52% of the participants were women; patients were randomly assigned to sacubitril-valsartan or valsartan; the tolerability of the therapies was roughly equivalent; sacubitril-valsartan was associated with fewer admissions for heart failure but the difference was not statistically significant; some measures of quality of life were better with sacubitril-valsartan than with valsartan alone; sacubitril-valsartan is still is the best medication available for the treatment of HFpEF; the Food and Drug Administration (FDA) is deliberating whether to authorize or approve sacubitril-valsartan for the treatment of HFpEF

Transthyretin (TTR) cardiac amyloidosis: caused by misfolding of the TTR protein; TTR has a tendency to misfold and be deposited in tissues including the heart, kidneys, and nervous system; the prevalence of TTR amyloidosis in patients with HFpEF is 10% to 15%, with a male predominance (>80%); includes wild-type and hereditary forms; the hereditary form is less common but is an important cause of HFpEF in the Black population; other manifestations of TTR amyloidosis are bilateral carpal tunnel syndrome, peripheral neuropathy, and orthostatic hypotension

Pharmacotherapy of cardiac amyloidosis: includes tafamidis, which has been approved by the FDA for the treatment of cardiac amyloid; delays progression of the disease, reduces mortality and heart failure symptoms, and improves quality of life

Device therapy for heart failure: implantable cardioverter–defibrillators (ICDs) — are beneficial in patients with HFrEF with ejection fraction <35%; benefits are evident in patients <65 yr of age, with a 35% reduction in mortality; in adults >65 yr of age, the benefit is no longer statistically significant (reduction in mortality of 19%); results of observational studies suggest that the benefit of ICD therapy declines progressively with increasing age; benefit in older adults is affected by competing risk for mortality, ie, the probability of dying of conditions not related to heart failure is increased in adults >80 yr of age; heart transplantation and durable mechanical circulatory support — the upper age limit for heart transplantation is 70 yr at most centers in the United States; left ventricular assist devices (LVAD) provide durable mechanical support; they are used in older adults with end-stage heart failure in whom all other therapeutic options have failed; outcomes in patients >75 yr of age (even adults in their early 80s) are generally favorable, with improvements in quality of life and ability to manage normal daily activities; rates of some complications such as gastrointestinal bleeding and strokes may be higher in older adults

Heart failure in patients with multimorbidity: 65% of patients ≥65 yr of age have ≥5 other medical conditions in addition to heart failure; 25% have ≥3 conditions and 25% have ≤2 comorbid conditions; no patient has heart failure as the only medical problem; multimorbidity has important implications for the management of patients with heart failure; multimorbidity is a driver of readmission rates, cost, and mortality; comorbidity complicates management owing to polypharmacy related to the treatment of multiple conditions; risks for drug interactions and diminished adherence to GDMT for heart failure in patients with multimorbidity are high

Frailty in patients with heart failure: reflects a state of decreased physiological reserve and increased vulnerability to stressors; frailty criteria — include 5 main components, ie, slowness (defined by slow gait speed), weakness (defined by grip strength), unintentional weight loss, low physical activity, and self-reported exhaustion; individuals with ≥3 features are considered frail and those with 1 to 2 are considered prefrail; frailty is common in older adults with heart failure and portends increased risk for decompensation, iatrogenic complications, delayed recovery, functional decline, disability, and death

End-of-life preferences: some older adults favor quality of life over length of life whereas others favor the opposite; clinicians should clarify the patient’s goals of care

Summary: care for older patients with heart failure must be individualized; applicability of guidelines to older patients is less clear; the clinician should take comorbidities and frailty into account, minimize polypharmacy whenever possible, and consider deprescribing nonessential cardiac and noncardiac medications

Readings


Atluri P et al. Ventricular assist device implant in the elderly is associated with increased, but respectable risk: a multi-institutional study. Ann Thorac Surg. 2013;96(1):141-147. doi:10.1016/j.athoracsur.2013.04.010; Borghi C, Cicero AFG. Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med. 2020;382:972; doi:10.1056/NEJMc1917241; Breitenstein A, Steffel J. Devices in heart failure patients-who benefits from ICD and CRT? Front Cardiovasc Med. 2019:111; doi:10.3389/fcvm.2019.00111; Butrous H, Hummel SL. Heart failure in older adults. Can J Cardiol. 2016;32:1140-1147; doi:10.1016/j.cjca.2016.05.005; Fala L. Entresto (Sacubitril/Valsartan): first-in-class angiotensin receptor neprilysin inhibitor FDA approved for patients with heart failure. Am Health Drug Benefits 2015;8:330-334; Lim WY et al. Implantable cardiac electronic devices in the elderly population. Arrhythm Electrophysiol Rev. 2019;8(2):143-146. doi:10.15420/aer.2019.3.4; Macedo AVS et al. Advances in the treatment of cardiac amyloidosis. Curr Treat Options Oncol. 2020;21:36; doi:10.1007/s11864-020-00738-8; Martinez-Naharro A et al. Cardiac amyloidosis. Clin Med (Lond). 2018;18:s30-s35; doi:10.7861/clinmedicine.18-2-s30; Reddy YN, Borlaug BA. Heart failure with preserved ejection fraction. Curr Probl Cardiol. 2016;41:145-188; doi:10.1016/j.cpcardiol.2015.12.002; Shah KS et al. Heart Failure with preserved, borderline, and reduced ejection fraction: 5-year outcomes. J Am Coll Cardiol. 2017;70(20):2476-2486. doi:10.1016/j.jacc.2017.08.074; Strait JB, Lakatta EG. Aging-associated cardiovascular changes and their relationship to heart failure. Heart Fail Clin. 2012;8:143-164; doi:10.1016/j.hfc.2011.08.011; Yamamoto H, Yokochi T. Transthyretin cardiac amyloidosis: an update on diagnosis and treatment. ESC Heart Fail. 2019;6:1128-1139; doi:10.1002/ehf2.12518; Yeom SY et al. Heart transplantation in the elderly patients: midterm results. Korean J Thorac Cardiovasc Surg. 2013;46:111-116; doi:10.5090/kjtcs.2013.46.2.111.

 

Disclosures


For this program, members of the faculty and planning committee reported nothing to disclose.

Acknowledgements


Dr. Rich was recorded exclusively for Audio Digest using virtual teleconference software, in compliance with current social-distancing guidelines during the COVID-19 pandemic. Audio Digest thanks Dr. Rich for his cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

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Lecture ID:

FP691601

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.

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