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Review
, 71 (18), 2041-2057

Arrhythmias in Patients ≥80 Years of Age: Pathophysiology, Management, and Outcomes

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Review

Arrhythmias in Patients ≥80 Years of Age: Pathophysiology, Management, and Outcomes

Anne B Curtis et al. J Am Coll Cardiol.

Abstract

Advances in medical care have led to an increase in the number of octogenarians and even older patients, forming an important and unique patient subgroup. It is clear that advancing age is an independent risk factor for the development of most arrhythmias, causing substantial morbidity and mortality. Patients ≥80 years of age have significant structural and electrical remodeling of cardiac tissue; accrue competing comorbidities; react differently to drug therapy; and may experience falls, frailty, and cognitive impairment, presenting significant therapeutic challenges. Unfortunately, very old patients are under-represented in clinical trials, leading to critical gaps in evidence to guide effective and safe treatment of arrhythmias. In this state-of-the-art review, we examine the pathophysiology of aging and arrhythmias and then present the available evidence on age-specific management of the most common arrhythmias, including drugs, catheter ablation, and cardiac implantable electronic devices.

Keywords: ablation; antiarrhythmic drugs; electrophysiology; geriatrics; octogenarians.

Figures

FIGURE 1
FIGURE 1. Pathophysiology of Arrhythmias in Elderly
Aging hearts demonstrate a typical milieu of sterile inflammation, with enhanced proinflammatory (IL-1, IL-6, tumor necrosis factor-α, and CRP) and profibrotic (TGF-β) cytokine release. Proinflammatory activity leads to progressive loss of cardiomyocyte numbers. The reduction in the proteolytic activity of MPs with increased expression of the tissue inhibitor of MPs, in association with a pro-fibrotic cytokine TGF-β, promotes fibrosis. Ca = calcium; CRP = C-reactive protein; ECM = extracellular matrix; IL = interleukin; MMP = matrix metalloproteinase; Na = sodium; TIMP = tissue inhibitor of matrix metalloproteinase; TGF = transforming growth factor;.
FIGURE 2
FIGURE 2. Age-Associated Pathological Changes and Their Effect on the Initiation, Manifestation, and Recurrence of Cardiac Arrhythmias
The major culprit mechanisms are related to cellular oxidative damage, cardiomyocyte apoptosis, and increased extracellular matrix volume that can lead to abnormal automaticity, re-entry, and repolarization abnormalities. In addition, ischemic and inflammatory mechanisms are responsible for fluctuating membrane potentials, ectopic pacemakers, and ultimately, myocardial fibrosis. Overall, aging hearts show electrical signal heterogeneity, abnormal electromechanical coupling, atrial and ventricular remodeling, low conduction voltage, and an increased incidence of both atrial and ventricular arrhythmias. Fibrofatty changes of the conduction system lead to bradycardia, AV block, and chronotropic incompetence. AV = atrioventricular; Ca2+ = calcium; EADs = early afterdepolarizations; EM = electromechanical; HR = heart rate; MPs = membrane potentials; VF = ventricular fibrillation; VT = ventricular tachycardia.
FIGURE 3
FIGURE 3. Role of Advanced Age and Existing Medical Comorbidities in Predicting Mortality Rate After Pacemaker Implantation
The bar diagrams represent mortality rates in patients with mild (group 1), moderate (group 2), and severe (group 3) Charlson comorbidity indexes. In each group, patients who are 90 years of age and older had significantly increased mortality rates after initial pacemaker implantation (age–comorbidity level interactions, p = 0.004). Study results are from a cross-sectional analysis of 2004 to 2008 hospital discharge information from the Healthcare Cost and Utilization Projection Nationwide Inpatient Sample administrative database. Reproduced with permission from Mandawat et al. (35).
FIGURE 4
FIGURE 4. Prevalence of Diagnosed Atrial Fibrillation Stratified by Age and Sex
Reproduced with permission from Go et al. (49).
FIGURE 5
FIGURE 5. Risk of Stopping Warfarin in the First Year on the Basis of Perceived Safety Concerns by Age
The y-axis represents the smoothed hazard estimates over time for the 2 age groups (<80 and ≥80 years). Numbers below the graph are the number of patients on warfarin at that time point (p < 0.001, log-rank test). The risk of stopping warfarin peaked early and then, beginning at 6 months, approximated that of younger patients. Reproduced with permission from Hylek et al. (61).
FIGURE 6
FIGURE 6. Annual Sudden and All-Cause Death Rate in Amiodarone Trialists Meta-Analysis Database of 6,252 Patients With Structural Heart Disease
Both sudden death and nonsudden death rates increased with age, although the increase of nonsudden death with age was more dramatic. Reproduced with permission from Krahn et al. (85).
CENTRAL ILLUSTRATION
CENTRAL ILLUSTRATION. Effects of Aging on Cardiac Arrhythmias: Etiology, Clinical Presentation, and Management
Aging leads to progressive degenerative changes of the contractile and conduction systems of the heart. Since the reparative process is slow, there is replacement fibrosis, which leads to structural and electrical conduction heterogeneity. Supraventricular and ventricular arrhythmias are then triggered. Pharmacotherapy can be challenging due to a narrow therapeutic window and risk of toxicity. Elderly patients often have concomitant structural heart disease requiring transcatheter or surgical procedures, which can lead to new arrhythmias requiring catheter ablation or implantable devices. AF = atrial fibrillation; AV = atrioventricular; TAVR = transcatheter aortic valvular replacement.

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