Atrial Fibrillation in the Elderly

Nantsupawat, Teerapat; Nugent, Kenneth; Phrommintikul, Arintaya

doi:10.1007/s40266-013-0094-8

Cited by 31 publications

(26 citation statements)

References 78 publications

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“…While not solely a disease of the elderly, the risk of all types of heart disease, including atrial fibrillation (AF) increases with age (39). AF is the most common arrhythmia in older adults, with a prevalence of 9% in adults aged 80 yr or older (40). Similar trends for AF to increase with age have also been documented before in mice (24 compared with 2 mo) (35).…”

Section: Discussionsupporting

confidence: 72%

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling

Liu

Sirenko

Juhaszova

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Lakatta EG. Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca 2ϩ signaling. Am J Physiol Heart Circ Physiol 306: H1385-H1397, 2014. First published March 14, 2014 doi:10.1152/ajpheart.00088.2014.-A reduced sinoatrial node (SAN) functional reserve underlies the age-associated decline in heart rate acceleration in response to stress. SAN cell function involves an oscillatory coupled-clock system: the sarcoplasmic reticulum (SR), a Ca 2ϩ clock, and the electrogenic-sarcolemmal membrane clock. Ca 2ϩ -activated-calmodulin-adenylyl cyclase/CaMKII-cAMP/PKA-Ca 2ϩ signaling regulated by phosphodiesterase activity drives SAN cells automaticity. SR-generated local calcium releases (LCRs) activate Na ϩ /Ca 2ϩ exchanger in the membrane clock, which initiates the action potential (AP). We hypothesize that SAN cell dysfunctions accumulate with age. We found a reduction in single SAN cell AP firing in aged (20 -24 mo) vs. adult (3-4 mo) mice. The sensitivity of the SAN beating rate responses to both muscarinic and adrenergic receptor activation becomes decreased in advanced age. Additionally, age-associated coincident dysfunctions occur stemming from compromised clock functions, including a reduced SR Ca 2ϩ load and a reduced size, number, and duration of spontaneous LCRs. Moreover, the sensitivity of SAN beating rate to a cAMP stress induced by phosphodiesterase inhibitor is reduced, as are the LCR size, amplitude, and number in SAN cells from aged vs. adult mice. These functional changes coincide with decreased expression of crucial SR Ca 2ϩ -cycling proteins, including SR Ca 2ϩ -ATPase pump, ryanodine receptors, and Na ϩ /Ca 2ϩ exchanger. Thus a deterioration in intrinsic Ca 2ϩ clock kinetics in aged SAN cells, due to deficits in intrinsic SR Ca 2ϩ cycling and its response to a cAMP-dependent pathway activation, is involved in the age-associated reduction in intrinsic resting AP firing rate, and in the reduction in the acceleration of heart rate during exercise.aging; Ca 2ϩ transient; intrinsic heart rate; pacemaker function; PKA signaling AN AGE-ASSOCIATED REDUCTION in heart rate acceleration in response to stress is a major factor underlying the age-associated decline in cardiovascular reserve (29). Specifically, the heart rate increase in response to perturbations from the supine basal state, e.g., on assuming an upright posture or during exercise, is reduced in older vs. younger persons (43). That an exaggerated increase in plasma catecholamines accompanies the reduction in heart rate reserve in older persons suggests that the age-associated reduction in heart rate reserve, in part at least, is attributable to postsynaptic mechanisms that reside within the sinoatrial node (SAN) (14). Broadly, these postsynaptic mechanisms include intrinsic mechanisms that control the rate and rhythm of spontaneous action potential (AP) firing of SAN pacemaker cells, and autonomic receptor signaling that modulates these intrinsic pacemaker cell mechanisms (3, 22, 37). The...

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Section: Discussionsupporting

confidence: 72%

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling

Liu

Sirenko

Juhaszova

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…Anticoagulant medications can reduce stroke risk by 60-70% [20]. Scoring systems, such as CHADS2 and, more recently, CHA2DS2-VASc, can be used to calculate stroke risk CHA2DS2-VASc places extra weight on advanced age and is useful in further identifying the truly low stroke risk patient [21,22]. With a CHADS2 score of zero or one before initiation of anticoagulation, recompute with the CHA2DS2-VASc scale.…”

Section: Stroke and Anticoagulationmentioning

confidence: 99%

“…With a CHA2DS2-VASc of zero, patients do not require anticoagulation. With a score of one, anticoagulation with warfarin or NOACs should be undertaken [22]. Just over half of elderly patients who are at very high risk for stroke are anticoagulated.…”

Section: Stroke and Anticoagulationmentioning

confidence: 99%

“…Fall risk is perhaps the most common reason for avoiding warfarin or NOACs. However, current evidence suggests that, even in patients at risk of falls, protective benefit against stroke outweighs risk of fall-induced intracranial hemorrhage [22]. As with scoring to calculate stroke risk, scoring systems can be utilized to calculate bleeding risk.…”

Section: Stroke and Anticoagulationmentioning

confidence: 99%

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Acute cardiac disease in elder patients

DeMeester

Mattu

Grossman

et al. 2016

Geriatric Emergencies

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“…Regardless of the HAS-BLED score, when it is ≥3 caution and efforts to correct reversible risk factors are advised, oral anticoagulants are recomended in all CHADS 2 scores of ≥2, with a Ia recomendation 1A [19]. However, it has been shown that estimates of bleeding risks by treating physicians are overstated, by as much as 18% [20] and as such under-usage is frequent.…”

Section: Introductionmentioning

confidence: 99%

Anticoagulation for Chronic Non Valvular Atrial Fibrillation in the Elderly: A Review

Murray¹

2015

HBTD

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Atrial Fibrillation (AF) is a major risk factor for disabling ischaemic stroke due to embolism from the left atrium. AF is the most frequent arrhymia in the elderly and its prevalence increases with age [1]. The true prevalence is difficult to determine as a substantial proportion of patients will be asymptomatic or have subclinical disease. However, two thirds of patients with AF will be at least 75 years old [2], and of the patients over 75 years 10% will have AF. The influence of AF on health outcomes increases with age in that 71% of strokes that occur in patients with AF are over 70 years [3] and that patient outcomes are worse in patients with AF than in those without AF [4].Current guidelines recommend the use of anticoagulants to reduce the risk of embolic stroke in patients with AF [5,6]. As with any pharmacological intervention there are risk and benefits with anticoagulant therapy. The benefit is the decrease in stroke at the *Corresponding author: Nigel P Murray, Department of Medicine, University Finis Terrae, Providencia, Santiago, Chile, Tel: +56 274980507; E-mail: nigelpetermurray@gmail.com There are simple clinical tools to assess the benefits and risks of anticoagulant therapy using easily available clinical data in the older patient.To assess benefit due to stroke risk, the CHADS2 score (congestive heart failure, hypertension, age >75 years, diabetes mellitus and previous stroke or transient ischemic attack) is commonly used [7]. This tool which was developed in a population of elderly patients, gives one point for the presence of each risk factor and two points for a previous stroke or TIA. The risk of embolic stroke increases with each point of the CHADS 2 tool, from 1.9% annual stroke risk with 0 points to 18.2% anual stroke risk in patients with a score of 6 points [8]. Most guidelines recomend the use of anticoagulation in patients with a CHADS 2 score of 1 or greater. In a study of 773 patients older than 75 years with AF, 49% had congestive heart failure, 83% hypertension, 21% diabetes and 32% previous stroke or TIA [9]. Or in other words nearly all patients over 75 years meet the recomendations for anticoagulation.To assess the risk for hemorrhage there are three prediction tools; firstly the HAS-BLED score [10], which includes hypertension; abnormal renal/liver function, stroke, bleeding history or predisposition, Labile International Normalized Ratio, elderly (>65 years), drugs/alcohol concomitantly and has been incorporated into the European and Canadian guidelines on the management of patients with AF [6,11]. The HAS-BLED score is designed to estimate the 1 year risk of major bleeding (intracranial, hospitalization, hemoglobin decrease of >2gr/dl or need for transfusion) in patients older than 65 years. It is simple to use, and the trade-off in terms of the benefits and risks of oral anticoagulation demonstrates that in the majority of patients with AF, the risk of bleeding outweighs the potential benefit of anticoagulation if the HAS-BLED score excedes the CHADS2 2 score. The HEMO...

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Atrial Fibrillation in the Elderly

Cited by 31 publications

References 78 publications

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling

Acute cardiac disease in elder patients

Anticoagulation for Chronic Non Valvular Atrial Fibrillation in the Elderly: A Review

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Atrial Fibrillation in the Elderly

Cited by 31 publications

References 78 publications

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca2+signaling

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca2+signaling

Acute cardiac disease in elder patients

Anticoagulation for Chronic Non Valvular Atrial Fibrillation in the Elderly: A Review

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Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling