what are the risk factors that predispose an individual to suffer a stroke
J Geriatr Cardiol. 2017 Mar; 14(iii): 179–184.
Predisposing factors for atrial fibrillation in the elderly
Received 2017 Jan 25; Revised 2017 Mar 10; Accustomed 2017 Mar 20.
Abstruse
Atrial fibrillation (AF) in the elderly occurs every bit a consequence of cardiovascular crumbling and an age related increase of comorbidity. Several predisposing factors for AF have been identified for the overall AF population. Near of them, cardiovascular disease in detail, play a function in younger and older patients. The longer fourth dimension menstruum during which these risk factors can crusade structural changes that ultimately atomic number 82 to AF may, at least in part, explicate the association betwixt age and AF. In addition, less well defined historic period-related changes in cellular electrophysiologic properties and structure predispose to AF in the elderly.
Keywords: Atrial fibrillation, Atrial fibrosis, Mechanisms, Risk factors, Stroke, The elderly
1. Introduction
Atrial fibrillation (AF) is the most frequent clinically significant arrhythmia and its incidence is continuously rising.[1] This increment is at least in part due to the aging of the population. Studies have also demonstrated an increase in AF incidence after age adjustment, which is probably a reflection of comorbidities and cardiovascular take chances factors, in addition to other factors such equally lifestyle changes.[1] , [2] It is expected that in the Eu the number of subjects age ≥ 55 years with AF will more than than double between 2010 and 2060, from 8.8 to 17.ix million.[iii] Likewise, information technology is expected that in the Us more than five.6 one thousand thousand people will have AF in 2050, and one-half of them will be older than 80 years.[4] The anticipated increase in AF may too be related to an before and more frequent diagnosis beyond all historic period groups due to meliorate awareness of the arrhythmia and its complications and more than frequent ECG monitoring over longer periods of time. In add-on, improved treatment and afterward improved survival of patients with cardiovascular disease may pb to an increase in individuals with AF compared to the by.
The association of AF with increasing age is well recognized and has been shown by several epidemiological studies.[5] – [7] The risk of developing AF doubles with each progressive decade of gaining and exceeds xx% by age eighty years.[8] Although important and well established, historic period is not the only take a chance gene associated with AF. The arrhythmia shows wide heterogeneity regarding comorbidities and historic period.[9] While it is observed ofttimes in older patients, it is also observed in immature people and those without any comorbidity.
AF etiology in the elderly likely differs from younger patients.[x] The EORP-AF general pilot registry was designed to proceeds information regarding AF direction in Europe. Based on these registry data, Fumagalli, et al.,[11] analyzed differences in presentation, co-morbidities and treatment of AF co-ordinate to age. One third of patients in this registry, more than than yard were ≥ 75 years of historic period. Older patients more often had persistent or permanent AF compared with younger patients. They besides had a higher prevalence of comorbidities, including coronary avenue illness, chronic centre failure including a substantial proportion of patients with middle failure with preserved ejection fraction, chronic kidney affliction, chronic obstructive pulmonary disease (COPD), valvular heart disease and hypertension. Previous hemorrhagic events and transient ischemic attack (TIA) were reported more than often in older patients. All these comorbidities led to college CHAtwoDS2-VASc and HAS-BLED scores. With regard to symptoms, older patients reported palpitations less frequently, but reported dyspnea more often. They appeared to do better with rate rather than rhythm command,[12] which was also the preferred management in older patients.[11]
This article summarizes run a risk factors for AF and associated pathophysiological changes, both in the general AF population, and with respect to the elderly patient.
2. Risk factors for development of AF
For the overall population, several take chances factors for AF development have been identified. They all contribute to AF, each factor individually, and in combination with each other.[13] Risk factors for incident AF (subsequently age-aligning) in the Framingham cohort were cigarette smoking, diabetes mellitus, hypertension, and prevalent CAD. Combined, they explained 44% of the brunt of AF in men and 58% in women.[14] The accented and attributable risks of AF in relation to optimal and borderline risk factors were studied in The Atherosclerosis Risk in Communities (ARIC) Written report.[fifteen] Overall, 56.5% of AF cases could be explained by i borderline or elevated risk factor of which elevated claret pressure level was the near important correspondent.[xvi] Thus, in a high number of cases, AF is associated with acquired take chances factors that should be amenable to preventive measures.
While some risk factors are well established, others are rather new. Because different adventure factors may cause the same electrical and structural changes that predispose for AF and several factors are oft present in an individual patient, quantification of a given factor's specific impact on AF development is a futile effort.
Beyond all historic period groups, the incidence of AF is higher in men than in women.[5] It is unknown whether this difference is due to sex itself or just a phenomenon of nether-diagnosed AF in women and/or over-diagnosed AF in men due to different symptom intensity or/and differing medical attention. Hypertension is the number one take chances factor globally.[ii] The higher the blood pressure, the greater is the risk for incident AF.[xiii] , [17]
Like hypertension, heart failure is associated with an increment in atrial pressure and/or volume overload and diastolic ventricular dysfunction, which may lead to atrial dilatation and fibrosis, the electrical and structural changes providing the ground for AF development. While hypertension is an important and well established take chances factor for AF, heart failure is less well defined and has non been studied as extensively. Valvular heart affliction, particularly left sided disease, leads to atrial pressure and volume overload and is associated with AF evolution. Both passive atrial stretch and an increase in atrial pressure during atrial contraction have been institute to stimulate the release of atrial natriuretic gene. The level of this neurohormonal activation was found to be a predictor of paroxysmal AF. Diabetes mellitus and hyperthyroidism take also been recognized as independent gamble factors for AF. Coronary artery illness and chronic kidney disease are risk markers for AF as well.[fourteen] , [xviii] Loftier body mass index (BMI) which is oft associated with slumber apnea ranks 6th in the global list.[2] High BMI is also associated with increased left atrial book. COPD appears to be associated with progression from paroxysmal to persistent and permanent AF.
Less well-established take chances factors are tall stature, increased epicardial fat, loftier birth weight, booze consumption, smoking and loftier-level endurance training. Obesity has recently received increasing attention every bit a take chances factor for AF based on epidemiological, mechanistic and clinical prove.[19] It carries a strong link to metabolically agile atrial epicardial fat tissue.[xx]
Genetic factors, both monogenic and polygenic, have recently been identified as adventure factors for AF. A positive family unit history of AF about doubles the run a risk of developing AF.[21] Early-onset AF in particular appears to accept a potent heritable component that is independent of concomitant cardiovascular weather.[22] , [23] Upwards to one third of AF patients comport common genetic variants that predispose to AF.
Inflammation has been suggested as pathophysiological mechanism in AF evolution and perpetuation.[24] The causal role of inflammation in structural atrial damage has been reinforced by experimental studies.[23] Inflammation has been studied predominantly in post-operative AF, and its office is less well established for other forms of AF.
Left atrial (LA) enlargement has also been described every bit risk factor for AF.[18] In a report past Tsang, et al.,[25] LA volume was confirmed to be independent of both clinical take chances factors and diastolic role profile for the prediction of AF. Whether LA enlargement is the hen or the egg with regard to AF is not known, only patients with new onset of AF were included in the study. Still information technology is possible that patients already had asymptomatic episodes of AF over some time that led to left atrial enlargement.
There is also an association between sick sinus syndrome (SSS) and AF. Like AF, SSS is diagnosed more often in men, increases with age and is associated with several cardiovascular risk factors like hypertension, diabetes and higher body mass index.[26] In addition, SSS tin can have a genetic background. It can manifest as bradycardia with or without tachycardia-bradycardia syndrome.[27] Both forms of SSS, with and without tachycardia-bradycardia syndrome, are correlated with severe structural and electrical remodeling, thereby predisposing for AF.
Recently, advanced interatrial block, kickoff described by Bayes de Luna., et al.,[28] has been shown in the ARIC study to be associated with an increased risk for AF after aligning for socio-demographics, cardiovascular take a chance factors, and potential confounders.[29]
Cardiovascular comorbidities and other risk factors too every bit AF itself induce a slow but progressive procedure of structural remodeling in the atria.[22] Activation of fibroblasts, enhanced connective tissue degradation, and fibrosis are the hallmarks of this process. In addition, atrial fat infiltrations, inflammatory infiltrates, myocyte hypertrophy, necrosis and amyloidosis are found in patients with concomitant atmospheric condition predisposing to AF. In many patients, the structural remodeling procedure occurs before the onset of AF.[22] In addition to structural changes, AF induces electrical and autonomic tone remodeling. The relative contribution of underlying primary conditions versus AF itself to the clinical progression of AF is presently unclear.[30]
In the High german Atrial Fibrillation Network (AFNET) registry, the likelihood that patients had persistent or permanent AF increased with the number of risk factors in a given patient.[31] The "HATCH" score, including the run a risk factors eye failure, age, previous TIA or stroke, COPD and hypertension, was proposed to identify patients with AF progression.[32] This emphasizes the fact that several risk factors typically coexist and act in combination.
The impact of each risk factor may vary by historic period. Genetic factors, obesity and endurance sports likely play a larger role in younger patients, while other factors are more prevalent and relevant in older patients. Their contribution to AF in an individual patient, especially in combination with the risk factor "historic period" which discussed below, is unknown, but likely depends on affliction severity and consequent handling.
3. "Age" every bit a risk factor for AF
Crumbling involves a relentless and systematic process of degeneration in living organisms leading to attenuation of about biochemical and physiological functions.[33] "Historic period" as risk gene remains to be defined and the charge per unit at which aging occurs is unlike between individuals. Virtually studies ascertain "elderly" every bit those patients older than 65 years.[18] At the aforementioned time, it is generally accepted that calendar historic period and biological age are not synonymous. At least from an epidemiological standpoint, in that location is a marked increase in AF between sixty and 65 years (Figure i).[33]
Depiction of the AF prevalence in different studies.
There is a steep increase in AF prevalence across all studies between 60 and 65 years of age (blood-red line). Adjusted from citation [31] with permission. AF: atrial fibrillation.
It is well known that aging increases the propensity for occurrence of AF.[34] , [35] The pathophysiologic mechanisms, though, by which aging increases the likelihood for AF development remain poorly understood.[36] A longer time flow during which the atrial myocardium is exposed to external stressors, i.e., risk factors, probable plays a function in the association of age and AF likewise. Most elderly patients nowadays with ane or more than comorbidities. It appears very difficult if non incommunicable to distinguish the affect of these comorbidities from truthful "age" related factors.
At that place are only limited experimental and fifty-fifty less clinical data that chronicle to "age" equally a predisposing factor for AF despite the overwhelming evidence of the shut association between increasing age and AF. While AF generally is more prevalent in men than in women in the AFNET registry, women outnumber men in the historic period group above 80years,[31] probable because they live longer than men. Since men typically acquire more cardiovascular risk factors, it could exist hypothesized, that theses comorbidities play a larger function for AF than the hazard cistron "age".
The atrial myocardium undergoes electric and structural remodeling with age, both of which may play an of import role in the initiation and/or perpetuation of atrial arrhythmias.[34] , [37] Changes in atrial tissue structure appear to be of major importance in providing a substrate for AF.
Structurally aged atrial bundles are characterized past enhancement of the fibrous tissue that is interspersed between myocytes.[34] Cardiac fibrosis is characterized by excessive accumulation of fibrillary collagen in the extracellular space. It may result from historic period-dependent cardiomyocyte loss (replacement fibrosis),[38] or it may be an interstitial response to chronic diseases such as hypertension, myocarditis, and congestive heart failure (reactive fibrosis).[34] Fibrosis is ubiquitous in the atria of the aging centre and the authentication of the structural AF substrate.[xxx] Both, increased non-compatible atrial interstitial fibrosis[39] and atrial conduction slowing have been shown in patients with AF.[40]
Age-related electrical changes due to ionic current alterations include modifications in the cellular activity potential shape and elapsing as well equally an enhanced dispersion of cardiac repolarization.[34] This has been shown in canine models and in homo tissue. Anyukovsky, et al.,[41] showed that conduction velocity for premature beats was reduced in older canine hearts and occurred during a wider time window. Again, they constitute a twofold increase in the amount of fibrous tissue. In a rat model, Hayashi, et al.,[42] showed that old rats had significantly longer interatrial conduction fourth dimension and P moving ridge durations compared with immature rats. AF was inducible in erstwhile rats, simply not young rats. As reported past others, histology revealed a meaning increase in interstitial atrial fibrosis, atrial cell size, and eye weight.
Arterial stiffness increases with age and predicts coronary avenue disease, stroke and mortality.[43] Fumagalli, et al.,[44] reported a significant association between arterial stiffness (measured equally cardio-ancle vascular alphabetize on both upper and lower extremities) and historic period in a pocket-sized group of patients. Of note, this alphabetize was not afflicted by hypertension, coronary artery illness, cerebrovascular disease, chronic renal failure and heart failure, all known to exist risk factors for AF. Arterial stiffness was also associated with increased left atrial diameters, but the verbal interaction between arterial stiffness, left atrial and left ventricular backdrop (i.e., stiffness) could not be fully explained by their observations. The majority of AF cases may be the issue of risk factors causing increased arterial stiffness, diastolic dysfunction, and atrial book overload.[45] , [46] Recently, the association between historic period-related arterial stiffness and persistence or recurrence of AF has been studied.[46] For each one-unit increase in cardio-ancle vascular index, the gamble of finding AF at the command visit was 2.31 times higher. When using pulse pressure as marker of arterial stiffness, participants of the Framingham Centre Study were found to have an increased run a risk for AF besides.[47]
Diastolic left ventricular dysfunction with aberrant left ventricular relaxation is very common in the elderly and has been regarded equally office of the normal aging procedure.[48] Although this form of left ventricular relaxation aberration is considered the mildest i, patients with this form of diastolic dysfunction take a greater adventure for AF independent of the effects of age. Pathophysiologically, LV relaxation abnormalities may lead to the evolution of higher atrial pressures during atrial diastole past reducing passive LA emptying. Over time, LA and pulmonary veins could amplify and potentiate electric and structural remodeling thereby increasing vulnerability to AF. In a study by Tsang, et al.,[25] the diastolic dysfunction profile was incremental to clinical chance factors and left atrial volume. Furthermore, the gradient of risk appeared to be related to the severity of diastolic dysfunction.
4. AF progression
AF is typically seen every bit a progressive arrhythmia, where structural and electrophysiological changes lead to persistent and permanent AF over time. This progression, though, differs widely between patients. Progression of AF from paroxysmal to persistent is faster in older patients and those with underlying center disease.[xxx] , [49] Saksena, et al.,[50] analyzed data of patients (mean age of 70 ± 10 years) with paroxysmal AF and a dual chamber pacemaker. AF progression was observed in 24% of patients and associated with a progressive increase in AT (atrial tachyarrhythmia)/AF burden. This increase was highly correlated with the presence of structural middle disease, which was interpreted equally a relation between AF progression and substrate rather than trigger-based progression. However information technology remains unclear, why paroxysmal AF may remain cocky-terminating for decades in some patients, but progresses to persistent AF inside weeks in others.[l]
Footnotes
This article is role of a Special Issue "Atrial fibrillation in the elderly".
Guest Editors: Manuel Martínez-Sellés & Antoni Bayés de Luna
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Articles from Journal of Geriatric Cardiology : JGC are provided here courtesy of Constitute of Geriatric Cardiology, Chinese PLA General Hospital
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5460064/
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