New Biomarkers and Risk Stratification in Atrial Fibrillation

Griffiths, Helen R.; Lip, Gregory Y.H.

doi:10.1161/circulationaha.114.012870

Cited by 11 publications

(9 citation statements)

References 19 publications

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“…In AF patients, it was found that most of the previously described risk factors of the vascular dysfunction are elevated [10][11][12]. AF is also strongly associated with elevated thromboembolic risk.…”

Section: Introductionmentioning

confidence: 94%

Can thromboembolic risk be associated with erectile dysfunction in atrial fibrillation patients?

et al. 2015

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Section: Introductionmentioning

confidence: 94%

Can thromboembolic risk be associated with erectile dysfunction in atrial fibrillation patients?

et al. 2015

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“…Although one might assume that biomarker abnormalities would simply reflect the degree of comorbidity severity, such as LV dysfunction, hypertrophy, inflammation, fibrosis and the like, [39][40][41][42] and therefore would have to be increased in patients with higher CHA 2 DS 2 -VASc scores and higher stroke risk, it is of interest that in the dabigatran versus warfarin AF trial where this was examined, troponin I and NT-proBNP levels were additive to the CHADS 2 score in correlating with stroke and systemic embolism, pulmonary embolism, myocardial infarction and non-hemorrhagic vascular death. 40 The biomarkers raised the c-statistic for these endpoints from 0.68 to 0.72 (p<0.0001).…”

Section: Biomarkersmentioning

confidence: 99%

Optimum Risk Assessment for Stroke in Atrial Fibrillation: Should We Hold the Status Quo or Consider Magnitude Synergism and Left Atrial Appendage Anatomy?

Reiffel

2017

Arrhythmia &Amp; Electrophysiology Review

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Thromboembolic stroke and systemic embolism are generally agreed to be the major morbidity/mortality concerns for patients with AF.However, the risk of thromboembolism (TE) is not the same for all AF patients. While ECG rhythm strips of patients with AF are generally indistinguishable, it has long been known that AF in younger patients without co-morbid factors ("lone AF") carries an extremely low risk for TE, whereas AF in older patients in the presence of specific comorbidities carries a high TE risk.1,2 Thus, AF alone cannot sufficiently explain the risk. However, it has also been long known that older patients with conditions such as hypertension, diabetes and atherosclerotic disease also have an important risk for stroke, even in the absence of AF, 3,4 but that these same conditions in the presence of AF have been associated with a two to seven times greater risk of stroke than when AF is absent. 5 Thus, the comorbidities themselves also do not fully explain the total risk. Consequently, both AF and comorbidities must interact synergistically to magnify the risk for TE.But, is the synergism dichotomous -AF present or absent, comorbid disorder present or absent -or does synergism have magnitude, depending on the number and severity of the associated disorders and the amount of time one is in AF (AF burden, AFB)? I believe the latter is the case and that clinical trials addressing this point are warranted.Moreover, left atrial appendage (LAA) anatomy and the risk for stasis therein may also be a contributory factor to cardioembolic risk in AF.Thus, the line from AF to stroke is far from straight.To best understand the risk for TE in patients with AF, both synergism and the magnitude of the underlying components must be recognised.Historically, based on the presence of specific comorbidities, we have determined the risk for TE in AF patients as being either high enough to warrant prophylactic chronic oral anticoagulation (OAC) or too low to justify the risk of OAC-associated bleeding. A decade or so ago, such risk was assessed by determining the CHADS 2 score (Table 1), congestive heart failure, a history of hypertension, age 75 years or higher, diabetes (each 1 point), or prior thromboembolic event, e.g. ischemic stroke (2 points), and the paradigm was to determine from the score calculated which AF patients were at high enough risk to warrant OAC -generally agreed to be a score of 2 or more. 2 More recently, as we have recognised that stroke is much more likely to be fatal or debilitating than is bleeding, and as we have developed newer oral anticoagulants with preferable efficacy and safety profiles as compared to warfarin, the paradigm has shifted. We now ask which AF patients are at too low a score to warrant avoidance of OAC, with the rest having OAC indicated, and current guidelines 1,2 recommend the CHA 2 DS 2 -VASc score (Table 1), congestive heart failure, history of hypertension, age 65-74 years (each 1 point) or 75 years and above (2 points), vascular disease and female gender (each 1 point) to mak...

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“…28 The HAS-BLED score should not be used to exclude patients from OAC therapy, but to address modifiable bleeding risks. 32 In summary, initiation of OAC therapy should be based on the individual assessment of stroke risk. According to the European Society of Cardiology (ESC) guidelines, in AF patients with a CHA 2 DS 2 -VASc score of 0 in males or 1 in females (annual stroke risk <1 %/year), initiation of OAC therapy is not recommended.…”

Section: Assessment Of Bleeding Riskmentioning

confidence: 99%

Individualising Anticoagulant Therapy in Atrial Fibrillation Patients

Alings

2016

Arrhythmia &Amp; Electrophysiology Review

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Non-vitamin K antagonist (VKA) oral anticoagulants (NOACs) have emerged as alternatives to VKAs for the prevention of stroke in patients with non-valvular atrial fibrillation. Four NOACS: dabigatran, apixaban, rivaroxaban and edoxaban, have received regulatory approval in Europe from the European Medicines Agency. Numerous factors can influence the decision to prescribe a NOAC, the most important of which are assessment of stroke and bleeding risks. Given the variation in design of the pivotal phase III clinical trials investigating the efficacy and safety of NOACs, and in the absence of head-to-head comparative data, it is impossible to recommend one NOAC over the other. However, NOACS offer the opportunity for individualised therapy based on factors such as renal function, age or patient/doctor preference for once- or twice-daily dosing regimens. Dose reduction of some NOACS should be considered in at-risk patient populations.

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New Biomarkers and Risk Stratification in Atrial Fibrillation

Cited by 11 publications

References 19 publications

Can thromboembolic risk be associated with erectile dysfunction in atrial fibrillation patients?

Can thromboembolic risk be associated with erectile dysfunction in atrial fibrillation patients?

Optimum Risk Assessment for Stroke in Atrial Fibrillation: Should We Hold the Status Quo or Consider Magnitude Synergism and Left Atrial Appendage Anatomy?

Individualising Anticoagulant Therapy in Atrial Fibrillation Patients

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