Arterial hypertension (HTN) and atrial fibrillation often coexist and the combination of these two conditions carries an increased risk of stroke. HTN is one of the most important risk factors included in the scores for stoke prediction in atrial fibrillation used to assess the need of anticoagulation, and HTN has also been strictly related to bleeding complications of antithrombotic therapy. Antithrombotic drugs options include vitamin K antagonists, or new oral anticoagulants, recently approved for stroke prevention in nonvalvular atrial fibrillation. More favorable new oral anticoagulant efficacy and safety, compared with warfarin, have been reported in hypertensive patients, making these drugs a first-line choice in this population to prevent cerebrovascular events and reduce the risk of major bleedings. The aim of this review is to explore the relationship among HTN, atrial fibrillation and the risk of stroke and to summarize the evidence on the impact of HTN on the choice of the most appropriate anticoagulation treatment.
aDepartment of Medical and Surgical Sciences, University of Bologna, Bologna
bIRCCS SDN, Institute of Research
cDepartment of Advanced Biomedical Sciences, Federico II University of Naples, Naples, Italy
Correspondence to Prof Pasquale Perrone Filardi, MD, PhD, Department of Advanced Biomedical Sciences, Federico II University of Naples, Via Pansini 5, 80131 Naples, Italy. Tel: +39 081 7462224; fax: +39 081 7462224; e-mail: firstname.lastname@example.org
Abbreviations: AF, atrial fibrillation; BP, blood pressure; CHA2DS2-VASc, congestive heart failure, hypertension, age ≥75 (doubled), diabetes, stroke (doubled), vascular disease, age 65–74, and sex category (female); CHADS, cardiac failure, hypertension, age, diabetes stroke; HAS-BLED, hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, Labile INR, elderly, drugs/alcohol concomitantly; HTN, hypertension; LV, left ventricular; LVH, left ventricular hypertrophy; NOACs, new oral anticoagulants; RAS, renin–angiotensin system; TOD, target organ damage
Received 29 June, 2016
Accepted 28 November, 2016