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This article has been accepted for publication and undergone full peer review but has not

been through the copyediting, typesetting, pagination and proofreading process which may

lead to differences between this version and the Version of Record. Please cite this article as

doi: 10.1111/bcp.13837

This article is protected by copyright. All rights reserved.

Atrial fibrillation and Human Immunodeficiency Virus type-1 infection: a systematic

review. Implications for anticoagulant and antiarrhythmic therapy.

Running title: Atrial fibrillation/flutter and HIV-1 infection

Daniele Pastori(1,2), Ivano Mezzaroma(3), Pasquale Pignatelli(1),

Francesco Violi(1), Gregory Y H Lip(2).

(1) Department of Internal Medicine and Medical Specialties, Sapienza University of Rome,

Rome, Italy.

(2) Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool

Heart & Chest Hospital, Liverpool, United Kingdom; and Aalborg Thrombosis Research

Unit, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark;

(3) Department of Translational and Precision Medicine, Sapienza University of Rome,

Rome, Italy.

Corresponding Author

Professor Gregory Y.H. Lip.

gregory.lip@liverpool.ac.uk

Conflict of interest statements: none.

Word count: 2404.

Keywords: atrial fibrillation; atrial flutter; HIV-1; antiretroviral; stroke; anticoagulants.

This article is protected by copyright. All rights reserved.

direct oral anticoagulant; NRTI: nucleoside reverse transcriptase inhibitor; PI: protease

inhibitor; RTV or r: ritonavir; TPV: tipranavir; VKA: vitamin K antagonist.

1. Introduction: cardiovascular disease risk in HIV-1 infection

The availability of highly effective antiretroviral therapy (ART) has resulted in markedly

improved survival for people with Human Immunodeficiency Virus type-1 (HIV-1) infection.

While HIV-1 related mortality is declining, the incidence of new cases of HIV-1 infection

remains stable, resulting in a growing number of older adults living with HIV-1 infection[1].

As a consequence of the increased life expectancy, the effects of aging on HIV-1 infected

persons have begun to be evident. In particular, long-term effects of HIV-1 infection, ART

use, and traditional risk factors, may be significant contributors to the increased risk of

premature cardiovascular disease (CVD) described in this population.

A pathogenic relevant role in CVD risk development is played by the chronic immune

activation and inflammation caused by HIV-1 infection itself[2]. Indeed, monocytes are an

important source of inflammatory mediators that promote CVD, even in treated HIV-1

patients[3]. Moreover, low CD4+ T cell count and/or failure to restore normal CD4+ T cell

counts during ART have been associated with the occurrence of CVD and increased risk of

morbidity and mortality due to CV events[4].

In addition, several antiretroviral drugs, such as nucleoside reverse transcriptase inhibitors

(NRTIs) and protease inhibitors (PIs), could result in an altered fat redistribution that

characterizes the so-called ‘lipodystrophy syndrome’ (subcutaneous fat tissue atrophy in the

face, limbs and buttocks and/or lipo-accumulation in different body districts, i.e., neck, trunk,

abdomen and viscera)[5]. These fat alterations were frequently associated with several

metabolic and endocrine disorders similar to those present during the metabolic syndrome

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