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World J Cardiol. Sep 26, 2018; 10(9): 87-96
Published online Sep 26, 2018. doi: 10.4330/wjc.v10.i9.87
Established and novel pathophysiological mechanisms of pericardial injury and constrictive pericarditis
Vinasha Ramasamy, Bongani M Mayosi, Edward D Sturrock, Mpiko Ntsekhe
Vinasha Ramasamy, Bongani M Mayosi, Edward D Sturrock, Mpiko Ntsekhe, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa
Vinasha Ramasamy, Edward D Sturrock, Department of Integrative Biomedical Sciences, University of Cape Town, Observatory 7925, South Africa
Bongani M Mayosi, Mpiko Ntsekhe, Division of Cardiology, University of Cape Town, Observatory 7925, South Africa
Author contributions: All authors contributed to the manuscript.
Supported by The University of Cape Town’ s Research Committee (URC) and the South African National Research Foundation (NRF).
Conflict-of-interest statement: No potential conflicts of interest relevant to this article were reported.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Mpiko Ntsekhe, FACC, MD, MPhil, PhD, Professor, Division of Cardiology, University of Cape Town, Anzio Road, Observatory 7925, South Africa. mpiko.ntsekhe@uct.ac.za
Telephone: +27-21-4046183
Received: February 8, 2018
Peer-review started: February 8, 2018
First decision: April 4, 2018
Revised: April 6, 2018
Accepted: April 18, 2018
Article in press: April 22, 2018
Published online: September 26, 2018
Processing time: 234 Days and 0.3 Hours
Abstract

This review article aims to: (1) discern from the literature the immune and inflammatory processes occurring in the pericardium following injury; and (2) to delve into the molecular mechanisms which may play a role in the progression to constrictive pericarditis. Pericarditis arises as a result of a wide spectrum of pathologies of both infectious and non-infectious aetiology, which lead to various degrees of fibrogenesis. Current understanding of the sequence of molecular events leading to pathological manifestations of constrictive pericarditis is poor. The identification of key mechanisms and pathways common to most fibrotic events in the pericardium can aid in the design and development of novel interventions for the prevention and management of constriction. We have identified through this review various cellular events and signalling cascades which are likely to contribute to the pathological fibrotic phenotype. An initial classical pattern of inflammation arises as a result of insult to the pericardium and can exacerbate into an exaggerated or prolonged inflammatory state. Whilst the implication of major drivers of inflammation and fibrosis such as tumour necrosis factor and transforming growth factor β were foreseeable, the identification of pericardial deregulation of other mediators (basic fibroblast growth factor, galectin-3 and the tetrapeptide Ac-SDKP) provides important avenues for further research.

Keywords: Inflammatory pericarditis; Autoimmune disease; Tuberculous pericarditis; Fibrosis mechanism; Constrictive pericarditis

Core tip: Constrictive pericarditis arises as a complication of pericarditis from a wide range of aetiologies. A comprehensive understanding of the fibrotic process eventually leading to pathological symptoms is currently lacking.Through this review of the literature, we have identified various molecular mediators which are likely to play a role in the establishment of constriction and which warrant further studies.