Abstract
Atrial cardiomyopathy (ACM) represents a constantly evolving concept, with increasing importance in contemporary research and clinical practice. A better understanding of the mechanisms involved in atrial remodeling and its clinical correlations especially with atrial fibrillation (AF) and other cardiometabolic comorbidities may induce a significant impact on the diagnosis, prognosis, and therapeutic approach of ACM-related comorbidities. Although initially described several decades ago, investigators have only recently highlighted that several renal, metabolic, and cardiovascular diseases are determining factors for atrial remodeling and subsequent ACM. Based on data from multiple recent studies, our research emphasizes the correlations between ACM and other coexisting pathologies including cardiovascular, respiratory, or metabolic diseases, with fibrosis being the most incriminated pathophysiological mechanism. In addition to the usual tests, the paraclinical assessment of ACM is increasingly based on the use of various cardiac biomarkers, while the cardiac magnetic resonance (CMR) has become an increasingly tempting diagnostic too for describing morphofunctional aspects of the heart chambers, with the gadolinium contrast enhanced CMR (LGE-CMR) emerging as a commonly used technique aiming to identify and quantify the precise extent of atrial fibrosis. Further research should be conducted in order to clarify our knowledge regarding atrial remodeling and, therefore, to develop new and improved therapeutic approaches in these patients.
Highlights
Definitions and ClassificationAtrial cardiomyopathy (ACM) and its clinical importance were first described in 1972 by Nagle et al [1] in a study about a familial pathology concerning the atria, with first-degree heart block and supraventricular tachycardia degrading to a persistent atrial standstill
Diagnostics 2021, 11, x Diagnostics 2021, 11, 449 in many pathologies, such as hypertension, chronic heart failure (CHF), coronary artery disease, obesity, or D3 oMf 1.6 A number of studies indicate that oxidative reactions and chronic inflammation present in the conditions mentioned above can lead to atrial fibrillation; they are present as a mechanism of endothelial dysfunction and arterial damage in hypertension [9,13]. menAtitorinaeldfuanboctvioencaalnrleemadodtoelaintrgiailsfiebnrcilolautniotenr;etdheiyn amreanalysoppatrheoselongtiacsalasmysetcehmaincispmroo-f ceesnsdeostahnedliacladnycsafuunsectaioltneraantdionarsteinriaaltrdiaalmfuagnectiinonhiynpgerretegnasridolnes[s9,o1f3]t.he left atrium (LA) size [7,9]
Fibrosis is the most important pathophysiological mechanism of atrial remodeling, its accurate assessment representing the foundation for an adequate therapeutic approach and an improved long-term prognosis
Summary
Atrial cardiomyopathy (ACM) and its clinical importance were first described in 1972 by Nagle et al [1] in a study about a familial pathology concerning the atria, with first-degree heart block and supraventricular tachycardia degrading to a persistent atrial standstill. The aim of this review is to depict some coordinates of ACM, from the molecular level to the therapeutic approach, for a better understanding of the mechanisms involved in atrial remodeling. The EHRA histopathological classification was proposed for a better understanding of these differences that may influence the disease evolution and subsequent management. This descriptive classification does not provide information about the clinical severity or progression of the disease. Class I: primarily cardiomyocyte changes (isolated AF, genetic diseases, and DM); Class II: predominantly fibrotic changes (cigarette smokers and the elderly); Class III: combined cardiomyocyte-pathology/fibrosis (CHF and valvular pathology); Class IV: primarily non-collagen infiltration, with or without cardiomyocyte changes (accumulation of amyloid, fatty ACM, and inflammatory infiltrates) [2]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
