Ischemia with Nonobstructive Coronary Artery Disease and Atrial Cardiomyopathy—Two Sides of the Same Story?

Author:

Afrăsânie Irina12,Matei Iulian Theodor12,Leancă Sabina Andreea12ORCID,Chetran Adriana12,Costache Alexandru Dan23ORCID,Afrăsânie Vlad-Adrian45,Dmour Bianca-Ana2ORCID,Crișu Daniela1,Bădescu Minerva Codruța26ORCID,Șerban Lăcrămioara Ionela7,Costache Irina Iuliana12

Affiliation:

1. Cardiology Clinic, “St. Spiridon” County Clinical Emergency Hospital, 700111 Iași, Romania

2. Department of Internal Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iași, Romania

3. Department of Cardiovascular Rehabilitation, Clinical Rehabilitation Hospital, 700661 Iași, Romania

4. Department of Medical Oncology, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iași, Romania

5. Department of Oncology, The Regional Institute of Oncology, 700483 Iași, Romania

6. Internal Medicine Clinic, “St. Spiridon” County Clinical Emergency Hospital, 700111 Iași, Romania

7. Department of Physiology, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iași, Romania

Abstract

Ischemia with nonobstructive coronary artery disease (INOCA) is increasingly recognized as a significant cause of angina, myocardial remodeling, and eventually heart failure (HF). Coronary microvascular dysfunction (CMD) is a major endotype of INOCA, and it is caused by structural and functional alterations of the coronary microcirculation. At the same time, atrial cardiomyopathy (ACM) defined by structural, functional, and electrical atrial remodeling has a major clinical impact due to its manifestations: atrial fibrillation (AF), atrial thrombosis, stroke, and HF symptoms. Both these pathologies share similar risk factors and have a high comorbidity burden. CMD causing INOCA and ACM frequently coexist. Thus, questions arise whether there is a potential link between these pathologies. Does CMD promote AF or the reverse? Which are the mechanisms that ultimately lead to CMD and ACM? Are both part of a systemic disease characterized by endothelial dysfunction? Lastly, which are the therapeutic strategies that can target endothelial dysfunction and improve the prognosis of patients with CMD and ACM? This review aims to address these questions by analyzing the existing body of evidence, offering further insight into the mechanisms of CMD and ACM, and discussing potential therapeutic strategies.

Publisher

MDPI AG

Subject

Paleontology,Space and Planetary Science,General Biochemistry, Genetics and Molecular Biology,Ecology, Evolution, Behavior and Systematics

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