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

• Published in: Life (Basel, Switzerland) Switzerland), 2023-02, Vol.13 (2), p.443
• Main Authors: Afrăsânie, Irina, Matei, Iulian Theodor, Leancă, Sabina Andreea, Chetran, Adriana, Costache, Alexandru Dan, Afrăsânie, Vlad-Adrian, Dmour, Bianca-Ana, Crișu, Daniela, Bădescu, Minerva Codruța, Șerban, Lăcrămioara Ionela, Costache, Irina Iuliana
• Format: Article
• Language: English
• Subjects: Adenosine; Angina; Angina pectoris; atrial cardiomyopathy; Atrial fibrillation; Cardiac arrhythmia; Cardiomyopathy; Cardiovascular disease; Care and treatment; Comorbidity; Congestive heart failure; Coronary artery disease; Coronary heart disease; coronary microvascular dysfunction; Coronary vessels; Diagnosis; endothelial dysfunction; Endothelium; Heart diseases; Heart failure; Hypertension; Inflammation; INOCA; Ischemia; Microvasculature; Questions; Review; Risk factors; Shear stress; Signs and symptoms; Sleep apnea; Smooth muscle; Structure-function relationships; Thromboembolism; Thrombosis; Vein & artery diseases; Weight control
• ISSN: 2075-1729; 2075-1729
• DOI: 10.3390/life13020443

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.