Atrial cardiomyopathy is a new concept proposed in recent years. Comprehensive category. Atrial cardiomyopathy is the atrial matrix that occurs in atrial fibrillation and stroke. It is closely related to atrial fibrosis. Atrial fibrillation, atrial fibrosis and atrial cardiomyopathy form an organic whole. Such changes in the atrial matrix can be caused by long-term persistence of atrial fibrillation (AF), or may precede atrial fibrillation as a potential factor in the development and maintenance of atrial fibrillation, or even induce stroke independently of atrial fibrillation. It can be said that the introduction of the concept of atrial cardiomyopathy provides a new entry point for elucidating the pathogenesis of atrial fibrillation and stroke, and explores the mode of prevention and management of atrial fibrillation and stroke. It has also become a new challenge.
Definition
Proposed by Kottkamp et al in 2012, atrial cardiomyopathy is used to describe a specific form of bi-atrial pathology characterized by is extensive fibrosis as the basis for atrial arrhythmias and thromboembolism.
2016 EHRA/HRS/APHRS/SOLAECE expert consensus defines atrial cardiomyopathy as: Atrial cardiomyopathy that affects atrial structure, contractility, or electrophysiological characteristics, and leads to atrial remodeling, conduction abnormalities and other related clinical manifestations of a disease. At the same time, atrial cardiomyopathy was proposed as a term to describe atrial stromal and functional abnormalities, including atrial fibrosis, atrial mechanical dysfunction, atrial electrophysiological dysfunction, and hypercoagulability.
Classification
1. Mainly cardiomyopathy (type 1)
Definition: Histologically manifested as cardiomyocyte hypertrophy, cardiomyocyte lysis, etc., without obvious fibrosis.
more common in isolated atrial fibrillation, diabetes.
2. Mainly fibrotic lesions (type 2)
Definition: Histologically manifested as interstitial fibrosis with relatively normal cardiomyocytes.
more common in aging, smoking.
3. Both cardiomyopathy and fibrosis (type 3) >
Definition: Histologically manifested as the coexistence of cardiomyocyte lesions (cardiomyocyte hypertrophy, cardiomyocyte lysis) and interstitial fibrosis.
more common in heart failure, valvular heart disease.
4. with myocardial changes)
Definition: Histologically manifested as non-fibrotic changes in the interstitium of myocardial cells.
It is more common in isolated atrial amyloidosis, granulomatous lesions, and inflammatory infiltration.
cause
>
1. Solitary atrial fibrillation
Low risk of thromboembolism, about 15 years of cumulativeThe risk of stroke is only 1%-2%.
Most of them present as paroxysmal atrial fibrillation at first, and rarely develop into permanent atrial fibrillation
2. Solitary atrial amyloidosis
The incidence rate increases with age and exceeds 90% in the 90-year-old age group
3. ANP precursor protein encoding gene (NPPA) mutation
4. Hereditary muscular dystrophy
5. Congestive heart failure
6. Obstructive sleep apnea
7. Atrial fibrillation induction
8. Drug-related atrial fibrillation
9. Myocarditis
10. Hypertension
11. Advanced age
12. Hereditary repolarization disorder< /span>
SCN5A and connexin-40 gene heterozygous combined mutation
13.Obesity
< p>14. Diabetes
15. Valvular Heart Disease
Pathophysiology
1. Oxidative stress
Oxidative stress is the core mechanism of atrial structural and electrical remodeling in atrial fibrillation , resulting in shortened action potential duration, cardiomyocyte apoptosis, and endothelial cell remodeling (promoting thrombosis).
2. Inflammatory pathway activation
The interaction of atrial fibrillation, CaMKII, and NLRP3 inflammasome leads to structural remodeling, especially fibrosis, and induces cell damage and apoptosis, which in turn leads to atrial enlargement.
strong Atrial endocardial remodeling diabetes, heart failure and other CHA2DS2-VASc risk factors can increase the activation of oxidative stress pathway in endothelial cells, thereby further increasing the prothrombotic Expression of forming molecules, atrial endocardial remodeling is responsible for thrombosis and stroke. clinical manifestations 1. Atrial fibrillation and atrial tachycardia Atrial fibrillation and atrial tachycardia can lead to atrial electrical remodeling, Long-term atrial tachycardia can lead to atrial fibrosis, and atrial structural changes can perpetuate atrial fibrillation, so the two are mutually exacerbating factors. 2. Elevated biomarkers myeloperoxidase (MPO) , C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and other factors increased expression levels. 3. Thrombosis and Stroke Patients with atrial cardiomyopathy may have abnormal vessel walls (Structural heart disease), abnormal blood flow (turbulent or slow blood flow) and abnormal blood components (platelets, inflammatory factors, etc.), these three points constitute the three elements of thrombosis. P-wave terminal potential in lead V1 and NT-proBNP were associated with stroke risk, while left atrial size was not associated with stroke risk. Imaging 1. Echocardiography Due to the complex morphology of the atrial and the heterogeneous atrial remodeling, measurement of atrial diameter cannot accurately assess atrial size, so measurement of atrial volume is recommended. The upper limit of the left atrium is 34ml/m2 (for both men and women). 2. Doppler echocardiography Left atrial function can be measured by pulse wave Determination of late diastolic (mitral valve A wave) filling for evaluation 3. Cardiac CT < span> It can be used to accurately assess atrial volume and to screen for thrombus before ablation of atrial fibrillation. 4. Atrial Magnetic Resonance Cardiac Magnetic Resonance (CMR) has become an atrioventricular The gold standard for structural and functional assessment. Gadolinium contrast-enhanced CMR can effectively detect atrial fibrosis. 5. Electroanatomical Mapping Imaging (EAM) < span>Invasive imaging technology, but with very good clinical operability and imaging advantages, can clearly describe the atrial matrix of atrial fibrillation, atrial flutter, and atrial tachycardia. Treatment
1. Cause treatment: Manage hypertension, diabetes, obesity, valve disease , heart failure, myocarditis, obstructive sleep apnea, genetic diseases and other risk factors
2.
3. Shorten the duration of atrial fibrillation, which may lead to atrial remodeling if the duration of atrial fibrillation is too long< /p>
4. Aggressive anticoagulation therapy to reduce the risk of thromboembolism
References
[1] Goette A, Kalman JM, Aguinaga L, Akar J, Cabrera JA, Chen SA, Chugh SS, Corradi D, D’Avila A, Dobrev D, Fenelon G, Gonzalez M, Hatem SN, Helm R, Hindricks G, Ho SY, Hoit B, Jalife J, Kim YH, Lip GY, Ma CS, Marcus GM, Murray K, Nogami A, Sanders P, Uribe W, Van Wagoner DR, Nattel S; Document Reviewers:. EHRA/HRS/APHRS/ SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication. Europace. 2016 Oct;18(10):1455-1490. doi: 10.1093/europace/euw161. Epub 2016 Jul 8. PMID: 27402624; PMCID: PMC6392440< /span>.
[2] Goette A, Lendeckel U. Atrial Cardiomyopathy: Pathophysiology and ClinicalConsequences. Cells. 2021 Sep 30;10(10):2605. doi: 10.3390/cells10102605. PMID: 34685585; PMCID: PMC8533786.
Disclaimer: This article is original content, authorNuoxinto, only for learning and communication, and reprinting requires authorization.
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