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Updated: Jun 25, 2026
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Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Age-related atrial fibrosis
Felix Gramley1, Johann Lorenzen, Christian Knackstedt
1Department of Cardiology & Vascular Medicine, II. Medizinische Klinik und Poliklinik, Klinikum der Johannes Gutenberg-Universität, Langenbeckstrasse 1, 55131, Mainz, Germany. gramley@hotmail.com
Age (Dordrecht, Netherlands)
|February 24, 2009
Summary
Age significantly increases cardiac fibrosis in the atria, impacting cardiovascular health. This study links aging to fibrotic signaling changes, reduced hypoxic signaling, and altered matrix metalloproteinase activity, promoting atrial fibrogenesis.
Area of Science:
- Cardiology
- Pathology
- Aging Research
Background:
- Cardiac fibrosis is linked to age-related diseases.
- Transforming growth factor-beta (TGF-beta), hypoxia-induced factor (HIF), and matrix metalloproteinase (MMP) systems are implicated in fibrogenesis.
Purpose of the Study:
- To investigate the relationship between age, cardiac fibrosis, and related molecular signaling pathways in the right atrial appendage (RAA).
Main Methods:
- Analysis of RAAs from 115 patients across different age groups.
- Quantification of fibrosis using Sirius-red staining.
- Measurement of TGF-beta, HIF1 alpha, VEGF-receptor, CD34, FIH, PHD3, MMP-2, MMP-9, and TIMP-1 levels using RT-PCR, immunostaining, and zymography.
Main Results:
- Older individuals (>70 years) exhibited significantly higher atrial fibrosis compared to younger patients (<50 years).
- Age was identified as the sole factor influencing fibrogenesis.
- Changes in fibrotic and hypoxic signaling, microvessel density, and MMP/TIMP-1 expression were observed with increasing age, favoring fibrosis.
Conclusions:
- Increasing age leads to significantly more fibrosis in the right atrial appendage.
- Altered molecular signaling, including increased fibrotic and decreased hypoxic signaling, along with differential MMP/TIMP-1 expression, contributes to age-related atrial fibrogenesis.
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