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Atrial myopathy: a pathogenic mechanism linking atrial fibrillation and ischemic stroke

Heart Science Journal · Vol. 6 No. 2 (2025)

DOI
10.21776/ub.hsj.2025.006.02.2
ISSN
2721-9984, 2721-9976
Terbit
2025-04-30
Penerbit
Universitas Brawijaya
Bahasa
en
Lisensi
creativecommons.org/licenses/by/4.0

Abstrak

Atrial myopathy (AM) has become a topic of study for many years. Atrial Myopathy is characterized as "any variety of architectural, structural, electrophysiological, or contractile abnormalities altering the atria, which can result in clinically significant manifestations," and is associated with atrial dysfunction and dilatation. Evidence shows that atrial myopathy (AM) contributes to atrial fibrillation and embolic strokes of unknown origin. Atrial myopathy or disease provides a substrate leading to atrial fibrillation (AF) and contributes to a chance of atrial thrombus development and, finally, stroke. However, following clinical trials have opposed this point of view. Additionally, ischemic strokes are categorized as cryptogenic when an embolic stroke occurs without a known related etiology (embolic stroke of undetermined source, ESUS). This led to the concept of atrial myopathy, showing that a dysfunctional atrium may result in stroke without the incidence of atrial fibrillation. Atrial interstitial fibrosis, extracellular matrix deposition, and inflammation may trigger and perpetuate atrial myopathy, resulting in blood stasis inside the atria and potentially resulting in stroke without any intervening atrial fibrillation. This paper describes an overview of Atrial Myopathy in pathogenic mechanisms linking atrial fibrillation and ischemic stroke. Atrial myopathy is not only a substrate for atrial fibrillation and makes thrombus formation cause ischemic stroke, but also leads to blood stasis within the atria and makes ischemic stroke without intervening atrial fibrillation.

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  • University of Brawijaya
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Rekan penulisOrganisasiArtikel bersama
Mohammad Saifur RohmanUniversity of Brawijaya20
Anna Fuji RahimahUniversity of Brawijaya12
Sasmojo WiditoUniversity of Brawijaya9
Novi KurnianingsihUniversity of Brawijaya9
Setyasih AnjarwaniUniversity of Brawijaya9
Indra PrasetyaUniversity of Brawijaya9
Heny MartiniUniversity of Brawijaya7
Djanggan SargowoUniversity of Brawijaya4
Cholid Tri TjahjonoUniversity of Brawijaya4
Adhika Prastya WikanandaUniversity of Brawijaya4
Wella KarolinaUniversity of Brawijaya4
Yoga WaranugrahaUniversity of Brawijaya3
Budi SatrijoUniversity of Brawijaya3
Icmi Dian RochmawatiUniversity of Brawijaya3
Puspa LestariUniversity of Brawijaya2
Olivia HandayaniUniversity of Brawijaya2
Fahmy RusnantaUniversity of Brawijaya2
Anita Surya SantosoAfiliasi tidak diketahui2
Fitranti Suciati LaitupaUniversity of Brawijaya2
Muhammad Saifur RohmanAfiliasi tidak diketahui2
Valerinna YogibuanaAfiliasi tidak diketahui2
Tri AstiawatiUniversity of Brawijaya2
Valerinna Yogibuana Swastika PutriUniversity of Brawijaya2
N KaputrinUniversity of Brawijaya2
Nikhen NoverikeUniversity of Brawijaya2
Gebryel Dennis SaerangUniversity of Brawijaya2
Vemmy Lian SaputriUniversity of Brawijaya2
Putri Annisa KamilaUniversity of Brawijaya1
Djanggan SargowoAfiliasi tidak diketahui1
Jonny Karunia FajarUniversity of Brawijaya1
Aditha Satria MaulanaUniversity of Brawijaya1
Aris Munandar Zulkifli IsmailUniversity of Brawijaya1
Anna Fuji RahimahAfiliasi tidak diketahui1
Aris Munandar ZIAfiliasi tidak diketahui1
Tonny AdriyantoUniversity of Brawijaya1
Seprian WidasmaraUniversity of Brawijaya1
Heny MartiniAfiliasi tidak diketahui1
Faris Wahyu NugrohoUniversity of Brawijaya1

Afiliasi berasal dari OpenAlex; metadata OAI-PMH jurnal tidak memuatnya. Penulis tanpa ID OpenAlex dicocokkan berdasarkan nama, sehingga dua orang bisa tergabung atau satu orang bisa terpisah.

Sumber metadata: OAI-PMH (metadata jurnal) https://heartscience.ub.ac.id/index.php/heartscience/oai, pertama di-harvest 8 Nov 2026, terakhir terlihat 8 Nov 2026.
Metadata asli (oai_dc)
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	<dc:title xml:lang="en">Atrial myopathy: a pathogenic mechanism linking atrial fibrillation and ischemic stroke</dc:title>
	<dc:creator xml:lang="en">Kahadi, Cik</dc:creator>
	<dc:creator xml:lang="en">Rizal, Ardian</dc:creator>
	<dc:subject xml:lang="en">Atrial Myopathy</dc:subject>
	<dc:subject xml:lang="en">Atrial Cardiomyopathy</dc:subject>
	<dc:subject xml:lang="en">Atrial Fibrillation</dc:subject>
	<dc:subject xml:lang="en">Ischemic Stroke</dc:subject>
	<dc:description xml:lang="en">Atrial myopathy (AM) has become a topic of study for many years. Atrial Myopathy is characterized as "any variety of architectural, structural, electrophysiological, or contractile abnormalities altering the atria, which can result in clinically significant manifestations," and is associated with atrial dysfunction and dilatation. Evidence shows that atrial myopathy (AM) contributes to atrial fibrillation and embolic strokes of unknown origin. Atrial myopathy or disease provides a substrate leading to atrial fibrillation (AF) and contributes to a chance of atrial thrombus development and, finally, stroke. However, following clinical trials have opposed this point of view. Additionally, ischemic strokes are categorized as cryptogenic when an embolic stroke occurs without a known related etiology (embolic stroke of undetermined source, ESUS). This led to the concept of atrial myopathy, showing that a dysfunctional atrium may result in stroke without the incidence of atrial fibrillation. Atrial interstitial fibrosis, extracellular matrix deposition, and inflammation may trigger and perpetuate atrial myopathy, resulting in blood stasis inside the atria and potentially resulting in stroke without any intervening atrial fibrillation. This paper describes an overview of Atrial Myopathy in pathogenic mechanisms linking atrial fibrillation and ischemic stroke. Atrial myopathy is not only a substrate for atrial fibrillation and makes thrombus formation cause ischemic stroke, but also leads to blood stasis within the atria and makes ischemic stroke without intervening atrial fibrillation.</dc:description>
	<dc:publisher xml:lang="en">Universitas Brawijaya</dc:publisher>
	<dc:date>2025-04-30</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://heartscience.ub.ac.id/index.php/heartscience/article/view/20177</dc:identifier>
	<dc:identifier>10.21776/ub.hsj.2025.006.02.2</dc:identifier>
	<dc:source xml:lang="en">Heart Science Journal; Vol. 6 No. 2 (2025): The Complexity in the Management of Heart Rhythm Disorder</dc:source>
	<dc:source>2721-9984</dc:source>
	<dc:source>2721-9976</dc:source>
	<dc:source>10.21776/ub.hsj.2025.006.02</dc:source>
	<dc:language>en</dc:language>
	<dc:relation>https://heartscience.ub.ac.id/index.php/heartscience/article/view/20177/485</dc:relation>
	<dc:rights xml:lang="en">Copyright (c) 2025 Cik Kahadi</dc:rights>
	<dc:rights xml:lang="en">http://creativecommons.org/licenses/by/4.0</dc:rights>
</oai_dc:dc>