Atrial fibrillation is associated with cardiac hypoxia

Gramley, Felix; Lorenzen, Johann; Jedamzik, Britta; Gatter, Kevin C.; Koellensperger, Eva; Münzel, Thomas; Pezzella, Francesco

doi:10.1016/j.carpath.2008.11.001

Cited by 60 publications

(52 citation statements)

References 50 publications

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“…43 Gramley et al reported that AF is closely associated with the upregulation of hypoxic and angiogenic markers. 40 The results of the present study also support increases in the levels of expression of VEGF and HIF-1α as a cause of hypoxia induced AF. There is a possibility that the combination of hypoxia and AF could create a vicious cycle that sustains the AF.…”

Section: Hypoxia and Af Remodelingsupporting

confidence: 81%

“…Atrial hypoxia and the HIF pathway have been implicated in structural changes of the atria, such as cardiac fibrosis, that may lead to the continuance of AF. 38- 40 HIF-1α levels are regulated by proteolysis via an oxygensensitive mechanism. The HIF-1α protein undergoes prolyl hydroxylation and is rapidly degraded by the ubiquitin -proteasome system under normoxic conditions.…”

Section: Discussionmentioning

confidence: 99%

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Is Structural Remodeling of Fibrillated Atria the Consequence of Tissue Hypoxia?

Ogi

Nakano

Niida

et al. 2010

Circ J

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Section: Hypoxia and Af Remodelingsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Is Structural Remodeling of Fibrillated Atria the Consequence of Tissue Hypoxia?

Ogi

Nakano

Niida

et al. 2010

Circ J

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“…Although microcirculation dysfunction in the atrium is still controversial in AF, 7 capillary rarefaction has been frequently found in the LA posterior wall of AF patients. 8 Additionally, chronic AF patients have a lower LA capillary density.…”

mentioning

confidence: 99%

Aging Modulates the Substrate and Triggers Remodeling in Atrial Fibrillation

Lin

Chen

Lee

et al. 2018

Circ J

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how aging and AF are connected and highlight the potential role of aging in AF substrate and triggered remodeling. Effects of Aging on Structural RemodelingStructural remodeling is characterized by histopathological changes, such as cellular hypertrophy, apoptosis, or myocardial fibrosis, and anatomical changes, such as chamber dilatation. 5 Anatomical Changes With Dilation of PV and Atria in AgingThe left atrium (LA) anteroposterior diameter and wall thickness increase with aging, and the 4 PVs become dilated in patients older than 50 years (Figure 1), 3 which suggests mechanical effects of aging on AF triggers and substrates. 3 Clinical data indicate that PV size correlates with PV arrhythmogenesis. Therefore, larger PVs may correlate with a higher PV arrhythmogenesis resulting in AF. Histopathological Changes With AgingBoth animal and human studies had shown that loss of cardiomyocytes by apoptosis and necrosis produces compensatory cellular hypertrophy, which may represent the structural basis of the aged heart, and contribute to cardiac dysfunction in the elderly. 5 Aging increases the rate of ventricular cardiomyocyte death caused by enhanced vulnerability to stress such as oxidative stress. 6 These histopathological changes at the microscopic level potentially T he prevalence and severity of arrhythmias increase with age. Advancing age is independently associated with the prevalence of atrial fibrillation (AF). 1 Aging and aging-related underlying diseases frequently result in structural remodeling as cardiac morphological changes either grossly or at the histological and ultrastructural levels, or they induce electrophysiological remodeling with changes in cardiac electrical properties in response to a functional insult, or as a result of a structural alteration. Aging-associated cardiac anatomical and functional remodeling may enhance the occurrence or the persistence of AF.Ectopic impulses generated from the pulmonary veins (PVs) play a key role in the genesis and maintenances of AF. 2 Elimination of PV arrhythmogenic foci or targeting atrial substrate abnormalities reduces the AF burden or cures AF. 2 PVs contain complex electrical activity because of their distinctive anatomical and physiological characteristics. 3 Aging-associated electrophysiological or structural changes in the atria or PVs may facilitate AF occurrence. 3 Age is an independent predictor of AF recurrence in lone AF patients after undergoing the first circumferential PV isolation. 4 AF may coexist with cardiovascular disorders, which may potentiate its occurrence, and these are also more prevalent with increased age. Together with agingrelated myocardial degeneration or anatomical changes, both inflammation and oxidative stress, as consequences of aging, enhance the occurrence and maintenance of AF. The aim of this review is to update the understanding of Aging plays a critical role in the genesis of atrial fibrillation (AF) and also increases the risks of cardiac dysfunction and stroke in AF patients. AF is caused by increased AF t...

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“…Por otro lado, la medición de MVEC de plasma demostró que en el momento del ingreso los pacientes con SCA tuvieron una concentración signifi-vante que demuestra que en las primeras 2 hrs de iniciado un SCA, hay un incremento estadísticamente significativo de vesículas circulantes de tamaño 91-120nm, característico de la población de exosomas 10,15 y que este aumento de MVEC ocurre antes que el incremento de TnI plasmática. La evidencia de la literatura demuestra que la principal causa del IAM es la falta de oxígeno suministrado por la circulación al tejido cardíaco 1,3,26 . En esta condición la elevación de TnI plasmática se debe a la destrucción de los cardiomiocitos y, por otro lado, como se ha descrito, las MVEC son secretados por célu-las vivas como mecanismo de comunicación y respuesta frente a la agresión 7,9 .…”

Section: Discussionunclassified

En el Infarto agudo al miocardio los niveles plasmáticos de microvesículas extracelulares se elevan más precozmente que el aumento de la Troponina-I

et al. 2017

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En el Infarto agudo al miocardio los niveles plasmáticos de microvesículas extracelulares se elevan más precozmente que el aumento de la Troponina-I Métodos: Plasma de 22 pacientes controles se recolectó 0-2hrs post-ingreso a urgencia. Plasma de 45 pacientes SCA se recolectó 0-2, 6-8 y 10-14hrs post ingreso, junto con la toma de muestra para estudio de TnI. Las MVECs plasmáticas fueron enriquecidas mediante kit comercial. La determinación de la concentración y tamaño MVECs se realizó por NTA (Nanoparticles Tracking Assay) usando el equipo Nanosight. Resultados: La concentración promedio de MVECs0-2 hrs post ingreso fue 7,2 veces superior en plasma de pacientes con SCA vs controles y la moda del tamaño disminuyó en pacientes con SCA. La TnI no mostró diferencias significativas en 0-2 hrs post ingreso en el grupo estudiado. La concentración de las MVEC disminuyó significativamente después de 10-14 hrs post ingreso, mientras que la concentración promedio TnI se mantuvo invariable demostrando el aumento de MVECs previo al incremento de TnI. Conclusión. El aumento de MVECs previo al in-cremento de la TnI en pacientes infartados, sugiere que las MVECs aumentan en la fase previa del IAM, como respuesta al daño tisular. Actualmente, estudiamos el contenido molecular de las MVECs, para establecer un método diagnóstico del Síndrome Coronario Agudo basado en MVECs. Financiado por proyecto Corfo 14IDL2-30168.

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Atrial fibrillation is associated with cardiac hypoxia

Cited by 60 publications

References 50 publications

Is Structural Remodeling of Fibrillated Atria the Consequence of Tissue Hypoxia?

Is Structural Remodeling of Fibrillated Atria the Consequence of Tissue Hypoxia?

Aging Modulates the Substrate and Triggers Remodeling in Atrial Fibrillation

En el Infarto agudo al miocardio los niveles plasmáticos de microvesículas extracelulares se elevan más precozmente que el aumento de la Troponina-I

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