Enhancement of Endothelial Function Inhibits Left Atrial Thrombi Development in an Animal Model of Spontaneous Left Atrial Thrombosis

Mawatari, Kazuaki; Yoshioka, Emiko; Toda, Satomi; Yasui, Sonoko; Furukawa, Hideki; Shimohata, Takaaki; Ohnishi, Takamasa; Miyamoto, Masaki; Harada, Nagakatsu; Takahashi, Akira; Sakaue, Hiroshi; Nakaya, Yutaka

doi:10.1253/circj.cj-13-1398

Cited by 13 publications

(6 citation statements)

References 48 publications

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“…Further supporting this evidence, in the present study, we demonstrated a 3.5-fold higher rate of thrombotic events in patients with LAT compared with subjects without LAT. The potential explanation of this finding could be that free floating atrial thrombi can reach peripheral tissues through blood flow and subsequently induce secondary embolisms, including cerebrovascular events (90). Extending this evidence, previous data suggested that the risk of LAT is not negligible among patients who have been therapeutically anticoagulated (12).…”

Section: Discussionmentioning

confidence: 89%

Prevalence of left atrial thrombus in patients with non-valvular atrial fibrillation

Minno¹,

Ambrosino²,

Russo³

et al. 2016

Thromb Haemost

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We performed a meta-analysis about the prevalence of left atrial thrombus (LAT) in patients with atrial fibrillation (AF) undergoing trans-esophageal echocardiography (TEE). Studies reporting on LAT presence in AF patients were systematically searched in the PubMed, Web of Science, Scopus and EMBASE databases and the pooled LAT prevalence was evaluated as weighted mean prevalence (WMP). Seventy-two studies (20,516 AF patients) showed a LAT WMP of 9.8 % (95 %CI: 7.6 %-12.5 %). LAT presence was associated with a higher age (mean difference: 2.56, 95 %CI: 1.49-3.62), and higher prevalence of female gender (OR: 1.35, 95 %CI: 1.04-1.75), hypertension (OR: 1.78, 95 %CI: 1.38-2.30), diabetes mellitus (OR: 1.86, 95 %CI: 1.33-2.59) and chronic heart failure (OR: 3.67, 95 %CI: 2.40-5.60). Overall, LAT patients exhibited a higher CHADS2-score (mean difference 0.88, 95 %CI: 0.68-1.07) and a higher risk of stroke/systemic embolism (OR: 3.53, 95 %CI: 2.24-5.56) compared with those without LAT. A meta-regression showed an inverse association between LAT prevalence and the presence of anticoagulation (Z-value: -7.3, p< 0.001). Indeed, studies in which 100 % of patients received oral anticoagulation reported a 3.4 % WMP of LAT (95 %CI: 1.3 %-8.7 %), whereas studies in which 0 % of patients received anticoagulation showed a LAT WMP of 7.4 % (95 %CI: 2.3 %-21.5 %). Our data suggest that LAT is present in ≍10 % of AF patients, and is associated with a 3.5-fold increased risk of stroke/systemic embolism. Interestingly, LAT is also reported in some of patients receiving anticoagulation. The implementation of the screening of LAT in AF patients before cardioversion/ablation could be useful for the prevention of vascular events.

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Section: Discussionmentioning

confidence: 89%

Prevalence of left atrial thrombus in patients with non-valvular atrial fibrillation

Minno¹,

Ambrosino²,

Russo³

et al. 2016

Thromb Haemost

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“…NO synthesized by vascular endothelial cells wields a significant influence in regulating vasomotion and maintaining blood coagulation-thrombolysis balance. Hyposecretion or inactivation of NO which is induced by vascular endothelial dysfunction is regarded as the important virulence factor involved in the pathogenesis and progression of vascular diseases [ 10 , 11 ]. Activating the endothelial nitric oxide synthase (eNOS) in the vascular endothelial cells will promote the synthesis and release of NO which can penetrate the cell membrane and diffuse to the adjacent smooth muscle cells.…”

Section: Introductionmentioning

confidence: 99%

Effects of Electroacupuncture Stimulation at “Zusanli” Acupoint on Hepatic NO Release and Blood Perfusion in Mice

Wang

Zhang

Tang

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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The study is to observe the influence of electroacupuncture (EA) stimulation at “Zusanli” (ST36) on the release of nitric oxide (NO) and blood perfusion (BP) in the liver and further explore whether the hepatic blood perfusion (HBP) changes were regulated by EA ST36 induced NO in nitric oxide synthase inhibited mice. The HBP change of the mice was detected by laser speckle perfusion imaging (LSPI) before and after being given interventions, and the NO in liver tissue was detected by nitric acid reductase in each group. The NO levels and HBP in the L-NAME group were significantly lower than those in the control group (P < 0.01). The NO level and HBP increase in EA group were significantly higher than those in control group (P < 0.05). The NO level in the L-NAME EA group was slightly higher than that in the L-NAME group. The HBP increase in the L-NAME EA group was not statistically significant. These results showed that EA could accelerate the synthesis of NO and thereby increase HBP via vasodilation in liver tissue.

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“…To test the impact of LPS and thrombin activation on pEV function, we incubated the pEVs with otherwise native HCAECs and performed a migration assay. Endothelial regeneration is an important factor involved in left atrial thrombus formation and thus particularly relevant in this context [ 9 ]. We found that both, LPS and thrombin activation of platelets, induced the release of pEVs, which significantly inhibited endothelial cell migration.…”

Section: Resultsmentioning

confidence: 99%

“…The most serious consequence of AF is thrombus formation in the left atrium, which typically takes place in the left atrial appendage (LAA). Along with stasis of the blood in the LAA, impaired endothelial function has been shown to be an important trigger and a hallmark for atrial thrombus formation in atrial fibrillation [8][9][10]. Embolization of these thrombi into the cerebral arteries leads to stroke and makes AF the most important cause of embolic stroke [11,12].…”

Section: Introductionmentioning

confidence: 99%

Large extracellular vesicles in the left atrial appendage in patients with atrial fibrillation—the missing link?

et al. 2021

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Atrial fibrillation (AF) is the most frequent arrhythmic disease in humans, which leads to thrombus formation in the left atrial appendage and stroke through peripheral embolization. Depending on their origin, large extracellular vesicles (lEVs) can exert pro-coagulant functions. In the present study, we investigated how different types of AF influence the levels of large EV subtypes in three distinct atrial localizations. Blood samples were collected from the right and left atrium and the left atrial appendage of 58 patients. 49% of the patients had permanent AF, 34% had non-permanent AF, and 17% had no history of AF. Flow cytometric analysis of the origin of the lEVs showed that the proportion of platelet-derived lEVs in the left atrial appendage was significantly higher in permanent AF patients compared to non-permanent AF. When we grouped patients according to their current heart rhythm, we also detected significantly higher levels of platelet-derived lEVs in the left atrial appendage (LAA) in patients with atrial fibrillation. In vitro studies revealed, that platelet activation with lipopolysaccharide (LPS) leads to higher levels of miR-222-3p and miR-223-3p in platelet-derived lEVs. Treatment with lEVs from LPS- or thrombin-activated platelets reduces the migration of endothelial cells in vitro. These results suggest that permanent atrial fibrillation is associated with increased levels of platelet-derived lEVs in the LAA, which are potentially involved in LAA thrombus formation.

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Enhancement of Endothelial Function Inhibits Left Atrial Thrombi Development in an Animal Model of Spontaneous Left Atrial Thrombosis

Cited by 13 publications

References 48 publications

Prevalence of left atrial thrombus in patients with non-valvular atrial fibrillation

Prevalence of left atrial thrombus in patients with non-valvular atrial fibrillation

Effects of Electroacupuncture Stimulation at “Zusanli” Acupoint on Hepatic NO Release and Blood Perfusion in Mice

Large extracellular vesicles in the left atrial appendage in patients with atrial fibrillation—the missing link?

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