2019
DOI: 10.1016/j.ijcard.2019.06.004
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Left atrial microvascular endothelial dysfunction, myocardial inflammation and fibrosis after selective insular cortex ischemic stroke

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Cited by 33 publications
(31 citation statements)
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“…CRP accumulates at sites of endothelial inflammation, which results in enhanced leukocyte adhesion (Figure 2). Moreover, the border area between the left atrium and pulmonary vein have significantly greater myocardial inflammatory infiltration and fibrosis than the distal left atrium 19 . As a result, PVI using radiofrequency catheter might tend to cause greater inflammation than cryoballoon ablation.…”
Section: Discussionmentioning
confidence: 99%
“…CRP accumulates at sites of endothelial inflammation, which results in enhanced leukocyte adhesion (Figure 2). Moreover, the border area between the left atrium and pulmonary vein have significantly greater myocardial inflammatory infiltration and fibrosis than the distal left atrium 19 . As a result, PVI using radiofrequency catheter might tend to cause greater inflammation than cryoballoon ablation.…”
Section: Discussionmentioning
confidence: 99%
“…This ganglion will selectively mediate any negative inotropic effect from vagal innervation to the left ventricle, independent from vagal stimulation to the sinoatrial node, which controls rate. Furthermore, there are significantly more post-ganglionic sympathetic nerves at the atria than the ventricles implicating less potential sympathetic damage to the ventricles than sinoatrial node following AIS autonomic dysregulation ( Balint et al, 2019 ). Consequently, multiple studies have shown that autonomic changes to HRV did not correspond to changes in cardiac stroke volume variability ( Toska and Eriksen, 1993 ; Akselrod et al, 2000 ; Liu et al, 2004 ).…”
Section: Discussionmentioning
confidence: 99%
“…Balint et al showed with a rat model that insular cortex ischemic stroke results in three histological features, namely, coronary microvascular endothelial dysfunction, myocardial inflammatory infiltration, and myocardial fibrosis. They also found that the fibrosis occurs downstream of the first two events [36]. Moreover, obesity-induced cardiovascular dysfunction associates with both endothelial dysfunction (excessive endothelium-dependent relaxation) and fibrosis, as indicated by increased cardiac expression of collagen 1α1, collagen 3α1, and periostin [37].…”
Section: Endothelial Dysfunction In Cardiac Fibrosismentioning
confidence: 94%