QRS fragmentation as a marker of arrhythmias in coronary artery disease, in cardiomyopathies and ion channel diseases

2012 ◽  
Vol 158 (1) ◽  
pp. 176-177 ◽  
Author(s):  
Stefan Peters
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Ion Channel ◽  
Qrs Fragmentation ◽  
Artery Disease ◽  
Ion Channel Diseases

Mutation Analysis Ion Channel Genes Ventricular Fibrillation Survivors with Coronary Artery Disease

2011 ◽  
Vol 34 (6) ◽  
pp. 742-749 ◽  
Author(s):  
TOMAS NOVOTNY ◽  
JITKA KADLECOVA ◽  
MARTINA RAUDENSKA ◽  
ALEXANDRA BITTNEROVA ◽  
IRENA ANDRSOVA ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Ion Channel ◽  
Mutation Analysis ◽  
Artery Disease

scholarly journals Mutation analysis of ion channel genes promoters in ventricular fibrillation survivors with coronary artery disease

Cor et Vasa ◽  
2013 ◽  
Vol 55 (5) ◽  
pp. e419-e423
Author(s):  
Tomáš Novotný ◽  
Martina Raudenská ◽  
Jitka Kadlecová ◽  
Irena Andršová ◽  
Alena Floriánová ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Ion Channel ◽  
Mutation Analysis ◽  
Artery Disease

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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