Intramyocardial echo‐free space with a turbulent flow within, suggestive of an aneurysmal coronary artery

2022 ◽  
Author(s):  
Negar Omidi ◽  
Golnaz Houshmand ◽  
Hamidreza Pourhosseini ◽  
Ali Hosseinsabet
Keyword(s):  
Coronary Artery ◽  
Turbulent Flow ◽  
Free Space

Turbulent flow inside coronary artery mimicking acute coronary syndrome in multislice computed tomography

2012 ◽  
Vol 157 (2) ◽  
pp. e38-e39
Author(s):  
Tsuyoshi Ito ◽  
Hitoshi Matsuo ◽  
Mitsuyasu Terashima ◽  
Kenya Nasu ◽  
Yoshihisa Kinoshita ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Turbulent Flow ◽  
Multislice Computed Tomography ◽  
Coronary Syndrome

scholarly journals Intracoronary cavitation as a cause of plaque rupture and thrombosis propagation in patients with acute myocardial infarction: A computational study

2019 ◽  
Vol 7 (2) ◽  
pp. 69-75 ◽  
Author(s):  
Gianluca Rigatelli ◽  
Marco Zuin ◽  
Tra T. Ngo ◽  
Hung T. Nguyen ◽  
Aravinda Nanjundappa ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Turbulent Flow ◽  
Coronary Artery Stenosis ◽  
Plaque Rupture ◽  
Computational Study ◽  
Fluid Pressure ◽  
Artery Stenosis

Abstract Background and Objectives Significant rather than moderate coronary artery stenosis has been postulated to be the main substrate of plaque rupture in acute myocardial infarction (AMI). We evaluate if cavitation could influence the coronary artery plaque rupture contributing to the progression of thrombotic process. Methods We reconstructed a 3D model of the left anterior descending coronary artery (LAD) after reviewing the intravascular ultrasound (IVUS) data of 30 consecutive patients with mild to severe coronary artery disease. Results Turbulent flow or cavitation occurs in both concentric and eccentric coronary artery stenosis (≥ 75% for the former and ≥ 50% for the latter). The analysis of vapor phase demonstrated that cavitation propagated downstream, creating microbubbles, which exploded when the fluid pressure was lower than the vapor pressure at a local thermodynamic state. The relative higher vorticity magnitude (as turbulent flow in vivo angiogram) observed on the distal cap of the atherosclerotic plaque created a higher turbulence, probably able to destabilize the plaque through a micro-erosion process. Conclusions Cavitation seems to be able to promote the thrombotic occlusion within the coronary vessels due the ‘constant injuries’ created by the micro-explosion of bubbles.

scholarly journals Transitional turbulent flow in a stenosed coronary artery with a physiological pulsatile flow

2020 ◽  
Vol 36 (7) ◽  
Author(s):  
Navid Freidoonimehr ◽  
Maziar Arjomandi ◽  
Nima Sedaghatizadeh ◽  
Rey Chin ◽  
Anthony Zander
Keyword(s):  
Coronary Artery ◽  
Turbulent Flow ◽  
Pulsatile Flow ◽  
Stenosed Coronary Artery

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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