Intimal Intussusception in Aortic Dissection and Coexisting Coronary Artery Disease

Abstract Over the past three decades, the implantation of coronary stents has revolutionized the management of coronary artery disease. We present a rare case of coronary stent migration in an asymptomatic 72-year-old male, incidentally discovered 9 years after revascularization of the left anterior descending coronary artery for unstable angina. Although a linear echodensity within the aortic root is highly suggestive of an aortic dissection flap, a coronary stent “on the move” should be considered in the differential diagnosis.

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Acute, Severe Chest Pain in the Presence of Known Coronary Artery Disease: New Myocardial Ischemia, Aortic Dissection, or Some Other Evolving Cardiovascular Catastrophe?

Journal of Cardiothoracic and Vascular Anesthesia ◽

10.1053/j.jvca.2015.08.011 ◽

2016 ◽

Vol 30 (3) ◽

pp. 841-844

Author(s):

Brent T. Boettcher ◽

Shaun M. Irish ◽

Mohamed Algahim ◽

Chris K. Rokkas ◽

Christopher J. Plambeck ◽

...

Keyword(s):

Coronary Artery Disease ◽

Chest Pain ◽

Coronary Artery ◽

Myocardial Ischemia ◽

Aortic Dissection ◽

Severe Chest Pain ◽

Artery Disease

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

Clinical Science ◽

10.1042/cs20190999 ◽

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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