Medical and Invasive Management of Coronary Artery Disease in Patients on Anticoagulants

2015 ◽  
pp. 163-174
Author(s):  
Ryan Berg ◽  
Nabil Shafi
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Artery Disease ◽  
Invasive Management

Non-invasive management of coronary artery disease

The Lancet ◽  
1995 ◽  
Vol 346 (8977) ◽  
pp. 750-753 ◽  
Author(s):  
K.L Gould ◽  
S.W Casscells ◽  
L.M Buja ◽  
D.C Goff
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Non Invasive ◽  
Artery Disease ◽  
Invasive Management

scholarly journals Invasive Management of Coronary Artery Disease in Advanced Renal Disease

2021 ◽  
Author(s):  
Keyvan Karimi Galougahi ◽  
Steven Chadban ◽  
Roxana Mehran ◽  
Sripal Bangalore ◽  
Glenn M. Chertow ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Renal Disease ◽  
Artery Disease ◽  
Invasive Management

A cloud-based platform for the non-invasive management of coronary artery disease

2020 ◽  
Vol 14 (8) ◽  
pp. 1102-1123 ◽  
Author(s):  
Antonis Sakellarios ◽  
Joao Correia ◽  
Savvas Kyriakidis ◽  
Elena Georga ◽  
Nikolaos Tachos ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Non Invasive ◽  
Artery Disease ◽  
Invasive Management

scholarly journals Angina, quality of life and prognosis: prospective comparison of patients undergoing invasive management

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T.J Ford ◽  
E Yii ◽  
A Morrow ◽  
N Sidik ◽  
R Good ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Treatment Response ◽  
Obstructive Coronary Artery Disease ◽  
Funding Source ◽  
Artery Disease ◽  
Invasive Management

Abstract Background Angina is associated with impaired quality of life and an adverse prognosis. Purpose Prospectively evaluate quality of life and clinical outcomes in patients with angina undergoing invasive coronary angiography according to endotype: symptoms and/or signs of ischaemia and no obstructive coronary artery disease (INOCA) compared to obstructive coronary artery disease subjects managed by medical therapy, revascularization with percutaneous coronary intervention (PCI) and coronary artery bypass graft (CABG) surgery, respectively. Methods We conducted a prospective clinical evaluation of patients with angina undergoing clinically indicated invasive management (NCT03193294). Symptom severity and quality of life were assessed at baseline and repeated after 6 months. Comparisons between treatment groups were based on analysis of covariance general linear models adjusting for baseline score, sex, and cardiovascular risk. INOCA subjects were considered as one diagnostic group and not all subjects had invasive vasoreactivity testing. Results 391 patients (mean age 62±10 years, 52% female) were enrolled over 12 months and classified into one of four groups: INOCA (N=185; 47%), obstructive CAD treated by PCI (N=126; 32%), obstructive CAD treated by CABG (N=48; 12%) and obstructive CAD managed with medical therapy (N=32; 8%). After adjusting for between group differences and overall risk, INOCA subjects had worse angina and worse treatment response at follow up (21% and 27% reduction in angina score compared to CAD patients revascularized with PCI and CABG respectively). INOCA subjects had numerically lower treatment response than CAD patients managed with medications (6.4 units, −12%; P=0.181). Population baseline mean Seattle Angina Questionnaire (SAQ) frequency score (60±26) and SAQ summary score (52.5±19) were similar between groups. The absolute difference was 6.4 units versus medically managed CAD (95% CI: −3.0 to 15.9; P=0.181), 11.3 units versus the CAD group undergoing PCI (6.1 to 16.5; P<0.001) and 14.3 units versus CABG (6.2 to 22.3; P=0.001). INOCA subjects had overall reduced quality of life (EQ5D index) and increased psychological distress scores versus all CAD groups at 6 months. During longer-term follow-up (median 18 months), 23 (6%) MACE events occurred with no differences between the groups (Kaplan Meier log-rank P=0.890). Conclusion(s) Patients with INOCA had more severe angina symptoms reflecting worse quality of life and treatment response at 6 months with similar MACE as CAD subjects even after adjustment for confounding factors. This study highlights the need for evidence-based antianginal therapies and disease-modifying treatments for angina patients regardless of the presence of obstructive coronary disease. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): This work was funded by the British Heart Foundation (PG/17/2532884; RE/13/5/30177; RE/18/6134217)

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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