Thrombin Activatable Fibrinolysis Inhibitor (TAFI) Levels in Patients with Coronary Artery Disease Investigated by Angiography

2002 ◽  
Vol 88 (12) ◽  
pp. 1020-1025 ◽  
Author(s):  
Verena Schroeder ◽  
Tushar Chatterjeel ◽  
Haresh Mehta ◽  
Stephan Windecker ◽  
Trinh Pham ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Coronary Atherosclerosis ◽  
Fibrinogen Concentration ◽  
Plasma Samples ◽  
Thrombin Activatable Fibrinolysis Inhibitor ◽  
Acute Phase Reactants ◽  
Fibrinolysis Inhibitor ◽  
Artery Disease

SummaryDue to its role in the balance between coagulation and fibrinolysis, thrombin activatable fibrinolysis inhibitor (TAFI) may be involved in the development of cardiovascular diseases. We studied 362 patients with coronary artery disease (CAD) and 134 control subjects free of CAD, both groups investigated by angiography. TAFI antigen levels were determined in venous and intracoronary plasma samples and were related to metabolic and hemostatic risk factors and extent of coronary atherosclerosis. Venous TAFI levels tended to be higher in CAD patients compared to controls, whereas this difference was significant in intracoronary samples. A subgroup of patients who had not experienced acute myocardial infarction or undergone previous cardiac interventions showed significantly higher TAFI levels in both venous and intracoronary plasma samples. TAFI levels correlated with acute phase reactants indicating a role for TAFI in inflammation. However, TAFI levels did not correlate with extent of coronary atherosclerosis and among the classical cardiovascular risk factors TAFI levels only correlated with total cholesterol and fibrinogen concentration. Our results suggest that TAFI might be a risk factor for the development of CAD.

Abstract 6133: Microvascular Dysfunction and Chronic Inflammation in Patients without Cardiovascular Risk Factors

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Alejandro Recio-Mayoral ◽  
Justin C Mason ◽  
Juan C Kaski ◽  
Michael B Rubens ◽  
Olivier A Harari ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Cardiovascular Risk ◽  
Coronary Artery ◽  
Cardiovascular Risk Factors ◽  
Chronic Inflammation ◽  
Coronary Atherosclerosis ◽  
Microvascular Dysfunction ◽  
Early Marker ◽  
Artery Disease

Premature coronary atherosclerosis, which is actually seen as an active inflammatory process, is an established complication of systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). We hypothesized that exposure to chronic inflammation, even in the absence of classical cardiovascular risk factors (CVRF), could result in coronary microvascular dysfunction (CMD), an early marker of coronary atherosclerosis. By means of positron emission tomography in combination with oxygen-15 labeled water, myocardial blood flow (MBF) was measured at rest and during iv adenosine infusion (140 μg/kg/min) in 13 SLE and 12 RA patients (mean [±SD] age 44±10 years) without CVRF. All patients underwent coronary angiography using multi-slice (64 slices) computed tomography and only those with none or trivial coronary artery disease (<30% luminal stenosis) were included. A group of 25 age- and gender-matched controls were also studied. There were no differences between patients and controls regarding body-mass index, blood pressure and lipid parameters. RA and SLE patients showed similar mean disease duration (16±11 and 11±7 years, respectively; p=0.12). Resting MBF was similar in patients and controls (1.25±0.27 vs 1.15±0.24 ml/min/g, p=0.15). However, during adenosine stress patients had lower MBF compared with controls (2.94±0.83 vs 4.11±0.84 ml/min/g, p<0.001). As result, coronary flow reserve (CFR; adenosine/resting MBF) was significantly reduced in patients (2.44±0.78) compared with controls (3.81±1.07; p<0.001). Seven patients showed ischemic electrocardiographic changes during adenosine and had a more severe reduction in CFR (1.76±0.81) and more years of disease (21±7 years) compared with those patients without ischemic changes (CFR 2.49±0.54; p=0.006; duration of disease 14±5 years; p=0.03). CFR was inversely correlated with years of disease (r=−0.65, p<0.001), but not with corticosteroid cumulative dose (r=0.20, p=0.39). Chronic inflammation in the absence of traditional CVRF is characterized by severe CMD. This may represent an early marker of disease which precedes and contributes to premature coronary artery disease in patients with RA and SLE.

Personalized management of coronary artery disease

ESC CardioMed ◽  
2018 ◽  
pp. 2989-2991
Author(s):  
Thorsten Kessler ◽  
Heribert Schunkert
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Genetic Risk ◽  
Coronary Atherosclerosis ◽  
Treatment Strategies ◽  
Integrated Approach ◽  
Genetic Risk Factors ◽  
Research Field ◽  
Artery Disease

Coronary artery disease and myocardial infarction are main causes of morbidity and mortality. In the past decades, several modifiable and non-modifiable risk factors underlying the disease have been identified. Recently, genome-wide association studies and next generation sequencing led to the discovery of genetic risk factors. Knowledge of these genetic risk factors has been shown to help to understand the pathophysiology of coronary atherosclerosis. Their knowledge might also be useful in risk prediction and diagnostics. Ultimately, an integrated approach using genetic information and novel imaging technologies should improve treatment strategies towards a personalized medicine. Here, we want to summarize recent findings in this research field and provide insight how these developments could be used to improve prevention and treatment of coronary atherosclerosis and its sequelae.

Thrombin-activatable fibrinolysis inhibitor antigen level in coronary artery disease

2015 ◽  
Vol 40 (2) ◽  
pp. 49
Author(s):  
Deena MohamedMohamed Habashy ◽  
HebatallahAdel Sedky ◽  
Walid AbdelSalam Ammar ◽  
Eman FathyMohamed El-Ashmawy
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Antigen Level ◽  
Thrombin Activatable Fibrinolysis Inhibitor ◽  
Fibrinolysis Inhibitor ◽  
Artery Disease

P6167Low leptin plasma levels are associated with progression of coronary atherosclerosis in patients with stable coronary artery disease from the SMARTool Study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Caselli ◽  
S Rocchiccioli ◽  
A Rosendael ◽  
R Buechel ◽  
A Teresinska ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Plasma Levels ◽  
Coronary Atherosclerosis ◽  
Atherosclerotic Burden ◽  
Artery Disease ◽  
Stable Cad ◽  
Plasma Leptin

Abstract Background Leptin is an adipokine involved in energy homeostasis and has been related with established vascular risk factors. However, studies on the association of leptin plasma levels with coronary artery disease (CAD) have yielded conflicting results. Purpose Aim of the present study was to evaluate the association between leptin plasma levels and presence, severity and progression of coronary atherosclerosis in patients with suspected stable CAD. Methods In a cohort of 257 patients with symptoms of stable CAD enrolled in the SMARTool study, coronary computed tomography angiography (CTA), plasma leptin levels and clinical and bio-humoral CAD risk profile (including glucose, lipid and inflammation variables) were obtained at enrolment and after 6±1yrs of follow-up. Sixty-four patients were revascularized and the remaining 193 represent the population for the present study. CTA findings were categorised as no-minimal CAD (<30% stenosis), non-obstructive CAD (30%-50% stenosis) and obstructive CAD (≥50% stenosis in at least one major coronary vessel). A CTA risk score (based on plaque extent, severity, composition, and location) was calculated at baseline and at follow-up to assess coronary atherosclerotic burden and its progression (Δ CTA score≥5). Results CTA findings showed obstructive CAD in 11% of patients at baseline and in 15% at follow-up (p<0.0001). CTA risk score, was 8.03±7.80 at baseline and increased to 10.33±8.17 at follow-up (p<0.0001) with CAD progression in 20% of patients. Leptin plasma levels were inversely related with CTA findings both at baseline and follow-up (Figure). In a Cox model, baseline plasma leptin was an independent predictor of CAD progression, after adjustment for clinical risk factors, biomarkers, and treatment (HR 0.572, 95% CI 0.393–0.834, P=0.0037). Figure 1 Conclusion Plasma leptin is inversely associated with coronary atherosclerotic burden and disease progression in patients with stable CAD. This association is independent of known factors affecting leptin levels. These results could prompt further investigations on the pathophysiological mechanisms of this association. Acknowledgement/Funding EU H2020 research and innovation program under grant agreement No 689068

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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