scholarly journals Serum Proprotein Convertase Subtilisin/ Kexin Type 9 Levels are Increased in Patients with Transient Ischemic Attack

2020 ◽  
pp. 5-11
Author(s):  
Thomas Tzimas ◽  
Eleni Pappa ◽  
Sebastien Filippas-Ntekouan ◽  
Maria Georgoula ◽  
Angelos Liontos ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Transient Ischemic Attack ◽  
Stable Coronary Artery Disease ◽  
Symptom Duration ◽  
Proprotein Convertase ◽  
Mean Values ◽  
Coronary Syndromes ◽  
Artery Disease ◽  
Ischemic Attack

Background: Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) is associated with hypercholesterolemia and atherosclerotic disease while its inhibition reduces cardiovascular risk. There is some evidence that serum PCSK9 concentrations are higher in patients with acute coronary syndromes compared with those with stable coronary artery disease, which has been attributed to a proatherogenic and prothrombotic state. Objective: This case-control pilot study investigated potential associations of PCSK9 in patients with transient ischemic attack (TIA). Methods: A total of 20 patients with a first-ever atherosclerotic non-cardioembolic TIA and 20 controls of similar age and sex were enrolled. Clinical characteristics, metabolic parameters, including serum PCSK9 within 24 hours from the onset of TIA symptoms were recorded. Results: The serum PCSK9 concentration was higher in TIA patients vs. controls (mean values, 248 ng/mL vs. 196 ng/mL, p = 0.02). In patients with TIA, serum PCSK9 correlated with age (r=0.603, p=0.03), history of coronary artery disease (r=0.515, p=0.020) and ABCD2 score (Age, Blood pressure, Clinical features, symptom Duration, Diabetes – a future stroke prediction tool) (r=0.512, p=0.021). In multivariate analysis, serum PCSK9 was independently associated with higher odds of TIA (1.16 per 10 ng/mL increase, 95% CI 1.01-1.34, p=0.035). Conclusions: Our findings indicate that serum PCSK9 levels are independently associated with atherosclerotic TIA and the risk of future stroke. Further investigation is needed to confirm these findings or to assess the use of PCSK9 as a target for early treatment as well as for secondary stroke prevention.

Circulating levels of proprotein convertase subtilisin/kexin type 9 (PCSK9) are associated with monocyte subsets in patients with stable coronary artery disease

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
KA Krychtiuk ◽  
M Lenz ◽  
P Hohensinner ◽  
K Distelmaier ◽  
L Schrutka ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Stable Coronary Artery Disease ◽  
Statin Treatment ◽  
Lipid Lowering ◽  
Monocyte Subsets ◽  
Proprotein Convertase ◽  
Artery Disease ◽  
Circulating Levels ◽  
Classical Monocytes

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): FWF Background and aims Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis and can be divided into three subsets. The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets. Methods We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14 + CD16++; NCM). Results Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n = 55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p = 0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R = 0.29; p = 0.04), while NCM showed an inverse correlation with PCSK9 levels (R=-0.33; p = 0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK-9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p = 0.05). Conversely, PCSK9 levels >median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 <median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p = 0.02). In contrast, IM showed no association with PCSK-9 levels. Conclusions We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.

Early Engagement in Exercise Improves Coronary Artery Disease Risk in Newly Diagnosed Transient Ischemic Attack Patients

2013 ◽  
Vol 8 (6) ◽  
pp. E29-E29 ◽  
Author(s):  
James Faulkner ◽  
Danielle Lambrick ◽  
Brandon Woolley ◽  
Lee Stoner ◽  
Laikin Wong ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Transient Ischemic Attack ◽  
Disease Risk ◽  
Coronary Artery Disease Risk ◽  
Newly Diagnosed ◽  
Artery Disease ◽  
Ischemic Attack

scholarly journals Essen Risk Score in Prediction of Myocardial Infarction After Transient Ischemic Attack or Ischemic Stroke Without Prior Coronary Artery Disease

Stroke ◽  
2019 ◽  
Vol 50 (12) ◽  
pp. 3393-3399 ◽  
Author(s):  
Marion Boulanger ◽  
Linxin Li ◽  
Shane Lyons ◽  
Nicola G. Lovett ◽  
Magdalena M. Kubiak ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Ischemic Stroke ◽  
Coronary Artery ◽  
Risk Score ◽  
Transient Ischemic Attack ◽  
Artery Disease ◽  
Ischemic Attack

scholarly journals Coronary Artery Disease in Patients Presenting With Acute Ischemic Stroke or Transient Ischemic Attack and Elevated Troponin Levels

2022 ◽  
Vol 12 ◽  
Author(s):  
Mathieu Kruska ◽  
Anna Kolb ◽  
Christian Fastner ◽  
Iris Mildenberger ◽  
Svetlana Hetjens ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Ischemic Stroke ◽  
Cardiovascular Risk ◽  
Coronary Artery ◽  
Transient Ischemic Attack ◽  
Large Artery ◽  
Elevated Troponin ◽  
Stroke Patients ◽  
Artery Disease ◽  
Ischemic Attack

Background: There is little information concerning the invasive coronary angiography (ICA) findings of patients with acute ischemic stroke (AIS) or transient ischemic attack (TIA) with elevated troponin levels and suspected myocardial infarction (MI). This study analyzed patient characteristics associated with ICA outcomes.Methods: A total of 8,322 patients with AIS or TIA, treated between March 2010 and May 2020, were retrospectively screened for elevated serum troponin I at hospital admission. Patients in whom ICA was performed, due to suspected type 1 MI based on symptoms, echocardiography, and ECG, were categorized according to ICA results (non-obstructive coronary artery disease (CAD): ≥1 stenosis ≥50% but no stenosis ≥80%; obstructive CAD: any stenosis ≥80% or hemodynamically relevant stenosis assessed by FFR/iwFR).Results: Elevated troponin levels were detected in 2,205 (22.5%) patients, of whom 123 (5.6%) underwent ICA (mean age 71 ± 12 years; 67% male). CAD was present in 98 (80%) patients, of whom 51 (41%) were diagnosed with obstructive CAD. Thus, ICA findings of obstructive CAD accounted for 2.3% of patients with troponin elevation and 0.6% of all stroke patients. The clinical hallmarks of myocardial ischemia, including angina pectoris (31 vs. 15%, p < 0.05) and regional wall motion abnormalities (49 vs. 32%, p = 0.07), and increased cardiovascular risk indicated obstructive CAD. While there was no association between lesion site or stroke severity and ICA findings, causal large-artery atherosclerosis was significantly more common in patients with obstructive coronary disease (p < 0.05).Conclusion: The rate of obstructive CAD in patients with stroke or TIA and elevated troponin levels with suspected concomitant type I MI is low. The cumulation of several cardiovascular risk factors and clinical signs of MI were predictive. AIS patients with large-artery atherosclerosis and elevated troponin may represent an especially vulnerable subgroup of stroke patients with risk for obstructive CAD.

Abstract 1521: Platelet RNA Content is Increased in Patients with Acute Coronary Syndromes Compared to Patients with stable Coronary Artery Disease and Healthy Individuals

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Erik L Grove ◽  
Anne-Mette Hvas ◽  
Steen D Kristensen
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Acute Coronary Syndromes ◽  
Thrombus Formation ◽  
Stable Coronary Artery Disease ◽  
Healthy Individuals ◽  
Coronary Thrombus ◽  
Coronary Syndromes ◽  
Immature Platelets ◽  
Artery Disease

Background: Platelets newly released from the bone marrow are characterized by large cell volumes and, contrary to mature platelets, contain RNA, which might reflect an increased capacity of producing proaggregatory proteins. We hypothesized that the fraction of RNA-containing, immature platelets (Immature Platelet Fraction = IPF) is a marker for acute coronary thrombus formation. Methods: Flow cytometric determination of immature platelets was conducted using a RNA fluorescent dye and an automated analyzer (Sysmex XE-2100). Measurements were performed in a total of 426 individuals (365 patients with acute coronary syndromes (ACS), 39 patients with stable coronary artery disease (CAD) and 22 healthy individuals). Results: Geometric mean IPF was 2.5 (CV = 0.37) in the control group, 2.9 (0.43) in patients with stable CAD, 3.0 (0.55) in the non-STEMI/Unstable Angina group and 3.7 (0.56) in patients with STEMI. IPF was significantly increased in STEMI patients compared to all other groups (t-test for log-transformed data: p < 0.004), and the overall difference between groups was significant (ANOVA: p < 0.0001). IPF was increased in active smokers among patients with ACS (3.2 vs 3.6, p=0.02), whereas no relation with age, sex, body mass index or CRP levels was observed. Conclusion: The fraction of RNA-containing platelets is increased in ACS, especially in the acute phase of STEMI. Immature platelets with an increased haemostatic potential may contribute to coronary thrombus formation and may partly explain previous findings of temporary resistance to anti-platelet therapy.

Sign in / Sign up

Export Citation Format

Share Document