Cardiovascular events occur independently of high on-aspirin platelet reactivity and residual COX-1 activity in stable cardiovascular patients

2016 ◽  
Vol 116 (08) ◽  
pp. 356-368 ◽  
Author(s):  
Kazuyuki Nagatsuka ◽  
Shigeki Miyata ◽  
Akiko Kada ◽  
Atsushi Kawamura ◽  
Jyoji Nakagawara ◽  
...  
Keyword(s):  
Cardiovascular Events ◽  
Cox Regression ◽  
Platelet Reactivity ◽  
Thrombus Formation ◽  
Cardiovascular Death ◽  
Characteristic Analysis ◽  
Cardiovascular Patients ◽  
Definition Of ◽  
Induced Aggregation ◽  
Cox 1

SummarySeveral studies have indicated that approximately 25% of patients treated with aspirin exhibit high on-treatment platelet reactivity (HTPR), which is potentially associated with cardiovascular events (CVEs). However, this association is still controversial, since the mechanisms by which HTPR contributes to CVEs remain unclear and a no standardised definition of HTPR has been established. To determine whether HTPR is associated with CVE recurrence and what type of assay would best predict CVE recurrence, we conducted a multicentre prospective cohort study of 592 stable cardiovascular outpatients treated with aspirin monotherapy for secondary prevention. Their HTPR was determined by arachidonic acid- or collagen-induced aggregation assays using two different agonist concentrations. Residual cyclooxygenase (COX)-1 activity was assessed by measuring serum thromboxane (TX)B2 or urinary 11-dehydro TXB2. Shear-induced platelet thrombus formation was also examined. We followed all patients for two years to evaluate how these seven indexes were related to the recurrence of CVEs (cerebral infarction, transient ischaemic attack, myocardial infarction, unstable angina, revascularisation, other arterial thrombosis, or cardiovascular death). Of 583 patients eligible for the analysis, CVEs occurred in 69 (11.8%). A Cox regression model identified several classical risk factors associated with CVEs. However, neither HTPR nor high residual COX-1 activity was significantly associated with CVEs, even by applying cut-off values suggested in previous reports or a receiver-operating characteristic analysis. In conclusion, recurrence of CVEs occurred independently of HTPR and residual COX-1 activity. Thus, our findings do not support the use of platelet or COX-1 functional testing for predicting clinical outcomes in stable cardiovascular patients.Supplementary Material to this article is available at www.thrombosis-online.com.

Platelet reactivity in patients with aortic stenosis depends on LV-AO angle

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P Mourikis ◽  
S Zako ◽  
L Dannenberg ◽  
R M'Pembele ◽  
T Hohlfeld ◽  
...  
Keyword(s):  
Aortic Stenosis ◽  
Platelet Activation ◽  
Platelet Function ◽  
Cox Regression ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Funding Source ◽  
Local Inflammation ◽  
German Research Foundation ◽  
Induced Aggregation

Abstract Background The pathogenesis of aortic stenosis (AS) is not fully understood. However, local inflammation of the valve appears to be a main player. Except haemostasis, platelets contribute to inflammatory processes in various ways. Furthermore, platelet function is altered in patients with AS. Moreover, a steep angle between the left ventricle and the aorta (LV-AO-angle) leads to turbulent blood flow. However, it is not known if platelet reactivity is associated with steep LV_AO angle in patients with AS. Methods We included 289 patients with severe AS and performed cardiac computertomography to assess the LV-AO-angle. Platelet function was evaluated by light transmission aggregometry by using collagen and adenosine-diphosphate to induce platelet activation Results ADP- and collagen induced aggregation showed a significant negative correlation with LV-AO-angle (ADP: r=−0.19, p=0.0009, R2=0.022; collagen: r=−0.21, p=0.0004, R2=0.027). ADP-induced MoA was significant higher in patients with a LV-AO-angle <160° in comparison to patients with an angle ≥160° (<160°: 66.99±20.72% vs. ≥160°: 60.66±19.85%, p=0.009). Collagen-induced platelet reactivity was significant higher in patients with a LV-AO-angle <160° in comparison to patients with an angle ≥160° (<160°: 78.67±13.19% vs. ≥160°: 73.85±14.44%, p=0.003). Multivariate cox-regression revealed that LV-AO angle <160 was a robust predictor of ADP- and collagen-induced platelet aggregation Conclusion A steep LV-AO-angle is associated with enhanced platelet reactivity in patients with AS. Platelet activation is known to lead to local inflammation. Therefore, enhanced platelet reactivity could play crucial in the progression of AS. The clinical significance of a steep LV-AO-angle needs be evaluated in further trials. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): German Research Foundation

P1930Pharmacodynamic effects of vorapaxar as an add-on antiplatelet therapy in patients with and without diabetes mellitus: the optimizing anti-platelet therapy in diabetes mellitus (OPTIMUS)-5 study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
F Franchi ◽  
F Rollini ◽  
V Kairouz ◽  
J Rivas ◽  
A Rivas ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Triple Therapy ◽  
Antiplatelet Therapy ◽  
Primary Endpoint ◽  
Platelet Reactivity ◽  
Dual Therapy ◽  
Mean Difference ◽  
Adjunctive Treatment ◽  
Induced Aggregation ◽  
Cox 1

Abstract Background Vorapaxar (Vora) is a protease-activated receptor (PAR)-1 inhibitor which when added to dual antiplatelet therapy (DAPT) in patients with a history of myocardial infarction (MI) or with peripheral arterial (PAD) reduces thrombotic cardiovascular events at the expense of increased bleeding. The efficacy of Vora is enhanced in patients with diabetes mellitus (DM) compared to non-DM. However, the differential pharmacodynamic (PD) effects of Vora in DM vs non-DM patients are unknown. Moreover, although withdrawal of aspirin has emerged as a strategy to reduce bleeding when adjunctive antithrombotic therapies are used, the PD effects of Vora after stopping aspirin in DAPT treated patients is unknown. Purpose To assess the PD effects of Vora in addition to standard DAPT as well as in combination with clopidogrel following aspirin withdrawal in patients with and without DM. Methods This was a prospective parallel-design PD study conducted in post-MI or PAD patients with and without DM. Patients on DAPT with aspirin (81mg/qd) and clopidogrel (75mg/qd) were divided in two groups according to DM status. Each cohort was treated with Vora (2.5mg/qd) in addition to DAPT (i.e., triple therapy) for 30 days and afterwards stopped aspirin and maintained treatment with Vora plus clopidogrel (i.e., dual therapy) for other 30 days. PD testing using 5 different assays was conducted at 3 time-points: baseline (while on DAPT); after 30 days of triple therapy; after 30 days of dual therapy. The primary endpoint was the non-inferiority of CAT (Collagen-ADP-TRAP)-induced aggregation, a marker of global platelet reactivity, of Vora plus clopidogrel (dual therapy) vs Vora plus DAPT (triple therapy). Results The PD population was composed of a total of 64 patients (DM, n=30; non-DM, n=34). Although adding Vora to DAPT significantly reduced CAT-induced aggregation, stopping aspirin was associated with an increase in CAT-induced aggregation in both DM (mean difference=12; 95% CI: 3 to 21; p=0.010) and non-DM (mean difference=10; 95% CI: 4 to 16; p=0.003), thus not meeting the primary endpoint of non-inferiority (Figure). The magnitude of such increase was higher in DM compared with non-DM (p=0.036). Although Vora abolished TRAP-induced aggregation in both DM and non-DM patients, it did not affect markers of clot kinetics including speed of thrombin generation. Aspirin withdrawal was associated with a marked increase in makers sensitive to cyclooxygenase-1 (COX-1) blockade; markers of P2Y12 signaling were higher in DM compared to not DM after aspirin withdrawal. CAT-induced aggregation Conclusion Adjunctive treatment with Vora reduces platelet-mediated thrombogenicity without affecting clot kinetics in both DM and non-DM patients while on DAPT. However, platelet-mediated thrombogenicity is increased after aspirin withdrawal, a phenomenon which is enhanced in DM patients underscoring the pivotal contribution of the COX-1 signaling pathway in these high risk patients. Acknowledgement/Funding The study was supported in part by an investigator initiated study grant from Merck

Mean Corpuscular Volume Predicts Adverse Outcomes Following Peripheral Angioplasty With Stenting and Is Associated With On-Treatment Platelet Reactivity

Angiology ◽  
2020 ◽  
Vol 72 (1) ◽  
pp. 16-23
Author(s):  
Maximilian Tscharre ◽  
Silvia Lee ◽  
Christoph W. Kopp ◽  
Simon Panzer ◽  
Thomas Gremmel
Keyword(s):  
Mean Corpuscular Volume ◽  
Cox Regression ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Adenosine Diphosphate ◽  
Adverse Outcomes ◽  
Corpuscular Volume ◽  
Characteristic Analysis ◽  
Cox Regression Analysis ◽  
Increased Risk

Structural aspects of red blood cells have been associated with cardiovascular disease. No data linking mean corpuscular volume (MCV) to clinical outcomes and on-treatment platelet reactivity in patients with peripheral artery disease (PAD) are available. We investigated a composite of atherothrombotic events and target vessel restenosis or reocclusion following infrainguinal stenting for stable PAD. Residual platelet reactivity was measured by light transmission aggregometry (LTA) and the VerifyNow assays. We included 104 patients receiving dual antiplatelet therapy (DAPT) with aspirin and clopidogrel. In receiver-operating characteristic analysis, MCV effectively discriminated between patients with and without adverse outcomes and identified a MCV ≤90.8 fL as optimal cutoff. Adverse outcomes occurred significantly more often in patients with low MCV (log-rank P = .002). In univariable Cox regression analysis, low MCV was associated with an increased risk of future adverse outcomes (hazard ratio [HR]: 2.662 [95%CI: 1.304-5.434]; P = .007) and remained significantly associated after adjustment (HR: 2.591 [95%CI: 1.242-5.403]; P = .011). Mean corpuscular volume was inversely correlated with arachidonic acid (AA)- and adenosine diphosphate (ADP)-inducible platelet reactivity by LTA and with the VerifyNow aspirin assay. Low MCV is associated with adverse outcomes over 2 years following infrainguinal stenting. Mean corpuscular volume correlates inversely with AA- and ADP-inducible platelet reactivity during DAPT.

Abstract 33: Platelet 12-lipoxygenase is a Key Regulator of Platelet Reactivity and Thrombus Formation in vivo

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Reheman Adili ◽  
Katherine Mast ◽  
Theodore R Holman ◽  
Michael Holinstat
Keyword(s):  
Platelet Aggregation ◽  
Ex Vivo ◽  
Platelet Reactivity ◽  
Thrombus Formation ◽  
High Shear ◽  
Vessel Occlusion ◽  
12 Lipoxygenase ◽  
Induced Aggregation

Background: Platelet reactivity is required to maintain hemostasis, however high platelet reactivity leads to thrombus formation, myocardial infarction, and stroke. Platelet 12-lipoxygenase (12-LOX) has been demonstrated by our lab and others to regulate agonist-mediated platelet reactivity suggesting a role for 12-LOX in regulation of in vivo thrombosis. The ability to target 12-LOX in vivo has not been established to date. Therefore, we sought to determine if 12-LOX regulates platelet reactivity and thrombus formation in vivo using the selective 12-LOX inhibitor ML355 to determine whether platelet 12-LOX is an effective target for anti-platelet therapeutics. Methods: ML355 effects on human platelet function was assessed in vitro by platelet aggregometry, ex vivo by perfusion chamber, and in vivo by thrombus formation and vessel occlusion in small and large vessels in 12-LOX -/- , WT mice, and mice treated with ML355 via intravital microscopy using the FeCl 3 and laser injury models. Results: In in vitro platelet aggregation, ML355 dose-dependently inhibited agonist-induced aggregation. In ex vivo flow chamber assays, platelet adhesion and thrombus formation on collagen-coated surfaces at high shear was attenuated in both mouse and human whole blood after incubation with ML355. Further, platelet aggregation and thrombus growth in 12-LOX -/- mice were impaired in both laser and FeCl 3 -induced mesenteric, carotid artery and cremaster arteriole thrombosis models. Thrombi in 12-LOX -/- mice were unstable and frequently formed emboli, which resulted in impaired vessel occlusion or reopening. Additionally, thrombus formation and vessel occlusion was impaired in ML355 treated WT mice. Conclusions: The 12-LOX inhibitor ML355 inhibits platelet aggregation induced by a number of platelet agonists. Ex vivo high shear conditions in both mice and human was attenuated in the presence of ML355. Thrombus formation and vessel occlusion were impaired in mice deficient in 12-LOX. Finally, ML355 attenuates thrombus formation and prevents vessel occlusion in vivo . Our data strongly indicates 12-LOX is an important determinant of platelet reactivity and inhibition of platelet 12-LOX may represent a new target for anti-platelet therapeutics.

Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin

Pharmacology ◽  
2017 ◽  
Vol 100 (3-4) ◽  
pp. 127-130 ◽  
Author(s):  
Annemarie Mohring ◽  
Kerstin Piayda ◽  
Lisa Dannenberg ◽  
Saif Zako ◽  
Theresa Schneider ◽  
...  
Keyword(s):  
Gold Standard ◽  
Cardiovascular Events ◽  
Platelet Reactivity ◽  
Area Under The Curve ◽  
Platelet Inhibition ◽  
Light Transmittance ◽  
Characteristic Analysis ◽  
Specific Test ◽  
Current Gold Standard ◽  
Light Transmittance Aggregometry

Platelet inhibition by aspirin is indispensable in the secondary prevention of cardiovascular events. Nevertheless, impaired aspirin antiplatelet effects (high on-treatment platelet reactivity [HTPR]) are frequent. This is associated with an enhanced risk of cardiovascular events. The current gold standard to evaluate platelet hyper-reactivity despite aspirin intake is the light-transmittance aggregometry (LTA). However, pharmacologically, the most specific test is the measurement of arachidonic acid (AA)-induced thromboxane (TX) B2 formation. Currently, the optimal cut-off to define HTPR to aspirin by inhibition of TX formation is not known. Therefore, in this pilot study, we aimed to calculate a TX formation cut-off value to detect HTPR defined by the current gold standard LTA. We measured platelet function in 2,507 samples. AA-induced TX formation by ELISA and AA-induced LTA were used to measure aspirin antiplatelet effects. TX formation correlated nonlinearly with the maximum of aggregation in the AA-induced LTA (Spearman's rho R = 0.7396; 95% CI 0.7208-0.7573, p < 0.0001). Receiver operating characteristic analysis and Youden's J statistics revealed 209.8 ng/mL as the optimal cut-off value to detect HTPR to aspirin with the TX ELISA (area under the curve: 0.92, p < 0.0001, sensitivity of 82.7%, specificity of 90.3%). In summary, TX formation ELISA is reliable in detecting HTPR to aspirin. The calculated cut-off level needs to be tested in trials with clinical end points.

Enhanced platelet MRP4 expression and correlation with platelet function in patients under chronic aspirin treatment

2016 ◽  
Vol 116 (12) ◽  
pp. 1100-1110 ◽  
Author(s):  
Isabella Massimi ◽  
Lavinia Lotti ◽  
Flavia Temperilli ◽  
Massimo Mancone ◽  
Gennaro Sardella ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Platelet Reactivity ◽  
Thrombus Formation ◽  
Independent Mechanism ◽  
Mrna And Protein Expression ◽  
Low Levels ◽  
Cox 1

SummaryPlatelet multidrug resistance protein4 (MRP4)-overexpression has a role in reducing aspirin action. Aspirin in vivo treatment enhances platelet MRP4 expression and MRP4 mediated transport inhibition reduces platelet function and delays thrombus formation. The aim of our work was to verify whether MRP4 expression is enhanced in platelets obtained from patients under chronic aspirin treatment and whether it correlates with residual platelet reactivity. We evaluated changes on mRNA and protein-MRP4 expression and platelet aggregation in four populations: healthy volunteers (HV), aspirin-free control population (CTR), patients who started the treatment less than one month ago (ASA<1 month patients) and aspirinated patients who started the treatment more than two months ago (ASA>2 months patients). In platelets obtained from ASA>2 months patients, it was found a statistically significant MRP4 enhancement of both mRNA and protein expression compared to HV, CTR and ASA<1 month patients. Platelets obtained from ASA>2 months patients that present high levels of platelet MRP4, have higher serum TxB2 levels and collagen-induced platelet aggregation compared to patient with low levels of MRP4 in platelets. In addition collagen induced platelet aggregation is higher in in vitro aspirinated platelets obtained from patients with high levels of MRP4 patients compared to those obtained from patients with low MRP4 levels. We can assert that, in patients under chronic aspirin treatment, platelets that present high MRP4 levels have an increase of residual platelet reactivity, which is due in part to incomplete COX-1 inhibition, and in part to COX-1–independent mechanism.

In vivo platelet activation and platelet hyperreactivity in abacavir-treated HIV-infected patients

2013 ◽  
Vol 110 (08) ◽  
pp. 349-357 ◽  
Author(s):  
Barbara Belfiori ◽  
Eleonora Petito ◽  
Giuseppe Guglielmini ◽  
Lisa Malincarne ◽  
AnnaMaria Mezzasoma ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Cardiovascular Events ◽  
Light Transmission ◽  
Ex Vivo ◽  
Platelet Reactivity ◽  
Retrospective Case ◽  
Activation Markers ◽  
Induced Aggregation

SummaryAbacavir (ABC) has been associated with ischaemic cardiovascular events in HIV-infected patients, but the pathogenic mechanisms are unknown. Aim of our study was to assess whether ABC induces in vivo platelet activation and ex vivo platelet hyper-reactivity. In a retrospective, case-control study, in vivo platelet activation markers were measured in 69 HIV-infected patients, before starting therapy and after 6–12 months of either ABC (n=35) or tenofovir (TDF) (n=34), and compared with those from 20 untreated HIV-infected patients. A subgroup of patients was restudied after 28–34 months for ex vivo platelet reactivity. In vivo platelet activation markers were assessed by ELISA or flow cytometry, ex vivo platelet reactivity by light transmission aggregometry (LTA) and PFA-100®. The in vitro effects of the ABC metabolite, carbovir triphosphate, on aggregation and intra-platelet cGMP were also studied. sPLA2, sPsel and sGPV increased significantly 6–12 months after the beginning of ABC, but not of TDF or of no treatment. Ex vivo platelet function studies showed enhanced LTA, shorter PFA-100® C/ADP closure time and enhanced platelet expression of P-sel and CD40L in the ABC group. The intake of ABC blunted the increase of intraplatelet cGMP induced by nitric oxide (NO) and acutely enhanced collagen-induced aggregation. Preincubation of control platelets with carbovir triphosphate in vitro enhanced platelet aggregation and blunted NO-induced cGMP elevation. In conclusion, treatment with ABC enhances in vivo platelet activation and induces platelet hyperreactivity by blunting the inhibitory effects of NO on platelets. These effects may lead to an increase of ischaemic cardiovascular events.

Thrombosis in diabetes: a shear flow effect?

2017 ◽  
Vol 131 (12) ◽  
pp. 1245-1260 ◽  
Author(s):  
Erik Westein ◽  
Thomas Hoefer ◽  
Anna C. Calkin
Keyword(s):  
Type 2 Diabetes ◽  
Shear Stress ◽  
Cardiovascular Events ◽  
Recurrent Events ◽  
New Technologies ◽  
Platelet Reactivity ◽  
Thrombus Formation ◽  
Diagnostic Systems ◽  
Novel Therapeutic

Cardiovascular events are the major cause of morbidity and mortality in Type 2 diabetes (T2D). This condition is associated with heightened platelet reactivity, contributing to increased atherothrombotic risk. Indeed, individuals with diabetes respond inadequately to standard antiplatelet therapy. Furthermore, they often experience recurrent events as well as side effects that include excess bleeding. This highlights the need for identification of novel regulators of diabetes-associated thrombosis to target for therapeutic intervention. It is well established that platelet aggregation, a process essential for thrombus formation, is tightly regulated by shear stress; however, the mechanisms underlying shear activation of platelets, particularly in the setting of diabetes, are still poorly understood. This review will address the limitations of current diagnostic systems to assess the importance of shear stress in the regulation of thrombus formation in T2D, and the inability to recapitulate the pro-thrombotic phenotype seen clinically in the setting of T2D. Moreover, we will discuss recent findings utilizing new technologies to define the importance of shear stress in thrombus formation and their potential application to the setting of diabetes. Finally, we will discuss the potential of targeting shear-dependent mechanisms of thrombus formation as a novel therapeutic approach in the setting of T2D.

scholarly journals Association of Baseline HbA1c With Cardiovascular and Renal Outcomes: Analyses From DECLARE-TIMI 58

Diabetes Care ◽  
2022 ◽  
Author(s):  
Avivit Cahn ◽  
Stephen D. Wiviott ◽  
Ofri Mosenzon ◽  
Erica L. Goodrich ◽  
Sabina A. Murphy ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Events ◽  
Cox Regression ◽  
Cardiovascular Death ◽  
Atherosclerotic Cardiovascular Disease ◽  
Baseline Hba1c ◽  
Renal Outcomes ◽  
Increased Risk ◽  
Hba1c Levels

OBJECTIVE Current guidelines recommend prescribing SGLT2 inhibitors to patients with type 2 diabetes and established or at high risk for atherosclerotic cardiovascular disease (ASCVD), irrespective of HbA1c levels. We studied the association of HbA1c with cardiovascular and renal outcomes and whether the benefit of dapagliflozin varies by baseline HbA1c. RESEARCH DESIGN AND METHODS In the Dapagliflozin Effect on Cardiovascular Events trial (DECLARE-TIMI 58), 17,160 patients with type 2 diabetes were randomly assigned to dapagliflozin or placebo for a median follow-up of 4.2 years. Cardiovascular and renal outcomes by baseline HbA1c in the overall population and with dapagliflozin versus placebo in HbA1c subgroups were studied by Cox regression models. RESULTS In the overall population, higher baseline HbA1c was associated with a higher risk of cardiovascular death or hospitalization for heart failure (HHF); major adverse cardiovascular events (MACE), including cardiovascular death, myocardial infarction, and ischemic stroke; and cardiorenal outcomes (adjusted hazard ratios 1.12 [95% CI 1.06–1.19], 1.08 [1.04–1.13], and 1.17 [1.11–1.24] per 1% higher level, respectively). Elevated HbA1c was associated with a greater increased risk for MACE and cardiorenal outcomes in patients with multiple risk factors (MRF) than in established ASCVD (P-interaction = 0.0064 and 0.0093, respectively). Compared with placebo, dapagliflozin decreased the risk of cardiovascular death/HHF, HHF, and cardiorenal outcomes, with no heterogeneity by baseline HbA1c (P-interaction &gt; 0.05). CONCLUSIONS Higher HbA1c levels were associated with greater cardiovascular and renal risk, particularly in the MRF population, yet the benefits of dapagliflozin were observed in all subgroups irrespective of baseline HbA1c, including patients with HbA1c &lt;7%.

4078Lipoprotein(a) and clinical outcomes in patients after revascularization of peripheral arteries

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N A Tmoyan ◽  
M V Ezhov ◽  
O I Afanasieva ◽  
E A Klesareva ◽  
M I Afanasieva ◽  
...  
Keyword(s):  
Cardiovascular Events ◽  
Cox Regression ◽  
Cardiovascular Death ◽  
Cardiovascular Outcomes ◽  
Lower Limbs ◽  
Limb Amputation ◽  
Peripheral Arteries ◽  
Cox Regression Analysis ◽  
Secondary Endpoints

Abstract Background Randomized trials have proved the reduction of cardiovascular events due to LDL-cholesterol level decrease. However, despite high-intensity statin therapy, there is a residual risk, that could be associated with lipoprotein(a) [Lp(a)]. It has been shown that there is an association between elevated Lp(a) level and cardiovascular outcomes in patients with coronary heart disease. Data about the role of Lp(a) in the development of cardiovascular events after revascularization of peripheral arteries are scarce. Purpose To evaluate the relationship of Lp(a) level with cardiovascular outcomes after revascularization of carotid and lower limbs arteries. Methods The study included 258 patients with severe carotid and/or lower extremity artery disease, who underwent successful elective revascularization. The primary endpoint was the composite of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. The secondary endpoint was the composite of transitory ischaemic attack, limb amputation, hospitalization for unstable angina, or revascularization surgery. Results During 36 months follow-up 29 (11%) primary and 113 (44%) secondary endpoints were registered. It was noted greater rate of primary (21 [8%] vs. 8 [3%]; hazard ratio [HR], 3.0; 95% confidence interval [CI] 1.5–6.3; p<0.01) and secondary endpoints (72 [28%] vs. 41 (16%], HR, 2.5; 95% CI 1.7–3.7; p<0.01) in patients with elevated Lp(a) level (≥30 mg/dl) compared to patients with Lp(a) <30 mg/dl (Picture). Multivariable-adjusted Cox regression analysis revealed that Lp(a) was independently associated with incidence of cardiovascular outcomes. Conclusions Patients with peripheral artery diseases have a high risk of cardiovascular events and the level of Lp(a) ≥30 mg/dl is an independent predictor of cardiovascular events in prospective 3-year follow-up after revascularization of carotid and lower limbs arteries.

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