Platelet aggregability and anticoagulant proteins activity during dobutamine stress echocardiography in asymptomatic patients  four months after percutaneous coronary intervention

Zoran Jović; Vesna Subota; Boris Džudović; Zorica Mladenović; Jelena Marić Kocijančić; Predrag Djurić; Marijan Spasić; Nemanja Djenić; Radoslav Romanović; Vladimir Miloradović; Radomir Matunović; Slobodan Obradović

doi:10.2298/VSP170204110J

Zoran Jović Military Medical Academy, Clinic of Cardiology, Belgrade, Serbia
Vesna Subota Military Medical Academy, Institute of Clinical Biochemistry, Belgrade, Serbia
Boris Džudović University of Defence, Faculty of Medicine of the Military Medical Academy, Belgrade, Serbia
Zorica Mladenović University of Defence, Faculty of Medicine of the Military Medical Academy, Belgrade, Serbia
Jelena Marić Kocijančić University of Defence, Faculty of Medicine of the Military Medical Academy, Belgrade, Serbia
Predrag Djurić University of Defence, Faculty of Medicine of the Military Medical Academy, Belgrade, Serbia
Marijan Spasić University of Defence, Faculty of Medicine of the Military Medical Academy, Belgrade, Serbia
Nemanja Djenić Military Medical Academy, Clinic of Emergency Internal Medicine, Belgrade, Serbia
Radoslav Romanović Military Medical Academy, Clinic of Emergency Internal Medicine, Belgrade, Serbia
Vladimir Miloradović University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
Radomir Matunović Military Medical Academy, Clinic of Emergency Internal Medicine, Belgrade, Serbia
Slobodan Obradović Military Medical Academy, Clinic of Emergency Internal Medicine, Belgrade, Serbia

DOI: https://doi.org/10.2298/VSP170204110J

Keywords: antithrombins;, echocardiography, stress;, percutaneous coronary intervention;, platelet aggregation.

Abstract

Background/Aim. Platelets aggregability (PA) and the activation of hemostasis during myocardial ischemia within physical or mental stress, can be one of many factors that influence the process of stent thrombosis after the percutaneous coronary intervention (PCI). The aim of the study is to investigate the relationship between the PA and activity of anticoagulant proteins with myocardial ischemia during the dobutamine stress echocardiography (DSE) in the asymptomatic patients 4 months after the PCI. Methods. The study population included 74 asymptomatic patients who had a successful PCI 4 months before a high-dose DSE. PA on epinephrine (EPI) and adenosine diphosphate (ADP) were determined by the Light Transmission Aggregometry (LTA), together with plasma activity of protein C and antithrombin before the DSE and at the peak stage of the stress test. The patients were divided into several groups on the basis of whether they have baseline or induced disturbance of segmental myocardial kinetics or not. All patients were on the clopidogrel and aspirin therapy at the time of DSE. Results. There were no statistically significant difference in the PA ADP (47.50% vs 50.20%; p = 0.970) as well as on EPI (59.30% vs 60.30%, p = 0.600) before and at the peak of DSE. A statistically significant difference was found in the anticoagulant activity of the antithrombin (84.85% vs 74.75%, p = 0.001) and protein C (77.75% vs 67.60%, p < 0.001). A significance of differences in antithrombin and the protein C, refered to the result before and at the peak levels of the test. There was no significant difference in the PA and plasma activity of anticoagulant proteins in the patients with or without induced myocardial ischemia at the peak of DSE. The patients who had an increased wall motion score index at the peak of DSE, had a higher EPI induced PA than the patients with normal myocardial contractility (68.60% vs 54.70%, respectively; p = 0.017). Conclusion. There are no changes in the PA before and after DSE, however, plasma activity of anticoagulant proteins decreased at the peak level of the test. The PA on EPI significantly increases at the peak of DSE in the patients with segmental myocardial hypocontractility.

Author Biography

Zoran Jović, Military Medical Academy, Clinic of Cardiology, Belgrade, Serbia

References

REFERENCES

Rosamond W, Flegal K, Furie K, Go A, Greenlund K, Haase N, et al. American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke sta-tistics--2008 update: a report from the American Heart Asso-ciation Statistics Committee and Stroke Statistics Subcommit-tee. Circulation 2008; 117(4): e25-146.

Lloyd-Jones D, Adams RJ, Brown TM, Carnethon M, Dai S, De Simone G, et al. Executive summary: heart disease and stroke statistics-2010 update: a report from the American Heart As-sociation. Circulation 2010; 121(7): 948‒54.

Angiolillo DJ, Fernandez-Ortiz A, Bernardo E, Alfonso F, Macaya C, Bass TA, et al. Variability in individual responsiveness to clopidogrel: clinical implications, management, and future per-spectives. J Am Coll Cardiol 2007; 49(14): 1505‒16.

Obradovic S, Subota V, Baskot B, Dopudja M, Antonijević N, Djenić N, et al. Changes in platelets and anticoagulant protein activity during adenosine-exercise single-photon emission computed tomography stress test. Srp Arh Celok Lek 2010; 138(1 Suppl): 28‒32.

Furie B, Furie BC. Mechanisms of thrombus formation. N Engl J Med 2008; 359(9): 938‒49.

Volpi E, Giusti L, Ciregia F, Da VY, Giannaccini G, Berti S, et al. Platelet proteome and clopidogrel response in patients with stable angina undergoing percutaneous coronary intervention. Clin Biochem 2012; 45(10‒11): 758‒65.

Braunwald E, Angiolillo D, Bates E, Berger PB, Bhatt D, Cannon CP, et al. Investigating the mechanisms of hyporesponse to an-tiplatelet approaches. Clin Cardiol 2008; 31(3 Suppl 1): I21‒7.

Pavlović P, Tavcioski D, Stamenković E. Thrombocyte aggrega-tion, endothelial dysfunction and acute myocardial infarction. Vojnosanit Pregl 2009; 66(4): 323‒7.

Folsom AR, Ohira T, Yamagishi K, Cushman M. Low protein C and incidence of ischemic stroke and coronary heart disease: the Atherosclerosis Risk in Communities (ARIC) Study. J Thromb Haemost 2009; 7(11): 1774‒8.

Bruley DF. Anticoagulant blood factor deficiencies (protein C). Adv Exp Med Biol 2007; 599: 1‒6.

Soare AM, Popa C. Deficiencies of proteins C, S and an-tithrombin and activated protein C resistance--their involve-ment in the occurrence of Arterial thromboses.J Med Life 2010; 3(4): 412‒5.

Maqbool S, Rastogi V, Seth A, Singh S, Kumar V, Mustaqueem A. Protein-C deficiency presenting as pulmonary embolism and myocardial infarction in the same patient. Thromb J 2013; 11(1): 19.

Previtali E, Bucciarelli P, Passamonti SM, Martinelli I. Risk fac-tors for venous and arterial thrombosis. Blood Transfus 2011; 9(2): 120‒38.

Sicari R, Nihoyannopoulos P, Evangelista A, Kasprzak J, Lancellotti P, Poldermans D, et al. Stress echocardiography expert consen-sus statement European Association of Echocardiography (EAE) (a registered branch of the ESC). Eur J Echocardiogr 2008; 9(4): 415‒37.

Gilstrap LG, Bhatia RS, Weiner RB, Dudzinski DM. Dobuta-mine stress echocardiography: A review and update. Res Rep Clin Cardiol 2014; 5: 69‒81.

Price MJ, Endemann S, Gollapudi RR, Valencia R, Stinis CT, Levisay JP, et al. Prognostic significance of post-clopidogrel platelet reactivity assessed by a point-of-care assay on throm-botic events after drug-eluting stent implantation. Eur Heart J 2008; 29(8): 992‒1000.

Fleischmann KE, Hunink MG, Kuntz KM, Douglas PS. Exercise echocardiography or exercise SPECT imaging? A meta-analysis of diagnostic test performance. JAMA 1998; 280(10): 13‒20.

Roger VL, Pellikka PA, Oh JK, Bailey KR, Tajik AJ. Identifica-tion of multivessel coronary artery disease by exercise echo-cardiography. J Am Coll Cardiol 1994; 24(1): 109‒14.

Pamukcu B, Oflaz H, Acar RD, Umman S, Koylan N, Umman B, et al. The role of exercise on platelet aggregation in patients with stable coronary artery disease: exercise induces aspirin re-sistant platelet activation. J Thromb Thrombolysis 2005; 20(1): 17‒22.

Hüfner K, Koudouovoh-Tripp P, Kandler C, Hochstrasser T, Malik P, Giesinger J, et al. Differential changes in platelet reactivity in-duced by acute physical compared to persistent mental stress. Physiol Behav 2015; 151: 284‒91.

El-Sayed MS, Ali N, El-Sayed AZ. Aggregation and activation of blood platelets in exercise and training. Sports Med 2005; 35(1): 11‒22.