The importance of platelet aggregability in different presentations of Coronary Artery Disease: from subclinical Atherosclerosis to Acute Coronary Syndromes

• Grant number: 17/26922-2
• Support type: Scholarships in Brazil - Post-Doctorate
• Effective date (Start): April 01, 2018
• Effective date (End): March 31, 2021
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal researcher: José Carlos Nicolau
• Grantee: María Del Rocío Salsoso Rodríguez
• Home Institution: Instituto do Coração Professor Euryclides de Jesus Zerbini (INCOR). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil
• Associated research grant: 14/01021-4 - Platelet aggregation and antiaggregation in coronary artery disease patients, AP.TEM

Abstract

There is evidence that platelets participate from the beginning of the atherosclerotic process (pre-clinical stage) to late stage of Coronary Disease, in which rupture or erosion of atherosclerotic plaque occurs, with consequent development of some form of Acute Coronary Syndromes(ACS): a) platelets may be involved in Atherosclerosis and formation of the foam cell, even in the absence of dyslipidemia; b) at the beginning of atherosclerotic plaque formation, platelets attached to injured endothelium and releases vasoactive substances stimulating migration and proliferation of smooth muscle cells; c) in patients with established Atherosclerotic Disease, plaque rupture or erosion leads to platelet adhesion, followed by release of mediators, such as ADP and thromboxane leading to platelet activation, modifications in platelet cytoskeleton wich ultimately causes platelet aggregation and thrombus formation. Obviously platelets have also important participation in other pathophysiological mechanisms, like inflammation, endothelial dysfunction and activation of the coagulation system. Interactions between these mechanisms are poorly understood, configuring a wide field of research in the cardiovascular area. On the other hand, from the therapeutic point of view, there are now several proven effective antiplatelet options, while very little is known about possible actions of interventions proven to be useful in the treatment of coronary disease (medicines or not), on the platelet aggregation. In general, there are much more questions than answers, further expanding the research opportunities in the area.In this thematic project, different aspects of platelet aggregation, both mechanistically/pathophysiologically and therapeutically, will be analyzed in different populations of patients with Atherosclerotic Coronary Disease: asymptomatic subjects with intermediate cardiovascular risk with and without subclinical Atherosclerosis, patients with stable coronary disease, and patients with ACS. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

SALSOSO, ROCIO; DALCOQUIO, TALIA F.; FURTADO, REMO H. M.; FRANCI, ANDRE; BARBOSA, CARLOS J. D. G.; GENESTRETI, PAULO R. R.; STRUNZ, CELIA M. C.; LIMA, VIVIANE; BARACIOLI, LUCIANO M.; GIUGLIANO, ROBERT P.; et al. Relation of High Lipoprotein (a) Concentrations to Platelet Reactivity in Individuals with and Without Coronary Artery Disease. ADVANCES IN THERAPY, SEP 2020. (14/01021-4, 14/03742-0, 17/26922-2)

GUTIERREZ, JAIME A.; GOMEZ, ISABEL; CHIARELLO, I, DELIA; SALSOSO, ROCIO; KLEIN, ANDRES D.; GUZMAN-GUTIERREZ, ENRIQUE; TOLEDO, FERNANDO; SOBREVIA, LUIS. Role of proteases in dysfunctional placental vascular remodelling in preeclampsia. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, v. 1866, n. 2, FEB 1 2020. (17/26922-2)

SALSOSO, ROCIO; MATE, ALFONSO; TOLEDO, FERNANDO; VAZQUEZ, CARMEN M.; SOBREVIA, LUIS. Insulin requires A(2B) adenosine receptors to modulate the L-arginine/nitric oxide signalling in the human fetoplacental vascular endothelium from late-onset preeclampsia. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, v. 1867, n. 1, JAN 1 2021. (17/26922-2)