0000000000131816

AUTHOR

Fausto J. Pinto

0000-0002-8034-4529

showing 4 related works from this author

Cardiovascular Damage Induced by Anti-VEGF Therapy

2018

Vascular endothelial growth factor (VEGF) plays an important role in maintaining the regular homeostasis of vascular walls. VEGF binds its receptor (VEGFR) promoting the regular survival and function of endothelial cells. Anti-VEGF and anti-VEGFR drugs inhibit the action of VEGF and VEGFR. These drugs can cause cardiovascular toxic effects such as arterial hypertension, thromboembolism, myocardial ischemia and heart failure. The monoclonal antibody bevacizumab and tyrosine kinase inhibitors (sorafenib, sunitinib, pazopanib, regorafenib, axitinib, cabozantinib, ponatinib) are the main inhibitors of VEGF, VEGFR and other tyrosine kinases. In this chapter we will illustrate the cardiovascular …

SorafenibCabozantinibSunitinibbusiness.industryAxitinibVascular endothelial growth factorPazopanibchemistry.chemical_compoundchemistryRegorafenibmedicineCancer researchbusinessTyrosine kinasemedicine.drug
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Right Ventricle Function in Patients With Anterior Myocardial Infarction: Are We Sure it Is Not Involved?

2022

Copyright © 2022, Elsevier

Right Ventricle FunctionHeart VentriclesMyocardial InfarctionVentricular Function RightHumansGeneral MedicineCardiology and Cardiovascular MedicineCurrent problems in cardiology
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Antithrombotic Therapy after Acute Coronary Syndrome or PCI in Atrial Fibrillation

2019

Background: Appropriate antithrombotic regimens for patients with atrial fibrillation who have an acute coronary syndrome or have undergone percutaneous coronary intervention (PCI) are unclear. Methods: In an international trial with a two-by-two factorial design, we randomly assigned patients with atrial fibrillation who had an acute coronary syndrome or had undergone PCI and were planning to take a P2Y12 inhibitor to receive apixaban or a vitamin K antagonist and to receive aspirin or matching placebo for 6 months. The primary outcome was major or clinically relevant nonmajor bleeding. Secondary outcomes included death or hospitalization and a composite of ischemic events. Results: Enroll…

Malemedicine.medical_specialtyAcute coronary syndromeVitamin KPyridonesmedicine.medical_treatmentMEDLINEHemorrhage030204 cardiovascular system & hematologylaw.invention03 medical and health sciencesPercutaneous Coronary Intervention0302 clinical medicinePharmacotherapyDouble-Blind MethodRandomized controlled triallawInternal medicineAtrial FibrillationAntithromboticmedicineHumans03.02. Klinikai orvostancardiovascular diseases030212 general & internal medicineAcute Coronary SyndromeAgedAged 80 and overAspirinbusiness.industryatrial fibrillation ; anticoagulant therapy ; acute coronary syndrome ; apixabanAnticoagulantsPercutaneous coronary interventionAtrial fibrillationGeneral MedicineMiddle Agedmedicine.diseaseConventional PCIPurinergic P2Y Receptor AntagonistsCardiologyPyrazolesDrug Therapy CombinationFemalebusinessPlatelet Aggregation InhibitorsFactor Xa InhibitorsNew England Journal of Medicine
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Cardiovascular Damage Induced by Anti-BCR-ABL TKIs

2018

Anti-BCR-ABL TKIs (tyrosine kinase inhibitors) are drugs that inhibit BCR ABL tyrosine. They are used especially in the treatment of hematological cancer and gastrointestinal stromal tumors (GIST). Anti-BCR-ABL TKIs include first (imatinib), second (nilotinib, dasatinib, bosutinib) and third-generation drugs (ponatinib). Especially second- and third-generation drugs can cause cardiovascular complications such as arterial thrombosis, myocardial ischemia, peripheral arterial diseases, QTc prolongation, and pulmonary hypertension. Nilotinib and ponatinib can cause thrombotic arterial events with various mechanisms. Particularly dasatinib can cause pulmonary hypertension. Compared to convention…

Oncologymedicine.medical_specialtyCardiotoxicitybusiness.industryPonatinibImatinibDasatinibchemistry.chemical_compoundchemistryNilotinibhemic and lymphatic diseasesInternal medicinemedicineAdverse effectbusinessBosutinibTyrosine kinasemedicine.drug
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