Leila Fernandes Araujo

[Cardiovascular events: a class effect by COX-2 inhibitors].

Non-steroidal anti-inflamatories (NSAIDs) are widely used in the treatment of post-surgery pain1, osteoarthritis2, rheumatoid arthritis3 and muscle-skeletal pain4,5, in different conditions. Major effects are: anti-inflammatory, analgesic, and antipyretic6. Generally speaking, such effects are associated to the inhibition of the enzyme cyclooxygenase (COX). COX catalyzes the transformation of arachidonic acid into different lipid mediators called prostaglandins and thromboxanes2. Those substances play a relevant hemostatic role in protecting gastric mucosa, renal physiology, and platelet aggregation, in addition to having their production induced under conditions such as inflammation and cancer7. Two isozymes – or forms of the COX enzyme – have been characterized: cyclooxygenase-1 (COX-1) and cycloxygenase-2(COX-2)2. COX-1 has shown to be constitutive in all body tissues8. It is the only isozyme found in platelets, leading to the formation of TXA2. It is found in gastric mucosa, among other tissues, where it catalyzes the biosynthesis of cytoprotective prostaglandins in vascular endotelium and in renal tissue. Finally, it is believed that COX-1 also plays a role in pathologic conditions such as inflammation7. On the other hand, COX-2 is shown to be increased in inflammatory and cell transformation processes particularly9-12, although its constitutive expression has been demonstrated in some CNS and kidney tissues7.

Lack of clopidogrel-statin interaction in patients undergoing coronary stent implantation

BACKGROUND Some studies have suggested reduced activity of clopidogrel on platelet activation and adherence in patients using statins. OBJECTIVE To assess whether platelet activation and aggregation decrease with clopidogrel, and whether there is a reduction of the action of clopidogrel when associated with atorvastatin or simvastatin. METHODS This prospective study included 68 patients with stable angina with previous use of simvastatin, atorvastatin, or no statin (control group), with previous elective indication of percutaneous coronary intervention (PCI). Platelet activation was analyzed by means of platelet count, levels of P-selectin and glycoprotein IIb/IIIa (with and without ADP stimulation) by flow cytometry. The findings were analyzed before and after percutaneous coronary intervention and the administration of clopidogrel. RESULTS We observed reduction in platelet activity with use of clopidogrel. Furthermore, no differences were found between the variables analyzed to prove reduced activity of clopidogrel when combined with statins. We observed levels of p-selectin (pre-angioplasty: 14.23 ± 7.52 x 8.83 x 11.45 ± 7.65 ± 7.09; after angioplasty: 21.49 ± 23.82 x 4 37 ± 2.71 x 4.82 ± 4.47, ρ < 0.01) and glycoprotein IIb/IIIa (pre-angioplasty: 98.97 ± 0.43 ± 1.25 x 98.79 x 99.21 ± 0.40 after angioplasty: 99.37 ± 0.29 ± 1.47 x 98.50 x 98.92 ± 0.88, ρ = 0.52), respectively, in the control, atorvastatin and simvastatin groups. CONCLUSION We concluded that platelet activation decreases with administration of clopidogrel, and clopidogrel has no antiplatelet effect reduced in the presence of simvastatin or atorvastatin.FUNDAMENTO: Alguns estudos tem sugerido reducao da atividade do clopidogrel sobre a ativacao e adesao plaquetarias em pacientes em uso de estatinas. OBJETIVO: Avaliar se a ativacao e agregacao plaquetarias diminuem com clopidogrel, e se ocorre reducao da acao do clopidogrel quando associado a atorvastatina ou a sinvastatina. METODOS: Estudo prospectivo que incluiu 68 pacientes com angina estavel em uso previo de sinvastatina, atorvastatina, ou nenhuma estatina (grupo controle), com indicacao previa eletiva de realizacao de intervencao coronaria percutânea. Foi analisada a ativacao plaquetaria atraves do numero de plaquetas, niveis de P-selectina e glucoproteina IIb/IIIa (com e sem estimulo de ADP) atraves de citometria de fluxo. Os resultados foram analisados antes e apos a intervencao coronaria percutânea e da administracao de clopidogrel. RESULTADOS: Observamos reducao da atividade plaquetaria com uso de clopidogrel. Alem disso, nao houve diferencas entre as variaveis analisadas que comprovassem reducao da atividade do clopidogrel quando associado a estatinas. Observou-se niveis de p-selectina (pre-angioplastia: 14,23±7,52 x 11,45±8,83 x 7,65±7,09; pos angioplastia: 21,49±23,82 x 4,37±2,71 x 4,82±4,47, ρ<0,01) e glicoproteina IIb/IIIa (pre-angioplastia: 98,97±0,43 x 98,79±1,25 x 99,21±0,40; pos angioplastia: 99,37±0,29 x 98,50±1,47 x 98,92±0,88, ρ=0,52), respectivamente nos grupos controle, atorvastatina e sinvastatina. CONCLUSAO: Concluimos que a ativacao plaquetaria diminui com a administracao de clopidogrel, e que o clopidogrel nao tem seu efeito antiplaquetario reduzido na presenca de sinvastatina ou atorvastatina.

Ausência de interação clopidogrel-estatina em pacientes submetidos a implante de "stent" coronário

BACKGROUND Some studies have suggested reduced activity of clopidogrel on platelet activation and adherence in patients using statins. OBJECTIVE To assess whether platelet activation and aggregation decrease with clopidogrel, and whether there is a reduction of the action of clopidogrel when associated with atorvastatin or simvastatin. METHODS This prospective study included 68 patients with stable angina with previous use of simvastatin, atorvastatin, or no statin (control group), with previous elective indication of percutaneous coronary intervention (PCI). Platelet activation was analyzed by means of platelet count, levels of P-selectin and glycoprotein IIb/IIIa (with and without ADP stimulation) by flow cytometry. The findings were analyzed before and after percutaneous coronary intervention and the administration of clopidogrel. RESULTS We observed reduction in platelet activity with use of clopidogrel. Furthermore, no differences were found between the variables analyzed to prove reduced activity of clopidogrel when combined with statins. We observed levels of p-selectin (pre-angioplasty: 14.23 ± 7.52 x 8.83 x 11.45 ± 7.65 ± 7.09; after angioplasty: 21.49 ± 23.82 x 4 37 ± 2.71 x 4.82 ± 4.47, ρ < 0.01) and glycoprotein IIb/IIIa (pre-angioplasty: 98.97 ± 0.43 ± 1.25 x 98.79 x 99.21 ± 0.40 after angioplasty: 99.37 ± 0.29 ± 1.47 x 98.50 x 98.92 ± 0.88, ρ = 0.52), respectively, in the control, atorvastatin and simvastatin groups. CONCLUSION We concluded that platelet activation decreases with administration of clopidogrel, and clopidogrel has no antiplatelet effect reduced in the presence of simvastatin or atorvastatin.FUNDAMENTO: Alguns estudos tem sugerido reducao da atividade do clopidogrel sobre a ativacao e adesao plaquetarias em pacientes em uso de estatinas. OBJETIVO: Avaliar se a ativacao e agregacao plaquetarias diminuem com clopidogrel, e se ocorre reducao da acao do clopidogrel quando associado a atorvastatina ou a sinvastatina. METODOS: Estudo prospectivo que incluiu 68 pacientes com angina estavel em uso previo de sinvastatina, atorvastatina, ou nenhuma estatina (grupo controle), com indicacao previa eletiva de realizacao de intervencao coronaria percutânea. Foi analisada a ativacao plaquetaria atraves do numero de plaquetas, niveis de P-selectina e glucoproteina IIb/IIIa (com e sem estimulo de ADP) atraves de citometria de fluxo. Os resultados foram analisados antes e apos a intervencao coronaria percutânea e da administracao de clopidogrel. RESULTADOS: Observamos reducao da atividade plaquetaria com uso de clopidogrel. Alem disso, nao houve diferencas entre as variaveis analisadas que comprovassem reducao da atividade do clopidogrel quando associado a estatinas. Observou-se niveis de p-selectina (pre-angioplastia: 14,23±7,52 x 11,45±8,83 x 7,65±7,09; pos angioplastia: 21,49±23,82 x 4,37±2,71 x 4,82±4,47, ρ<0,01) e glicoproteina IIb/IIIa (pre-angioplastia: 98,97±0,43 x 98,79±1,25 x 99,21±0,40; pos angioplastia: 99,37±0,29 x 98,50±1,47 x 98,92±0,88, ρ=0,52), respectivamente nos grupos controle, atorvastatina e sinvastatina. CONCLUSAO: Concluimos que a ativacao plaquetaria diminui com a administracao de clopidogrel, e que o clopidogrel nao tem seu efeito antiplaquetario reduzido na presenca de sinvastatina ou atorvastatina.

Ausencia de interacción clopidogrel-estatina en pacientes sometidos a implante de "Stent" coronario

BACKGROUND Some studies have suggested reduced activity of clopidogrel on platelet activation and adherence in patients using statins. OBJECTIVE To assess whether platelet activation and aggregation decrease with clopidogrel, and whether there is a reduction of the action of clopidogrel when associated with atorvastatin or simvastatin. METHODS This prospective study included 68 patients with stable angina with previous use of simvastatin, atorvastatin, or no statin (control group), with previous elective indication of percutaneous coronary intervention (PCI). Platelet activation was analyzed by means of platelet count, levels of P-selectin and glycoprotein IIb/IIIa (with and without ADP stimulation) by flow cytometry. The findings were analyzed before and after percutaneous coronary intervention and the administration of clopidogrel. RESULTS We observed reduction in platelet activity with use of clopidogrel. Furthermore, no differences were found between the variables analyzed to prove reduced activity of clopidogrel when combined with statins. We observed levels of p-selectin (pre-angioplasty: 14.23 ± 7.52 x 8.83 x 11.45 ± 7.65 ± 7.09; after angioplasty: 21.49 ± 23.82 x 4 37 ± 2.71 x 4.82 ± 4.47, ρ < 0.01) and glycoprotein IIb/IIIa (pre-angioplasty: 98.97 ± 0.43 ± 1.25 x 98.79 x 99.21 ± 0.40 after angioplasty: 99.37 ± 0.29 ± 1.47 x 98.50 x 98.92 ± 0.88, ρ = 0.52), respectively, in the control, atorvastatin and simvastatin groups. CONCLUSION We concluded that platelet activation decreases with administration of clopidogrel, and clopidogrel has no antiplatelet effect reduced in the presence of simvastatin or atorvastatin.FUNDAMENTO: Alguns estudos tem sugerido reducao da atividade do clopidogrel sobre a ativacao e adesao plaquetarias em pacientes em uso de estatinas. OBJETIVO: Avaliar se a ativacao e agregacao plaquetarias diminuem com clopidogrel, e se ocorre reducao da acao do clopidogrel quando associado a atorvastatina ou a sinvastatina. METODOS: Estudo prospectivo que incluiu 68 pacientes com angina estavel em uso previo de sinvastatina, atorvastatina, ou nenhuma estatina (grupo controle), com indicacao previa eletiva de realizacao de intervencao coronaria percutânea. Foi analisada a ativacao plaquetaria atraves do numero de plaquetas, niveis de P-selectina e glucoproteina IIb/IIIa (com e sem estimulo de ADP) atraves de citometria de fluxo. Os resultados foram analisados antes e apos a intervencao coronaria percutânea e da administracao de clopidogrel. RESULTADOS: Observamos reducao da atividade plaquetaria com uso de clopidogrel. Alem disso, nao houve diferencas entre as variaveis analisadas que comprovassem reducao da atividade do clopidogrel quando associado a estatinas. Observou-se niveis de p-selectina (pre-angioplastia: 14,23±7,52 x 11,45±8,83 x 7,65±7,09; pos angioplastia: 21,49±23,82 x 4,37±2,71 x 4,82±4,47, ρ<0,01) e glicoproteina IIb/IIIa (pre-angioplastia: 98,97±0,43 x 98,79±1,25 x 99,21±0,40; pos angioplastia: 99,37±0,29 x 98,50±1,47 x 98,92±0,88, ρ=0,52), respectivamente nos grupos controle, atorvastatina e sinvastatina. CONCLUSAO: Concluimos que a ativacao plaquetaria diminui com a administracao de clopidogrel, e que o clopidogrel nao tem seu efeito antiplaquetario reduzido na presenca de sinvastatina ou atorvastatina.