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1.
Alger. J. health sci. (Online. Oran) ; 3(3): 88-94, 2021. Tables, figures
Artigo em Inglês | AIM (África) | ID: biblio-1292605

RESUMO

L'expansion planétaire du covid19 représente une crise sans précèdent ; cette pandémie a fait plus d'un million de mort en une année. En plus de l'atteinte pulmonaire, le virus a des implications majeures sur le système cardiovasculaire : les maladies cardiovasculaires pré existantes représentent un facteur de risque d'infection sévère avec augmentation de la mortalité, d'autre part l'infection entraine des complications cardiovasculaires qui aggravent le pronostic. Le lien entre le Covid19 et le système cardiovasculaire découle principalement de la voie d'entrée cellulaire du virus qui est assurée par sa liaison à une protéine membranaire l'enzyme de conversion de l'angiotensine (ECA), qui joue un rôle clé dans la régulation neurohumorale ; cette protéine est très présente au niveau du cœur et du poumon, d'où le tropisme du virus qui entraine la dysrégulation de cette voie cellulaire avec des répercussion sur la fonction cardiaque et respiratoire. Une polémique a déferlé concernant les traitements anti hypertenseurs et notamment les inhibiteurs du système rénine angiotensine aldostérone mais après évaluation des données actuelles, il est de consensus de ne pas arrêter ou changer les traitements anti hypertenseurs. L'augmentation des troponines cardiaques est un facteur de mauvais pronostic qui aggrave le tableau. La myocardite est définie par une inflammation myocardique, Les tableaux cliniques sont variables de la forme légère à la forme grave ; les biomarqueurs myocardiques restent un test incontournable en cas de suspicion clinique, le pronostic est incertain avec des formes fulminantes qui peuvent régresser et enfin pour le traitement les corticoïdes semblent être efficaces. Une autre complication du virus sont les accidents thrombo-emboliques et le dilemme occasionné par le risque accru aux thromboses et la thrombopénie induite par l'utilisation de l'héparine (TIH). On note une augmentation de l'incidence des syndromes coronaires aigus chez les sujets atteints du covid19.


The global expansion of covid19 represents a global crisis; this pandemic killed more than a million people in one year. In addition to pulmonary involvement, the virus has major implications on the cardiovascular system: pre-existing cardiovascular diseases represent a risk factor for severe infection with increased mortality, on the other hand the infection causes cardiovascular complications which worsen the prognosis. The link between the Covid19 and the cardiovascular system stems primarily from the virus's cellular entry pathway, which is provided by its binding to a membrane protein, the angiotensin converting enzyme (ACE) wich plays a key role in neurohumoral regulation; this protein is very present in the heart and lungs, hence the tropism of the virus which causes the dysregulation of this cellular pathway with repercussions on cardiac and respiratory function. A controversy broke out concerning the antihypertensive treatments and in particular the inhibitors of the renin angiotensin aldosterone system but after evaluation of the current data, there is a consensus not to withhold or change the treatments. The increase in cardiac troponins is a factor of poor prognosis which worsens the picture. Myocarditis is defined by myocardial inflammation, its clinical form ranges from the mild form to the severe one; the myocardial biomarkers remain an essential when the clinical suspicion rise, the prognosis is uncertain with fulminant forms which can regress; for treatment corticosteroids seem to be effective. Another complication of the virus are thromboembolic events and the dilemma caused by the increased risk of thrombosis and thrombocytopenia induced by the use of heparin (TIH), and there is an increase in the incidence of acute coronary syndromes in patients affected by covid19.


Assuntos
COVID-19 , Trombose , Sistema Cardiovascular , Argélia , Teste de Ácido Nucleico para COVID-19 , Miocardite
2.
Cardiovasc J Afr ; 30(1): 45-51, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30460974

RESUMO

OBJECTIVE: To test whether aspiration thrombectomy with intracoronary (IC) instead of intravenous (IV) administration of abciximab could reduce the no-reflow phenomenon in patients undergoing primary percutaneous intervention (PCI) for ST-elevation myocardial infarction (STEMI). BACKGROUND: Despite recanalisation with PCI, failure to restore microvascular flow may affect the prognosis of patients with STEMI. A combination of aspiration thrombectomy with IC abciximab may improve distal perfusion. METHODS: After aspiration thrombectomy during primary PCI for STEMI, 160 patients were randomly assigned to either an IV or IC abciximab bolus delivered through the aspiration catheter, both followed by a 12-hour IV abciximab infusion. RESULTS: ST-segment resolution ≥ 70% was achieved in 36 of 78 patients with IC versus 30 of 82 patients with IV abciximab (46.1 vs 36.6%, p = 0.368), and partial resolution in 28 of 78 versus 31 of 82 patients (35.9 vs 37.8%, p = 0.368). Postprocedural myocardial blush grade (MBG) 3 was obtained in 62.8 vs 63.4% (p = 0.235) and MBG ≥ 2 in 89.7 vs 81.7% (p = 0.148) of patients given IC and IV abciximab, respectively. There were three deaths in each group (3.8%). Major adverse cardiac events occurred in six of 78 patients given the IC and seven of 82 patients given the IV abciximab bolus (7.6 vs 8.5%, p = 0.410). One stroke occurred in each group, and two patients in the IC and nine in the IV group developed renal failure (2.5 vs 10.9%, p = 0.414). CONCLUSIONS: IC versus IV abciximab did not enhance myocardial reperfusion in non-selected patients with STEMI undergoing primary PCI after aspiration thrombectomy had successfully been performed.


Assuntos
Abciximab/administração & dosagem , Fenômeno de não Refluxo/prevenção & controle , Intervenção Coronária Percutânea , Inibidores da Agregação Plaquetária/administração & dosagem , Infarto do Miocárdio com Supradesnível do Segmento ST/terapia , Trombectomia/métodos , Abciximab/efeitos adversos , Adulto , Idoso , Argélia , Circulação Coronária/efeitos dos fármacos , Feminino , Humanos , Infusões Intravenosas , Masculino , Microcirculação/efeitos dos fármacos , Pessoa de Meia-Idade , Fenômeno de não Refluxo/diagnóstico por imagem , Fenômeno de não Refluxo/etiologia , Fenômeno de não Refluxo/fisiopatologia , Intervenção Coronária Percutânea/efeitos adversos , Intervenção Coronária Percutânea/instrumentação , Inibidores da Agregação Plaquetária/efeitos adversos , Estudos Prospectivos , Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico por imagem , Infarto do Miocárdio com Supradesnível do Segmento ST/fisiopatologia , Método Simples-Cego , Stents , Sucção , Trombectomia/efeitos adversos , Fatores de Tempo , Resultado do Tratamento
3.
Arch Cardiovasc Dis ; 110(11): 626-633, 2017 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-28583820

RESUMO

BACKGROUND: High P2Y12 platelet reactivity (PR) level after primary percutaneous coronary intervention (PPCI) for ST-segment elevation myocardial infarction (STEMI) affects prognosis and may induce the no-reflow phenomenon. AIM: To investigate the role of PR in the genesis of microvascular obstruction. METHODS: Patients with STEMI undergoing PPCI within 12hours of symptoms onset were included prospectively. All patients received a 600mg clopidogrel-loading dose before PPCI and 250mg aspirin. PR was measured thereafter during PPCI while wiring the culprit lesion and before coronary dilatation, using the P2Y12 VerifyNow® assay. No-reflow was defined as ST-segment regression<50% observed 90minutes after PPCI. RESULTS: Between January 2014 and November 2015, 140 STEMI patients were included, and divided into two groups: a low PR group (LPR) defined as PR<209P2Y12 reaction units (PRU); and a high PR group (HPR) defined as PR≥209PRU. There were no differences in baseline characteristics between LPR and HPR groups, including age (57.8±11.9 vs. 59.4±13.2 years, respectively; P=0.44) and weight (76.1±15.1 vs. 74.8±10.9kg, respectively; P=0.55). Delay to revascularization was 270.1±175.5 vs. 295.6±206.2minutes (P=0.49) and time between clopidogrel-loading and PR measurement was 53±37 vs 65±54minutes (P=0.29) in the LPR and HPR groups, respectively. No-reflow was more frequent in the HPR group (44 [47.3%] vs. 9 [19.1%]; P=0.0012). Mean PR was higher in patients with no-reflow: 268.3±53 vs. 223.8±50.1 PRU (P=0.002). In multivariable analysis, HPR was an independent predictor of no-reflow. Area under the receiver operating characteristic curve was 0.745 (0.654, 0.835); the cut-off value predicting no-reflow was 254PRU. CONCLUSION: High PR level measured at PPCI is independently associated with no-reflow.


Assuntos
Aspirina/uso terapêutico , Plaquetas/efeitos dos fármacos , Fenômeno de não Refluxo/etiologia , Intervenção Coronária Percutânea , Inibidores da Agregação Plaquetária/uso terapêutico , Antagonistas do Receptor Purinérgico P2Y/uso terapêutico , Infarto do Miocárdio com Supradesnível do Segmento ST/terapia , Ticlopidina/análogos & derivados , Idoso , Área Sob a Curva , Aspirina/efeitos adversos , Plaquetas/metabolismo , Distribuição de Qui-Quadrado , Clopidogrel , Angiografia Coronária , Circulação Coronária , Resistência a Medicamentos , Feminino , Humanos , Masculino , Microcirculação , Pessoa de Meia-Idade , Análise Multivariada , Fenômeno de não Refluxo/diagnóstico por imagem , Fenômeno de não Refluxo/fisiopatologia , Razão de Chances , Intervenção Coronária Percutânea/efeitos adversos , Inibidores da Agregação Plaquetária/efeitos adversos , Testes de Função Plaquetária , Valor Preditivo dos Testes , Estudos Prospectivos , Antagonistas do Receptor Purinérgico P2Y/efeitos adversos , Curva ROC , Receptores Purinérgicos P2Y12/sangue , Receptores Purinérgicos P2Y12/efeitos dos fármacos , Fatores de Risco , Infarto do Miocárdio com Supradesnível do Segmento ST/sangue , Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico por imagem , Infarto do Miocárdio com Supradesnível do Segmento ST/fisiopatologia , Ticlopidina/efeitos adversos , Ticlopidina/uso terapêutico , Fatores de Tempo , Resultado do Tratamento
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