RESUMO
Presentamos el caso de varón joven que ingresa en Unidad Cuidados Intensivos con dolor torácico como manifestación de insuficiencia aórtica masiva secundaria a endocarditis infecciosa sobre válvula aórtica bicúspide. El ecocardiograma transesofágico muestra además como complicación grave pseudoaneurisma en seno de Valsalva que comunica tanto con raíz aórtica como con ventrículo izquierdo
We present the case of a young man who is admitted in Intensive Care Unit with chest pain as manifestation of masive aortic regurgitation due to infective endocarditis in bicuspid aortic valve. The transesophageal echocardiography also shows, as severe complication, pseudoaneurysm of the sinus of Valsalva that communicates with both aortic root as left ventricle
Assuntos
Humanos , Masculino , Adulto Jovem , Estenose da Valva Aórtica/complicações , Estenose da Valva Aórtica/diagnóstico , Lesões das Artérias Carótidas/diagnóstico , Endocardite/complicações , Estenose da Valva Aórtica/metabolismo , Estenose da Valva Aórtica , Estenose da Valva Aórtica/cirurgia , Lesões das Artérias Carótidas/complicações , Endocardite/prevenção & controleRESUMO
Stent thrombosis (ST) is an uncommon but potentially lethal complication of coronary endoprothesis. Clinical trials have not shown differences in the incidence of early and late thrombosis among bare-metal stents and drug-eluting stents. Very late stent thrombosis occurs more than a year after stent implantation and is more specific of drug-eluting stents. Factors related to the patient, the stent, the coronary lesion and the technique are involved in the pathogenesis of ST. The main risk factor ST is the premature discontinuation of antiplatelet therapy. Currently, patients must receive aspirin and a thienopyridine for at least one month after the implantation of a bare-metal stent and 12 months after the implantation of a drug-eluting stent, then maintaining one antiplatelet agent indefinitely.
Assuntos
Stents/efeitos adversos , Trombose/etiologia , Humanos , Trombose/terapiaRESUMO
La trombosis del stent (TS) es una complicación infrecuente pero potencialmente letal de las endoprótesis coronarias. Los ensayos clínicos no han demostrado diferencias en la incidencia de trombosis temprana y tardía entre stents convencionales (SC) y stents liberadores de fármacos antiproliferativos (SLF). La trombosis muy tardía ocurre pasado un año de la implantación del stent y es más específica de los SLF. En la etiopatogenia de la trombosis del stent intervienen factores relacionados con el paciente, el stent, la lesión y la técnica de implante. El principal factor de riesgo para la TS es la suspensión prematura de los fármacos antiplaquetarios. Actualmente los pacientes deben recibir ácido acetilsalicílico y una tienopiridina por lo menos durante un mes tras el implante de un SC y durante 12 meses tras el implante de un SLF, manteniendo posteriormente un antiplaquetario de forma indefinida (AU)
Stent thrombosis (ST) is an uncommon but potentially lethal complication of coronary endoprothesis. Clinical trials have not shown differences in the incidence of early and late thrombosis among bare-metal stents and drug-eluting stents. Very late stent thrombosis occurs more than a year after stent implantation and is more specific of drug-eluting stents. Factors related to the patient, the stent, the coronary lesion and the technique are involved in the pathogenesis of ST. The main risk factor ST is the premature discontinuation of antiplatelet therapy. Currently, patients must receive aspirin and a thienopyridine for at least one month after the implantation of a bare-metal stent and 12 months after the implantation of a drug-eluting stent, then maintaining one antiplatelet agent indefinitely (AU)
