RESUMEN
Lemierre's syndrome (LS) is characterized by septic thrombophlebitis of the internal jugular vein with septicemia and metastatic infection following an oropharyngeal infection. LS is rare but can cause infective endocarditis (IE), complicating IE management. We report a case of IE secondary to thrombophlebitis in the left vertebral vein following pharyngitis (LS variant) with distinctively severe manifestations, including metastatic infection and severe neurological impairment with multiple cerebral infarctions. A pedunculated abscess was noted on the left ventricular free wall. Despite the patient's highly impaired consciousness level (i.e., comatose state), we performed early surgery to remove the abscess after excluding LS-related brain complications. Preoperative antibiotics included clindamycin to cover LS-related anaerobic bacteria, and thrombophlebitis required postoperative anticoagulation. By managing LS as well as IE, the infection was controlled, and the neurological status normalized. This report provides insights into the perioperative management of IE secondary to LS.
Asunto(s)
Endocarditis , Síndrome de Lemierre , Faringitis , Tromboflebitis , Humanos , Venas Yugulares/diagnóstico por imagen , Venas Yugulares/cirugía , Síndrome de Lemierre/complicacionesRESUMEN
We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative that is unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3) and prolonged the lifespan of heart failure mice with genetic dilated cardiomyopathy or transverse aortic constriction-induced left ventricular hypertrophy. However, it remained unclear how DM-celecoxib regulated structure and function of cardiomyocytes and cardiac fibroblasts involved in cardiac remodeling. In the present study, therefore, we investigated the effect of DM-celecoxib on isoprenaline-induced cardiomyocyte hypertrophy and cardiac fibroblast activation, because DM-celecoxib prevented isoprenaline-induced cardiac remodeling in vivo. DM-celecoxib suppressed isoprenaline-induced neonatal rat cardiomyocyte hypertrophy by the inhibition of Akt phosphorylation resulting in the activation of GSK-3 and the inhibition of ß-catenin and mammalian target of rapamycin (mTOR). DM-celecoxib also suppressed the proliferation and the production of matrix metalloproteinase-2 and fibronectin of rat cardiac fibroblasts. Moreover, we found that phosphatase and tensin homolog on chromosome 10 (PTEN) could be a molecule to mediate the effect of DM-celecoxib on Akt. These results suggest that DM-celecoxib directly improves the structure and function of cardiomyocytes and cardiac fibroblasts and that this compound could be clinically useful for the treatment of ß-adrenergic receptor-mediated maladaptive cardiac remodeling.
Asunto(s)
Cardiomegalia/inducido químicamente , Cardiomegalia/tratamiento farmacológico , Fibroblastos/efectos de los fármacos , Glucógeno Sintasa Quinasa 3/metabolismo , Isoproterenol/farmacología , Miocitos Cardíacos/efectos de los fármacos , Proteínas Proto-Oncogénicas c-akt/antagonistas & inhibidores , Pirazoles/uso terapéutico , Sulfonamidas/uso terapéutico , Animales , Animales Recién Nacidos , Modelos Animales de Enfermedad , Fibroblastos/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Miocitos Cardíacos/metabolismo , Fosforilación/efectos de los fármacos , Proteínas Proto-Oncogénicas c-akt/metabolismo , Pirazoles/farmacología , Ratas , Ratas Sprague-Dawley , Sulfonamidas/farmacología , Remodelación Ventricular/efectos de los fármacosRESUMEN
We report a case of aortic prosthetic valve endocarditis presenting with subaortic stenosis without perivalvular leakage and vegetations in the left ventricular outflow and right atrium, the latter being attached to the atrioventricular septum. Intraoperatively, an abscess that had formed on the aortic annulus and perforated to the right atrium was unexpectedly found, the fistula being occluded by vegetations. Even when no left-to-right shunts are detected by imaging, vegetations adjacent to the atrioventricular septum may conceal a left ventricle-right atrium fistula, resulting in prosthetic valve endocarditis presenting clinically as subaortic stenosis without perivalvular leakage.