RESUMO
In acute coronary syndromes inflammatory process plays an important role in atherosclerotic plaque instability. Our aim was to evaluate the presence and distribution of vulnerable plaques and inflammatory infiltrates in patients who died of acute myocardial infarction in comparison to patients who died of non-coronary heart disease. We analyzed pathologic studies of the heart of 68 patients who died of acute myocardial infarction and 15 patients who died of non-coronary heart disease. The presence of thrombus, intraplaque hemorrhage, endothelial rupture and inflammatory infiltrates were registered. In patients who died of myocardial infarction, we found thrombus in 73.5% of the involved arteries and in 28.7% of the non involved (p < 0.0001). Intraplaque hemorrhage was found in 70.5% of involved arteries and in 39.7% of the non involved (p < 0.0001); endothelial rupture in 29.4% of involved arteries and in 3.7% of non involved arteries (p < 0.0001). There was no difference in the presence of inflammatory infiltrates (76.5% versus 68.4%). Comparing with patients who have died of non-coronary heart disease, the presence of thrombus was significantly higher (73.5% vs. 13.3%; p < 0.0001), as well as the presence of intraplaque hemorrhage (70.5% vs. 0%; p < 0.0001) and of inflammatory infiltrates in atherosclerotic plaques (76.5% vs. 46.6%; p = 0.021). In patients who died of acute myocardial infarction we observed plaque instability and inflammatory activity, not only in the infarct related artery but also in the non involved arteries.
Assuntos
Infarto do Miocárdio/patologia , Placa Aterosclerótica/patologia , Autopsia , Vasos Coronários/patologia , Feminino , Humanos , Imuno-Histoquímica , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/mortalidade , Ruptura EspontâneaRESUMO
Los procesos inflamatorios en los síndromes coronarios agudos juegan un rol importante en la inestabilidad de la placa ateroesclerótica. Nuestro objetivo fue evaluar la presencia y distribución de placas vulnerables e infiltrados inflamatorios en pacientes fallecidos por infarto agudo de miocardio y su comparación con los hallazgos en pacientes fallecidos por cuadros no coronarios. Se analizaron los estudios anatomopatológicos de corazón de 68 pacientes fallecidos por infarto agudo de miocardio y 15 fallecidos por causa no coronaria. Se registró la presencia de trombo, hemorragia intraplaca, ruptura endotelial e infiltrado inflamatorio. Al evaluar los pacientes fallecidos por IAM, encontramos trombo en 73.5% de las arterias responsables del IAM y en 28.7% de las no responsables (p < 0.0001). La hemorragia intraplaca se halló en el 70.5% de las arterias responsables y en 39.7% de las no responsables, p < 0.0001; ruptura endotelial en el 29.4% de las arterias responsables y en 3.7% de las no responsables, p < 0.0001. No encontramos diferencias en la presencia de infiltrado inflamatorio (76.5% versus 68.4%). Comparando con los fallecidos por causas no coronarias, la presencia de trombo fue significativamente superior (73.5% vs. 13.3%; p < 0.0001), así como la de hemorragia intraplaca (70.5% vs. 0%; p < 0.0001) y de infiltrado inflamatorio en las placas ateroescleroticas (76.5% vs. 46.6%; p = 0.021). En los pacientes fallecidos por infarto agudo de miocardio se observa inestabilidad de placa y actividad inflamatoria, no sólo en la arteria responsable del infarto sino también en las arterias no responsables del infarto.
In acute coronary syndromes inflammatory process plays an important role in atherosclerotic plaque instability. Our aim was to evaluate the presence and distribution of vulnerable plaques and inflammatory infiltrates in patients who died of acute myocardial infarction in comparison to patients who died of non-coronary heart disease. We analyzed pathologic studies of the heart of 68 patients who died of acute myocardial infarction and 15 patients who died of non-coronary heart disease. The presence of thrombus, intraplaque hemorrhage, endothelial rupture and inflammatory infiltrates were registered. In patients who died of myocardial infarction, we found thrombus in 73.5% of the involved arteries and in 28.7% of the non involved (p < 0.0001). Intraplaque hemorrhage was found in 70.5% of involved arteries and in 39.7% of the non involved (p < 0.0001); endothelial rupture in 29.4% of involved arteries and in 3.7% of non involved arteries (p < 0.0001). There was no difference in the presence of inflammatory infiltrates (76.5% versus 68.4%). Comparing with patients whoo have died of non-coronary heart disease, the presence of thrombus was significantly higher (73.5% vs. 13.3%; p < 0.0001), as well as the presence of intraplaque hemorrhage (70.5% vs. 0%; p < 0.0001) and of inflammatory infiltrates in atherosclerotic plaques (76.5% vs. 46.6%; p = 0.021). In patients who died of acute myocardial infarction we observed plaque instability and inflammatory activity, not only in the infarct related artery but also in the non involved arteries.
Assuntos
Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/patologia , Placa Aterosclerótica/patologia , Autopsia , Vasos Coronários/patologia , Imuno-Histoquímica , Infarto do Miocárdio/mortalidade , Ruptura EspontâneaRESUMO
Primary antiphospholipid syndrome (APS) is a well-defined entity characterized by spontaneous and recurrent abortion, thrombocytopenia and recurrent vascular thromboses (arterial and venous). Left ventricular thrombus mimicking primary cardiac tumor with recurrent systemic embolism has not been previously reported. In this report we describe a 39 year-old man admitted to hospital presenting with left hemiparesis and a peripheral embolism. He had no history of thrombotic events. Transthoracic echocardiography showed a large, polypoid and mobile mass (4.0 x 1.2 cm) attached to the apex of the left ventricle, highly suggestive of primary cardiac tumor. The patient subsequently underwent open heart surgery. The histological examination showed an older thrombus and a fresh thrombus. Post-operative laboratory tests showed lupus anticoagulant activity, confirming the primary APS diagnosis. The patient initiated treatment with oral anticoagulation (INR levels between 2 and 3) and was discharged 29 days after surgery. At ten month follow-up, he was symptom-free with long-term anticoagulation therapy. No evidence of intracardiac mass recurrence on two-dimensional echocardiography was seen. Intracardiac thrombus has been rarely reported as a complication of primary APS. Left ventricular mass mimicking primary cardiac tumor with recurrent systemic embolism has not been previously reported. Pre-operative investigations could not distinguish such a thrombus from a cardiac tumor and the diagnosis was made post-operatively.
Assuntos
Síndrome Antifosfolipídica/diagnóstico , Embolia/etiologia , Cardiopatias/etiologia , Neoplasias Cardíacas/diagnóstico , Trombose/etiologia , Administração Oral , Adulto , Anticoagulantes/administração & dosagem , Síndrome Antifosfolipídica/complicações , Síndrome Antifosfolipídica/tratamento farmacológico , Procedimentos Cirúrgicos Cardíacos , Diagnóstico Diferencial , Embolia/diagnóstico por imagem , Embolia/terapia , Cardiopatias/diagnóstico por imagem , Cardiopatias/terapia , Ventrículos do Coração/diagnóstico por imagem , Humanos , Masculino , Recidiva , Trombose/diagnóstico por imagem , Trombose/terapia , Resultado do Tratamento , UltrassonografiaRESUMO
Introducción Estudios clínicos y anatomopatológicos sugieren que los procesos inflamatorios tienen un papel importante en la inestabilidad de la placa aterosclerótica, dado que en pacientes con síndromes coronarios agudos se observan infiltrados inflamatorios difusos en las arterias coronarias. Objetivos Evaluar y localizar la distribución de placas vulnerables e infiltrados inflamatorios en pacientes fallecidos por infarto agudo de miocardio. Material y métodos Mediante microscopia óptica se estudiaron las arterias coronarias de 58 pacientes fallecidos por infarto de miocardio. En las arterias coronarias relacionadas con el infarto y en las no relacionadas se registraron las siguientes variables: presencia de trombo, rotura de placa, hemorragia intraplaca y presencia de infiltrado inflamatorio. Resultados Al analizar las diferencias existentes entre las arterias responsables del infarto y en las no responsables se encontraron diferencias significativas con respecto a la presencia de trombo (69% versus 38%; p < 0,008) y de hemorragia intraplaca (69% versus 50%; p < 0,03). No se encontró una diferencia significativa entre la arteria responsable y la no responsable al evaluar la presencia de infiltrado inflamatorio en las placas ateroscleróticas (77% versus 71%; p = ns). Conclusión En el infarto agudo de miocardio se comprobó la presencia de actividad inflamatoria que afectaba a más de un vaso, con compromiso de otras arterias además de la responsable del infarto. Se detectó también accidente agudo de placa en más de una arteria coronaria.
Background Data from clinical and histopathologic studies suggest that inflammation plays a key role in instability of atherosclerotic plaque as patients with acute coronary syndromes present diffuse inflammatory infiltrates in the coronary arteries. Objectives To assess and locate the distribution of vulnerable plaques and inflammatory infiltrates in patients who died of acute myocardial infarction. Material and Methods We examined the coronary arteries from 58 patients who died of myocardial infarction using light microscopy. The following variables were evaluated in culprit and non-culprit coronary arteries: presence of thrombus, plaque rupture, intraplaque hemorrhage and inflammatory infiltrate. Results The presence of thrombus and intraplaque hemorrhage was significantly greater in culprit coronary arteries compared to non-culprit vessels (69% versus 38%; p<0.008, and 69% versus 50%; p<0.03, respectively). There were no significant differences in the presence of inflammatory infiltrates in atherosclerotic plaques from culprit and non-culprit coronary arteries (77% versus 71%; p=ns). Conclusion Inflammatory activity was demonstrated in acute myocardial infarction affecting not only the infarct-related artery but also other coronary vessels. Plaque accident was also present in more than one coronary artery.
RESUMO
Lamotrigine is a non-aromatic antiepileptic drug. Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a severe idiosyncratic reaction to drugs, especially anti-epileptic drugs. Associated clinical features include cutaneous eruption, fever, multiple peripheral lymphadenopathies, and potentially life-threatening damage of one or more organs. We report a case of DRESS syndrome induced by lamotrigine presenting with a hypersensitivity syndrome and fulminant hepatic failure requiring liver transplant. A 21-year old female patient presented an episode of seizure with loss of conscience. CT and EEG studies performed were normal. Treatment with lamotrigine was prescribed. In the course of 30 days, the patient developed skin lesions, pruritus, cholestatic hepatitis, and systemic symptoms -fever, lymphadenopathies, extensive exfoliative erythematous maculopapular rash, and jaundice. Serologic and laboratory tests showed no other causes responsible for the clinical spectrum. Hematologic tests revealed peripheral eosinophilia. Fulminant hepatic failure was diagnosed and an orthotopic liver transplant was performed. Histologic sections of the explanted liver demonstrated submassive hepatic necrosis, with the remnant portal spaces and lobules showing a mixed inflammatory infiltrate with lymphocytes and eosinophils. Lamotrigine treatment has been associated with multiorgan failure, DRESS syndrome, acute hepatic failure, and disseminated intravascular coagulation. In conclusion, we suggest that these potentially fatal side effects should be considered in any patient with clinical deterioration following administration of this drug.
Assuntos
Anticonvulsivantes/efeitos adversos , Hipersensibilidade a Drogas/etiologia , Falência Hepática Aguda/induzido quimicamente , Triazinas/efeitos adversos , Toxidermias/etiologia , Hipersensibilidade a Drogas/patologia , Hipersensibilidade a Drogas/cirurgia , Eosinofilia/induzido quimicamente , Feminino , Febre/induzido quimicamente , Humanos , Lamotrigina , Falência Hepática Aguda/patologia , Falência Hepática Aguda/cirurgia , Transplante de Fígado , Doenças Linfáticas/induzido quimicamente , Síndrome , Adulto JovemRESUMO
La miocarditis de células gigantes (MCG) es una entidad rara, de causa desconocida, de probable etiología autoinmune. Puede presentarse como insuficiencia cardíaca refractaria, asociarse con arritmias ventriculares y en otras ocasiones simular un infarto agudo de miocardio. Su pronóstico con frecuencia es ominoso, salvo que se realicen tratamiento inmunosupresor o trasplante cardíaco, este último con elevada recurrencia.
The giant cell myocarditis (GCM) is a rare disease, of unknown origin, and probably of autoimmune etiology. It can occur as refractory heart failure, associate with ventricular arrhythmias, and mimicking an acute myocardial infarction in certain cases. Its prognosis is usually ominous, unless immunosupressive therapy or cardiac transplant is performed, the latter with a high recurrence.
RESUMO
Thrombosis in a native aortic valve is a rare complication which may lead to systemic embolization. A few cases of aortic thrombosis in previously abnormal valves have been described. In this report, we describe a 42-year-old male who suffered two acute ischaemic attacks, one in the upper right limb and another in the cerebral territory supplied by the left sylvian artery, from a thrombus that developed in a bicuspid and stenotic aortic valve. The diagnosis was made with transthoracic and transoesophageal echocardiography, and the patient subsequently underwent surgery. In cases of bicuspid aortic valves, we should think of thrombosis as a possible complication with its resulting risk of embolism, and assess such patients with transthoracic and transoesophageal echocardiography, thus enabling their early detection and treatment.
Assuntos
Estenose da Valva Aórtica/diagnóstico por imagem , Embolia/etiologia , Trombose/diagnóstico por imagem , Adulto , Estenose da Valva Aórtica/complicações , Humanos , Masculino , Recidiva , Trombose/etiologia , UltrassonografiaRESUMO
Antiphospholipid syndrome is a well-defined entity that is characterized by spontaneous abortion, thrombocytopenia, and recurrent arterial and venous thromboses. A partially calcified right atrial thrombus mimicking myxoma with recurrent pulmonary embolism has not been previously reported in a patient who also had systemic lupus erythematosus and secondary antiphospholipid syndrome. Herein, we describe the case of a 37-year-old woman with systemic lupus erythematosus and secondary antiphospholipid syndrome who was admitted to the hospital with progressive exertional dyspnea. Ventilation-perfusion scanning showed multiple parenchymal defects in the lungs that portended pulmonary embolism. In addition, the scanning revealed normal regional ventilation. Transthoracic and transesophageal echocardiography showed a right atrial mass that was highly suggestive of myxoma, and the patient subsequently underwent surgery. A histologic examination showed an organized, partially calcified thrombus. Intracardiac thrombus has been rarely reported as a complication of antiphospholipid syndrome. In our patient, the preoperative investigations could not differentiate the partially calcified right atrial thrombus from a myxoma, and the diagnosis was made postoperatively.
Assuntos
Síndrome Antifosfolipídica/diagnóstico , Trombose Coronária/diagnóstico , Átrios do Coração/patologia , Lúpus Eritematoso Sistêmico/diagnóstico , Mixoma/diagnóstico , Embolia Pulmonar/diagnóstico , Adulto , Anticorpos Monoclonais/uso terapêutico , Anticorpos Monoclonais Murinos , Anticoagulantes/uso terapêutico , Antineoplásicos/uso terapêutico , Síndrome Antifosfolipídica/complicações , Síndrome Antifosfolipídica/diagnóstico por imagem , Trombose Coronária/diagnóstico por imagem , Trombose Coronária/fisiopatologia , Trombose Coronária/cirurgia , Diagnóstico Diferencial , Feminino , Humanos , Fatores Imunológicos/uso terapêutico , Lúpus Eritematoso Sistêmico/complicações , Lúpus Eritematoso Sistêmico/diagnóstico por imagem , Lúpus Eritematoso Sistêmico/fisiopatologia , Mixoma/diagnóstico por imagem , Mixoma/fisiopatologia , Mixoma/cirurgia , Perfusão , Embolia Pulmonar/diagnóstico por imagem , Embolia Pulmonar/fisiopatologia , Embolia Pulmonar/cirurgia , Fatores de Risco , Rituximab , Ultrassonografia , Varfarina/uso terapêuticoAssuntos
Perfuração Intestinal/cirurgia , Politetrafluoretileno , Próteses e Implantes , Idoso de 80 Anos ou mais , Evolução Fatal , Feminino , Seguimentos , Humanos , Mucosa Intestinal/patologia , Perfuração Intestinal/etiologia , Perfuração Intestinal/patologia , Pessoa de Meia-Idade , Úlcera Gástrica/complicações , Resultado do TratamentoRESUMO
FAP is an autosomal dominant inherited disease, characterized by systemic deposition of amyloid fibrils in various tissues. The purpose of this study is to describe the gross and microscopic findings of the explanted livers for FAP.10 patients were transplanted for FAP at our institution. Diagnosis was supported by positive familiar history, clinical data and detection of mutated TTR by electrospray ionization mass spectrometry with Val30Met mutation verified by PCR. All the explanted livers were photographed, fixed in formol and processed according to protocol. Later they were examined with HyE, reticulin, PAS diastasa, Masson trichromic, Congo red with polarised light and immunoreactivity against TTR. The gross aspect was normal. We obtained multiple samples representative of the organ and the hepatic hilium. All of the patients presented with deposits of amyloid substance in the lymph nodes and the nerves of the hepatic hilium These deposits were Congo red positive with a greenish birefringence to polarized light Deposits show immunoreactivity with antihuman TTR. Whereas liver transplantation restores hepatic function in patients with cirrhosis, liver transplantation cures the FAP patient of their genetic defect. Domino transplantation is a procedure in which the index patient receives an organ, while the explanted organ is reused for transplantation into another patient. In conclusion, exclusion of hepatic amyloid deposits which can cause functional alterations in the FAP liver is vital; and is important to study the explanted livers of patients with FAP to confirm the results of the scarce published series.