RESUMO
BACKGROUND: Infective endocarditis (IE) is a serious condition with a high mortality, represents a rare cause of stroke and an increased risk of intracranial hemorrhage. In this single center study, we characterize stroke patients with IE. We were interested in risk factors for intracranial hemorrhage and outcome of patients with intracranial hemorrhage compared to patients with ischemic stroke. METHODS: Patients with IE and symptomatic ischemic stroke or intracranial hemorrhage admitted to our hospital between January 2019 and December 2022 were included in this retrospective study. RESULTS: 48 patients with IE and ischemic stroke or intracranial hemorrhage were identified. 37 patients were diagnosed with ischemic stroke, 11 patients were diagnosed with intracranial hemorrhage. The intracranial hemorrhage occurred within the first 12 days after admission. We identified Staphylococcus aureus detection and thrombocytopenia as risk factors for hemorrhagic complications. An increased in-hospital mortality in patients with intracranial hemorrhage (63.6% vs. 22%, p = 0.022) was found, whereas patients with ischemic stroke and patients with intracranial hemorrhage do not differ regarding favorable clinical outcome (27% vs. 27.3%, p = 1.0). 27.3% patients with intracranial hemorrhage and 43.2% patients with ischemic stroke underwent cardiac surgery. Overall, 15.7% new ischemic strokes occurred after valve reconstruction, whereas no new intracranial hemorrhage was observed. CONCLUSIONS: We found an increased in-hospital mortality in patients with intracranial hemorrhage. Beside thrombocytopenia, we identified S. aureus detection as a risk factor for intracranial hemorrhage.
RESUMO
BACKGROUND: Elevated troponin levels are commonly found in patients with acute stroke and approximately 60 % of stroke patients suffer from an accompanying coronary artery disease. Troponin release can be caused either by an acute thrombotic myocardial infarction or by insufficient coronary perfusion due to neurocardiogenic causes like blood pressure or heart rate variability without thrombotic coronary occlusion. Due to the often unclear pathological cause of troponin release and the risk of secondary hemorrhage during dual antiplatelet therapy, the determination of the best time point for coronary diagnostics and therapy in stroke patients is a common challenge in clinical daily routine. MATERIALS AND METHODS: Based on the current literature, we describe a potential diagnostic and therapeutic approach in stroke patients with increased troponin levels. RESULTS: First, the probability of an acute thrombotic myocardial infarction should be evaluated based on clinical, laboratory, and electrocardiographic parameters. In case of suspected myocardial infarction, a diagnostic coronary angiography/CT angiography should be performed and dual antiplatelet therapy should be given depending on the intracranial bleeding risk. In patients with high risk of intracranial bleeding, thrombus aspiration and balloon dilatation should be considered. CONCLUSION: In patients with acute stroke and elevated troponin levels, a thorough diagnostic workup is necessary to estimate the probability for a thrombotic myocardial infarction and to prevent cardiac and neurologic complications.
Assuntos
Síndrome Coronariana Aguda/sangue , Síndrome Coronariana Aguda/diagnóstico , Acidente Vascular Cerebral/sangue , Acidente Vascular Cerebral/diagnóstico , Troponina/sangue , Síndrome Coronariana Aguda/tratamento farmacológico , Algoritmos , Hemorragia Cerebral/induzido quimicamente , Hemorragia Cerebral/prevenção & controle , Comorbidade , Angiografia Coronária , Diagnóstico Diferencial , Quimioterapia Combinada , Ecocardiografia , Eletrocardiografia , Humanos , Infarto do Miocárdio/sangue , Infarto do Miocárdio/diagnóstico , Infarto do Miocárdio/tratamento farmacológico , Intervenção Coronária Percutânea , Inibidores da Agregação Plaquetária/efeitos adversos , Inibidores da Agregação Plaquetária/uso terapêutico , Medição de Risco , Acidente Vascular Cerebral/tratamento farmacológicoAssuntos
Encefalopatias/patologia , Doenças da Medula Espinal/patologia , Adulto , Idade de Início , Química Encefálica , Encefalopatias/metabolismo , Tronco Encefálico/patologia , Feminino , Marcha Atáxica/etiologia , Humanos , Ácido Láctico/metabolismo , Espectroscopia de Ressonância Magnética , Masculino , Transtornos da Motilidade Ocular/etiologia , Paresia/etiologia , Doenças da Medula Espinal/metabolismoAssuntos
Imagem de Difusão por Ressonância Magnética/métodos , Encefalomielite Aguda Disseminada/patologia , Adolescente , Anti-Inflamatórios/uso terapêutico , Corpo Caloso/efeitos dos fármacos , Corpo Caloso/patologia , Encefalomielite Aguda Disseminada/tratamento farmacológico , Humanos , Masculino , Metilprednisolona/uso terapêutico , Análise de Regressão , Fatores de TempoRESUMO
The authors report a patient with familial hemiplegic migraine type II who developed a long-lasting attack including fever, right-sided hemiplegia, aphasia, and coma. Quantitative analysis of early gadolinium-enhanced MRI revealed a mild but significant left-hemispheric blood-brain barrier (BBB) opening limited to the cortex and preceding cortical edema. The findings suggest that the delayed cortical edema was vasogenic in the severe migraine aura variant of this ATP1A2 mutation carrier.
Assuntos
Barreira Hematoencefálica/fisiopatologia , Edema Encefálico/genética , Artérias Cerebrais/fisiopatologia , Córtex Cerebral/fisiopatologia , Enxaqueca com Aura/complicações , Adulto , Afasia/genética , Afasia/patologia , Afasia/fisiopatologia , Barreira Hematoencefálica/patologia , Edema Encefálico/patologia , Edema Encefálico/fisiopatologia , Artérias Cerebrais/patologia , Córtex Cerebral/irrigação sanguínea , Córtex Cerebral/patologia , Coma/genética , Coma/patologia , Coma/fisiopatologia , Análise Mutacional de DNA , Progressão da Doença , Febre/genética , Febre/patologia , Febre/fisiopatologia , Lateralidade Funcional/genética , Hemiplegia/genética , Hemiplegia/patologia , Hemiplegia/fisiopatologia , Humanos , Imageamento por Ressonância Magnética , Masculino , Meninges/patologia , Meninges/fisiopatologia , Enxaqueca com Aura/genética , Enxaqueca com Aura/fisiopatologia , Mutação/genética , ATPase Trocadora de Sódio-Potássio/genética , Fatores de TempoRESUMO
A1A2 Na+/K+-ATPase mutations cause familial hemiplegic migraine type 2 (FHM2). The authors identified three putative A1A2 mutations (D718N, R763H, P979L) and three that await validation (P796R, E902K, X1021R). Ten to 20% of FHM cases may be FHM2. A1A2 mutations have a penetrance of about 87%. D718N causes frequent, long-lasting HM, and P979L may cause recurrent coma. D718N and P979L may predispose to seizures and mental retardation. A1A2 does not play a major role in sporadic HM; only one variant, R383H, occurred in 1 of 24 cases.
