Early BBBD in focal cerebral ischemia initiates multifocally in the distal capillary and venular bed of the cerebral microvasculature. It is closely associated with perimicrovascular vasogenic edema and microglial activation and predicts the extent of final infarction.

Background Troponin elevation is common in ischemic stroke (IS) patients. The pathomechanisms involved are incompletely understood and comprise coronary and non-coronary causes, e.g. autonomic dysfunction. We investigated determinants of troponin elevation in acute IS patients including markers of autonomic dysfunction, assessed by heart rate variability (HRV) time domain variables. Methods Data were collected within the Stroke Induced Cardiac FAILure (SICFAIL) cohort study. IS patients admitted to the Department of Neurology, Würzburg University Hospital, underwent baseline investigation including cardiac history, physical examination, echocardiography, and blood sampling. Four HRV time domain variables were calculated in patients undergoing electrocardiographic Holter monitoring. Multivariable logistic regression with corresponding odds ratios (OR) and 95% confidence intervals (CI) was used to investigate the determinants of high-sensitive troponin T (hs-TnT) levels ≥14 ng/L. Results We report results from 543 IS patients recruited between 01/2014–02/2017. Of those, 203 (37%) had hs-TnT ≥14 ng/L, which was independently associated with older age (OR per year 1.05; 95% CI 1.02–1.08), male sex (OR 2.65; 95% CI 1.54–4.58), decreasing estimated glomerular filtration rate (OR per 10 mL/min/1.73 m2 0.71; 95% CI 0.61–0.84), systolic dysfunction (OR 2.79; 95% CI 1.22–6.37), diastolic dysfunction (OR 2.29; 95% CI 1.29–4.02), atrial fibrillation (OR 2.30; 95% CI 1.25–4.23), and increasing levels of C-reactive protein (OR 1.48 per log unit; 95% CI 1.22–1.79). We did not identify an independent association of troponin elevation with the investigated HRV variables. Conclusion Cardiac dysfunction and elevated C-reactive protein, but not a reduced HRV as surrogate of autonomic dysfunction, were associated with increased hs-TnT levels in IS patients independent of established cardiovascular risk factors. Registration-URL: https://www.drks.de/drks_web/; Unique identifier: DRKS00011615.

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ZusammenfassungDas Pyoderma gangraenosum (PG) ist eine neutrophile Dermatose unklarer Genese, die sowohl in Assoziation zu hämatologischen und neoplastischen Systemerkrankungen, chronisch-entzündlichen Darmerkrankungen und autoinflammatorischen Syndromen als auch idiopathisch auftreten kann. Sowohl die Diagnosestellung wie auch die Therapie des PG stellen aufgrund seiner Seltenheit, des Fehlens großer randomisierter kontrollierter Studien und der unzureichend verstandenen Pathogenese eine Herausforderung in der klinischen Praxis dar. Diese Übersichtsarbeit beschreibt und diskutiert aktuelle Erkenntnisse, die das PG als autoinflammatorische Erkrankung beschreiben. Durch eine Dysregulation von T-Lymphozyten und myeloiden Zellen wie den neutrophilen Granulozyten kommt es zur Entstehung von Pusteln und großflächigen Ulzera. Klassische Therapieansätze umfassen eine anti-inflammatorische topische Therapie, eine Analgesie sowie die systemische Gabe von Immunmodulantien oder -suppressiva. Neuere, bisher nicht zugelassene Therapieoptionen sind der Einsatz von Biologika und JAK-Inhibitoren.