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Paul Gressenberger

Bio: Paul Gressenberger is an academic researcher from Medical University of Graz. The author has contributed to research in topics: Interquartile range & Renal function. The author has an hindex of 3, co-authored 8 publications receiving 12 citations.

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Journal ArticleDOI
TL;DR: In this paper, the authors evaluated the contribution of COVID-19 to persisting vascular injury and identified parameters linked to COVID19-associated endothelial dysfunction and inflammatory vasculopathy.
Abstract: Background: Rising data suggest that COVID-19 affects vascular endothelium while the underlying mechanisms promoting COVID-19-associated endothelial dysfunction and inflammatory vasculopathy are largely unknown. The aim was to evaluate the contribution of COVID-19 to persisting vascular injury and to identify parameters linked to COVID-19-associated endothelial dysfunction and inflammatory vasculopathy. Methods: In a cross-sectional design, flow-mediated dilation (FMD), nitroglycerine-related dilation (NMD), pulse-wave velocity (PWV), augmentation index, intima-media thickness (IMT), compounds of the arginine and kynurenine metabolism, homocysteine, von Willebrand factor (vWF), endothelial microparticles (EMP), antiendothelial cell antibodies, inflammatory, and immunological parameters, as well as nailfold capillary morphology were measured in post-COVID-19 patients, patients with atherosclerotic cardiovascular diseases (ASCVD) and healthy controls without prior or recent SARS-CoV-2 infection. Results: Post-COVID-19 patients had higher values of PWV, augmentation index, IMT, asymmetric and symmetric dimethylarginine, vWF, homocysteine, CD31+/CD42b- EMP, C-reactive protein, erythrocyte sedimentation rate, interleukin-6, and β-2-glycoprotein antibodies as well as lower levels of homoarginine and tryptophan compared to healthy controls (all with p < 0.05). A higher total number of pathologically altered inflammatory conditions and higher rates of capillary ramifications, loss, caliber variability, elongations and bushy capillaries with an overall higher microangiopathy evolution score were also observed in post-COVID-19 patients (all with p < 0.05). Most parameters of endothelial dysfunction and inflammation were comparably altered in post-COVID-19 patients and patients with ASCVD, including FMD and NMD. Conclusion: COVID-19 may affect arterial stiffness, capillary morphology, EMP and selected parameters of arginine, kynurenine and homocysteine metabolism as well as of inflammation contributing to COVID-19-associated endothelial dysfunction and inflammatory vasculopathy.

25 citations

Journal ArticleDOI
08 Jul 2021
TL;DR: In this article, a 39-year-old woman with an unremarkable medical history was admitted with severe holocephalic headache since 2.5 days after vaccination with ChAdOx1 nCov-19 (AstraZeneca). Physical and neurological examination was normal.
Abstract: Very recently, unusual thrombotic events in combination with severe thrombocytopenia have been reported 1–2 weeks following SARS-CoV-2 vaccination with ChAdOx1 nCov-19 (AstraZeneca). This condition, termed VITT (vaccine-induced immune thrombotic thrombocytopenia), has been related to high risk of fatal outcome with both ischaemic and haemorrhagic complications.1 2 Optimal treatment strategies still need to be elucidated—especially in case of cerebral sinus venous thrombosis (CSVT) with associated brain haemorrhage as the underlying thrombotic event. We here report our clinical experience with two young women diagnosed with VITT-associated CSVT, treated with high-dose intravenous immunoglobulins (IVIGs), corticosteroids and argatroban in the hyperacute phase, followed by dabigatran resulting in excellent outcome. A 39-year-old woman with an unremarkable medical history was admitted with severe holocephalic headache since 2 days. Eight days earlier, she had received the first vaccination with ChAdOx1 nCov-19 (AstraZeneca). Physical and neurological examination was normal. Laboratory investigations revealed moderate thrombocytopenia (84×109/L) and significantly elevated D-dimer (14.2 mg/L; normal <0.5 mg/L). Fibrinogen and other routine parameters were normal (table 1). Brain CT including venography was unremarkable as were CT pulmonary angiography and compression ultrasound of both legs. Coincidentally, the patient had contact with a COVID-19-positive person a few days after vaccination and SARS-CoV-2 reverse transcription PCR (RT-PCR) on admission was positive with cycle threshold value 26 on a nasopharyngeal swab. Prophylactic treatment with danaparoid 750 IU two times per day subcutaneously and intravenous dexamethasone 40 mg were started. While the …

16 citations

Journal ArticleDOI
TL;DR: Treatment with platelet-rich plasma as a monotherapy does not improve hair growth in men with androgenetic alopecia, and no improvements were seen over the course of the trial.
Abstract: Platelet-rich plasma injections have been presented as an effective treatment for androgenetic alopecia; however, reliable study data concerning this therapy are lacking. The current randomized, placebo-controlled pilot study explored this novel therapy in 30 healthy male subjects with androgenetic alopecia. Five platelet-rich plasma treatments, at intervals of 4-6 weeks, and 2 follow-up examinations were performed. Twenty subjects were injected intracutaneously with platelet-rich plasma and 10 with physiological saline. Treatment efficacy was assessed by changes in hair number and diameter, measured with the TrichoScan system. A secondary objective was to assess clinical improvement, which was evaluated by an independent reviewer using patient photographs and a 5-point Likert scale. In addition, subject satisfaction was assessed by survey. No improvements were seen over the course of the trial, using TrichoScan measurements or visual assessment. In conclusion, these results suggest that treatment with platelet-rich plasma as a monotherapy does not improve hair growth in men with androgenetic alopecia.

12 citations

Journal ArticleDOI
TL;DR: Thoracic but not abdominal ADs occur more commonly in GCA patients, however, the subsequent risk for aortic repair, rupture or dissection is low and changes of T-cell subsets, presence of polymyalgia rheumatica and increased carotid IMT at disease onset are associated with AD development.

11 citations

Journal ArticleDOI
TL;DR: The white blood cell count to mean platelet volume ratio presents an easily obtainable and cost-effective parameter to identify LEAD patients at high risk for CLTI.
Abstract: Background: The white blood cell count to mean platelet volume ratio (WMR) is increasingly gaining importance as a promising prognostic marker in atherosclerotic disease, but data on lower extremity artery disease (LEAD) are not yet available. The principle aim of this study was to assess the association of the WMR with the occurrence of CLTI (chronic limb-threatening ischemia) as the most advanced stage of disease. Methods: This study was performed as a retrospective analysis on 2121 patients with a diagnosis of LEAD. Patients were admitted to the hospital for the reason of LEAD and received conservative or endovascular treatment. Blood sampling, in order to obtain the required values for this analysis, was implemented at admission. Statistical analysis was conducted by univariate regression in a first step and, in case of significance, by multivariate regression additionally. Results: Multivariate regression revealed an increased WMR (p < 0.001, OR (95%CI) 2.258 (1.460–3.492)), but also advanced age (p < 0.001, OR (95%CI) 1.050 (1.040–1.061)), increased CRP (p < 0.001, OR (95%CI) 1.010 (1.007–1.014)), and diabetes (p < 0.001, OR (95%CI) 2.386 (1.933–2.946)) as independent predictors for CLTI. Conclusions: The WMR presents an easily obtainable and cost-effective parameter to identify LEAD patients at high risk for CLTI.

9 citations


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TL;DR: A wide spectrum of neurological complications is continuously being reported following COVID-19 vaccination, such as cerebral venous sinus thrombosis, acute transverse myelitis, acute disseminated encephalomyelitis and acute demyelinating polyneuropathy.
Abstract: COVID-19 vaccines have brought us a ray of hope to effectively fight against deadly pandemic of COVID-19 and hope to save lives. Many vaccines have been granted emergency use authorizations by many countries. Post-authorization, a wide spectrum of neurological complications is continuously being reported following COVID-19 vaccination. Neurological adverse events following vaccination are generally mild and transient, like fever and chills, headache, fatigue, myalgia and arthralgia, or local injection site effects like swelling, redness, or pain. The most devastating neurological post-vaccination complication is cerebral venous sinus thrombosis. Cerebral venous sinus is frequently reported in females of childbearing age, generally following adenovector-based vaccination. Another major neurological complication of concern is Bell's palsy that was reported dominantly following mRNA vaccine administration. Acute transverse myelitis, acute disseminated encephalomyelitis, and acute demyelinating polyneuropathy are other unexpected neurological adverse events that occur as result of phenomenon of molecular mimicry. Reactivation of herpes zoster in many persons, following administration of mRNA vaccines, has been also recorded. Considering the enormity of recent COVID-19-vaccinated population, the number of serious neurological events is miniscule. Large collaborative prospective studies are needed to prove or disprove causal association between vaccine and neurological adverse events occurring vaccination.

104 citations

Journal ArticleDOI
TL;DR: In this paper , the immediate, intermediate, and long-term effects of COVID-19 on endothelial function were assessed by brachial artery flow-mediated dilation (FMD).

48 citations

Journal ArticleDOI
TL;DR: In this article , a review of reports of stroke associated with COVID-19 vaccines and provide a coherent clinical picture of this condition is presented, and the most common clinical symptom of CVST seen after COVID19 vaccination was headache.
Abstract: ObjectivesDevelopment of safe and effective vaccines against coronavirus disease 2019 (COVID-19) remains the cornerstone of controlling this pandemic. However, there are increasing reports of various types of stroke including ischemic stroke, and hemorrhagic stroke, as well as cerebral venous sinus thrombosis (CVST) after COVID-19 vaccination. This paper aims to review reports of stroke associated with COVID-19 vaccines and provide a coherent clinical picture of this condition.Materials and methodsA literature review was performed with a focus on data from recent studies.ResultsMost of such patients are women under 60 years of age and who had received ChAdOx1 nCoV-19 vaccine. Most studies reported CVST with or without secondary ischemic or hemorrhagic stroke, and some with Vaccine-induced Thrombotic Thrombocytopenia (VITT). The most common clinical symptom of CVST seen after COVID-19 vaccination was headache. The clinical course of CVST after COVID-19 vaccination may be more severe than CVST not associated with COVID vaccination. Management of CVST following COVID-19 vaccination is challenging and may differ from the standard treatment of CVST. Low molecular weight heparin is commonly used in the treatment of CVST; however, it may worsen outcomes in CVST associated with VITT. Furthermore, administration of intravenous immunoglobulin and high-dose glucocorticoids have been recommended with various success rates.ConclusionThese contradictory observations are a source of confusion in clinical decision-making and warrant further study and development of clinical guidelines. Clinicians should be aware of clinical presentation, diagnosis, and management of stroke associated with COVID-19 vaccination.

19 citations

Journal ArticleDOI
TL;DR: A reduction in cfPWV was related with MAP, and some indicators of arterial stiffness remain elevated for several months following SARS-CoV-2 infection, possibly contributing to prolonged recovery and increased cardiovascular health risks.
Abstract: INTRODUCTION Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can increase arterial stiffness 3-4 weeks following infection, even among young, healthy adults. However, the long-term impacts of SARS-CoV-2 infection on cardiovascular health and the duration of recovery remains unknown. PURPOSE The purpose of this study was to elucidate potential long-lasting effects of SARS-CoV-2 infection on markers of arterial stiffness among young adults during the six months following infection. METHODS Assessments were performed at months 1, 2, 3, 4, and ~6 following SARS-CoV-2 infection. Doppler ultrasound was utilized to measure carotid-femoral pulse wave velocity (cfPWV) and carotid stiffness, and arterial tonometry was used to measure central blood pressures and aortic augmentation index at a heart rate of 75 beats∙min-1 (AIx@HR75). Vascular (VCAM-1) and intracellular (ICAM-1) adhesion molecules were analyzed as circulating markers of arterial stiffness. RESULTS From months 1-6, a significant reduction in cfPWV was observed (month1: 5.70±0.73m·s-1; month6: 4.88±0.65m·s-1; p<0.05) without any change in carotid stiffness measures. Reductions in systolic blood pressure (month1: 123±8mmHg; month6: 112±11mmHg) and mean arterial pressure (month1: 97±6mmHg; month6: 86±7mmHg) were observed (p<0.05), although AIx@HR75 did not change over time. The month1-6 change in cfPWV and MAP were correlated (r=0.894; p<0.001). A reduction in VCAM-1 was observed at month 3 compared with month 1 (month1: 5575±2242pg·ml-1; month3: 4636±1621pg·ml-1; p<0.05) without a change in ICAM-1. CONCLUSION A reduction in cfPWV was related with MAP, and some indicators of arterial stiffness remain elevated for several months following SARS-CoV-2 infection, possibly contributing to prolonged recovery and increased cardiovascular health risks.

18 citations