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Prof. Dr. Dr. med. habil. Mathias Burgmaier

Fakultät Angewandte Gesundheitswissenschaften

Professor:innen

Professor

LA 27-2.14

0991/3615-8343

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Zeitschriftenartikel

  • N. Ganesh
  • Emiel van der Vorst
  • Jens Spiesshöfer
  • Shun He
  • Mathias Burgmaier
  • Hannes Findeisen
  • Michael Lehrke
  • Filip Swirski
  • Nikolaus Marx
  • Florian Kahles

Gut immune cells-A novel therapeutical target for cardiovascular disease?

In: Frontiers in Cardiovascular Medicine vol. 9 pg. 943214.

  • 15.08.2022 (2022)

DOI: 10.3389/fcvm.2022.943214

Despite scientific and clinical advances during the last 50 years cardiovascular disease continues to be the main cause of death worldwide. Especially patients with diabetes display a massive increased cardiovascular risk compared to patients without diabetes. Over the last two decades we have learned that cardiometabolic and cardiovascular diseases are driven by inflammation. Despite the fact that the gastrointestinal tract is one of the largest leukocyte reservoirs of our bodies, the relevance of gut immune cells for cardiovascular disease is largely unknown. First experimental evidence suggests an important relevance of immune cells in the intestinal tract for the development of metabolic and cardiovascular disease in mice. Mice specifically lacking gut immune cells are protected against obesity, diabetes, hypertension and atherosclerosis. Importantly antibody mediated inhibition of leukocyte homing into the gut showed similar protective metabolic and cardiovascular effects. Targeting gut immune cells might open novel therapeutic approaches for the treatment of cardiometabolic and cardiovascular diseases.
  • Angewandte Gesundheitswissenschaften
  • GESUND
Zeitschriftenartikel

  • P. Petsophonsakul
  • Mathias Burgmaier
  • B. Willems
  • S. Heeneman
  • N. Stadler
  • F. Gremse
  • S. Reith
  • Kathrin Burgmaier
  • Florian Kahles
  • Nikolaus Marx
  • Ehsan Natour
  • Elham Bidar
  • Michael Jacobs
  • Barend Mees
  • Chris Reutelingsperger
  • Malgorzata Furmanik
  • Leon Schurgers

Nicotine promotes vascular calcification via intracellular Ca2+-mediated, Nox5-induced oxidative stress, and extracellular vesicle release in vascular smooth muscle cells

In: Cardiovascular Research vol. 118 pg. 2196-2210.

  • (2022)

DOI: 10.1093/cvr/cvab244

AIMS Smokers are at increased risk of cardiovascular events. However, the exact mechanisms through which smoking influences cardiovascular disease resulting in accelerated atherosclerosis and vascular calcification are unknown. The aim of this study was to investigate effects of nicotine on initiation of vascular smooth muscle cell (VSMC) calcification and to elucidate underlying mechanisms. METHODS AND RESULTS We assessed vascular calcification of 62 carotid lesions of both smoking and non-smoking patients using ex vivo micro-computed tomography (µCT) scanning. Calcification was present more often in carotid plaques of smokers (n = 22 of 30, 73.3%) compared to non-smokers (n = 11 of 32, 34.3%; P < 0.001), confirming higher atherosclerotic burden. The difference was particularly profound for microcalcifications, which was 17-fold higher in smokers compared to non-smokers. In vitro, nicotine-induced human primary VSMC calcification, and increased osteogenic gene expression (Runx2, Osx, BSP, and OPN) and extracellular vesicle (EV) secretion. The pro-calcifying effects of nicotine were mediated by Ca2+-dependent Nox5. SiRNA knock-down of Nox5 inhibited nicotine-induced EV release and calcification. Moreover, pre-treatment of hVSMCs with vitamin K2 ameliorated nicotine-induced intracellular oxidative stress, EV secretion, and calcification. Using nicotinic acetylcholine receptor (nAChR) blockers α-bungarotoxin and hexamethonium bromide, we found that the effects of nicotine on intracellular Ca2+ and oxidative stress were mediated by α7 and α3 nAChR. Finally, we showed that Nox5 expression was higher in carotid arteries of smokers and correlated with calcification levels in these vessels. CONCLUSION In this study, we provide evidence that nicotine induces Nox5-mediated pro-calcific processes as novel mechanism of increased atherosclerotic calcification. We identified that activation of α7 and α3 nAChR by nicotine increases intracellular Ca2+ and initiates calcification of hVSMCs through increased Nox5 activity, leading to oxidative stress-mediated EV release. Identifying the role of Nox5-induced oxidative stress opens novel avenues for diagnosis and treatment of smoking-induced cardiovascular disease.
  • Angewandte Gesundheitswissenschaften
  • GESUND
Zeitschriftenartikel

  • A. Milzi
  • R. Dettori
  • R. Lubberich
  • Kathrin Burgmaier
  • N. Marx
  • S. Reith
  • Mathias Burgmaier

Coronary microvascular dysfunction as assessed by angiography-derived index of microvascular resistance co-localizes with and may explain the presence of ischemia in stress-cardiac magnetic resonance imaging in the absence of coronary artery disease

In: Frontiers in Cardiovascular Medicine vol. 9 pg. 1060764.

  • 24.11.2022 (2022)

DOI: 10.3389/fcvm.2022.1060764

INTRODUCTION Ischemia with no obstructive coronary disease (INOCA) is a frequent phenomenon in the cath lab. A possible cause is coronary microvascular dysfunction (CMD), which may be assessed by invasive testing with possible complications; therefore, less invasive approaches have emerged, such as the angiography-derived index of microvascular resistance (aIMR). The aim of our study was to investigate the association of single-vessel aIMR as a measure of CMD with areas of INOCA in stress testing. METHODS We measured aIMR in 286 vessels from 102 patients undergoing both stress cMRI and coronary angiography. Groups were (a) INOCA group (93 vessels, 32 patients); (b) coronary artery disease (CAD) control group (116 vessels, 42 patients) with ischemia due to relevant stenosis; and (c) control group (77 vessels, 28 patients) without ischemia or relevant stenosis. RESULTS INOCA patients presented higher mean aIMR (28.3 ± 5.7) compared to both CAD patients (17.4 ± 5.7, p < 0.001) and controls (22.1 ± 5.9, p < 0.001). Furthermore, in INOCA patients aIMR was significantly increased (33.0 ± 8.1 vs. 25.8 ± 6.3, p = 0.021) in vessels with vs. without ischemia. Single vessel aIMR presented a very good diagnostic efficiency in detecting INOCA [AUC 0.865 (0.804-0.925), optimal cut-off 27.1, p < 0.001]. CONCLUSION CMD, as assessed by 3-vessel aIMR, co-localizes with and may explain the presence of ischemia in stress-cMRI in INOCA.
  • Angewandte Gesundheitswissenschaften
  • GESUND
Zeitschriftenartikel

  • A. Milzi
  • R. Dettori
  • R. Lubberich
  • Kathrin Burgmaier
  • N. Marx
  • S. Reith
  • Mathias Burgmaier

Quantitative Flow Ratio Is Related to Anatomic Left Main Stem Lesion Parameters as Assessed by Intravascular Imaging

In: Journal of Clinical Medicine vol. 11

  • 12.10.2022 (2022)

DOI: 10.3390/jcm11206024

INTRODUCTION Previously, an association between anatomic left main stem (LMS) lesion parameters, as described by intravascular ultrasound (IVUS) and fractional flow reserve (FFR), was shown. Quantitative flow ratio (QFR) is a novel, promising technique which can assess functional stenosis relevance based only on angiography. However, as little is known about the relationship between anatomic LMS parameters and QFR, it was thus investigated in this study. METHODS In 53 patients with LMS disease, we tested the association between anatomic assessment using OCT (n = 28) or IVUS (n = 25) on the one hand and functional assessment as determined by QFR on the other hand. LMS-QFR was measured using a dedicated approach, averaging QFR over left anterior descending (LAD) and circumflex (LCX) and manually limiting segment of interest to LMS. RESULTS The minimal luminal area of the LMS (LMS-MLA) as measured by intravascular imaging showed a consistent correlation with QFR (R = 0.61, p < 0.001). QFR could predict a LMS-MLA < 6 mm2 with very good diagnostic accuracy (AUC 0.919) and a LMS-MLA < 4.5 mm2 with good accuracy (AUC 0.798). Similar results were obtained for other stenosis parameters. CONCLUSIONS QFR might be a valuable tool to assess LMS disease. Further studies focusing on patient outcomes are needed to further validate the effectiveness of this approach.
  • Angewandte Gesundheitswissenschaften
  • GESUND
Zeitschriftenartikel

  • E. Ferrannini
  • N. Marx
  • D. Andreini
  • B. Campi
  • A. Saba
  • M. Gorini
  • G. Ferrannini
  • A. Milzi
  • M. Magnoni
  • A. Maseri
  • A. Maggioni
  • Mathias Burgmaier

Mannose as a biomarker of coronary artery disease: Angiographic evidence and clinical significance

In: International Journal of Cardiology vol. 346 pg. 86-92.

  • 18.11.2021 (2022)

DOI: 10.1016/j.ijcard.2021.11.038

BACKGROUND High mannose has previously associated with insulin resistance and cardiovascular disease (CVD). Our objective is to establish whether mannose is associated with anatomical evidence of coronary artery disease (CAD). METHODS Plasma mannose concentrations were measured by liquid chromatography/tandem mass spectrometry in a discovery cohort (n = 513) and a validation cohort (n = 221) of carefully phenotyped individuals. In both cohorts CAD was quantitated using state-of-the-art imaging techniques (coronary computed coronary tomography angiography (CCTA), invasive coronary angiography and optical coherence tomography). Information on subsequent CVD events/death was collected. Associations of mannose with angiographic variables and biomarkers were tested using univariate and multivariate regression models. Survival analysis was performed using the Kaplan-Meier estimator. RESULTS Mannose was related to indices of CAD and features of plaque vulnerability. In the discovery cohort, mannose was a marker of quantity and quality of CCTA-proven CAD and subjects with a mannose level in the top quartile had a significantly higher risk of CVD events/death (p = 3.6e-5). In the validation cohort, mannose was significantly associated with fibrous cap thickness < 65 μm (odds ratio = 1.32 per each 10 μmol/L mannose change [95% confidence interval, 1.05-1.65]) and was an independent predictor of death (hazard ratio for mannose≥vs < 84.6 μmol/L: 4.0(95%CI, 1.4-11.3), p = 0.006). CONCLUSION The current data add novel evidence that high mannose is a signature of CAD with a vulnerable plaque phenotype, consistently across measures of severity of vessel involvement and independent of the traditional correlates of CVD, and that it is an independent predictor of incident adverse outcomes.
  • Angewandte Gesundheitswissenschaften
  • GESUND

Kernkompetenzen

Facharzt für Innere Medizin, Innere Medizin mit Schwerpunkt Kardiologie, Zusatzbezeichnungen Intensivmedizin, Notfallmedizin, Sportmedizin, Kardiovaskuläre Intensiv- und Notfallmedizin (DGK), Herzinsuffizienz (DGK), Sportkardiologie (DGK), Interventionelle Kardiologie (DGK), Fachkunde Strahlenschutz, Diplom IIa Tauchmedizin (GTÜM)