Paper of the Month

e-Health based management of patients receiving oral anticoagulation therapy: results from the observational thrombEVAL study

Journal of Thrombosis and Haemostasis
DOI 10.1111/jth.13727

Prochaska JH, Göbel S, Keller K, Coldewey M, Ullmann A, Lamparter H, Schulz A, Schinzel H, Bickel C, Lauterbach M, Michal M, Hardt R, Binder H, Espinola-Klein C, Lackner KJ, Ten Cate H, Münzel T, Wild PS.

Effects of noise on vascular function, oxidative stress, and inflammation: mechanic insight from studies in mice

European Heart Journal
DOI 10.1093/eurheart/ehx081

Thomas Münzel, Andreas Daiber, Sebastian Steven, Lan P. Tran, Elisabeth Ullmann, Sabine Kossmann, Frank P. Schmidt, Matthias Oelze, Ning Xia, Huige Li, Antonio Pinto, Philipp Wild, Kai Pies, Erwin R. Schmidt, Steffen Rapp und Swenja Kröller-Schön

Platelet-localized FXI promotes a vascular coagulation-inflammatory circuit in arterial Hypertension

Science Translational Medicine
DOI: Kossmann et al., Sci. Transl. Med. 9, eaah4923 (2017) 1 February 2017

Kossmann S, Lagrange J, Jäckel S, Jurk K, Ehlken M, Schönfelder T, Weihert Y, Knorr M, Brandt M, Xia N, Li H, Daiber A, Oelze M, Reinhardt C, Lackner K, Gruber A, Monia B, Karbach SH, Walter U, Ruggeri Z, Renné T, Ruf W, Münzel T, Wenzel P

Innate Effector-Memory T-Cell Activation Regulates Post-Thrombotic Vein Wall Inflammation and Thrombus Resolution

Circulation Research
doi: https://doi.org/10.1161/CIRCRESAHA.116.309301

Natascha Luther, Fatemeh Shahneh, Melanie Brähler, Franziska Krebs, Sven Jäckel, Saravanan Subramaniam, Christian Stanger, Tanja Schönfelder, Bettina Kleis-Fischer, Christoph Reinhardt, Hans C Probst, Philip Wenzel, Katrin Schäfer, Christian Becker

Hydroxychloroquine inhibits proinflammatory signalling pathways by targeting endosomal NADPH oxidase

Annals of the Rheumatic Diseases (IF 12.3)
doi: 10.1136/annrheumdis-2016-210012

Nadine Müller-Calleja, Davit Manukyan, Antje Canisius, Dennis Strand, Karl J Lackner

The role of perivascular adipose tissue in obesity-induced vascular dysfunction

British Journal of Pharmacology
doi: 10.1111/bph.13650

Xia N., Li H.

The perivascular adipose tissue (PVAT) is the tissue surrounding the blood vessels. Long time it was seen as a mechanical  "cushion" for the vessels. It is now known that the PVAT secretes a range of substances, which regulates the vascular function. The PVAT appears to play a very important role in connection with obesity.

Now research results from the research group headed by Professor Li show, that a vessel dysfunction of adipose mice only is verifiable, if the PVAT is intact. When it gets removed, the vascular function remains absolutely normal. This observation points to the fact that the causes of an vessel dysfunction induced by abnormally overweight (adipositas) are located in the vascular wall itself. To explain this phenomenon, it was now possible to show on molecular level, that an enzyme (the NO synthase) in the PVAT of adipose mice was defective; but in the vascular wall it shows an absolute normal activity.
The Enzyme eNOS is known for ist  protective role in the vascular endothelium. Here the produced NO protects against Hypertension, Atherosklerose and Thrombosis. Studies of the research group Li now show that the Enzyme eNOS is also of great importance for the PVAT function. If the eNOS-functionality gets improved by pharmacological measures, the vessel function of adipose mice returns to normal. It also works if the body weight and the fat mass of the adipose mice remain unchanged.

These data suggest that vascular damage under adipose conditions are not per se caused by body weight or fat mass, but arises from a PVAT dysfunction. So the PVAT could be a new therapeutic aim for prevention and therapy of adipositas caused vessel damages.

NOX2 amplifies acetaldehyde-mediated cardiomyocyte mitochondrial dysfunction in alcoholic cardiomyopathy

Scientific Reports

DOI: 10.1038/srep32554

Brandt M, Garlapati V, Oelze M, Sotiriou E, Knorr M, Kröller-Schön S, Kossmann S, Schönfelder T, Morawietz H, Schulz E, Schultheiss HP, Daiber A, Münzel T, Wenzel P

Depression, anxiety and suicidal Ideation among 1(st) and 2(nd) Generation migrants - results from the Gutenberg health study

BMC Psychiatry

DOI: 10.1186/s12888-016-0995-2

Beutel ME, Jünger C, Klein EM, Wild P, Lackner KJ, Blettner M, Banerjee M, Michal M, Wiltink J, Brähler E.

The mental health of people with migrant background, which are already born in Germany (Migrants of the 2. Generation) is comparable with the mental health of people without migrant background.
People with migrant background, who moved on their own after 1949 (Migrants of the 1. Generation) suffer from mental problems.

These are the findings of a recent research work in the course of the Gutenberg Health Study.

Although it’s internationally proven that people with migrant background are exposed to particular health and psychosocial burden, representative German studies don’t exist.
In the course of the Gutenberg Health Study the research team headed by Univ.-Prof. Dr. Beutel, Director of the Clinic and Polyclinic for psychosomatic medicine and psychotherapy at the University Medical Center Mainz compared a broad range of psychological stress in people with migrant background of the first and second generation and people with no migrant background. Cross section data of 14,943 participants of the Gutenberg Health Study, which represent a random sample of the Mainz and Mainz-Bingen population in the age between 35 and 74, were examined.

Environmental stressors and cardio-metabolic disease: part I–epidemiologic evidence supporting a role for noise and air pollution and effects of mitigation strategies

European Heart Journal

DOI:10.1093/eurheartj/ehw269

Thomas Münzel, Mette Sørensen, Tommaso Gori, Frank P. Schmidt, Xiaoquan Rao, Jeffrey Brook, Lung Chi Chen, Robert D. Brook and Sanjay Rajagopalan

Environmental stressors and cardio-metabolic disease: part II–mechanistic insights

European Heart Journal

DOI:10.1093/eurheartj/ehw294

Thomas Münzel, Mette Sørensen,, Tommaso Gori, Frank P. Schmidt, Xiaoquan Rao, Frank R. Brook, Lung Chi Chen, Robert D. Brook and Sanjay Rajagopalan

Environmental pollution and noise contribute to 75% of all diseases which are caused by environmental factors.

While environmental pollution is responsible for 6,6 million deaths worldwide, it is assumed that in western industrialized nations up to 1 million healthy years of life get lost. In a summary of the most important  new experimental and clinical findings in the recognized European Heart Journal (http://eurheartj.oxfordjournals.org/cgi/reprint/ehw269ijkey=Qgtj6vzq2pUHmOs&keytype=ref ; http://eurheartj.oxfordjournals.org/cgi/reprint/ehw294?ijkey=yOisu5ikv9HSw3W&keytype=ref) Professor Münzel, Director of the Center of Cardiology, Cardiology I and board member of the Foundation Mainzer Herz, pointed out that noise and environmental pollution are some of the most important risk factors for the development of cardiovascular diseases. Particularly alarming is the fact that both environmental factors cause vessel damages on the same mechanisms.  And if both risk factors get together it must be taken into consideration that the chance of developing a cardiovascular disease is higher.
In the two overview articles, the latest epidemiologic studies and the latest pathopsychologic studies are summarized.

“What is decisive is that both environmental factors, noise and fine dust, must be accepted as new cardiovascular risks, which can’t be reduced significantly by the treating doctor or the patient himself, but the politics”, says Münzel.

Because of that the Foundation Mainzer Herz intensifies research of noise induced vessel damage mechanisms and supports these projects with up to 100,000 Euros per year.

Nitroglycerin induces DNA damage and vascular cell death in the setting of nitrate tolerance

Basic Res Cardiol (2016) 111:52

DOI 10.1007/s00395-016-0571-4

Yuliya Mikhed, Jörg Fahrer, Matthias Oelze, Swenja Kröller-Schön, Sebastian Steven, Philipp Welschof, Elena Zinßius, Paul Stamm, Fatemeh Kashani, Siyer Roohani, Joana Melanie Kress, Elisabeth Ullmann, Lan P. Tran, Eberhard Schulz, Bernd Epe, Bernd Kaina, Thomas Münzel, Andreas Daiber

This study takes up previous findings of Andreassi et al. and shows that the classic and long proven antiischemic medication nitroglycerin, which is effective against insufficient blood supply (ischemia), induces oxidative damages of DNA in cell culture trials and in animal models. These damages lead to apoptosis, the programmed cell death, and may explain the partly unfavorable prognosis of patients during therapy with organic nitrates. The data also show that with exposure of the nitroglycerin therapy these oxidative damages continue to exist and condense in a permanent, even though lower deterioration of the endothelial function (eg the regulation of blood pressure and the activation or inhibition of the clotting process). Future studies have to verify these findings in clinical daily routine.

Mrs. Mikhed, the lead author of this study, had a doctoral fellowship of the Institute of Molecular Biology (IMB) at the Johannes Gutenberg University Mainz (financed by the Boehringer Ingelheim Foundation). Besides that the study was supported by the Research Center of Translational Vascular Biology (CTVB) and the location Rhein-Main of the German Center of Cardiovascular Research (DZHK).