13210
2013
eng
289-295
2
37
article
1
2016-04-14
--
--
Potential role of vitamin D deficiency on Fabry cardiomyopathy
Patients with Fabry disease frequently develop left ventricular (LV) hypertrophy and renal fibrosis. Due to heat intolerance and an inability to sweat, patients tend to avoid exposure to sunlight. We hypothesized that subsequent vitamin D deficiency may contribute to Fabry cardiomyopathy. This study investigated the vitamin D status and its association with LV mass and adverse clinical symptoms in patients with Fabry disease. 25-hydroxyvitamin D (25[OH]D) was measured in 111 patients who were genetically proven to have Fabry disease. LV mass and cardiomyopathy were assessed by magnetic resonance imaging and echocardiography. In cross-sectional analyses, associations with adverse clinical outcomes were determined by linear and binary logistic regression analyses, respectively, and were adjusted for age, sex, BMI and season. Patients had a mean age of 40 ± 13 years (42 % males), and a mean 25(OH)D of 23.5 ± 11.4 ng/ml. Those with overt vitamin D deficiency (25[OH]D ≤ 15 ng/ml) had an adjusted six fold higher risk of cardiomyopathy, compared to those with sufficient 25(OH)D levels >30 ng/ml (p = 0.04). The mean LV mass was distinctively different with 170 ± 75 g in deficient, 154 ± 60 g in moderately deficient and 128 ± 58 g in vitamin D sufficient patients (p = 0.01). With increasing severity of vitamin D deficiency, the median levels of proteinuria increased, as well as the prevalences of depression, edema, cornea verticillata and the need for medical pain therapy. In conclusion, vitamin D deficiency was strongly associated with cardiomyopathy and adverse clinical symptoms in patients with Fabry disease. Whether vitamin D supplementation improves complications of Fabry disease, requires a randomized controlled trial.
Journal of Inherited Metabolic Disease
10.1007/s10545-013-9653-8
urn:nbn:de:bvb:20-opus-132102
Journal of Inherited Metabolic Disease (2014) 37:289–295 DOI 10.1007/s10545-013-9653-8
Christiane Drechsler
Benjamin Schmiedeke
Markus Niemann
Daniel Schmiedeke
Johannes Krämer
Irina Turkin
Katja Blouin
Andrea Emmert
Stefan Pilz
Barbara Obermayer-Pietsch
Frank Wiedemann
Frank Breunig
Christoph Wanner
eng
uncontrolled
Fabry patient
eng
uncontrolled
urinary protein excretion
eng
uncontrolled
hypertrophic cardiomyopathy
eng
uncontrolled
renal fibrosis
eng
uncontrolled
left ventricular mass
eng
uncontrolled
LV mass
eng
uncontrolled
diabetic mouse
eng
uncontrolled
septal hypertrophy
eng
uncontrolled
Fabry nephropathy
eng
uncontrolled
cardiac hypertrophy
eng
uncontrolled
cornea verticillata
eng
uncontrolled
enzyme replacement therapy
Krankheiten
open_access
Medizinische Klinik und Poliklinik I
Institut für Klinische Epidemiologie und Biometrie
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/13210/163_Drechsler_Journal_of_inherited_Metabolic_Diseases.pdf
13449
2013
eng
356
108
article
1
2016-06-07
--
--
How can we cure a heart "in flame"? A translational view on inflammation in heart failure
The prevalence of chronic heart failure is still increasing making it a major health issue in the 21st century. Tremendous evidence has emerged over the past decades that heart failure is associated with a wide array of mechanisms subsumed under the term "inflammation". Based on the great success of immuno-suppressive treatments in auto-immunity and transplantation, clinical trials were launched targeting inflammatory mediators in patients with chronic heart failure. However, they widely lacked positive outcomes. The failure of the initial study program directed against tumor necrosis factor-a led to the search for alternative therapeutic targets involving a broader spectrum of mechanisms besides cytokines. We here provide an overview of the current knowledge on immune activation in chronic heart failure of different etiologies, summarize clinical studies in the field, address unresolved key questions, and highlight some promising novel therapeutic targets for clinical trials from a translational basic science and clinical perspective.
Basic Research in Cardiology
10.1007/s00395-013-0356-y
urn:nbn:de:bvb:20-opus-134497
Basic Research in Cardiology (2013) 108:356 DOI 10.1007/s00395-013-0356-y
Ulrich Hofmann
Stefan Frantz
eng
uncontrolled
cytokines
eng
uncontrolled
immuno-modulation
eng
uncontrolled
heart failure
Medizin und Gesundheit
open_access
Medizinische Klinik und Poliklinik I
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/13449/142_Hofmann_Basic_Research_in_Cardiology.pdf
13029
2013
eng
e56923
3
8
article
1
2016-03-18
--
--
Impact of Regional Left Ventricular Function on Outcome for Patients with AL Amyloidosis
Objectives
The aim of this study was to explore the left ventricular (LV) deformation changes and the potential impact of deformation on outcome in patients with proven light-chain (AL) amyloidosis and LV hypertrophy.
Background
Cardiac involvement in AL amyloidosis patients is associated with poor outcome. Detecting regional cardiac function by advanced non-invasive techniques might be favorable for predicting outcome.
Methods
LV longitudinal, circumferential and radial peak systolic strains (Ssys) were assessed by speckle tracking imaging (STI) in 44 biopsy-proven systemic AL amyloidosis patients with LV hypertrophy (CA) and in 30 normal controls. Patients were divided into compensated (n = 18) and decompensated (n = 26) group based on clinical assessment and followed-up for a median period of 345 days.
Results
Ejection fraction (EF) was preserved while longitudinal Ssys (LSsys) was significantly reduced in both compensated and decompensated groups. Survival was significantly reduced in decompensated group (35% vs. compensated 78%, P = 0.001). LSsys were similar in apical segments and significantly reduced in basal segments between two patient groups. LSsys at mid-segments were significantly reduced in all LV walls of decompensated group. Patients were further divided into 4 subgroups according to the presence or absence of reduced LSsys in no (normal), only basal (mild), basal and mid (intermediate) and all segments of the septum (severe). This staging revealed continuously worse prognosis in proportion to increasing number of segments with reduced LSsys (mortality: normal 14%, mild 27%, intermediate 67%, and severe 64%). Mid-septum LSsys<11% suggested a 4.8-fold mortality risk than mid-septum LSsys≥11%. Multivariate regression analysis showed NYHA class and mid-septum LSsys were independent predictors for survival.
Conclusions
Reduced deformation at mid-septum is associated with worse prognosis in systemic amyloidosis patients with LV hypertrophy.
PLoS ONE
10.1371/journal.pone.0056923
urn:nbn:de:bvb:20-opus-130293
PLoS ONE 8(3): e56923. doi:10.1371/journal.pone.0056923
Dan Liu
Kai Hu
Markus Niemann
Sebastian Herrmann
Maja Cikes
Stefan Störk
Meinrad Beer
Philipp Daniel Gaudron
Caroline Morbach
Stefan Knop
Eva Geissinger
Georg Ertl
Bart Bijnens
Frank Weidemann
eng
uncontrolled
regression analysis
eng
uncontrolled
ejection fraction
eng
uncontrolled
echocardiography
eng
uncontrolled
cardiac transplantation
eng
uncontrolled
deformation
eng
uncontrolled
amyloidosis
eng
uncontrolled
prognosis
eng
uncontrolled
stem cell transplantation
Medizin und Gesundheit
open_access
Institut für diagnostische und interventionelle Radiologie (Institut für Röntgendiagnostik)
Pathologisches Institut
Medizinische Klinik und Poliklinik I
Medizinische Klinik und Poliklinik II
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/13029/102_Liu_Impact_of_Regional.pdf
12869
2013
eng
67
14
article
1
2016-03-04
--
--
Predicting erythropoietin resistance in hemodialysis patients with type 2 diabetes
Background: Resistance to ESAs (erythropoietin stimulating agents) is highly prevalent in hemodialysis patients with diabetes and associated with an increased mortality. The aim of this study was to identify predictors for ESA resistance and to develop a prediction model for the risk stratification in these patients.
Methods: A post-hoc analysis was conducted of the 4D study, including 1015 patients with type 2 diabetes undergoing hemodialysis. Determinants of ESA resistance were identified by univariate logistic regression analyses. Subsequently, multivariate models were performed with stepwise inclusion of significant predictors from clinical parameters, routine laboratory and specific biomarkers.
Results: In the model restricted to clinical parameters, male sex, shorter dialysis vintage, lower BMI, history of CHF, use of ACE-inhibitors and a higher heart rate were identified as independent predictors of ESA resistance. In regard to routine laboratory markers, lower albumin, lower iron saturation, higher creatinine and higher potassium levels were independently associated with ESA resistance. With respect to specific biomarkers, higher ADMA and CRP levels as well as lower Osteocalcin levels were predictors of ESA resistance.
Conclusions: Easily obtainable clinical parameters and routine laboratory parameters can predict ESA resistance in diabetic hemodialysis patients with good discrimination. Specific biomarkers did not meaningfully further improve the risk prediction of ESA resistance. Routinely assessed data can be used in clinical practice to stratify patients according to the risk of ESA resistance, which may help to assign appropriate treatment strategies.
BMC Nephrology
10.1186/1471-2369-14-67
urn:nbn:de:bvb:20-opus-128695
BMC Nephrology 2013, 14:67. doi:10.1186/1471-2369-14-67
Andreas Schneider
Markus P. Schneider
Hubert Scharnagl
Alan G. Jardine
Christoph Wanner
Christiane Drechsler
eng
uncontrolled
type 2 diabetes
eng
uncontrolled
heodialysis patients
Medizin und Gesundheit
open_access
Medizinische Klinik und Poliklinik I
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/12869/013_Predicting_erythropoietin.pdf
13166
2013
eng
51-52
110
article
1
2016-04-10
--
--
Adrenal Cortical Insufficiency-a Life Threatening Illness With Multiple Etiologies
Background: The clinical signs of adrenal cortical insufficiency (incidence, ca. 25 per million per year; prevalence, ca. 400 per million) are nonspecific, and misdiagnoses are therefore common. Glucocorticoid substitution therapy has been in use for 50 years but is not a wholly adequate treatment. Our understanding of this disease remains incomplete in many ways.
Methods: We selectively searched the Medline database for publications on adrenal cortical insufficiency, with particular attention to studies from the year 2000 onward (search terms: "adrenal insufficiency" or "Addison's disease" or "hypopituitarism"). Results: Hydrocortisone substitution therapy is often given in doses of 10-25 mg/day, timed according to the circadian rhythm. Gastrointestinal and other, febrile infections account for 30-50% of life-threatening adrenocortical crises. Such crises affect 8 of 100 persons with adrenal cortical insufficiency per year and must be treated by the immediate administration of glucocorticoids and fluids. When persons with adrenal cortical insufficiency are acutely ill or are otherwise under unusual stress, they may need additional amounts of hydrocortisone, often in the range of 5-10 mg but occasionally as high as 200 mg. The sustained administration of excessive amounts of steroid can shorten patients' lives by several years. Inappropriate substitution therapy can cause other major medical conditions, such as metabolic syndrome and osteoporosis.
Conclusion: Important measures for the prevention of adrenocortical crises include improved care by treating physicians, education of patients and their families, the provision of emergency identifying documents, and the prescription of glucocorticoid emergency kits.
Deutsches Ärzteblatt International
10.3238/arztebl.2013.0882
urn:nbn:de:bvb:20-opus-131662
Deutsches Ärzteblatt International 2013; 110(51–52): 882–8. DOI: 10.3238/arztebl.2013.0882
Deutsches Urheberrecht
Marcus Quinkler
Felix Beuschlein
Stefanie Hahner
Gesine Meyer
Christof Schöfl
Günter K. Stalla
eng
uncontrolled
short term
eng
uncontrolled
subjective health-status
eng
uncontrolled
modified-release hydrocortisone
eng
uncontrolled
glucocorticoid replacement regimens
eng
uncontrolled
Addisons disease
eng
uncontrolled
therapeutic management
eng
uncontrolled
hypopituitary patients
eng
uncontrolled
premature mortality
eng
uncontrolled
circadian therapy
eng
uncontrolled
adult patients
Medizin und Gesundheit
open_access
Medizinische Klinik und Poliklinik I
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/13166/117_Qunikler_Deutsches_Aerzteblatt_International.pdf
13097
2013
eng
e63560
5
8
article
MMKD Study Group
1
2016-03-31
--
--
Homoarginine and Progression of Chronic Kidney Disease: Results from the Mild to Moderate Kidney Disease Study
Background: Homoarginine is an amino acid derivative mainly synthesized in the kidney. It is suggested to increase nitric oxide availability, enhance endothelial function and to protect against cardiovascular diseases. We aimed to investigate the relation between homoarginine, kidney function and progression of chronic kidney disease (CKD).
Methods: We measured plasma homoarginine concentrations in baseline samples of the Mild to Moderate Kidney Disease (MMKD) Study, a prospective cohort study of 227 patients with CKD in Europe. Homoarginine concentrations were available in 182 of the baseline samples and in 139 of the prospectively-followed patients. We correlated homoarginine concentrations to parameters of kidney function. The association between homoarginine and progression of CKD was assessed during a follow-up of up to seven years (median 4.45 years, interquartile range 2.54-5.19) using Cox regression analysis. Progression of CKD was defined as doubling of baseline serum creatinine and/or end-stage renal disease.
Results: Study participants were at baseline on average 47 \(\pm\)13 years old and 65% were male. Mean \(\pm\) standard deviation of homoarginine concentrations were \(2.5 \pm 1.1 \mu mol/L\) and concentrations were incrementally lower at lower levels of GFR with mean concentrations of \(2.90 \pm 1.02 \mu mol/L\) (GFR. 90 ml/min), \(2.64 \pm 1.06 \mu mol/L\) (GFR 60-90 ml/min), \(2.52 \pm 1.24 \mu mol/L\) (GFR 30-60 ml/min) and \(2.05 \pm 0.78 \mu mol/L\) (GFR, 30 ml/min), respectively (p = 0.002). The age-and sex-adjusted risk to reach the renal endpoint was significantly higher by 62% with each decrease by one standard deviation (\(1.1 \mu mol/L\)) of homoarginine (HR 1.62, 95% CI 1.16-2.27, p = 0.005). This association was independent of proteinuria (HR 1.56, 95% CI 1.11-2.20, p = 0.01), and was slightly attenuated when adjusting for GFR (HR 1.40 (95% CI 0.98-1.98, p = 0.06).
Conclusions: Homoarginine concentrations are directly correlated with kidney function and are significantly associated with the progression of CKD. Low homoarginine concentrations might be an early indicator of kidney failure and a potential target for the prevention of disease progression which needs further investigations.
PLoS ONE
10.1371/journal.pone.0063560
urn:nbn:de:bvb:20-opus-130979
PLoS ONE 8(5): e63560. doi:10.1371/journal.pone.0063560
Christiane Drechsler
Barbara Kolleritz
Andreas Meinitzer
Winfried März
Eberhard Ritz
Paul König
Ulrich Neyer
Stefan Pilz
Christoph Wanner
Florian Kronenberg
eng
uncontrolled
risk
eng
uncontrolled
alkaline phosphatase
eng
uncontrolled
cardiovascular events
eng
uncontrolled
nictric-oxide
eng
uncontrolled
induced insulin-release
eng
uncontrolled
creatine synthesis
eng
uncontrolled
renal function
eng
uncontrolled
heart failure
eng
uncontrolled
rat kidney
eng
uncontrolled
L-arginine
Krankheiten
open_access
Medizinische Klinik und Poliklinik I
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/13097/084_Drechsler_Plos_One.pdf
13058
2013
eng
16
Article ID 265182
article
1
2016-03-23
--
--
Identification of PDZ domain containing proteins interacting with \(Ca_v1.2\) and PMCA4b
PDZ (PSD-95/Disc large/Zonula occludens-1) protein interaction domains bind to cytoplasmic protein C-termini of transmembrane proteins. In order to identify new interaction partners of the voltage-gated L-type \(Ca^{2+}\) channel Cav1.2 and the plasma membrane \(Ca^{2+}\) ATPase 4b (PMCA4b), we used PDZ domain arrays probing for 124 PDZ domains. We confirmed this byGST pulldowns and immunoprecipitations. In PDZ arrays, strongest interactionswith \(Ca_v1.2\) and PMCA4b were found for the PDZ domains of SAP-102, MAST-205, MAGI-1, MAGI-2, MAGI-3, and ZO-1. We observed binding of the \(Ca_v1.2\) C-terminus to PDZ domains of NHERF1/2, Mint-2, and CASK. PMCA4b was observed to interact with Mint-2 and its known interactions with Chapsyn-110 and CASK were confirmed. Furthermore, we validated interaction of \(Ca_v1.2\) and PMCA4b with NHERF1/2, CASK,MAST-205 and MAGI-3 viaimmunoprecipitation. We also verified the interaction of \(Ca_v1.2\) and nNOS and hypothesized that nNOS overexpression might reduce \(Ca^{2+}\) influx through \(Ca_v1.2\). To address this, we measured \(Ca^{2+}\) currents in HEK 293 cells co-expressing \(Ca_v1.2\) and nNOS and observed reduced voltage-dependent \(Ca_v1.2\) activation. Taken together, we conclude that \(Ca_v1.2\) and PMCA4b bind promiscuously to various PDZ domains, and that our data provides the basis for further investigation of the physiological consequences of these interactions.
ISRN Cell Biology
10.1155/2013/265182
urn:nbn:de:bvb:20-opus-130585
ISRN Cell Biology Volume 2013, Article ID 265182, 16 pages http://dx.doi.org/10.1155/2013/265182
Doreen Korb
Priscilla Y. Tng
Vladimir M. Milenkovic
Nadine Reichhart
Olaf Strauss
Oliver Ritter
Tobias Fischer
Peter M. Benz
Kai Schuh
eng
uncontrolled
Cell
Humanphysiologie
open_access
Physiologisches Institut
Medizinische Klinik und Poliklinik I
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/13058/052_Korb_Tng_Milenkovic.pdf
12966
2013
eng
7
Article ID 716902
2013
article
1
2016-03-11
--
--
Complement C3c as a Biomarker in Heart Failure
Experimental data indicates an important role of the innate immune system in cardiac remodeling and heart failure (HF). Complement is a central effector pathway of the innate immune system. Animals lacking parts of the complement system are protected from adverse remodeling. Based on these data, we hypothesized that peripheral complement levels could be a good marker for adverse remodeling and prognosis in patients with HF. Methods and Results. Since complement activation converges on the complement factor C3, we measured serum C3c, a stable C3-conversion product, in 197 patients with stable systolic HF. Subgroups with normal and elevated C3c levels were compared. C3c levels were elevated in 17%of the cohort. Patients with elevated C3c levels exhibited a trend to better survival, slightly higher LVEF, and lower NTpro-BNP values in comparison to patients with normal C3c values. No differences were found regarding NYHA functional class. Significantly more patients with elevated C3c had preexisting diabetes. The prevalence of CAD, arterial hypertension, and atrial fibrillation was not increased in patients with elevated C3c. Conclusion. Elevated C3c levels are associated with less adverse remodeling and improved survival in patients with stable systolic heart failure.
Mediators of Inflammation
10.1155/2013/716902
urn:nbn:de:bvb:20-opus-129668
Mediators of Inflammation Volume 2013, Article ID 716902, 7 pages http://dx.doi.org/10.1155/2013/716902
A. Frey
G. Ertl
C. E. Angermann
U. Hofmann
S. Störk
S. Frantz
eng
uncontrolled
medicine
Medizin und Gesundheit
open_access
Medizinische Klinik und Poliklinik I
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/12966/066_Frey_Complement_C3c.pdf
12988
2013
eng
e78938
11
8
article
1
2016-03-13
--
--
Exogenous Administration of a Recombinant Variant of TWEAK Impairs Healing after Myocardial Infarction by Aggravation of Inflammation
Background: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factorinducible 14 (Fn14) are upregulated after myocardial infarction (MI) in both humans and mice. They modulate inflammation and the extracellular matrix, and could therefore be important for healing and remodeling after MI. However, the function of TWEAK after MI remains poorly defined.
Methods and results: Following ligation of the left coronary artery, mice were injected twice per week with a recombinant human serum albumin conjugated variant of TWEAK (HSA-Flag-TWEAK), mimicking the activity of soluble TWEAK. Treatment with HSA-Flag-TWEAK resulted in significantly increased mortality in comparison to the placebo group due to myocardial rupture. Infarct size, extracellular matrix remodeling, and apoptosis rates were not different after MI. However, HSA-Flag-TWEAK treatment increased infiltration of proinflammatory cells into the myocardium. Accordingly, depletion of neutrophils prevented cardiac ruptures without modulating all-cause mortality.
Conclusion: Treatment of mice with HSA-Flag-TWEAK induces myocardial healing defects after experimental MI. This is mediated by an exaggerated neutrophil infiltration into the myocardium.
PLoS ONE
10.1371/journal.pone.0078938
urn:nbn:de:bvb:20-opus-129889
PLoS ONE 8(11): e78938. doi:10.1371/journal.pone.0078938
Christina Pachel
Denise Mathes
Barbara Bayer
Charlotte Dienesch
Gaby Wangorsch
Wolfram Heitzmann
Isabell Lang
Hossein Ardehali
Georg Ertl
Thomas Dandekar
Harald Wajant
Stefan Frantz
eng
uncontrolled
apoptosis
eng
uncontrolled
myocardial infarction
eng
uncontrolled
neutrophils
eng
uncontrolled
cytokines
eng
uncontrolled
inflammation
eng
uncontrolled
myocardium
eng
uncontrolled
heart
eng
uncontrolled
extracellular matrix
Medizin und Gesundheit
open_access
Medizinische Klinik und Poliklinik I
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/12988/088_Exogenous Administration of a Recombinant Variant of.pdf
13006
2013
eng
e68275
8
8
article
1
2016-03-16
--
--
Impact of Thoracic Surgery on Cardiac Morphology and Function in Small Animal Models of Heart Disease: A Cardiac MRI Study in Rats
Background
Surgical procedures in small animal models of heart disease might evoke alterations in cardiac morphology and function. The aim of this study was to reveal and quantify such potential artificial early or long term effects in vivo, which might account for a significant bias in basic cardiovascular research, and, therefore, could potentially question the meaning of respective studies.
Methods
Female Wistar rats (n = 6 per group) were matched for weight and assorted for sham left coronary artery ligation or control. Cardiac morphology and function was then investigated in vivo by cine magnetic resonance imaging at 7 Tesla 1 and 8 weeks after the surgical procedure. The time course of metabolic and inflammatory blood parameters was determined in addition.
Results
Compared to healthy controls, rats after sham surgery showed a lower body weight both 1 week (267.5±10.6 vs. 317.0±11.3 g, n<0.05) and 8 weeks (317.0±21.1 vs. 358.7±22.4 g, n<0.05) after the intervention. Left and right ventricular morphology and function were not different in absolute measures in both groups 1 week after surgery. However, there was a confined difference in several cardiac parameters normalized to the body weight (bw), such as myocardial mass (2.19±0.30/0.83±0.13 vs. 1.85±0.22/0.70±0.07 mg left/right per g bw, p<0.05), or enddiastolic ventricular volume (1.31±0.36/1.21±0.31 vs. 1.14±0.20/1.07±0.17 µl left/right per g bw, p<0.05). Vice versa, after 8 weeks, cardiac masses, volumes, and output showed a trend for lower values in sham operated rats compared to controls in absolute measures (782.2±57.2/260.2±33.2 vs. 805.9±84.8/310.4±48.5 mg, p<0.05 for left/right ventricular mass), but not normalized to body weight. Matching these findings, blood testing revealed only minor inflammatory but prolonged metabolic changes after surgery not related to cardiac disease.
Conclusion
Cardio-thoracic surgical procedures in experimental myocardial infarction cause distinct alterations upon the global integrity of the organism, which in the long term also induce circumscribed repercussions on cardiac morphology and function. This impact has to be considered when analyzing data from respective animal studies and transferring these findings to conditions in patients.
PLoS ONE
10.1371/journal.pone.0068275
urn:nbn:de:bvb:20-opus-130064
PLoS ONE 8(8): e68275. doi:10.1371/journal.pone.0068275
Peter Nordbeck
Leoni Bönhof
Karl-Heinz Hiller
Sabine Voll
Paula Arias-Loza
Lea Seidlmaier
Tatjana Williams
Yu-Xiang Ye
Daniel Gensler
Theo Pelzer
Georg Ertl
Peter M. Jakob
Wolfgang R. Bauer
Oliver Ritter
eng
uncontrolled
heart rate
eng
uncontrolled
body weight
eng
uncontrolled
surgical and invasive medical procedures
eng
uncontrolled
magnetic resonance imaging
eng
uncontrolled
blood
eng
uncontrolled
vascular surgery
eng
uncontrolled
myocardial infarction
eng
uncontrolled
cardiac ventricles
Medizin und Gesundheit
open_access
Physikalisches Institut
Medizinische Klinik und Poliklinik I
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/13006/093_Impact of Thoracic Surgery.pdf