Cornelia Piper

Ruhr-Universität Bochum, Bochum, North Rhine-Westphalia, Germany

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Publications (119)274.99 Total impact

  • D Horstkotte, C Piper
    Herz 06/2015; 40(4):637-8. DOI:10.1007/s00059-015-4236-0 · 0.91 Impact Factor
  • D Horstkotte, C Piper
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    ABSTRACT: Colonization of native cardiac valves or polymer implants, e.g. valves, conduits, rings, electrode leads and polymer-associated endocarditis (PIE), by microorganisms, primarily gram-positive bacteria (infective endocarditis), constitutes a severe, prognostically unfavorable disease. Fever and in the majority of cases development of a valve regurgitant murmur are clinical landmark findings. The white blood cell count, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are regularly elevated. With a normal CRP level, infective endocarditis is extremely unlikely. Irrespective of body temperature, at least three blood cultures (aerobic and anaerobic) should be taken and if initiation of antimicrobial therapy is urgent, 1 h apart before therapy is initiated. Identification of the pathogen to the species level and testing antimicrobial susceptibility to antibiotics by a quantitative hemodilution test, not with agar diffusion tests, are obligatory. A minimum inhibitory concentration should be administered for antibiotics and usual combinations of antibiotics with an expected synergistic potential. Streptococci, staphylococci and enterococci are the most frequent causative organisms. Immediate initiation of transthoracic echocardiography (TTE) is mandatory followed by transesophageal echocardiography if imaging quality is poor, involvement of intracardiac implants is possible or TTE is insufficient to establish the diagnosis. An insufficiently long antimicrobial therapy promotes recurrent infections, thus a 4-week treatment is standard, while in special cases (e.g. PIE) treatment for 6 weeks should be the rule. If typical complications of infective endocarditis, such as uncontrolled local infection, systemic thromboembolism, central nervous involvement, development of a severe valve incompetence or mitral kissing vegetation in primary aortic valve endocarditis occur, urgent surgical intervention should be considered. If cardiac implants are involved, early surgical removal followed by a 6-week antimicrobial treatment is the rule. Adequate and timely diagnosis and treatment are the key to improve the overall prognosis.
    Herz 04/2015; 40(2):265-280. DOI:10.1007/s00059-015-4217-3 · 0.91 Impact Factor
  • Cornelia Piper, Lothar Faber, Dieter Horstkotte
    DMW - Deutsche Medizinische Wochenschrift 03/2015; 140(5):353-62. DOI:10.1055/s-0041-100499 · 0.55 Impact Factor
  • European Heart Journal – Cardiovascular Imaging 12/2014; 15 Suppl 2:ii57-ii59. DOI:10.1093/ehjci/jeu244 · 2.65 Impact Factor
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    ABSTRACT: The coxsackie and adenovirus receptor (CAR) mediates the entry of coxsackievirus B (CVB) and adenovirus into host cells and is, therefore, a key determinant for the molecular pathogenesis of viral diseases such as myocarditis. The aim was to investigate the influence of HMG-CoA reductase inhibitor lovastatin on CAR expression in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were exposed to different concentrations of lovastatin (0.05-5 μmol/l) for up to 48 h. Alterations in CAR expression were examined by quantitative real-time PCR (qRT-PCR) and flow cytometry. In addition, after treatment with 1 μmol/l lovastatin for 48 h, HUVECs were infected for 8 h with CVB3 and virus replication was detected by qRT-PCR using viral-specific TaqMan probes. We found that lovastatin decreases CAR mRNA expression by up to 80 % (p < 0.01) and CAR protein expression by up to 19 % (p < 0.01), in a concentration-dependent manner. Moreover, virus replication of CVB3 was significantly inhibited after lovastatin treatment (p < 0.05). The signaling mechanism of CAR down-regulation by lovastatin depends on the Rac1/Cdc42 pathway. This study shows for the first time that lovastatin reduces the expression of CAR and subsequently the replication of CVB3 in HUVECs. Full paper here: http://link.springer.com/article/10.1007/s00011-013-0695-z
    Agents and Actions 12/2013; DOI:10.1007/s00011-013-0695-z · 2.14 Impact Factor
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    ABSTRACT: We examined the prevalence of sleep-disordered breathing (SDB) in patients with severe aortic valve stenosis (AS) and the impact of transfemoral aortic valve implantation (TAVI) on SDB. 79 patients underwent cardiorespiratory polygraphy (PG) before TAVI (CoreValve™), 62 of them a second PG after the procedure. Forty-nine (62 %) patients had obstructive sleep apnea (OSA), 25 (32 %) central sleep apnea (CSA), and 5 (6 %) presented without significant SDB (apnea-hypopnea index (AHI) < 5/h). Among the 62 patients evaluated before and after TAVI, 36 (58 %) had OSA, 22 (36 %) CSA, and 4 patients (7 %) no SDB. AHI was significantly higher in CSA patients than in OSA patients (34.5 ± 18.3 vs. 18.0 ± 12.6/h, p < 0.001). Successful TAVI had a significant impact on CSA but not on OSA: CSA patients with optimal TAVI results experienced a significant reduction in central respiratory events (AHI 39.6 ± 19.6-23.1 ± 16.0/h, p = 0.035), while no changes were detected in OSA patients (AHI 18.8 ± 13.0-20.25 ± 13.4/h, p = 0.376). In contrast, in patients who developed at least moderate periprosthetic aortic regurgitation (AR > I), CSA increased significantly (AHI 26.3 ± 13.2-39.2 ± 18.4/h, p = 0.036), whereas no acute change was seen in patients with OSA (AHI 10.5 ± 7.8-12.5 ± 5.0/h, p = 0.5). OSA and CSA are prevalent in more than 90 % of patients undergoing TAVI for severe aortic valve stenosis. Successful TAVI had no significant impact on OSA but improved CSA. In case of an acute change from pressure overload (aortic stenosis) to acute volume overload (aortic regurgitation after TAVI), central, but not obstructive, sleep apnea deteriorated.
    Clinical Research in Cardiology 08/2013; DOI:10.1007/s00392-013-0603-0 · 4.17 Impact Factor
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    ABSTRACT: Fibroblast activity within the heart may be considered a basically constructive process. Hyperactivity of fibroblasts, however, may result in the accumulation of extracellular matrix proteins with adverse effects on cardiac structure and function including electrical instability and increased risk of arrhythmogenic cardiac death. The detection of cardiac fibrosis by dedicated imaging techniques, mainly gadolinium-enhanced MRI, holds promise to refine patient management in a variety of cardiac conditions. This review aims to summarize the current knowledge regarding fibrosis in hypertrophic cardiomyopathy.
    Expert Review of Cardiovascular Therapy 04/2013; 11(4):495-504. DOI:10.1586/erc.13.24
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    ABSTRACT: Psychological symptoms are common in patients with heart disease. Objective of this study was to analyse the effects of somatic factors on anxiety and depression in hospitalised patients with heart failure. We examined 150 patients by short-term interview and standardized questionaire (HADS-D) and performed a written survey 3 months later. In 47% of the patients signs of anxiety and in 30% signs of depression were present. Increased heart failures severity was associated with increased rates of anxiety and depression. 3 months after hospital discharge the percentage of patients who reported symptoms of anxiety had decreased, the percentage of depressive female patients had increased. The course of anxiety and depression was not affected by cardiologic treatment. Patients with severe signs of anxiety and/or depression should receive specific diagnostics and therapy.
    PPmP - Psychotherapie · Psychosomatik · Medizinische Psychologie 03/2013; 63(7). DOI:10.1055/s-0032-1316385 · 1.02 Impact Factor
  • D Horstkotte, C Prinz, C Piper
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    ABSTRACT: An intervention for chronic acquired valvular heart disease may either be indicated in symptomatic patients to relieve symptoms and improve quality of life or in asymptomatic patients to improve long-term prognosis, e.g., by preventing disease-related complications like chronic heart failure or arrhythmias. For proper action according to current guidelines, the systematic evaluation of symptoms related to the underlying valve disease is of utmost importance. If a discrepancy between symptoms reported or not reported by the patients and the severity of the valve disease is supposed, true absence of symptoms and exercise tolerance should be verified by spiroergometry. In the truly asymptomatic patient with a severe valvular lesion, preservation of myocardial adaption to the chronic volume or pressure overload should be tested utilizing appropriate imaging techniques like radionuclide ventriculography under exercise conditions. The proper evaluation of the functional status is of growing importance in our aging population with its sedentary lifestyle. In this context, the results of a survey should be kept in mind, which indicated that a significant proportion of patients still have interventions too late during the natural history of their valve disease with symptoms of congestive heart failure, arrhythmias, and the risk of sudden cardiac death persisting after a primarily successful valve repair or replacement.
    Der Internist 01/2013; 54(1). DOI:10.1007/s00108-012-3092-8 · 0.27 Impact Factor
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    ABSTRACT: Fragestellung: Veränderungen der Na+Ca2+-Exchanger (EXCH)-Expression werden als Ausdruck einer gestörten Calciumhomöostase angesehen. Da sich diastolische und systolische Funktionsstörungen lange vor Manifestation einer terminalen Herzinsuffizienz einstellen, untersuchten wir bei 22 Patienten mit chronischen Herzklappenfehlern (HKF), in welchem Stadium der myokardialen Funktionsstörung eine Hochregulation des EXCH erfolgt und ob diese ggf. frühzeitig eine Erschöpfung der myokardialen Adaptationsmechanismen an chronische Druck- und/oder Volumenbelastung anzeigt.¶   Methoden: Mittels quantitativer RT-PCR wurde die Transkriptionshöhe des EXCH in endomyokardialen Biopsien von 11 Patienten mit Aortenstenosen (AS), 5 mit Aorteninsuffizienzen (AI) und 6 mit primären Mitralinsuffizienzen (MI) unterschiedlicher hämodynamischer Schweregrade bestimmt. Zusätzlich wurde endomyokardiales Gewebe von 13 explantierten, terminal insufffizienten Herzen untersucht. Als Kontrollgruppe diente endomyokardiales Gewebe von sieben Individuen bei denen letztlich eine Herzerkrankung ausgeschlossen werden konnte.¶   Ergebnisse: Die Menge an EXCH mRNA betrug im Myokard der Kontrollgruppe 2,6±1,2amol/ng totaler RNA und unterschied sich nicht von der Menge an EXCH mRNA bei AS (1,8±1,4amol/ng totaler RNA), AI (1,9±0,8amol/ng) oder MI (2,2±2,1amol/ng). Im Myokard explantierter terminal insuffizienter Herzen fand sich dagegen eine deutlich erhöhte Menge an EXCH mRNA (8,9±1,9amol/ng).¶Zwischen der EXCH-Transkription und dem Schweregrad des Vitiums oder der konsekutiven Einschränkung der linksventrikulären Pumpfunktion bestand kein Zusammenhang: Cardiac Index (CI) >3,5l/min/m2 (EXCH 1,4±1,1amol/ng totaler RNA); CI 3,5–2,4 (EXCH 2,5±1,8); CI <2,4 (EXCH 1,8±1,0); EF-angio >50% (EXCH 1,9±1,8), EF-angio ≤50% (EXCH 1,9±0,9); EF-RNV >50% (EXCH 2,4±1,8), EF-RNV ≤50% (EXCH 1,7±1,0).¶   Schlussfolgerung: Die myokardialen EXCH-Transkriptionsmengen ändern sich bei HKF nicht parallel zur Ausbildung einer myokardialen Pumpfunktionsstörung. EXCH scheint daher nicht geeignet, eine beginnende Erschöpfung der myokardialen Adaptation an chronische Volumen- und/oder Druckbelastungen zu detektieren. Background: Na+-Ca2+ exchanger (EXCH) is an important regulator of intracellular calcium homeostasis. To maintain a normal intracellular Ca2+ concentration, EXCH expression may be upregulated before the onset of end-stage heart failure. We tested for a correlation between the EXCH transcription level and the degree of myocardial dysfunction as well as the suitability of EXCH transcription as a molecular marker for early detection of a transition from adequate to inadequate myocardial adaptation to chronic pressure and/or volume overload in valvular heart disease (VHD).¶   Methods: The level of EXCH transcription was analyzed in myocardial biopsies from eleven patients with aortic stenosis (AS), five with aortic regurgitation (AR) and six with primary mitral regurgitation (MR) of different hemodynamic severity and myocardial impairment using the quantitative rt-PCR technique. In addition, endomyocardial tissue from thirteen explanted hearts with end-stage heart failure and biopsies from seven individuals without heart disease were investigated.¶   Results: The mean level of EXCH transcription in patients with AS was: 1.8±1.4amol/ng total RNA, with AR: 1.9±0.8amol/ng and with MR: 2.2±+2.1 amol/ng. This was not from different controls (2.6±1.2 amol/ng total RNA). However, in myocardium from end-stage heart failure, EXCH transcription was increased fourfold amounting to 8.9±1.9amol/ng total RNA. No difference in the EXCH transcription was found in VHD with respect to the degree of myocardial dysfunction: cardiac index (CI) >3.5l/min/m2 (EXCH 1.4±1.1amol/ng total RNA); CI 3.5–2.4 (EXCH 2.5±1.8); CI <2.4 (EXCH 1.8±1.0); EF-angio >50% (EXCH 1.9±1.8); EF-angio ≤50% (EXCH 1.9±0.9); EF-RNV >50% (EXCH 2.4±1.8), EF-RNV ≤50% (EXCH 1.7±1.0).¶   Conclusion: Myocardial EXCH transcription does not change parallel to the degree of myocardial dysfunction in VHD. Consequently, myocardial EXCH transcription does not appear to be suitable as a parameter indicating the transition from adequate to inadequate myocardial adaptation to chronic volume and/or pressure overload. Schlüsselwörter Natrium-Calcium-Exchanger – Herzklappenfehler – myokardiale Adaptation – endomyokardiale Biopsie – terminale Herzinsuffizienz Key words Sodium-calcium exchanger – heart valve disease – endomyocardial biopsy – myocardial adaptation – end-stage heart failure
    Zeitschrift für Kardiologie 04/2012; 89(8):682-690. DOI:10.1007/s003920070196 · 0.97 Impact Factor
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    ABSTRACT: Die supravalvuläre Aortenstenose ist im Erwachsenenalter seltene Ursache einer Behinderung des linksventrikulären Blutausstroms. Sie tritt zum einen als isolierter Defekt sporadisch oder familiär mit autosomal-dominantem Erbgang ohne weitere phänotypische Anomalien und zum anderen im Rahmen des Williams-Syndroms mit geistiger Retardierung und multiplen weiteren Anomalien auf. Als Ursache ist ein Defekt des Elastin kodierenden Gens nachgewiesen. Die supravalvuläre Aortenstenose ist häufig mit kardiovaskulären Defekten assoziiert, insbesondere Anomalien der peripheren Pulmonalarterien, der thorakalen Aorta, der Carotiden, der Aa. subclaviae, der Koronarien und der Aortenklappe. Die Koronararterien sind einem erhöhten Perfusionsdruck ausgesetzt, was zu deren Dilatation, Schlängelung und beschleunigter Arteriosklerose beiträgt. Es wird über einen 35-jährigen Patienten berichtet, bei dem eine bisher asymptomatische supravalvuläre Aortenstenose mit einer exzessiven Dilatation von rechter Koronararterie und Ramus descendens anterior der linken Koronararterie sowie einer Ostiumstenose der linken A. carotis communis vergesellschaftet ist. Phänotypische Anomalien des Williams-Syndroms fanden sich bei dem Patienten nicht. Supravalvular aortic stenosis is a rare cause of left ventricular outflow obstruction in adults. It occurs as an isolated defect sporadically or on a hereditary basis with an autosomal dominant trait without further phenotypical anomalies, or as part of the Williams syndrome with mental retardation and multiple other anomalies. This lesion was proved to result from a defect of the elastin coding gene. Supravalvular aortic stenosis is frequently associated with cardiovascular defects, particularly of the peripheral pulmonary arteries, thoracic aorta, carotid, subclavian, and coronary arteries and the aortic valve. The coronary arteries are subject to an increased perfusion pressure leading to dilatation, tortuosity and acelerated arteriosclerosis. We give details of a 35-year-old patient in whom a previously asymptomatic supravalvular aortic stenosis is associated with an excessive dilatation of the right coronary artery and the left anterior descending coronary artery as well as an ostium stenosis of the left common carotid artery. The patient did not present any phenotypical anomalies of the Williams syndrome. Schlüsselwörter Supravalvuläre Aortenstenose – Williams-SyndromKey words Supravalvular aortic stenosis – Williams syndrome
    Zeitschrift für Kardiologie 04/2012; 89(3):199-205. DOI:10.1007/s003920050471 · 0.97 Impact Factor
  • Der Klinikarzt 04/2012; 41(S 01):44-50. DOI:10.1055/s-0032-1312462
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    ABSTRACT: Dysfunction of heart valve prostheses (VP) is a life-threatening complication and the diagnosis remains difficult. The motivation for this study was to improve the detection of dysfunctional VP by optimizing application of the prosthetic effective orifice area (VA). For this reason the minimal expected normal VA (VA(expected)) was introduced. We investigated echocardiographically 1,369 normally functioning aortic valve prostheses (AVP). Mean VA, transprosthetic peak (PPG) and mean pressure gradients (MPG) were evaluated to gain reference values depending on prosthetic size and construction principle. Mean VA(expected) was calculated by applying a simple formula that was developed empirically using statistical analyses. The results were compared with those of 65 dysfunctional AVPs. VA(expected) can be applied as a threshold between normal and dysfunctional stenotic AVP and showed a correct estimation in 87% of all normally functioning and 100% of dysfunctional stenotic VPs. The sensitivity for all prosthetic sizes is 1.0, independently of the constructional principle of the VP. Specificity ranged between 0.8 and 1.0, dependent on VP size. The formula representing VA(expected) is simple and can be executed easily. As nearly independent of stroke volume and in consideration of VA(expected), VA seems to have become one of the preferable parameters for detecting pathological stenotic AVPs echocardiographically. The additional application of PPG/MPG and other parameters permits prostheses with relevant isolated regurgitation and patient-prosthesis-mismatch to be distinguished.
    Echocardiography 02/2012; 29(6):713-9. DOI:10.1111/j.1540-8175.2011.01659.x · 1.25 Impact Factor
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    ABSTRACT: The Coxsackievirus and Adenovirus Receptor (CAR) is a transmembrane protein of the immunoglobulin superfamily and plays a physiological role in cellular adhesion on various cell types. Moreover, CAR mediates the entry of Coxsackievirus B (CVB) and Adenovirus (Ad) in host cells and is therefore a key determinant for the molecular pathogenesis of viral diseases like myocarditis. A down regulation of CAR expression could potentially affect the virus entry and subsequent the replication. Therefore we investigated in cultured human umbilical vein endothelial cells (HUVEC) whether CAR expression is influenced by the 3‑hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor Lovastatin and, if so, by which mechanisms. We could demonstrate for the first time that pre-incubation of HUVEC with Lovastatin dose-dependently decreases the mRNA and protein level of CAR resulting in a remarkable reduction of Coxsackievirus B3 replication. Moreover, the signalling mechanism of CAR down regulation by statins depends on the Rac1/Cdc42 pathway. Through the statin-mediated inhibition of G protein isoprenylation Rac1 and Cdc42 remain inactive and the gene expression is therefore down regulated. In summary, these results indicate potentially beneficial antiviral effects of Lovastatin which could be the basis for a new therapeutic strategy in viral myocarditis.
    Herbsttagung und Jahrestagung der Arbeitsgruppe Rhythmologie, Deutsche Gesellschaft für Kardiologie; 10/2011
  • Dieter Horstkotte, Cornelia Piper
    The Journal of heart valve disease 07/2011; 20(4):376-7. · 0.73 Impact Factor
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    ABSTRACT: There are as yet no data on the prevalence of sleep apnoea in patients with severe aortic stenosis (AS). To assess the occurrence, severity and clinical correlates of sleep apnoea in patients with AS. During a 4-month period in 2010, 67 patients were consecutively included in this study, 42 of which (19 men; mean±SD age 72±9 years) had severe AS (aortic valve opening area≤1.0 cm2); all were investigated with cardiorespiratory polygraphy. Sleep apnoea was diagnosed if the apnoea-hypopnoea index (AHI) (median (lower quartile, upper quartile)) was ≥5/h. The control group of 25 patients matched for age, body mass index and sex had angiographic exclusion of coronary artery disease, regular left ventricular ejection fraction, and no valve disease. Sleep apnoea was found in 30/42 patients with AS (71%; AHI=23/h (14/h, 36/h)). The severity was significantly greater in patients with severe AS than in the control group (AHI=12/h (8/h, 17/h)) (p<0.01). Half of the patients with sleep apnoea had obstructive sleep apnoea (OSA) (AHI=15/h (9/h, 28/h)), and half had central sleep apnoea (CSA) (AHI=25/h (18/h, 45/h)). New York Heart Association classification and severity of sleep apnoea correlated with η=0.5 (η2=0.3). The severity of CSA correlated with pulmonary artery pressure (r=0.7, p<0.01) and pulmonary capillary wedge pressure (r=0.7, p<0.01). Patients with AS and CSA had a lower PCO2 than those with OSA and those without sleep apnoea (p<0.01). Sleep apnoea is common in patients with severe AS. The severity of CSA correlates with pulmonary hypertension, which may suggest that myocardial adaptation is exhausting.
    Postgraduate medical journal 03/2011; 87(1029):458-62. DOI:10.1136/pgmj.2010.112052 · 1.55 Impact Factor
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    ABSTRACT: Purpose: Troponin is a well established marker in the diagnosis of acute coronary syndroms. In this study we analyzed the impact of troponin to detect bypass dysfunction early after coronary artery bypass surgery (CABG). Methods: During 334 consecutive days troponin I, CK, and CK-MB were measured every two hours for 24 hours in 1237 patients (949 men, 77%) after CABG (on pump 796 (64.3%), off pump 441). If troponin I was > 15 ng/ml, coronary angiography was performed within the first 24 hours after CABG. Results: In-hospital mortality of all patients was 2.1% (on pump 2.6%, off pump 1.1%). Coronary angiography was performed in 104 patients (on pump 80 (10.1%), off pump 24 (5.4%)). The mean value of cardiac enzymes was 33.2±25.1 ng/ml for troponin I, 1459±1114 U/l for CK, and 103.3±117.4 U/l for CK-MB. Dysfunction of at least one bypass graft was detected in 56 patients (53.8% of all examined, 4.5% of all patients). In this subgroup there was a tendency towards a higher average value of troponin I (34.8±30.4 ng/ml) than in the group of patients without bypass dysfunction (31.3±17.1 ng/ml, p=0.12, n.s.). The mean value of CK (1575±1178 U/l vs. 1323±1030 U/l, p=0.06, n.s.), and CK-MB (121.7±137.1 U/l vs. 81.7±85.7 U/l, p=0.08, n.s.) was increased as well. Percutaneous coronary intervention or re-operation was performed in 37 patients (35.6% of all examined, 3.0% of all patients). The mean value of troponin I in these patients was 38.2±36.2 ng/ml with a tendency towards higher values than in patients without bypass dysfunction (30.4±15.5 ng/ml, p=0.57, n.s.). There was a tendency towards higher CK (1498±1249 vs. 1437±1041 U/l, p=0.91, n.s.), and CK-MB (140.7±161.1 vs. 82.6±78.3 U/l, p=0.06, n.s.) values compared to those of the patients without bypass dysfunction. In all patients undergoing re-catheterization mean operative bypass time had been 101.4±38.3 minutes and mean aortic clamp time 40.4±22.7 minutes while in the group of patients with bypass dysfunction 103.0±40.0 and 41.8±27.2 minutes were documented, respectively (n.s.). Conclusions: Postoperative measurement of troponin is suitable to detect early bypass dysfunction. About 50% of the patients with an elevated postoperative troponin I above 15 ng/ml had bypass dysfunction and in 35% of these patients an indication for coronary intervention or re-operation was given. There was a tendency towards higher troponin levels in patients with bypass dysfunction independent from operative bypass and aortic clamp time.
    ESC 2010, Stockholm; 08/2010
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    ABSTRACT: In viral myocarditis, adeno- and enteroviruses have most commonly been implicated as causes of infection. Both viruses require the human coxsackie-adenovirus receptor (CAR) to infect the myocardium. Due to its crucial role for viral entry, CAR-downregulation may lead to novel approaches for treatment for viral myocarditis. In this study, we report on pharmaceutical drug influences on CAR levels in human umbilical vein endothelial cells (HUVEC) and cervical carcinoma cells (HeLa) detected by immunoblotting, quantitative real time-PCR and cellular susceptibility to the cardiotropic coxsackie-B3 virus strain Nancy (CVB3). Our results indicate, for the first time, a dose-dependent CAR mRNA and protein downregulation upon Valsartan and Bosentan treatment. Most interestingly, drug-induced CAR diminution significantly reduced the viral load in CVB3-infected HUVEC. In order to assess the regulatory effects of both drugs in detail, we knocked down their protein targets, the G-protein coupled receptors angiotensin-II type-1 receptor (AT(1)R) and endothelin-1 type-A and -B receptors (ET(A)R/ET(B)R) in HUVEC. Receptor-specific gene silencing indicates that CAR gene expression is regulated by agonistic and antagonistic binding to ET(B)R, but not ET(A)R. In addition, neither stimulation nor inhibition of AT(1)R seemed to be involved in CAR gene regulatory processes. Our study indicates that Valsartan and Bosentan protected human endothelial cells from CVB3-infection. Therefore, besides their well-known anti-hypertensive effects these drugs may also protect the myocardium and other tissues from coxsackie- and adenoviral infection.
    Journal of General Virology 08/2010; 91(Pt 8):1959-70. DOI:10.1099/vir.0.020065-0 · 3.53 Impact Factor
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    ABSTRACT: Sleep-disordered breathing (SDB) has a prognostic impact in patients with cardiac diseases. We included 257 patients with preserved left ventricular function and angiographically proven coronary artery disease (CAD). All patients underwent cardiorespiratory polygraphy. In 251 patients high-sensitive C-reactive protein and fibrinogen were measured. SDB was documented in 188 patients (apnea-hypopnea-index [AHI] 16.4+/- 1.9/h): 58 patients presented central sleep apnea (CSA) and 130 patients obstructive sleep apnea (OSA). All patients (73%) with SDB had higher blood fibrinogen levels than those without SDB (p = 0.01). We found 197 patients with CRP-values below the cut-off of 0.5 mg/dl (group 1) and 54 patients with no active infection but CRP>0.5 mg/dl (group 2). Severity of SDB was significantly higher in group 2 (p = 0.01). SDB has a high prevalence in CAD patients and seems to be associated with chronic inflammation, which may be linked to CAD progression and/or acute coronary events.
    Wiener Medizinische Wochenschrift 07/2010; 160(13-14):349-55. DOI:10.1007/s10354-009-0737-x
  • Wiener Medizinische Wochenschrift 07/2010; 160:349-355.

Publication Stats

974 Citations
274.99 Total Impact Points

Institutions

  • 2000–2015
    • Ruhr-Universität Bochum
      • • Institut für Klinische Chemie, Transfusions- und Laboratoriumsmedizin
      • • Medizinische Klinik II - Kardiologie und Angiologie
      Bochum, North Rhine-Westphalia, Germany
  • 2000–2012
    • Franziskus Hospital Bielefeld
      Bielefeld, North Rhine-Westphalia, Germany
  • 2001–2009
    • Herz- und Diabeteszentrum Nordrhein-Westfalen
      • Department of Cardiology, Heart and Diabetes Centre North Rhine-Westphalia
      Bad Oeyhausen, North Rhine-Westphalia, Germany
  • 2005
    • Institutul Național de Boli Infecțioase "Prof. Dr. Matei Balș"
      Bucureşti, Bucureşti, Romania
  • 2003
    • Krankenhaus Bad Oeynhausen
      Bad Oeyhausen, North Rhine-Westphalia, Germany
  • 1995–2003
    • Freie Universität Berlin
      Berlín, Berlin, Germany
  • 1994
    • Heinrich-Heine-Universität Düsseldorf
      • Klinik für Kardiologie, Pneumologie und Angiologie
      Düsseldorf, North Rhine-Westphalia, Germany