Archiv für Kreislaufforschung Journal Impact Factor & Information

Publisher: Deutsche Gesellschaft für Kreislaufforschung, Springer Verlag

Journal description

Basic Research in Cardiology is an international journal for cardiovascular research. It provides a forum for original and review articles related to experimental cardiology that meet its stringent scientific standards. Thus it comprises all aspects related to the physiology and pathology of the structure and function of the heart and the cardiovascular system including their regulation by neuronal and humoral mechanisms. The journal regularly receives articles from the fields of Molecular and cellular biology Biochemistry Biophysics Pharmacology Physiology and pathology Clinical cardiology Fields of interest: Cardiology physiology pathology.

Current impact factor: 5.41

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 5.414
2013 Impact Factor 5.955
2012 Impact Factor 5.904
2011 Impact Factor 7.348
2010 Impact Factor 6.128
2009 Impact Factor 5.973
2008 Impact Factor 5.407
2006 Impact Factor 3.798
2005 Impact Factor 2.806
2004 Impact Factor 3.009
2003 Impact Factor 2.993
2002 Impact Factor 1.994
2001 Impact Factor 1.729
2000 Impact Factor 1.49
1999 Impact Factor 1.148
1998 Impact Factor 1.573
1997 Impact Factor 1.141
1996 Impact Factor 0.978
1995 Impact Factor 0.915
1994 Impact Factor 0.873
1993 Impact Factor 0.991
1992 Impact Factor 0.636

Impact factor over time

Impact factor

Additional details

5-year impact 4.94
Cited half-life 5.10
Immediacy index 0.80
Eigenfactor 0.01
Article influence 1.53
Website Basic Research in Cardiology website
Other titles Basic research in cardiology (Online)
ISSN 0300-8428
OCLC 42790143
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Springer Verlag

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Author's pre-print on pre-print servers such as
    • Author's post-print on author's personal website immediately
    • Author's post-print on any open access repository after 12 months after publication
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification
    ​ green

Publications in this journal

  • Archiv für Kreislaufforschung 11/2015; 110(6). DOI:10.1007/s00395-015-0512-7
  • Archiv für Kreislaufforschung 11/2015; 110(6). DOI:10.1007/s00395-015-0511-8
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    ABSTRACT: Cyclic GMP-dependent protein kinase (PKG) is a serine-threonine kinase that mediates the cardioprotective effect of ischemic and pharmacologic preconditioning. Since hydrogen sulfide (H2S) has been implicated in mediating the cardioprotective effects of the cGMP modulators tadalafil and cinaciguat, we tested the hypothesis that myocardial gene therapy with PKG exerts cardioprotection against ischemia/reperfusion (I/R) injury through a mechanism involving H2S. Adult rat cardiomyocytes were infected with adenoviral vector encoding PKGIα or inactive mutant PKGIαK390A (K390A) for 24 h. Necrosis and apoptosis (n = 6/group) were determined after 90 min of simulated ischemia and 1 or 18 h of reoxygenation, respectively. To study the effect of PKGIα in vivo, mice received intramyocardial injections of adenoviral PKGIα or K390A. Four days later, the hearts were subjected to 30 min of ischemia followed by reperfusion for 24 h. The inhibitor of H2S-producing enzyme, cystathionine-γ-lyase (CSE), dl-propargylglycine (PAG, 50 mg/kg, ip) was given 30 min before ischemia. PKGIα overexpression induced CSE expression, whereas cystathionine-β-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase expression was not changed. PKGIα overexpression increased H2S in the heart and cardiomyocytes in relation to control and PKGIαK390A. Moreover, PAG abolished protection with PKGIα in vitro by increasing necrosis (35.2 ± 1.7 %, P P P 2S signaling.
    Archiv für Kreislaufforschung 07/2015; 110(4). DOI:10.1007/s00395-015-0500-y
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    ABSTRACT: Hypoadiponectinemia is an independent predictor of cardiovascular disease, impairs mitochondrial function in skeletal muscle, and has been linked to the pathogenesis of Type 2 diabetes. In models of Type 2 diabetes, myocardial mitochondrial function is impaired, which is improved by increasing serum adiponectin levels. We aimed to define the roles of adiponectin receptor 1 (AdipoR1) and 2 (AdipoR2) in adiponectin-evoked regulation of mitochondrial function in the heart. In isolated working hearts in mice lacking AdipoR1, myocardial oxygen consumption was increased without a concomitant increase in cardiac work, resulting in reduced cardiac efficiency. Activities of mitochondrial oxidative phosphorylation (OXPHOS) complexes were reduced, accompanied by reduced OXPHOS protein levels, phosphorylation of AMP-activated protein kinase, sirtuin 1 activity, and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) signaling. Decreased ATP/O ratios suggested myocardial mitochondrial uncoupling in AdipoR1-deficient mice, which was normalized by lowering increased mitochondrial 4-hydroxynonenal levels following treatment with the mitochondria-targeted antioxidant Mn (III) tetrakis (4-benzoic acid) porphyrin. Lack of AdipoR2 did not impair mitochondrial function and coupling in the heart. Thus, lack of AdipoR1 impairs myocardial mitochondrial function and coupling, suggesting that impaired AdipoR1 signaling may contribute to mitochondrial dysfunction and mitochondrial uncoupling in Type 2 diabetic hearts.
    Archiv für Kreislaufforschung 07/2015; 110(4). DOI:10.1007/s00395-015-0495-4
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    ABSTRACT: Recent reports indicate that elevating DNA glycosylase/AP lyase repair enzyme activity offers marked cytoprotection in cultured cells and a variety of injury models. In this study, we measured the effect of EndoIII, a fusion protein construct that traffics Endonuclease III, a DNA glycosylase/AP lyase, to the mitochondria, on infarct size in a rat model of myocardial ischemia/reperfusion. Open-chest, anesthetized rats were subjected to 30 min of occlusion of a coronary artery followed by 2 h of reperfusion. An intravenous bolus of EndoIII, 8 mg/kg, just prior to reperfusion reduced infarct size from 43.8 ± 1.4 % of the risk zone in control animals to 24.0 ± 1.3 % with no detectable hemodynamic effect. Neither EndoIII's vehicle nor an enzymatically inactive EndoIII mutant (K120Q) offered any protection. The magnitude of EndoIII's protection was comparable to that seen with the platelet aggregation inhibitor cangrelor (25.0 ± 1.8 % infarction of risk zone). Because loading with a P2Y12 receptor blocker to inhibit platelets is currently the standard of care for treatment of acute myocardial infarction, we tested whether EndoIII could further reduce infarct size in rats treated with a maximally protective dose of cangrelor. The combination reduced infarct size to 15.1 ± 0.9 % which was significantly smaller than that seen with either cangrelor or EndoIII alone. Protection from cangrelor but not EndoIII was abrogated by pharmacologic blockade of phosphatidylinositol-3 kinase or adenosine receptors indicating differing cellular mechanisms. We hypothesized that EndoIII protected the heart from spreading necrosis by preventing the release of proinflammatory fragments of mitochondrial DNA (mtDNA) into the heart tissue. In support of this hypothesis, an intravenous bolus at reperfusion of deoxyribonuclease I (DNase I) which should degrade any DNA fragments escaping into the extracellular space was as protective as EndoIII. Furthermore, the combination of EndoIII and DNase I produced additive protection. While EndoIII would maintain mitochondrial integrity in many of the ischemic cardiomyocytes, DNase I would further prevent mtDNA released from those cells that EndoIII could not save from propagating further necrosis. Thus, our mtDNA hypothesis would predict additive protection. Finally to demonstrate the toxicity of mtDNA, isolated hearts were subjected to 15 min of global ischemia. Infarct size doubled when the coronary vasculature was filled with mtDNA fragments during the period of global ischemia. To our knowledge, EndoIII and DNase are the first agents that can both be given at reperfusion and add to the protection of a P2Y12 blocker, and thus should be effective in today's patient with acute myocardial infarction.
    Archiv für Kreislaufforschung 03/2015; 110(2):459. DOI:10.1007/s00395-014-0459-0
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    ABSTRACT: The genetic underpinnings of heart rate regulation are only poorly understood. In search for genetic regulators of cardiac pacemaker activity, we isolated in a large-scale mutagenesis screen the embryonic lethal, recessive zebrafish mutant schneckentempo (ste). Homozygous ste mutants exhibit a severely reduced resting heart rate with normal atrio-ventricular conduction and contractile function. External electrical pacing reveals that defective excitation generation in cardiac pacemaker cells underlies bradycardia in ste−/− mutants. By positional cloning and gene knock-down analysis we find that loss of dihydrolipoyl succinyltransferase (DLST) function causes the ste phenotype. The mitochondrial enzyme DLST is an essential player in the citric acid cycle that warrants proper adenosine-tri-phosphate (ATP) production. Accordingly, ATP levels are significantly diminished in ste−/− mutant embryos, suggesting that limited energy supply accounts for reduced cardiac pacemaker activity in ste−/− mutants. We demonstrate here for the first time that the mitochondrial enzyme DLST plays an essential role in the modulation of the vertebrate heart rate by controlling ATP production in the heart. Electronic supplementary material The online version of this article (doi:10.1007/s00395-015-0468-7) contains supplementary material, which is available to authorized users.
    Archiv für Kreislaufforschung 03/2015; 110(2):468. DOI:10.1007/s00395-015-0468-7
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    ABSTRACT: Melusin is a protein selectively expressed in skeletal muscles and heart and highly conserved in vertebrates. Melusin is part of the heat shock protein 90 machinery and acts as molecular chaperone in controlling cardiomyocyte survival and adaptive hypertrophy signaling pathways in the heart in response to different stress conditions. The role of melusin has been extensively investigated in genetically modified mice over the past years disclosing an important cardioprotective function of this unique muscle-specific chaperone protein in different pathological conditions. This review highlights the findings in animal models and the molecular mechanisms underlying melusin cardioprotective function.
    Archiv für Kreislaufforschung 03/2015; 110(2):466. DOI:10.1007/s00395-015-0466-9
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    ABSTRACT: It is generally held that inhibition of mammalian sterile 20-like kinase 1 (Mst1) protects the heart through reducing myocyte apoptosis. We determined whether inhibition with a dominant-negative Mst1 (DN-Mst1) would protect against the cardiomyopathy induced by chronic β1-adrenergic receptor (β1-AR) stimulation by preventing myocyte apoptosis. DN-Mst1 mice were mated with β1-AR transgenic (Tg) mice and followed for 20 months. β1-AR Tg mice developed cardiomyopathy as they aged, as reflected by premature mortality and depressed cardiac function, which were rescued in β1-AR × DN-Mst1 bigenic mice. Surprisingly, myocyte apoptosis did not significantly decrease with Mst1 inhibition. Instead, Mst1 inhibition predominantly reduced non-myocyte apoptosis, e.g., fibroblasts, macrophages, neutrophils and endothelial cells. Fibrosis in the hearts with cardiomyopathy increased fivefold and this increase was nearly abolished in the bigenic mice with Mst1 inhibition. Regression analysis showed no correlation between myocyte apoptosis and cardiac function or myocyte number, whereas the latter two correlated significantly, p < 0.05, with fibrosis, which generally results from necrosis. To examine the role of myocyte necrosis, chronic β-AR stimulation with isoproterenol was induced for 24 h and myocyte necrosis was assessed by 1 % Evans blue dye. Compared to WT, DN-Mst1 mice showed significant inhibition, p < 0.05, of myocyte necrosis. We confirmed this result in Mst1-knockout mice, which also showed significant protection, p < 0.05, against myocyte necrosis compared to WT. These data indicate that Mst1 inhibition rescued cardiac fibrosis and myocardial dysfunction in β1-AR cardiomyopathy. However, this did not occur through Mst1 inhibition of myocyte apoptosis but rather by inhibition of cardiomyocyte necrosis and non-myocyte apoptosis, features of Mst1 not considered previously.
    Archiv für Kreislaufforschung 03/2015; 110(2):461. DOI:10.1007/s00395-015-0461-1
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    ABSTRACT: Conflicting results exist regarding the role of A3 adenosine receptors (A3ARs) in mediating cardioprotection during reperfusion following myocardial infarction. We hypothesized that the effects of the A3AR agonist IB-MECA to produce cardioprotection might involve activation of other adenosine receptor subtypes. C57Bl/6 (B6), A3AR KO, A2AAR KO, and A2AAR KO/WT bone marrow chimeric mice were assigned to 12 groups undergoing either hemodynamic studies or 45 min of LAD occlusion and 60 min of reperfusion. IB-MECA (100 μg/kg) or vehicle was administered by iv bolus 5 min before reperfusion. Radioligand binding assays showed that IB-MECA has high affinity for the mouse A3AR (K i = 0.17 ± 0.05 nM), but also can bind with lower affinity to the A1AR (9.0 ± 2.4nM) or the A2AAR (56.5 ± 10.2nM). IB-MECA caused bi-phasic hemodynamic changes, which were completely absent in A3AR KO mice and were modified by A2AAR blockade or deletion. IB-MECA stimulated histamine release, increased heart rate, and significantly reduced IF size in B6 mice from 61.5 ± 1.4 to 48.6 ± 2.4 % of risk region (RR; 21 % reduction, p < 0.05) but not in A3AR KO mice. Compared to B6, A3AR KO mice had significantly reduced IF size (p < 0.05). In B6/B6 bone marrow chimeras, IB-MECA caused a 47 % reduction of IF size (from 47.3 ± 3.9 to 24.7 ± 4.5, p < 0.05). However, no significant cardioprotective effect of IB-MECA was observed in A2AARKO/B6 mice, which lacked A2AARs only on their bone marrow-derived cells. Activation of A3ARs induces a bi-phasic hemodynamic response, which is partially mediated by activation of A2AARs. The cardioprotective effect of IB-MECA is due to the initial activation of A3AR followed by activation of A2AARs in bone marrow-derived cells.
    Archiv für Kreislaufforschung 03/2015; 110(2):473. DOI:10.1007/s00395-015-0473-x
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    ABSTRACT: Remote ischemic conditioning (RIC) represents an innovative cardioprotective method that has been investigated in numerous clinical studies providing miscellaneous results. This systematic review and meta-analysis sought to assess RIC-induced effects on myocardial injury biomarkers and clinical outcomes in clinical situations at risk of myocardial ischemia/reperfusion damage. PubMed and Cochrane databases were searched for randomized clinical trials testing any RIC protocol versus a control in a situation or procedure at risk of cardiac ischemia/reperfusion damage, including coronary angioplasty and cardiac or major vascular surgery. Data were collected from publications reporting biological markers of myocardial injury or clinical events, including major adverse cardiovascular and cerebral events (MACCE), all-cause mortality, myocardial infarction incidence, and repeat revascularization. Standardized mean difference (SMD) (continuous outcomes) and odds ratios (OR) (dichotomous outcomes) were compared between groups. Heterogeneity was investigated by means of meta-analysis regression. A total of 53 articles (44 studies) were identified by the search, with 5,317 patients included in the systematic meta-analysis. RIC significantly reduced troponin area under curve (AUC) (SMD -0.27, 95 % confidence interval (CI): [-0.36, -0.18]; p < 0.01) and troponin peak (SMD: -0.22, 95 % CI: [-0.30, -0.15]; p < 0.01). The same reduction was observed with creatine kinase MB (CK-MB) AUC and peak. Long-term MACCE and all-cause mortality were significantly lower in the RIC group (OR: 0.42, 95 % CI [0.28, 0.64]; p < 0.01 vs. OR: 0.27, 95 % CI [0.13, 0.58]; p < 0.01, respectively), as was myocardial infarction incidence (OR: 0.54, 95 % CI [0.40, 0.73]; p < 0.01). We observed no difference regarding repeat revascularization. RIC appears to be an effective method for reducing ischemia/reperfusion myocardial injury, and our findings suggest that it may reduce long-term clinical events.
    Archiv für Kreislaufforschung 03/2015; 110(2):467. DOI:10.1007/s00395-015-0467-8
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    ABSTRACT: Myocardial infarction (MI) leads to necrosis and uncontrolled release of cellular content. Binucleated and polyploid cardiomyocytes contain high amounts of chromatin, a DNA polymer of histones which are cytotoxic. We hypothesized that chromatin from necrotic cells accumulates in the non-perfused, ischemic infarct region, causing local high concentrations of cytotoxic histones, thereby potentiating damage to the heart after MI. The endonuclease DNase1 is capable of dispersing extracellular chromatin through linker DNA digestion which could lead to a decrease in local histone concentrations and cytotoxicity. It was confirmed that after permanent coronary artery ligation in mice, extracellular histones accumulated within the infarcted myocardium. In vitro, histones caused myocyte cytotoxicity. For protection against histone-mediated cytotoxicity after MI in vivo, DNase1 was administered within the first 6 h after induction. Indeed, DNase1 accumulation in the infarcted region of the heart was observed, as well as effective disruption of extracellular cytotoxic chromatin and subsequent reduction of high local histone concentrations. Functionally, acute DNase1 treatment resulted in significantly improved left ventricular remodeling in mice as measured by serial echocardiography, while mortality, infarct size and inflammatory parameters were unaffected. Notably, improved cardiomyocyte survival within the infarct region was observed and might account for the protective effects in acutely DNase1-treated animals. Disruption of extracellular cytotoxic chromatin within the infarcted heart by acute DNase1 treatment is a promising approach to protect myocytes from histone-induced cell death and subsequent left ventricular dysfunction after MI.
    Archiv für Kreislaufforschung 03/2015; 110(2):472. DOI:10.1007/s00395-015-0472-y
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    ABSTRACT: Ischemic heart disease (IHD) is a leading cause of death worldwide, and regenerative therapies through exogenous stem cell delivery hold promising potential. One limitation of such therapies is the vulnerability of stem cells to the oxidative environment associated with IHD. Accordingly, manipulation of stem cell mitochondrial metabolism may be an effective strategy to improve survival of stem cells under oxidative stress. MitoNEET is a redox-sensitive, mitochondrial target of thiazolidinediones (TZDs), and influences cellular oxidative capacity. Pharmacological targeting of mitoNEET with the novel TZD, mitoNEET Ligand-1 (NL-1), improved cardiac stem cell (CSC) survival compared to vehicle (0.1 % DMSO) during in vitro oxidative stress (H2O2). 10 μM NL-1 also reduced CSC maximal oxygen consumption rate (OCR) compared to vehicle. Following treatment with dexamethasone, CSC maximal OCR increased compared to baseline, but NL-1 prevented this effect. Smooth muscle α-actin expression increased significantly in CSC following differentiation compared to baseline, irrespective of NL-1 treatment. When CSCs were treated with glucose oxidase for 7 days, NL-1 significantly improved cell survival compared to vehicle (trypan blue exclusion). NL-1 treatment of cells isolated from mitoNEET knockout mice did not increase CSC survival with H2O2 treatment. Following intramyocardial injection of CSCs into Zucker obese fatty rats, NL-1 significantly improved CSC survival after 24 h, but not after 10 days. These data suggest that pharmacological targeting of mitoNEET with TZDs may acutely protect stem cells following transplantation into an oxidative environment. Continued treatment or manipulation of mitochondrial metabolism may be necessary to produce long-term benefits related to stem cell therapies.
    Archiv für Kreislaufforschung 03/2015; 110(2):471. DOI:10.1007/s00395-015-0471-z