Cardiology Journal Impact Factor & Information

Publisher: Karger

Journal description

Cardiologyí features high-quality papers from all over the world to keep its readers regularly informed of current strategies in the prevention, diagnosis and treatment of heart disease. These papers not only describe but offer critical appraisals of new developments in non-invasive, invasive, diagnostic and therapeutic methods. The importance of experimental work is also acknowledged through reports covering the function and metabolism of the heart and the morphology and physiology of cardiovascular disease. Special sections in a variety of subspecialty areas reinforce the journalís value as a complete record of recent progress for all cardiologists, internists, cardiac surgeons and clinical physiologists.

Current impact factor: 2.04

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.044
2012 Impact Factor 1.519
2011 Impact Factor 1.705
2010 Impact Factor 1.982
2009 Impact Factor 1.637
2008 Impact Factor 1.837
2006 Impact Factor 1.795
2005 Impact Factor 2.092
2004 Impact Factor 1.585
2003 Impact Factor 1.127
2002 Impact Factor 0.952
2001 Impact Factor 0.757
2000 Impact Factor 0.678
1999 Impact Factor 0.739
1998 Impact Factor 0.784
1997 Impact Factor 0.692
1996 Impact Factor 0.676
1995 Impact Factor 0.425
1994 Impact Factor 0.538
1993 Impact Factor 0.621
1992 Impact Factor 0.563

Impact factor over time

Impact factor

Additional details

5-year impact 1.45
Cited half-life 6.70
Immediacy index 0.59
Eigenfactor 0.00
Article influence 0.46
Website Cardiology website
ISSN 1421-9751
OCLC 66586947
Material type Periodical
Document type Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's server or institutional server
    • Server must be non-commercial
    • Publisher's version/PDF cannot be used
    • Publisher copyright and source must be acknowledged
    • Must link to publisher version
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: With the present therapeutic advances in the era of primary percutaneous coronary intervention (PCI), the role of β-blockers in ST elevation acute myocardial infarction (STEMI) has remained contentious. We analyzed the data and clinical outcomes of 901 STEMI patients who had undergone primary PCI. We classified the patients into β-blocker (n = 598) and non-β-blocker groups (n = 303). The cumulative incidence of all-cause death was 10.0% in the β-blocker group and 25.4% in the non-β-blocker group (p < 0.001). The incidence of major adverse cardiac events (MACE) was 22.1% in the β-blocker group and 34.3% in the non-β-blocker group (p < 0.001). The relative hazard ratio (HR) of β-blockers for all-cause death and MACE with low left ventricle ejection fraction (LVEF; <50%) was 0.55 [95% confidence interval (CI) 0.35-0.86, p = 0.009] and 0.75 (95% CI 0.51-1.09, p = 0.125), respectively. In patients with normal LVEF (≥50%), the relative HR of β-blockers for death and MACE were 0.50 (95% CI 0.29-0.88, p = 0.016) and 0.75 (95% CI 0.51-1.12, p = 0.162), respectively. After propensity score matching of the difference of the baseline characteristics, the Kaplan-Meier survival curve demonstrated lower mortality in the β-blocker group than in the non-β-blocker group with both low LVEF and normal LVEF (p = 0.02 and p = 0.001, respectively). β-Blockers have beneficial clinical outcomes in the era of primary PCI for STEMI, regardless of the LVEF. © 2015 S. Karger AG, Basel.
    Cardiology 06/2015; 132(2):91-100. DOI:10.1159/000431077
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    ABSTRACT: Myocardial fibrosis causes deterioration of myocardial function in carcinoid intestinal disease (CID). We assessed the ability of myocardial function and various biomarkers to predict mortality in patients with CID. A total of 71 patients with small intestinal carcinoid tumours were included, and underwent echocardiography at baseline. Systolic function was assessed by two-dimensional speckle tracking echocardiography as left ventricular (LV) and right ventricular (RV) strain, and as mitral annular displacement (MAD), by tissue Doppler imaging. Parameters of diastolic function, the amount of liver metastases, and various biomarkers were also analysed. During 1,274 ± 368 days of follow-up, 18 patients (25%) died. Of the 53 survivors, 46 patients (87%) were available for follow-up echocardiography. Baseline LV strain and MAD was reduced in those who died compared to those who survived (p < 0.001). Baseline plasma levels of activin A were markedly higher in patients who died during follow-up than those who survived (p = 0.001). In multivariate Cox hazard models (A, B, C and D), LV strain, age, the amount of liver metastases, MAD, and activin A were independent predictors of mortality. Assessment of myocardial function by echocardiography, and the biomarker activin A, can be very useful in the risk stratification of patients with CID. © 2015 S. Karger AG, Basel.
    Cardiology 06/2015; 132(2):81-90. DOI:10.1159/000431076
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    ABSTRACT: The landmark Dual Antiplatelet Therapy (DAPT) trial revealed an impressive reduction of stent thrombosis and myocardial infarction after prolonged 30-month DAPT compared to the conventional 12-month regimen. However, aside from the expected extra bleeding risks, more cancers and noncardiovascular deaths (NCVD) were observed in the 30-month DAPT arm. We aimed to comprehend the totality of DAPT trial evidence in the light of the FDA medical review. A significant excess of solid cancers that was picked up after prasugrel treatment in the TRITON trial (Prasugrel versus Clopidogrel in Patients with Acute Coronary Syndromes) and later observed with vorapaxar treatment in the TRACER trial (Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome) has now been confirmed by the FDA DAPT review for 30-month therapy with prasugrel [hazard ratio (HR) 1.3] and clopidogrel (HR 1.2). The latest randomized evidence with antiplatelet agents rejected the drug-specific cancer risks, clearly indicating the class effect. The NCVD risks were elevated after treatment with both thienopyridines, but were more prominent after clopidogrel treatment (HR 1.91) than prasugrel treatment (HR 1.17). About half of the NCVD were considered to be caused by cancers occurring after the 24 months of extended antiplatelet therapy. Impression: The DAPT trial confirmed that long-term antiplatelet therapy is associated with cancer that contributes to NCVD. Based on the full disclosure of cancer data by the DAPT study, it can be reflected that the optimal duration of antiplatelet therapy with thienopyridines should be limited to no more than 2 years. This duration allows the preservation of most vascular benefits while avoiding additional cancers and NCVD. © 2015 S. Karger AG, Basel.
    Cardiology 06/2015; 132(2):74-80. DOI:10.1159/000431356
  • Cardiology 06/2015; 132(2):71-73. DOI:10.1159/000431034
  • Cardiology 06/2015; 132(1):68-70. DOI:10.1159/000431252
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    ABSTRACT: The purpose of this study was to evaluate the associations of fasting plasma glucose (FPG) and hypertension (HTN) with cardiovascular autonomic neuropathy (CAN) and to estimate the extent to which the synergistic effects of FPG and HTN affect outcomes in a Chinese population. We conducted a large-scale, population-based study to analyze the association and interaction of the two factors with CAN in a sample of 2,092 Chinese people. Univariate and multiple linear regression (MLR) analyses were employed to detect these relationships. Interaction on an additive scale can be calculated by using the relative excess risk due to interaction, the proportion attributable to interaction (AP), and the synergy index (S). After adjusting for confounding factors, MLR showed that FPG and HTN were independently associated with CAN (p < 0.001 for both). A significant synergistic effect of FPG and HTN on CAN was detected (p = 0.046, RETI = 0.733, 95% CI 0.059-1.450; AP = 0.167, 95% CI -0.033 to 0.367; S = 1.275, 95% CI 0.140-2.410). Our findings suggest that FPG and HTN are independently associated with CAN, and they offer evidence to support the hypothesis that FPG and HTN have synergistic effects that influence the progression of CAN. © 2015 S. Karger AG, Basel.
    Cardiology 06/2015; 132(1):58-64. DOI:10.1159/000381013
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    ABSTRACT: Coronary stent infections in general and stent abscesses (SAs) in particular are rare but often deadly complications. Most SAs manifest with fever and chest pain within 30 days after intervention and require antibiotics and stent removal. A 45-year-old man with second ST elevated myocardial infarction and cardiogenic shock was admitted to a hospital that had no cardiac catheterization laboratory. The patient underwent fibrinolytic therapy with alteplase but died 1 h later. His medical history revealed posterior myocardial infarction 7 years before, which had been successfully treated with a bare metal stent of the right coronary artery. The post-discharge observation had been unremarkable with no evidence of ischaemia or infection but gross non-compliance. Autopsy revealed complete closure of the left main coronary artery and a surprise additional finding, namely SA; the stented portion of the artery was enveloped by an abscess, and purulent material completely occluded the stent, which was floating in pus. Impressions: Since coronary angioplasty is so common, the incidence of late silent SA is probably higher than expected, especially considering that there is often a lack of clinical manifestations. Clinicians should be cognizant of this complication. More attention may be required to assess the condition of existing stents during repeated interventions. Gross non-compliance and/or early withdrawal from dual anti-platelet therapy may be directly responsible for the development of silent delayed SA. © 2015 S. Karger AG, Basel.
    Cardiology 06/2015; 132(1):65-67. DOI:10.1159/000398789
  • Cardiology 06/2015; 132(1):45-48. DOI:10.1159/000430783
  • Cardiology 06/2015; 131(1):42-43.
  • Cardiology 06/2015; 131(1):42.
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    ABSTRACT: We aimed to investigate the role of mShox2 in generating If pacemaker current in vitro by means of electric-pulse current stimulation (EPCS) of canine mesenchymal stem cells (cMSCs). mShox2 genetically modified cMSCs were prepared with pLentis-mShox2 red fluorescent protein. After EPCS induction, we examined the kinetic characteristics of generated inward current by means of a patch clamp. We then evaluated the expression of pacemaker-related genes, such as Nkx2.5, Tbx3, HCN4, Cx43 and Cx45, by means of qRT-PCR and Western blotting. The morphological changes and the cardiomyogenic differentiation marker cTnT were investigated at the same time. The time- and voltage-dependent inward current recorded after mShox2 infection was confirmed to be If current. After EPCS induction, the detection rate of this If current was increased. The current amplitude and density were increased, and the channel activation curve shifted to the right. The pacemaker markers Tbx3, HCN4 and Cx45 were significantly upregulated, but the working myocardium markers Nkx2.5 and Cx43 were downregulated after mShox2 infection, and were more remarkable after EPCS induction. The cells became larger and assumed spindle and spider-like morphologies. cTnT was also detected in the experimental cells. Our results suggest that EPCS promotes the differentiation of mShox2 genetically modified cMSCs into pacemaker-like cells, which generates more If current. © 2015 S. Karger AG, Basel.
    Cardiology 06/2015; 132(1):49-57. DOI:10.1159/000398784
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    ABSTRACT: Congress abstract. DOI:10.1159/000431110
    Cardiology 06/2015; 131(Suppl 1):11.
  • Cardiology 05/2015; 131(4):260-264. DOI:10.1159/000381303
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    ABSTRACT: The aim of this study was to assess the recovery of regional myocardial function of the left-ventricular septal wall and the septal site of the mitral valve (MV) annulus by tissue Doppler imaging (TDI). In 63 (32 diabetic and 31 control) patients having off-pump coronary artery bypass grafting (OPCABG), including the left internal mammary artery (LIMA) and the left anterior descending coronary artery (LAD), TDI measurements were performed before operation (baseline), 5 min after LIMA-LAD revascularization (early reperfusion) and after completion of all anastomoses (after revascularization). Compared to the patients with diabetes, the controls had higher peak systolic velocities of the mid septal segments in the early reperfusion measurement (p = 0.002). After revascularization, values of peak systolic strain at the basal (-10.13 vs. -13.36%, p = 0.044) and mid septal segments (-8.25 vs. -12.69%, p = 0.009) were decreased in the diabetic patients compared to the controls. There was no difference between the groups with respect to the velocities acquired at the septal site of the MV annulus. This study demonstrates an insufficient recovery of regional myocardial function in patients with type II diabetes undergoing OPCABG. © 2015 S. Karger AG, Basel.
    Cardiology 05/2015; 132(1):34-44. DOI:10.1159/000380811
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    ABSTRACT: Granulomatosis with polyangiitis (GPA) is a systemic necrotizing vasculitis, associated with antineutrophil cytoplasmic autoantibody-associated systemic vasculitis, and it can affect many organ systems via the inflammation of small-to-medium-sized vessels. Cardiac involvements in GPA are relatively rare. We report a 75-year-old woman who was diagnosed with GPA and rapid progressive glomerulonephritis that resulted in a partial posteromedial papillary muscle rupture, but with no coronary angiographic findings. The surgical and pathological findings with regard to the ruptured papillary muscle revealed necrotic muscle and acute ischemic change. The mechanism of papillary muscle rupture in GPA is coronary vasculitis leading to myocardial infarction. The ischemic change is not always detected on coronary angiography, so assessment using an echocardiogram is important. © 2015 S. Karger AG, Basel.
    Cardiology 05/2015; 132(1):22-25. DOI:10.1159/000382096
  • Cardiology 05/2015; 132(1):26. DOI:10.1159/000381825
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    ABSTRACT: Oxidized low-density lipoprotein (ox-LDL) may induce autophagy, apoptosis, necrosis or proliferation of cultured endothelial cells depending on the concentration and exposure time. Our previous studies found that ox-LDL exposure for 6 h increases the autophagic level of human umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner. The present study investigates the relationship between autophagy and apoptosis in HUVECs exposed to ox-LDL. Flow cytometry and Western blot were used to study the apoptotic and autophagic phenomena. The contribution of autophagic and apoptotic mechanisms to ox-LDL-induced upregulation of MAP1-LC3, beclin1 and p53 protein levels were assessed by pretreatment with the autophagic inhibitors 3-MA and Atg5 small interfering (si)RNA, as well as z-vad-fmk, an apoptosis inhibitor. ox-LDL induced the apoptosis of HUVECs in a concentration-dependent way. The increased expression of the autophagic proteins, LC3-II and beclin1, can be reversed by 3-MA and z-vad-fmk pretreatment. 3-MA and Atg5 siRNA increased the ox-LDL-induced increases of the p53 protein level and the annexin V-positive staining, which was decreased by z-vad-fmk. These results suggest that overstimulation of ox-LDL can induce autophagy and apoptosis in HUVECs. Inhibition of apoptosis leads to an inhibition of autophagy induced by ox-LDL. However, inhibition of autophagy leads to an increase in the ox-LDL-induced apoptosis. © 2015 S. Karger AG, Basel.
    Cardiology 05/2015; 132(1):27-33. DOI:10.1159/000381332
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    ABSTRACT: Despite a lack of scientific evidence, oxygen has long been a part of standard treatment for patients with acute myocardial infarction (AMI). However, several studies suggest that oxygen therapy may have negative cardiovascular effects. We here describe a randomized controlled trial, i.e. Supplemental Oxygen in Catheterized Coronary Emergency Reperfusion (SOCCER), aiming to evaluate the effect of oxygen therapy on myocardial salvage and infarct size in patients with ST elevation myocardial infarction (STEMI) treated with a primary percutaneous coronary intervention (PCI). One hundred normoxic STEMI patients accepted for a primary PCI are randomized in the ambulance to either standard oxygen therapy or no supplemental oxygen. All patients undergo cardiovascular magnetic resonance imaging (CMR) 2-6 days after the primary PCI, and a subgroup of 50 patients undergo an extended echocardiography during admission and at 6 months. All patients are followed for 6 months for hospital admission for heart failure and subjective perception of health. The primary endpoint is the myocardial salvage index on CMR. Even though oxygen therapy is a part of standard care, oxygen may not be beneficial for patients with AMI and is possibly even harmful. The results of the present and concurrent oxygen trials may change international treatment guidelines for patients with AMI or ischemia. © 2015 S. Karger AG, Basel.
    Cardiology 05/2015; 132(1):16-21. DOI:10.1159/000398786
  • Cardiology 05/2015; 132(1):9-10. DOI:10.1159/000398788
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    ABSTRACT: Atherosclerosis and osteoporosis are the leading causes of mortality and morbidity. The objective of this study was to test this hypothesis in experimental hypercholesterolemia to determine whether statins play a protective role in this process. LDLR(-/-) mice (n = 60) were allocated to the following groups: group I (n = 20), normal diet; group II (n = 20), 0.25% (w/w) cholesterol diet (w/w), and group III (n = 20), 0.25% (w/w) cholesterol diet + atorvastatin for 48 weeks. Examination of aortic valves (AVA) and femurs for atherosclerosis and calcification markers included micro-CT, special stains, and calcein incorporation. The cholesterol diet induced bone formation in calcified AVA and an increase in macrophage infiltration. Hyperlipidemic bones expressed an increase in osteoclast cells and a decrease in bone formation. Atorvastatin reduced atherosclerosis and bone mineralization in AVA and increased mineralization within femur bones (p < 0.05). Atherosclerosis is present in hyperlipidemic bones and valves as characterized by macrophage and osteoclast infiltration, and it is attenuated by atorvastatin, which may have implications for therapy in the future. © 2015 S. Karger AG, Basel.
    Cardiology 05/2015; 132(1):11-15. DOI:10.1159/000381703