From abstract to impact in cardiovascular research: factors predicting publication and citation

Aims Through a 4-year follow-up of the abstracts submitted to the European Society of Cardiology Congress in 2006, we aimed at identifying factors predicting high-quality research, appraising the quality of the peer review and editorial processes, and thereby revealing potential ways to improve future research, peer review, and editorial work. Methods and results All abstracts submitted in 2006 were assessed for acceptance, presentation format, and average reviewer rating. Accepted and rejected studies were followed for 4 years. Multivariate regression analyses of a representative selection of 10% of all abstracts (n= 1002) were performed to identify factors predicting acceptance, subsequent publication, and citation. A total of 10 020 abstracts were submitted, 3104 (31%) were accepted for poster, and 701 (7%) for oral presentation. At Congress level, basic research, a patient number ≥ 100, and prospective study design were identified as independent predictors of acceptance. These factors differed from those predicting full-text publication, which included academic affiliation. The single parameter predicting frequent citation was study design with randomized controlled trials reaching the highest citation rates. The publication rate of accepted studies was 38%, whereas only 24% of rejected studies were published. Among published studies, those accepted at the Congress received higher citation rates than rejected ones. Conclusions Research of high quality was determined by study design and largely identified at Congress level through blinded peer review. The scientometric follow-up revealed a marked disparity between predictors of full-text publication and those predicting citation or acceptance at the Congres

Intravenous and intramyocardial injection of apoptotic white blood cell suspensions prevents ventricular remodelling by increasing elastin expression in cardiac scar tissue after myocardial infarction

Congestive heart failure developing after acute myocardial infarction (AMI) is a major cause of morbidity and mortality. Clinical trials of cell-based therapy after AMI evidenced only a moderate benefit. We could show previously that suspensions of apoptotic peripheral blood mononuclear cells (PBMC) are able to reduce myocardial damage in a rat model of AMI. Here we experimentally examined the biochemical mechanisms involved in preventing ventricular remodelling and preserving cardiac function after AMI. Cell suspensions of apoptotic cells were injected intravenously or intramyocardially after experimental AMI induced by coronary artery ligation in rats. Administration of cell culture medium or viable PBMC served as controls. Immunohistological analysis was performed to analyse the cellular infiltrate in the ischaemic myocardium. Cardiac function was quantified by echocardiography. Planimetry of the infarcted hearts showed a significant reduction of infarction size and an improvement of post AMI remodelling in rats treated with suspensions of apoptotic PBMC (injected either intravenously or intramoycardially). Moreover, these hearts evidenced enhanced homing of macrophages and cells staining positive for c-kit, FLK-1, IGF-I and FGF-2 as compared to controls. A major finding in this study further was that the ratio of elastic and collagenous fibres within the scar tissue was altered in a favourable fashion in rats injected with apoptotic cells. Intravenous or intramyocardial injection of apoptotic cell suspensions results in attenuation of myocardial remodelling after experimental AMI, preserves left ventricular function, increases homing of regenerative cells and alters the composition of cardiac scar tissue. The higher expression of elastic fibres provides passive energy to the cardiac scar tissue and results in prevention of ventricular remodelling

Neuromuscular comorbidity, atrial fibrillation and left bundle branch block predict the prognosis of left ventricular hypertrabeculation/noncompaction

Abstract Background The prognosis of patients with left ventricular hypertrabeculation/noncompaction (LVHT) is controversially assessed. LVHT is frequently associated with neuromuscular disorders (NMDs). Aim of the study was to assess cardiac and neurological findings as predictors of mortality in LVHT-patients. Methods Included were patients with LVHT diagnosed between June 1995 and December 2019 in one echocardiographic laboratory. They underwent a baseline cardiologic examination and were invited for a neurological investigation. In January 2020, their survival status was assessed. Results LVHT was diagnosed in 310 patients (93 female, aged 53±18 years) with a prevalence of 0.4%/year. A neurologic investigation was performed in 205 patients (67%). A specific NMD was found in 33 of the investigated patients (16%), NMDs of unknown etiology in 123 (60%) and the neurological investigation was normal in 49 (24%) patients. During 86 months of follow-up, 59 patients received implanted electronic devices (cardioverter/defibrillator n=21, antibradycardic pacemakers n=11, cardiac resynchronization device/defibrillator n=22, cardiac resynchronization device n=4). During follow-up 105 patients died and 6 patients underwent heart transplantation. The mortality was 4.7%/year. By multivariate analysis, the following baseline parameters were identified as predictors of mortality: increased age (p=0.0005), inpatient-status when LVHT was diagnosed (p=0.0050), presence of a specific NMD (p=0.0187) or NMD of unknown etiology (p=0.0052), atrial fibrillation (p=0.0007) and left bundle branch block (p=0.0168). Conclusions LVHT patients should be systematically investigated neurologically since neurological comorbidity has a prognostic impact. Electrocardiographic abnormalities like atrial fibrillation and left bundle branch block should be considered when planning pharmacotherapy and device-therapy. It has to be assessed by prospective studies, which measures improve the prognosis of LVHT. Funding Acknowledgement Type of funding source: None </jats:sec