bluuebunny/crossref_metadata_2025_split huggingface dataset:
The mortality outcome after implantable cardioverter-defibrillator implantation according to indication for implantation and underlying etiology: a Nationwide Cohort study
Authors: Yang P.S , Kang Y , Park H.D , Sung J.H , Joung B 
Published: November 2020

Abstract

Background and objectives
There are few nationwide data about the mortality outcome after implantable cardioverter-defibrillator (ICD) implantation. The aim of this study was to evaluate the mortality outcome after ICD implantation according to indication for implantation (primary vs. secondary prevention) and underlying etiology (non-ischemic vs. ischemic heart disease) with a nationwide cohort data of Korea.

Methods
During the period from January 1, 2008 to December 31, 2017, 3,558 patients (mean age, 67.7±11.4 years) with newly-implanted ICD who were aged 19 years or older were identified by 50-percents random sampling from the Korean National Health Insurance Service database.

Results
Patients with primary and secondary prevention ICD were 1,097 (30.8%) and 2,461 (69.2%), respectively. Patients with non-ischemic and ischemic heart disease were 2,487 (69.9%) and 1,071 (30.1%), respectively. Overall all-cause mortality was 20.4% during the follow-up period (mean 24 months). The mortality rates in patients with primary and secondary prevention ICD were 26.2% and 17.9%, respectively. The mortality rates in patients with non-ischemic and ischemic heart disease were 16.1% and 30.4%, respectively. In Kaplan-Meier estimates of survival according to both indication for implantation and underlying etiology, the best prognostic group was patients with secondary prevention ICD and having non-ischemic etiology. The worst prognostic group was patients with primary prevention ICD and having ischemic etiology. The survival probability was below 50% (45.2%) 5 years after ICD implantation in patients with primary prevention ICD and having ischemic etiology.

Conclusions
In Korean nationwide data, patients with primary prevention ICD and having ischemic etiology show the worst prognosis. About half of these patients died of any cause within five years.

Funding Acknowledgement
Type of funding source: None
Echocardiographic assessment of CRT candidates. Does it work equally well in intermediate QRS duration?
Authors: Duchenne J , Cvijic M , Aalen J.M , Larsen C.K , Galli E , Penicka M , Fehske W , Hopp E , Stankovic I , Smiseth O.A , Donal E , Voigt J.U 
Published: November 2020

Abstract

Background
The presence of mechanical dyssynchrony – such as apical rocking (ApRock) and septal flash (SF) – on echocardiography is associated with favourable outcome after cardiac resynchronization therapy (CRT). Myocardial scar on the other hand, has a considerable negative impact on CRT response. There is growing evidence that a visual echocardiographic assessment of mechanical dyssynchrony by ApRock, SF and scar predicts CRT response. Little is known however if this works equally well in patients with intermediate QRS duration (120–150ms), where guideline recommendation for CRT is weaker.

Methods
A total of 400 unselected patients referred for CRT, who fulfil the contemporary guidelines, were enrolled in this multicentre study. Echocardiographic images were visually assessed before CRT implantation, focussing on the presence of ApRock, SF and location and extent of scar segments in the left ventricle (LV), resulting in a CRT response prediction (i.e. Reader Interpretation). Readers were blinded to all patient information other than ischaemic aetiology of heart failure. CRT response was defined as ≥15% reduction in LV end-systolic volume on echocardiography, on average 15 months after device implantation.

Results
Overall, 321 (80%) patients had a left bundle branch block (LBBB), with an average QRS duration of 166±25ms. Ischemic aetiology of heart failure was found in 131 (33%) patients. Before CRT, ApRock and SF were present in 254 (64%) and 244 (61%) patients, respectively. ApRock and SF alone predicted CRT response with an area under the curve (AUC) of 0.79 (95% CI: 0.74–0.84) and 0.78 (95% CI: 0.73–0.83) (Figure A), while the echocardiographic Reader Interpretation had an AUC of 0.85 (95% CI: 0.81–0.89), with a sensitivity of 89% and a specificity of 82% for the prediction of CRT response (Figure B) (p&lt;0.0001 vs. ApRock and SF alone). A total of 92 patients had a QRS duration of 120–150ms, and 48 of them responded to CRT. In these patients, the AUC of Reader Interpretation was comparable to that of the entire study cohort [0.83 (95% CI: 0.75–0.92)], as was sensitivity and specificity (90% and 79%, respectively, p=0.717 vs. the AUC of the entire cohort) (Figure C).

Conclusions
A visual assessment of LV function, by means of mechanical dyssynchrony and scar, has an excellent predictive value for CRT response, and requires only apical echocardiographic images. Responders were identified equally well in the challenging subgroup of patients with a QRS duration of 120–150 ms.

Funding Acknowledgement
Type of funding source: Public Institution(s). Main funding source(s): KU Leuven
Essential role of PET-CT in the management of patients with severe infectious complication CIEDS: multicentre study
Authors: Taborsky M , Latal J , Fedorco M , Skala T , Novak M , Kozak M , Krivan L , Gloger V , Schee A 
Published: November 2020

Abstract

Background
With the increasing number of implanted cardiac pacemakers, ICDs and CRTs, the number of serious infectious complications of these procedures increases significantly, especially in the longer term from the primary implantation. The systematic solution is in most cases endovasal extraction of these systems.

Methods
In a multicenter, prospective, randomized, controlled trial evaluating the benefit of CIEDS infection management in 277 patients, a conventional approach using blood cultures, microbiological examinations and TEE versus innovative management of these patients using PET-CT was compared. PET-CT examination is able to differentiate very well the infection of the implant pocket (Figure A) against bacterial endocarditis (Figure B). Thanks to this, it is possible to individualize the management of the patient and to shorten the dates of hospitalization, resp. time to re-implantation of the new system in patients without the presence of bacterial endocarditis.

Results
The results of the multicentre study are summarized in Table 1.

Conclusions
A comprehensive examination of patients with CDRIE using PET-CT significantly shortens hospital stay, time of antibiotic therapy and, as a consequence, leads to a lower incidence of serious complications of extraction procedures.
PET-CT in CDRIE patients

Funding Acknowledgement
Type of funding source: None
AIM2-driven inflammasome activation in chronic heart failure
Authors: Ruppert M , Onodi Z.S , Leszek P , Toth V.E , Koncsos G , Merkely B , Ferdinandy P , Radovits T , Varga Z 
Published: November 2020

Abstract

Background
Inflammation and cytokine release have been implicated in the pathogenesis of chronic heart failure (CHF). Of particular interest, Canakinumab, a monoclonal antibody against interleukin-1b (IL-1β), had provided benefit against cardiovascular events, suggesting that blockade of IL-1β secretion and signaling might be a promising new therapeutic target. Although, recent studies have provided evidence that inflammasome activation is the main contributor to IL-1β maturation, the role of inflammasome activation in CHF remains unknown.

Objective
Therefore, we aimed to assess inflammasome activation in myocardial samples from end-stage failing hearts.

Methods
Inflammasome activation was assessed by immunoblotting in left ventricular myocardial specimens harvested from patients with end-stage CHF. Furthermore, immunoblot measurements were also performed on translational animal models of CHF (e.g. rat models of permanent coronary artery ligation and transverse aortic constriction). Left ventricular monocyte and macrophage infiltration was detected by immunohistochemistry. To investigate the molecular background of inflammasome activation, a series of cell culture experiments were performed on AC16 human cardiomyocytes and THP-1 human monocytic cell lines.

Results
Out of the 4 major inflammasome sensors tested, expression of the inflammasome protein absent in melanoma 2 (AIM2) and NLR family CARD domain-containing protein 4 (NLRC4) increased in human CHF while the NLRP1 and NLRP3 (NLR family, pyrin domain containing 1 and 3) inflammasome showed no change. A similar expression pattern in AIM2 and NLRC4 was also noted in CHF animal models. Furthermore, robust infiltration of Iba1+ monocytes/macrophages was observed in human failing hearts as well as in different animal models of CHF. In vitro AIM2 inflammasome activation, as induced by transfection with double-stranded DNA [poly(deoxyadenylic-deoxythymidylic)] was reduced significantly by the pharmacological blockade of pannexin-1 channels.

Conclusions
AIM2 and NLRC4 inflammasome activation might contribute to chronic inflammation in CHF. Our findings suggest that pannexin-1 channels might be a promising novel target to reduce inflammasome activation.

Funding Acknowledgement
Type of funding source: Public grant(s) – National budget only. Main funding source(s): NVKP_16-1-2016-0017
Shear wave elastography by high frame rate echocardiography can detect diffuse myocardial fibrosis after heart transplantation
Authors: Petrescu A , Bezy S , Cvijic M , Santos P , Duchenne J , Orlowska M , Van Keer J , Von Bardeleben S , Droogne W , Bogaert J , Van Cleemput J , D'hooge J , Voigt J.-U 
Published: November 2020

Abstract

Background
Myocardial fibrosis is fundamental in the development of cardiac failure, regardless of ethiology. In both animal models and humans it has been shown that diffuse myocardial fibrosis (DMF) contributes to functional impairment, especially to increased passive myocardial stiffness, which is an important pathophysiological determinant of left ventricular diastolic dysfunction. Histological examination is the gold standard for myocardial fibrosis quantification, however, it requires endomyocardial biopsies which are invasive and not without risk. Echocardiographic shear wave (SW) elastography, based on high frame rate imaging, is an emerging approach for measuring myocardial stiffness in vivo. Natural SWs occur after mechanical excitation of the myocardium, e.g. after mitral valve closure (MVC) and their propagation velocity is directly related to myocardial stiffness, thus providing an opportunity to assess myocardial stiffness at end-diastole.

Purpose
The aim was to investigate if propagation velocities of natural SWs can be used to detect diffuse myocardial fibrosis in a cohort of heart transplant recipients.

Methods
We prospectively enrolled 22 patients (10.3±6.3 years after HTx) that underwent CMR during their annual check-up. We performed SW elastography in parasternal long axis views of the left ventricle using a fully programmable experimental scanner (HD-PULSE) equipped with a clinical phased array transducer (Samsung Medison P2–5AC) at 1100±250 frames per second. The SW propagation velocities at MVC were measured in the basal LV septum. Native T1 and extracellular volume (ECV) were measured at the same segment to evaluate DMF. A cut-off value for native T1 of 1040 ms and for ECV of 29% was used to define DMF in our cohort.

Results
We found good correlations between SW velocities and both myocardial T1 (r=0.80, p&lt;0.0001, Figure A) and ECV (r=0.64, p=0.003, Figure B) measured with CMR. Further, we derived reference thresholds of natural SW velocities to identify DMF in HTx patients. The optimal cut-off value of SW velocity to identify patients with nativT1&gt;1040 ms was 4.84 m/s (AUC 0.81, sensitivity 82%, specificity 82%, Figure C). To identify patients with ECV&gt;0.29 the cut-off value of SW velocity was 4.74 m/s (AUC 0.74, sensitivity 73%, specificity 78%, Figure D).

Conclusions
End-diastolic shear wave propagation velocities, as measure of myocardial stiffness, showed a good correlation with CMR defined diffuse myocardial injury. Values higher than 4.74 m/s could identify diffuse myocardial injury in HTX patients with a good sensitivity and good specificity. These findings thus suggest that shear wave elastography has the potential to become a valuable non-invasive method for the detection of diffuse myocardial fibrosis.

Funding Acknowledgement
Type of funding source: None
Weight loss early after discharge predicts the risk of rehospitalization in non-obese patients with heart failure preserved ejection fraction
Authors: Kamisaka K , Kamiya K , Iwatsu K , Iritani N , Iida Y , Adachi T , Yamada S 
Published: November 2020

Abstract

Background
Weight loss (WL) has been considered as a prognostic factor in heart failure with reduced ejection fraction (HFrEF). However, the prognosis and associated factors of WL in heart failure with preserved ejection fraction (HFpEF) have remained unclear.

Purpose
This study aimed to examine the prevalence, prognosis, and clinical characteristics of worse prognosis based on the identified WL after discharge in HFpEF.

Methods
The study was conducted as a part of a multicenter cohort study (Flagship). The cohort study enrolled ambulatory HF who hospitalized due to acute HF or exacerbation of chronic HF. Patients with severe cognitive, psychological disorders or readmitted within 6-month after discharge were excluded in the study. WL was defined as ≥5% weight loss in 6-month after discharge and HFpEF was defined as left ventricular ejection fraction (LVEF) ≥50% at discharge. Age, gender, etiology, prior HF hospitalization, New York Heart Association (NYHA) class, brain natriuretic peptide (BNP) or N-terminal-proBNP (NT-proBNP), anemia (hemoglobin; male &lt;13g/dL, female &lt;12g/dL), serum albumin, Geriatric Depression Scale, hand grip strength and comorbidities were collected at discharge. Patients were stratified according to their body mass index (BMI) at discharge as non-obese (BMI &lt;25) or obese (BMI ≥25). We analyzed the association between WL and HF rehospitalization from 6 month to 2 years after discharge using Kaplan-Meier curve analysis and Cox regression analysis adjusted for age and gender, and clinical characteristics associated to worse prognosis in WL using logistic regression analysis adjusted for potential confounders in HFpEF.

Results
A total of 619 patients with HFpEF were included in the analysis. The prevalence of WL was 12.9% in 482 non-obese and 15.3% in 137 obese patients. During 2 years, 72 patients were readmitted for HF (non-obese: 48, obese: 24). WL in non-obese independently associated with poor prognosis (hazard ratio: 2.2: 95% confidence interval: 1.13–4.25) after adjustment for age and sex, while WL in obese patients did not. Logistic regression analysis chose age (odds ratio 1.02 per 1 year; 1.00–1.05), anemia (2.14; 1.32–3.48), and BNP ≥200pg/mL or NT-proBNP ≥900pg/mL (1.83; 1.18–2.86) as independent associated factors for worse prognosis of WL in non-obese patients.

Conclusion
In HFpEF, WL in early after discharge in non-obese elderly patients may be a prognostic indicator for HF rehospitalization. HF management including WL prevention along with controlling anemia is likely to improve prognosis in this population.
Kaplan Meier survival curves

Funding Acknowledgement
Type of funding source: Public grant(s) – National budget only. Main funding source(s): A Grant-in-Aid for Scientific Research (A) from the Japan Society for the Promotion of Science
Correlation between procollagen propeptides end echocardiography indices in patients with ST segment elevation myocardial infarction (STEMI)
Authors: Osokina A , Karetnikova V.N , Polikutina O.M , Slepynina Y.S , Artemova T.P , Ryzhenkova S.A , Chukalenko D.A , Barbarash O.L 
Published: November 2020

Abstract

Objective
To investigate the correlation between Procollagen I C-Terminal Propeptide (PICP), Procollagen III N-Terminal Propeptide (PIIINP), indices of echocardiography and anamnestic data in patients with ST segment elevation myocardial infarction (STEMI) and preserved myocardial contractility.

Materials and methods
60 men and 23 women diagnosed with STEMI were examined. Echocardiographic studies were performed using SONOS 2500 Cardiac – Vascular Ultrasound (Hewlett Packard, USA). Myocardial contractility was considered to be preserved with left ventricular ejection fraction (LVEF) ≥50%. In addition to standard indices of echocardiography, mitral flow propagation velocity (FPV) was evaluated to diagnose diastolic dysfunction. Coronary angiography was performed using INNOVA 3100 Cardiovascular Imaging System (USA). All patients, during the first twelve hours of the disease, underwent percutaneous coronary intervention (PCI) with stenting of the occluded culprit infarct-related artery. On the 1st and 12th days of hospitalization, the concentrations of PICP and PIIINP were determined for all patients by enzyme-linked immunosorbent assay (ELISA) using laboratory BCM Diagnostics kits (USA). All patients at the hospital received standard therapy.

Results
The following marker values were obtained: 1st day: PICP 609 (583; 635) ng/ml, PIIINP 26 (18.9; 34.9) ng/ml; 12th day: PICP 588 (580; 561) ng/ml, PIIINP 24.2 (18.6; 30.3) ng/ml. The following significant correlations were revealed: PICP 1st day / isovolumic contraction time – IVCT (m/s) 12th day, r=−0.68, p=0.042; PICP 1st day / Tei Index 12th day, r=−0.72, p=0.028; PICP 1st day / diastolic rigidity 12th day, r=−0.74, p=0.021; PIIINP 1st day/age, r=0.55, p=0.016; PIIINP 1st day/ body mass index (BMI), r=−0.59, p=0.009; PIIINP 1st day / E (cm/s) 1st day, r=0.72, p=0.018; PIIINP 1st day / Em /FPV 1st day, r=0.78, p=0.007; PIIINP 12th day / Em / FPV 1st day, r=0.65, p=0.041; PIIINP 12th day / E (cm/s) 1st day, r=0.67, p=0.033; PIIINP 12th day / E / Em) 12th day, r=0.70, p=0.023; PIIINP 12th day / Em/FPV 12th day, r=0.73, p=0.014.

Conclusions
The data obtained indicates the correlation between serum markers of myocardial fibrosis and the indices of echocardiography, as well as age. We conclude that, all the markers listed above, are able to represent myocardial remodeling in patients with STEMI.

Funding Acknowledgement
Type of funding source: None
Impact of arterial stiffness on diastolic function and outcomes of heart failure in patients presenting with acute myocardial infarction
Authors: Kim K , Kang M.G , Koh J.S , Park J.R , Hwang S.J , Hwang J.Y , Park H.W 
Published: November 2020

Abstract

Background
Relation of arterial stiffness and cardiovascular disease is well-known. However, there is no data on association between diastolic function and brachial-ankle pulse wave velocity (baPWV) and influence on heart failure outcomes in patients with acute myocardial infarction (AMI).

Methods
Among patients presenting with AMI, all subjects underwent baPWV and echocardiography were recruited. Diastolic function was categorized by 2016 guideline of ASE/EACVI left ventricular diastolic function. Heart failure outcomes were defined 1) hospitalization for heart failure, 2) cardiac death and 3) sudden cardiac arrest.

Results
Totally 1,016 subjects were enrolled (FU duration; 3.5±2.0 years, mean age 65±13, predominant male 71.3% and STEMI 40.8%) from 2012 to 2015 in the our University Hospital. Elderly, female, low BMI, higher PWV, HTN, DM and stroke were associated with higher baPWV. Increased arterial stiffness (defined as baPWV ≥1700) had higher prevalence of diastolic dysfunction compared with baPWV &lt;1700 (98.3% vs 86.2%). HF outcomes of 69 events were identified (HF; n=48, cardiac death; n=16, sudden cardiac arrest; n=2, death d/t HF; n=3). In the multivariate analysis, baPWV ≥1700, HTN and low BMI (23 kg/m2) were independent predictors for HF outcomes after adjustment with age, LVEF, DM and stroke (Table 1). Furthermore, KM curve showed that increased arterial stiffness was associated with higher prevalence of diastolic dysfunction and poor outcomes of heart failure (Figure 1).

Conclusions
In patients with AMI, arterial stiffness was associated with higher prevalence of diastolic dysfunction an independent predictor for heart failure hospitalization and cardiac death.
Figure 1. Diastolic dysfunction and HF in AMI

Funding Acknowledgement
Type of funding source: None
Genome wide association analysis in dilated cardiomyopathy revealed two new susceptibility loci for systolic heart failure
Authors: Garnier S , Harakalova M , Weiss S , Mokry M , Van Setten J , Proust C , Duboscq-Bidot L , Boland A , Deleuze J.-F , Dorr M , Asselbergs F.-W , Cambien F , Villard E , Tregouet D.-A , Charron P 
Published: November 2020

Abstract

We conducted the largest Genome Wide Association Study performed so far in Dilated Cardiomyopathy (DCM), a leading cause of systolic heart failure and cardiovascular death. Using a discovery phase of 2,719 cases and 4,440 controls and a replication phase of 584 independent cases and 966 controls, we identified and replicated two new DCM-associated loci, one on chromosome 3p (meta-analysis OR = 1.36 [1.25 - 1.48], p=5.3 10–13) and the second on chromosome 22q (meta-analysis OR = 1.33 [1.22 - 1.46], p=5.0 10–10), while confirming the two previously identified DCM loci on chromosome 10 and 1, BAG3 and HSPB7. We estimated the global heritability to 31% ± 8%. The genetic risk score constructed from the number of lead risk-alleles at these 4 loci revealed a 27% risk increased in individuals with 8 risk-alleles compared to the 5 risk alleles reference group (OR = 1.27 [1.14–1.42]).
The two association signals were then fine-mapped by combining in silico and functional genomics investigations (as 4C-sequencing on iPSC-derived cardiomyocytes). While a few genes remain candidates at the second locus and deserve further investigations, our work clearly identified one gene as responsible for the association at the first locus whose role in the pathophysiology of DCM is supported by recent observations in human and mice. As the biological pathway in which this gene is involved is a potential target for pharmacological agents, our finding opens novel therapeutic perspectives for treating or preventing heart failure.
We are convinced that these results provide new findings that add both on the understanding of the genetic architecture of heart failure and on potential new players involved in the pathophysiology of this devastating disease.

Funding Acknowledgement
Type of funding source: Public grant(s) – National budget only. Main funding source(s): GENMED Laboratory of Excellence on Medical Genomics, DETECTIN-HF project (ERA-CVD framework), Assistance Publique-Hôpitaux de Paris, Délégation à la recherche clinique, the “Fondation LEDUCQ”, the PROMEX charitable foundation, the Société Française de Cardiologie/Fédération Française de Cardiologie, the Deutsche Forschungsgemeinschaft, The Federal Ministry of Education and Research and the Ministry of Cultural Affairs and the Social Ministry of the Federal State of Mecklenburg-West Pomerania, The German Center for Cardiovascular Research (DZHK), Hospitals NIHR Biomedical Research Centre, NWO VENI grant (no. 016.176.136)