bluuebunny/crossref_metadata_2025_split huggingface dataset:
P4134Impaired left ventricular systolic function in alcohol abusers expressed by both 3D calculated ejection fraction and longitudinal strain by AFI
Authors: Hamala P , Kasprzak J D , Lipiec P , Wierzbowska-Drabik K 
Published: October 2019

Abstract

Aim
Despite knowledge regarding the existence of alcohol cardiomyopathy the exact impact of alcohol abuse in consecutive subject is poorly examined.
We aimed to evaluate the left ventricle (LV) function in chronic abusers group and compared classical and novel echocardiography parameters in alcohol abusers (ALC) and control group (C).

Methods
We compared 75 adults (mean age 48±12, 60 male) without other overt heart disease, coronary artery disease excluded, but with alcohol abuse history: average alcohol intake 32 alcohol unit per week (AUW) with control group consisted of 40 subjects without history of excessive drinking, abstinents or drinking ≤8 AUW (mean age 50±4, 16 men). One unit was defined as 10 grams of pure etanol. All patients underwent TTE examination including ejection fraction (EF) calculation with 3D and longitudinal strain assessment by AFI method.

Results
ALC group showed LV systolic dysfunction expressed as EF 48±14 vs 60±9%, global longitudinal strain (AFI GLS) −15.6±6.6 vs −18.7±3.4; p<0.0001 and p 0.0064, respectively. On the other hand the LV and left atrial diameters as well as diastolic function were similar in both groups, indicating on relatively low advancement of heart remodeling.
ALC vs Control group comparison ALC N75 C N40 p value Age 48±12 50±4 ns BMI 24±6 28±6 0.0009 LVd 48±13 47±4 ns LVs 34±15 32±4 ns LA 38±9 38±3 ns EF 48±14 60±9 <0.0001 E/A 1.1±0.6 1.1±0.3 ns E' lateral 10.6±3.9 10.6±2.9 ns AFI 2ch −15.9±6.9 −18.8±4.8 0.0143 AFI 3ch −15.9±6.9 −18.9±3.6 0.0116 AFI 4ch −15.2±7.1 −18.6±3.5 0.0053 AFI GLS −15.6±6.6 −18.7±3.4 0.0064

Conclusions
Chronic alcohol abuse revealed harmful effect on LV systolic function which can be assessed quantitatively by both decreased EF and absolute values of myocardial longitudinal strain. This systolic function impairment seems to anticipate the overt remodelling of the heart.
P4142PI3-kinase delta protects against atherosclerosis progression by governing regulatory T-cell biology
Authors: Zierden M , Millarg C , Baldus S , Rosenkranz S , Berghausen E M , Vantler M 
Published: October 2019

Abstract

Introduction and purpose
Atherosclerosis is a chronic inflammatory disease of arteries and represents the main underlying cause of death worldwide. Macrophages are major drivers of atherosclerosis by ingestion of lipoproteins, foam cell formation, and secretion of pro-inflammatory mediators. Although macrophages outnumber other leukocytes in atherosclerotic plaques, T and B lymphocytes can shape the course of disease by promoting or mitigating inflammatory responses. Leukocytes highly express the phosphoinositide 3-kinase isoform delta (PI3Kd), exerting a key role in the regulation of immune responses including the activation, proliferation, differentiation, and effector function of lymphocytes. Since macrophages and lymphocytes are all major effectors of atherosclerosis, we aimed to understand the role of PI3Kd in these leukocytes during atherogenesis.

Methods and results
To investigate the role of haematopoietic PI3Kd in atherosclerosis, bone marrow from PI3Kd−/− or PI3Kd+/+ mice was transplanted into LDLR−/− mice. After 6 weeks of feeding on an atherogenic diet, PI3Kd−/− recipient LDLR−/− mice displayed significantly impaired CD4+ and CD8+ T-cell numbers, CD4+ T-cell activation, CD4+ effector T cells, and proatherogenic CD4+ T helper (Th) 1 responses in para-aortic lymph nodes and spleen compared with PI3Kd+/+ transplanted controls. Surprisingly, the net effect of PI3Kd deficiency was a substantial increase of aortic inflammation and atherosclerosis in LDLR−/− mice. Moreover, haematopoietic PI3Kd deficiency augmented macrophage accumulation in atherosclerotic plaques of LDLR−/− mice, whereas major macrophage functions including foam cell formation, efferocytosis, and cytokine secretion were unaffected by PI3Kd inactivation in these phagocytes. However, haematopoietic PI3Kd deficiency led to depletion of atheroprotective B-1 cells and reduction of proatherogenic B-2 cells in LDLR−/− mice. Moreover, haematopoietic PI3Kd deficiency caused a significant reduction of regulatory CD4+ T cells (Tregs) in plaques, para-aortic lymph nodes, and spleen of LDLR−/− mice. Furthermore, PI3Kd−/− Tregs exhibited reduced secretion of anti-inflammatory cytokines IL-10 and TGF-b as well as impaired suppression of CD4+ T-cell proliferation. Consequently, adoptive transfer of PI3Kd+/+ Tregs fully constrains the atherosclerotic burden in PI3Kd−/− transplanted LDLR−/− mice without affecting B cell numbers.

Conclusions
We demonstrate that PI3Kd plays a crucial role in B lymphocytes, Th1 cells, and Tregs during atherogenesis. Lack of PI3Kd signalling in atheroprotective Treg responses outplays its impact on proatherogenic Th1 responses, thus leading to aggravated atherosclerosis. Hence, PI3Kd is a key regulator of Treg biology and thereby protects against atherosclerosis progression.

Acknowledgement/Funding
Center for Molecular Medicine Cologne (CMMC) and the Marga and Walter Boll-Stiftung
P4150Causes of death in a heart failure clinic in Spain along 17 years
Authors: Moliner P , Lupon J , De Antonio M , Domingo M , Santiago-Vacas E , Zamora E , Santesmases J , Diez-Quevedo C , Troya M I , Boldo M , Altimir S , Alonso N , Gonzalez B , Nunez J , Bayes-Genis A 
Published: October 2019

Abstract

Background
Advances in heart failure (HF) treatment have achieved a reduction of death in HF patients in the last two decades. Indeed, not only mortality has been reduced but also the mode of death might have been modified through these years.

Purpose
To assess the causes of death in outpatients attended in a HF Unit since the year 2002 up to the year 2018.

Methods
Causes of death were classified as follows: progression of HF (worsening HF or treatment-resistant HF, in the absence of another cause); sudden death (any unexpected death, witnessed or not, of a previously stable patient with no evidence of worsening HF or any other known cause of death); acute myocardial infarction; stroke; procedural (post-diagnostic or post-therapeutic); other cardiovascular causes (e.g., rupture of an aneurysm, peripheral ischemia, or aortic dissection), and non-cardiovascular. Patients who died of unknown cause were excluded from the analysis. Fatal events were identified from the clinical records of patients with HF, hospital wards, the emergency room, general practitioners, or by contacting the patient's relatives. Furthermore, data were verified from the databases of the Catalan and Spanish Health Systems. Trends on every cause of death were assessed by linear regression.

Results
Since August 2001 to May 2018, 2295 HF patients were admitted to the HF clinic (age 66.4±12.8 years, 71% men, 49% from ischemic aetiology, mean LVEF 35.2% ± 14). During the 17 years of the study, 1201 deaths were recorded. Seventy-eight patients (6.5% of deaths) were excluded due to unknown cause of death. The evolution in the mode of death by years is shown in the figure. Two trends were observed: a decrease in sudden death (p=0.05) and a very significant linear increase in non-cardiovascular causes of death (p<0.001). The decrease of sudden death was mainly driven from changes observed in the first 10 years (p=0.014); thereafter the incidence of sudden death remained stable (p=0.18). Remarkably we did not observe significant changes in HF progression as mode of death (p=0.17).

Conclusions
During the 17 years of the study, a very significant trend towards higher percentage of non-cardiovascular deaths was progressively observed. On the other hand, percentage of sudden death showed a gradual decrease, mainly driven from the changes observed in the first 10 years.
P4158Marked impairment of endothelium-dependent digital vasodilatations in patients with microvascular angina compared with those with vasospastic angina
Authors: Kajitani S , Shiroto T , Godo S , Ito A , Ikumi Y , Sugisawa J , Suda A , Shindo T , Ikeda S , Hao K , Kikuchi Y , Nochioka K , Matsumoto Y , Takahashi J , Shimokawa H 
Published: October 2019

Abstract

Background/Introduction
Nitric oxide (NO) and endothelium-dependent hyperpolarization (EDH) factor are the major endothelium-derived relaxing factors. NO plays an important role in conduit arteries, while the importance of EDH factor increases as the vessel size decrease in patients with microvascular angina (MVA) compared with those with vasospastic angina (VSA) remains to be fully elucidated.

Purpose
We evaluated the roles of NO and EDH factor in conduit (brachial) arteries and resistance (digital) arteries of the patients with MVA, VSA and comorbid MVA+VSA patients.

Methods
We enrolled 39 patients who underwent diagnostic cardiac catheterization and divided them into 3 groups based on acetylcholine (ACh) provocation test, index of microcirculation resistance (IMR), and coronary flow reserve (CFR); MVA (N=9, mean age 59.9±3.5 years), VSA (N=12, mean age 61.3±1.8 years), and comorbid MVA+VSA (N=18, mean age 64.0±2.2 years). Endothelium-dependent brachial and digital vasodilatations in response to intra-arterial infusion of bradykinin (BK, 25, 50, and 100 ng/min for 2 min) were simultaneously measured by ultrasonography and peripheral arterial tonometry, respectively. Measurements were repeated after oral administration of aspirin (486 mg) and intra-arterial infusion of NG-monomethyl-L-arginine (L-NMMA, 8μmol/min for 5 min) in order to inhibit the effects of vasodilator prostaglandins and NO, respectively. Finally, endothelium-independent brachial and digital vasodilatations in response to sublingual nitroglycerin (NTG, 0.3 mg) were measured in the same manner.

Results
In the brachial artery, dose-dependent vasodilatations to BK were comparable among the 3 groups, and L-NMMA equally attenuated the responses to BK (Figure 1). Endothelium-independent brachial vasodilatation in response to NTG was also comparable among the 3 groups. Surprisingly, dose-dependent digital vasodilatations to BK were almost absent in MVA patients compared with VSA or comorbid MVA+VSA group (Figure 2). Furthermore, the digital vasodilatations were unaffected by L-NMMA in VSA group, but were significantly reduced in comorbid MVA+VSA group (VSA, 16.8±15.1% vs. MVA+VSA, −0.23±6.2%, P<0.05), suggesting reduced EDH and compensatory role of NO in the latter group. In contrast, endothelium-independent digital vasodilatation in response to NTG was comparable among the 3 groups.
The main results of this study

Conclusions
These results provide the first evidence that endothelium-dependent digital vasodilatations (both NO and EDH factor) are markedly impaired in MVA patients compared with VSA or comorbid MVA+VSA patients, whereas the responses are comparable in the brachial artery among the 3 groups, suggesting the involvement of severe endothelial dysfunction in the pathogenesis of MVA.
P4170Survival after dispatcher assisted CPR in out of hospital cardiac arrest compared to CPR without dispatcher assistance and no CPR before emergency medical services arrival – a nationwide study
Authors: Riva G , Jonsson M , Ringh M , Claesson A , Djarv T , Nordberg P , Hollenberg J 
Published: October 2019

Abstract

Background
Cardiopulmonary resuscitation (CPR) before arrival of emergency medical services (EMS) is associated with survival in out-of hospital cardiac arrest. Dispatcher assisted CPR (DA-CPR) has been shown to increase CPR rates. However there are several challenges to successful DA-CPR, such as identification of cardiac arrest, time delays to CPR instructions, time delays to start of chest compression and quality of CPR.

Purpose
The aim of this study is to assess survival in out of hospital cardiac arrest after no CPR, DA-CPR and CPR without dispatcher assistance before EMS arrival in a nationwide cardiac arrest register.

Methods
A register based observational study. All consecutive Out of Hospital Cardiac Arrests reported to the Swedish Register for Cardiopulmonary Resuscitation in 2010–2017 were collected. Patients with cardiac arrest witnessed by EMS, who received CPR by off-duty medical professionals, missing data on CPR, DA-CPR or survival were excluded. Exposure was categorized as either; no CPR before EMS arrival (NO-CPR), dispatcher assisted CPR before EMS arrival (DA-CPR) and CPR before EMS arrival without dispatcher assistance, spontaneous CPR (S-CPR). Propensity score matched cohorts were used for comparison between groups. Primary endpoint was 30-day survival.

Results
Out of 36309, a total of 15471 patients were included, 41.6% received NO-CPR 31.0% received DA-CPR and 27.4% received S-CPR. In propensity score matched cohorts survival to 30-days was 9.0% after NO-CPR, 13.6% after DA-CPR and 15.8% after S-CPR. Using DA-CPR as reference, NO-CPR was associated with lower survival (Conditional OR 0.61, 95% CI 0.52–0.72), absolute difference 4.6% (95% CI 3.0%-6.2%) and S-CPR was associated with higher survival (Conditional OR 1.21 (95% CI 1.05–1.39), absolute difference 2.3% (95% CI 0.5%-4.0%).
30-day survival

Conclusion
In this nationwide study spontaneous CPR was associated with the highest survival. When spontaneous CPR is not initiated DA-CPR is a reasonable option.

Acknowledgement/Funding
Swedish Heart and Lung Foundation
P4335The incidence of acute rheumatic fever in indigenous adults in the Northern Territory, South Australia and Western Australia
Authors: De Angelis C , Giles L , Roberts-Thomson R , Brown A 
Published: October 2019

Abstract

Background
Worldwide, knowledge of the contemporary incidence of acute rheumatic fever (ARF) in Indigenous adult populations is limited, with little understanding of patterns of ARF recurrence according to age and geographical location. This has created uncertainty in the development of rheumatic heart disease (RHD) guidelines surrounding the appropriate duration of antibiotic prophylaxis for these patients.

Purpose
This study aimed to describe the incidence rates of ARF in Indigenous Australian adults, analyse patterns of recurrence according to sex, age and geographical location, and assess adherence to secondary prophylaxis.

Methods
ARF episodes in Indigenous adults, aged 18 years and older, recorded within three Australian jurisdictions (Northern Territory, South Australia and Western Australia) ARF registers, diagnosed between 2007 to 2017, were included. Poisson and negative binomial regression were used to estimate incidence rate ratios (IRR) and 95% confidence intervals (CI) for first and recurrent episodes according to age, sex and remoteness. Adherence rates to secondary prophylaxis was described in the 12 months preceding recurrent ARF episodes in the Northern Territory.

Results
481 episodes were analysed. The incidence of ARF episodes in these jurisdictions from 2007 to 2017 was relatively constant. The overwhelming burden of disease occurred in remote areas (105 episodes per 100,000 people). An increased rate occurred in females (IRR 2.34, 95% CI 1.81–3.03). The 18–24 year olds had the highest incidence rates (115 episodes per 100,000 people). High rates of recurrence were also observed in those aged 25–34 years (96 episodes per 100,000 people). Adherence to secondary prophylaxis in those having a recurrent episode was only achieved in 10% of cases.

Conclusions
The incidence of ARF remains very high amongst adult Indigenous Australians. Adherence to secondary prophylaxis continues to play a role in recurrent episodes. RHD guidelines should take into account remoteness as a significant risk factor when deciding the duration of secondary prophylaxis.
P4342How burnout affects errors among physicians: meta-analysis
Authors: Olszewski R , Owoc J , Manczak M , Tombarkiewicz M 
Published: October 2019

Abstract

Burnout among physician is a growing and widespread phenomenon that seriously affects various aspects of healthcare delivery. A growing number of studies suggest that it significantly impacts quality of patient care and safety in various ways. This meta-analysis takes a narrowed approach to estimate association of burnout with self-perceived medical errors.

Purpose
To examine and quantify an overall effect of burnout on self-perceived errors among physicians.

Methods
The PubMed, Web of Science, Scopus, MEDLINE and Google Scholar databases were searched using various combinations of key terms: burnout, error, quality of care, patient safety. The inclusion criteria focused on prevalence of burnout among physicians and their self-reported errors in quantitative, observational studies that measured prevalence of self-reported errors in relation to physician burnout. We used Odds Ratio (OR) with 95% CI in the statistical analysis.

Results
The meta-analysis eventually covered 19,932 physicians from 10 studies (Tab. 1). The overall effect of burnout on self-reported errors was 2.72 (OR; 95% CI, 2.19–3.37) for burnout vs non-burnout physicians (Fig. 1). In none of the analysed studies was the effect of overall burnout neutral or negative.
Table 1. Characteristics of studies in the meta-analysis Study Year No. of physicians OR (95% CI) p weight % Shanafelt 1 2002 115 5.37 (1.71–16.81) 0.0039 3,02% Fahrenkopf 2008 123 3.68 (1.03–13.15) 0.0452 3,42% Toral-Villanueva 2009 312 8.90 (3.97–19.95) <0.001 5,26% Klein 2010 1,311 2.07 (1.50–2.86) <0.001 14,02% Tawfik 2018 6,695 3.25 (2.70–3.92) <0.001 17.73% O'Connor 2017 168 2.16 (1.08–4.30) 0.029 6.58% Baer 2017 258 7.32 (2.03–26.42) 0.002 2.47% Shanafelt 2 2010 7,905 2.34 (2.00–2.73) <0.001 18.42% Oliveira 2013 1,508 1.92 (1.44–2.56) <0.001 14.97% Wen 2016 1,537 2.79 (2.03–3.83) <0.001 14.11% Overall 19932 2.72 (2.19–3.37) 0.ehz745.0750 100.00%
Figure 1. Associations between burnout and errors.

Conclusions
This study provides evidence that burnout among physicians increases the likelihood of errors and thus may seriously affect patient safety at hospitals. The results suggest that it may be one of the key aspects in terms of patient safety and quality of care and should be considered a priority in patient safety improvement programs and policies.
P4353Global longitudinal strain is a measure of subclinical left ventricular dysfunction in chronic inflammatory autoimmune conditions
Authors: Khanna S , Newman J M , Gan G , Bhat A , Chen H , Tan T 
Published: October 2019

Abstract

Background
Myocardial deformation indices are proposed to be a more sensitive marker of subclinical dysfunction compared to standard measures of left ventricular (LV) systolic function. We hypothesize that subclinical myocardial dysfunction is present in chronic inflammatory autoimmune diseases such as Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA), despite both conditions being mediated by different pro-inflammatory modulators.

Purpose
Identify subclinical myocardial dysfunction through assessment of global longitudinal strain in two different chronic autoimmune conditions, SLE and RA.

Methods
Consecutive patients admitted to our institution with known history of SLE or RA (>1 year disease activity) were examined. Patients with preexisting cardiac disease, LVEF <50% and those without comprehensive transthoracic echocardiograms (TTE) were excluded. Mean longitudinal LV strain was performed offline using vendor-independent software (TomTec v4.6) and compared to age- and gender-matched controls with normal LV function and no history of cardiac disease.

Results
Of the 86 patients examined (mean age 53.01±21.74, 85.4% female), 51 (59.3%) had SLE and 35 (40.7%) had RA. No significant difference in BMI, hypertension, hypercholesterolemia, diabetes, obesity, obstructive sleep apnea and stroke was observed between controls and patients with SLE or RA. While there was no significant difference in LVEF between RA patients and matched controls, there was a significantly lower GLS in the RA cohort. Conversely, patients with SLE had significantly lower LVEF and GLS when compared to matched controls, despite LVEF being in the normal range. See Table 1. Receiver operator curve analysis revealed that mean GLS is a better discriminator for autoimmune disease with an area under the curve of 0.829 (95% CI, 0.77 to 0.89; p<0.01) compared to LVEF with an area under the curve of 0.632 (95% CI, 0.55 to 0.72; p<0.01).
Echocardiographic Parameters SLE (n=51) Controls (n=51) Sig (p value) RA (n=35) Controls (n=35) Sig (p value) LVEDV (mls) 102±30 85±20 <0.01 84±28 89±30 0.43 LVESV (mls) 36±17 29±9 0.02 26±14 30±12 0.24 Biplane LVEF % 59±6 63±4 <0.01 62±6 62±5 0.81 LV Mass (grams/m2) 96±34 72±20 <0.01 79±26 82±23 0.67 LV Mean GLS % 16.7±2.8 21.3±2 <0.01 17.8±1.7 19.1±2.5 0.02

Conclusions
Our results suggest that chronic inflammatory conditions (SLE and RA) are associated with subclinical cardiac dysfunction. Impaired GLS may reflect early myocardial damage and be used as a tool for screening of patients with inflammatory conditions.

Acknowledgement/Funding
None
P4354Regional Strain Pattern Index - A novel technique to predict CRT response
Authors: Orszulak M , Mizia-Stec K , Wrobel W , Berger-Kucza A , Orszulak W , Filipecki A , Urbanczyk-Swic D , Kwasniewski W 
Published: October 2019

Abstract

Background
Cardiac resynchronization therapy (CRT) reduces morbidity and mortality in heart failure individuals. Despite many efforts 30–40% patients with CRT still do not respond to therapy.

Purpose
The purpose was to propose and evaluate a novel dyssynchrony scoring system – Regional Strain Pattern Index (RSPI) in prediction of response to CRT.

Methods
Forty-nine HF patients (age: 66.5±10 years, LV ejection fraction: 24.9±6.4%, QRS: 173.1±19.1 ms, NYHA class II/III: 34.7%/63.3%, ischemic aetiology: 57.1%) underwent CRT implantation. Transthoracic echocardiography was performed before and 15±7 months after CRT implantation. Baseline dyssynchrony was studied by standard indices, strain pattern analysis and novel, author's index- RSPI. RSPI constitutes a method of quantification of LBBB-related strain curve pattern analysis. RSPI was calculated using longitudinal strain by 2D speckle tracking as the sum of dyssynchronous components across 12 segments from all three apical views. In one view, four components were assessed: 1) the contraction of the early-activated wall, 2) the prestretching of the late activated wall, 3) the contraction of the early-activated wall in the first 70% of the systolic ejection phase and 4) the peak contraction of the late-activated wall after aortic valve closure. One point was attributed to each component, thus the maximum was 12 points. RSPI was prospectively evaluated in predicting response to CRT. The response to CRT was defined as ≥15% reduction in the left ventricular end-systolic volume after 15 month follow-up.

Results
Thirty-six (73.5%) patients were responders. There were no significant differences in the baseline demographics, clinical, echocardiographic parameters between responders and non-responders. The mean RSPI in the overall population was 5.39±2.9 and higher RSPI values were observed in responders (5.86±2.9) than in non-responders (4.08±2.4, p=0.044). The ROC curve indicated that RSPI significantly predicted CRT response (area under curve, AUC=0.691, p=0.014) with the cut-off value at 7 points. Therefore, study population was divided into two groups according to RSPI score: ≥7 points (19 patients, 38.8% of population) and <7 points (30 patients, 61.2%). In univariate logistic regression analysis, among all of the dyssynchrony indices only RSPI≥7 points predicted the positive response to CRT (OR: 12; 95% CI=1.33–108.17; p=0.0036) with specificity of 92.3%, sensitivity of 50%, positive of 64.7% and negative of 40% predictive value for CRT response.
ROC curve for RSPI

Conclusion
RSPI constitutes a novel, valuable predictor for CRT response.

Acknowledgement/Funding
Grant for scientific research in the field of CRT efficacy funded by Medical University of Silesia.