bluuebunny/crossref_metadata_2025_split huggingface dataset:
P4420Is exercise-induced cardiac troponin release caused by skeletal muscle injury?
Authors: Paana T , Jaakkola S , Tuunainen E , Wittfooth S , Bamberg K , Petterson K , Kallio P , Heinonen O , Airaksinen K E J 
Published: October 2019

Abstract

Background
Cardiac troponins (cTn) are highly sensitive and specific markers for cardiac injury and a key element in the diagnosis of acute coronary syndrome. Strenuous exercise is known to induce increases in cTn, but the causative factors remain ambiguous. It is also equivocal whether exercise induced skeletal muscle injury is associated with cTn elevation.

Purpose
The aim of this study was to identify independent predictors for the rise in cardiac troponin T (cTnT) and I (cTnI) concentration and to focus on the relationship between skeletal muscle injury measured by skeletal troponin I (skTnI) and cTn elevations after a marathon race in a large group of male recreational runners.

Methods
A total of 40 recreational runners participating in the marathon in our city were recruited. The study included baseline visit (prerace) and immediate post-race sampling.

Results
The post-marathon cTnT concentration rose above the reference limit in 38 (95%) participants and the detection limit for cTnI was exceeded in 34 (85%) participants. Similarly, a 10-fold increase in skTnI concentration was observed and elevated post-race values were seen in all participants. There was no significant correlation between the post-race cTnT or cTnT change and post-race skTnI (Spearman's rho = 0.249, p=0.122, rho = 0.285, p=0.074). However, post-race cTnI and change in cTnI were associated with post-race skTnI (rho = 0.404, p=0.01, rho = 0.460, p=0.003) and creatine kinase (r=0.368, p=0.019) concentration. Subjective exertion or self-reported muscle symptoms did not correlate with post-race cTnT, cTnI or skTnI levels.
Post-Race cTnT <40 Post-Race cTnT ≥40 p-value n=18 n=22 Age, years 53.3±12.2 44.0±11.9 0.002 Active training, years 12.0 (9.3) 17.0 (15.8) 0.190 Muscle symptoms 7 (38.9) 11 (52.4) 0.523 Creatinine kinase, ug/l 406 (137) 399 (319) 0.163 N-terminal proBNP ng/l 137±168 158±277 0.783 Skeletal Troponin I, ng/ml 28.6 (41) 56.7 (143) 0.199
Figure 1

Conclusions
Cardiac troponin became abnormal in almost all runners after marathon race. The exercise-induced rise in cardiac troponin I is related to simultaneous release of skeletal troponin I. The mechanism of this association remains uncertain, but clinicians should be cautious when interpreting post-exercise troponin levels without clinical symptoms and signs of myocardial ischemia.
P4430Physical activity in leisure time: complying with the recommendations of clinical practice guidelines increases maximum oxygen consumption
Authors: Tojal Sierra L , Garcia Mancebo S , Torres Fernandez M , Juanes Dominguez I , Saez De Buruaga E , Salaverria I , Alonso Gomez A , Aros F 
Published: October 2019

Abstract

Introduction/Objectives
The promotion of physical activity is a universal recommendation for prevention of cardiovascular diseases. Clinical practice guidelines recommend at least 150 min/week of moderate or severe physical activity or ≥75 min of severe intensity.Our objective was to analyze whether reaching the physical activity levels recommended in the clinical practice guidelines evaluated by validated questionnaires and accelerometry, is associated with higher level of VO2 max.

Methods
We conducted a prospective cross-sectional study of 243 participants in the PREDIMED PLUS study (site: Vitoria-Gasteiz), (82 women), 65±4,9 years old, with metabolic syndrome and overweight/obesity. They performed a maximum exercise testing with expired gas analyses. Physical activity in leisure time was evaluated using subjective methods: self-reported questionnaires REGICOR and RAPA 1 and objective methods: chair test and accelerometry (91 subjects). Sedentarism was analyzed with the Nurses Health Study questionnaire and accelerometry

Results
Subjects who claimed to comply with the recommendations of the PA guidelines in the REGICOR questionnaire achieved higher maximum oxygen consumption (21.3±4.6 vs 18±4.4 ml/kg/min; P<0.001) and those who reported more physical activity in the RAPA 1 test showed a maximum oxygen consumption 18% higher than the less active group (P < . 001). However, those who performed ≥150 min/week of moderate/intense physical activity by accelerometry did not differ significantly from those who did not (21.1±4.7 vs 19.9±4.7 ml/kg/min; P: 0.644).

Conclusions
Subjects with metabolic syndrome and overweight/obesity who claim to meet PA recommendations in the REGICOR and RAPA tests achieve higher máximum oxygen consumption
P4432Coronary microvascular dysfunction in inflammatory bowel disease: Restored after enterectomy
Authors: Kakuta K , Dohi K , Yamamoto T , Fujimoto N , Shimoyama T , Umegae S , Ito M 
Published: October 2019

Abstract

Background
Inflammatory bowel disease (IBD) is a complex multisystem disease characterized by chronic inflammation, which can lead to coronary microvascular dysfunction (CMD).

Purpose
We aimed to investigate the presence and the severity of CMD in Crohn's disease (CD) and ulcerative colitis (UC) by assessing coronary flow reserve (CFR) using transthoracic Doppler echocardiography, and to elucidate the influence of enterectomy on CMD.

Methods
Thirty-seven IBD patients (22 CD patients: 39±12 years, 15 UC patients: 52±17 years), and 30 age- and gender-matched control subjects (46±12 years) who have comparable risk factors for coronary artery disease were enrolled. Smokers were excepted from the present study. For CFR measurement, coronary flow velocity was recorded at rest and during hyperemia in the left anterior descending coronary artery induced by intravenous infusion of adenosine triphosphate (0.14 mg/kg/min), and a CFR ≤2.5 calculated as the ratio of hyperemic to basal peak and mean diastolic velocity defined CMD. CFR measurement was repeated before and within 1 year after enterectomy. Serum or plasma cytokines were also measured before and after enterectomy.

Results
The median disease duration of CD and UC patients were 12 and 6 years. Although none of control subjects had CMD, 38% in IBD patients (CD: 41%, UC: 33%) had CMD. CFR was similarly and significantly lower in CD and UC patients than Control subjects (CD: 2.92±1.03*, UC: 2.99±0.65*, and Control: 3.84±0.75, *p<0.05 vs. Control). Serum levels of TNF-α, IL-6 and hs-CRP were significantly higher in CD and UC patients than Control subjects. Multiple linear regression analysis showed that the presence of IBD and mean diastolic flow velocity at baseline were independently associated with reduced CFR among all study participants (β=−0.324 and −0.614, p=0.001, respectively). CFR in IBD patients with both CMD and non-CMD significantly improved after enterectomy, and the extent of CFR improvement was greater in patients with CMD than those with non-CMD (Figure). Serum levels of IL-6 and hs-CRP significantly reduced among all IBD patients.

Conclusion
IBD was associated with CMD, which improved after enterectomy.
P4439Increased risk of out-of-hospital cardiac arrest in patients with psoriasis - a nationwide case-control study
Authors: Mohr G H , Barcella C A , Kragholm K , Rajan S , Sondergaard K B , Pallisgaard J L , Wissenberg M , Lindhardsen J , Ahlehoff O , Skov L , Lippert F K , Torp-Pedersen C , Gislason G 
Published: October 2019

Abstract

Background
Chronic inflammatory disorders such as psoriasis have been associated with cardiovascular diseases and linked to proarrhythmogenic electrocardiographic changes, including QT-prolongation. However, evidence regarding the risk of out-of-hospital cardiac arrest with a history of psoriasis is lacking.

Purpose
To investigate the association between psoriasis and out-of-hospital cardiac arrest.

Methods
Through the nationwide Danish Cardiac Arrest Registry, we identified adult out-of-hospital cardiac arrest patients of presumed cardiac cause with and without psoriasis between June 2001 and December 2014. The odds of cardiac arrest were estimated using conditional logistic regression in a case-control design where we matched up to nine controls per case on age, sex and ischemic heart disease. The models were adjusted for comorbidities, concomitant pharmacotherapy and socioeconomic position.

Results
A total of 32,447 out-of-hospital cardiac arrest cases were included and matched with 291,999 controls from the general population. The median age was 72 years, 67% were male and 29% had ischemic heart disease. A total of 607 (1.9%) cases and 4662 (1.6%) controls had psoriasis. Compared with cardiac arrest cases without psoriasis, cases with psoriasis had same age (p=0.718) and gender distribution (p=0.794), higher prevalence of comorbidities such as congestive heart failure (25.7% vs 20.2%, p=0.001), chronic kidney disease (8.9% vs 6.2%, p=0.008) and chronic obstructive pulmonary disease (19.0% vs 14.7%, p=0.005) but had same prevalence of cerebral vascular disease (15.8% vs 14.5%, p=0.351) and peripheral vascular disease (13.3% vs 11.1%, p=0.078). In unadjusted and adjusted analyses, psoriasis was significantly associated with increased odds of cardiac arrest (odds ratio (OR) 1.18 [95% confidence interval (CI) 1.08–1.28] and OR 1.13 [95% CI 1.04–1.23], respectively) (Figure 1).

Conclusion
In this nationwide case-control study, psoriasis was significantly associated with increased odds of out-of-hospital cardiac arrest. Focus on risk factors and prevention of cardiovascular disease in patients with psoriasis is warranted.

Acknowledgement/Funding
None
P4455The controversial role of genetics behind premature CAD: a plausible excuse for the young?
Authors: Sousa J , Mendonca M , Pereira A , Mendonca F , Neto M , Monteiro J , Sousa A C , Freitas S , Henriques E , Freitas A I , Borges S , Ornelas I , Drumond A , Palma Dos Reis R 
Published: October 2019

Abstract

Introduction
The complex interaction between genes and environmental factors contribute to individual-level risk of coronary artery disease (CAD), often resulting in premature CAD. The role for genetic risk scores in premature CAD is still controversial.

Objective
To evaluate the importance of conventional risk factors and of a genetic risk score in younger and older patients with coronary artery disease

Methods
From a group of 1619 pts with angiographic documented CAD from the GENEMACOR study, we selected 1276 pts admitted for ACS and analysed them in 2 groups (group A: ≤50 years, n=491 pts, 87.2% male, mean age 44±4.9 and group B: >50 years, n=785 pts, 75.2% male, mean age 57±4.2). Univariate analysis was used to characterize the traits of each group and we used ROC curves and respective AUCs to evaluate the power of genetics in the prediction of CAD, through a Genetic Risk Score (GRS).

Results
99.3% of the young patients had at least one modifiable risk factor, 18.4% had 2 modifiable risk factors and 75.2% had 3 or more modifiable risk factors. The pattern of risk factors contributing to CAD were different among groups: family history (A: 27.5%, B: 21.4%, p=0.015) and smoking habits (A: 64.8%, B: 42.9%, p<0.001) were more frequent among patients under 50, and traditional age-linked factors like hypertension (A: 58%, B: 75.7%, p<0.001), diabetes (A: 21.6%, B: 38.6%, p<0.001) were more common in the older group. Acute ST-elevation myocardial infarction was more frequent among the young (A: 55.4%, B: 47.4%, p=0.006), as non-ST clinical presentation was higher among elder patients. Regarding angiographic presentation, single vessel CAD was higher in group A (A: 50.3%, B: 40.9%, p<0.001), while multivessel diasease was higher in group B (A: 33.3%, B: 53.9%, p<0.001). At a mean follow-up of 5 years, older patients had a worst prognosis, registering a higher rate of cardiovascular death (A: 4.1%, B: 8.6%, p=0.002) and higher MACE (A: 26.8%, B: 31%, p=0.128),. Adding the genetic risk score (GRS), we achieved only a slight improvement in the AUC for predicting CAD (0.796->0.805, p=0.0178 and 0.748->0.761, p=0.0007 in patients under and over 50, respectively).

Conclusion
Coronary artery disease is not all the same, as premature CAD shares a unique and specific pattern of risk factors, clinical presentation, angiographic severity and prognosis. Genetics should not be used as an excuse to justify premature CAD, as there is frequently more than one potentially reversible risk factor present even in young patients and the additive predictive value of GRS is modest.
P4457Cardiac screening is improved by the addition of vectorcardiography
Authors: Cortez D , Morrell H 
Published: October 2019

Abstract

Background
The most common cause of sudden cardiac death in the United State of America is hypertrophic cardiomyopathy, while other causes such as left ventricular hypertrophy, ion-channelopathies, and other causes are also significant. Screening programs typically involve electrocardiograms with mainly false positive results. Little data regarding EKG and echocardiographic screening combined have been published.

Methods
During 2016–2019, over 15000 patients were screened by the Heartfelt Cardiac screening program. Screening electrocardiograms and echocardiograms including parasternal short/long axis, 4-chamber views, coronary assessment with color doppler and subcostal views with color doppler for assessment of septal defects, were performed.

Results
15,329 patients were screened under 35 years of age, mean age 17 years, with 36 hypertrophic cardiomyopathy patients, 61 borderline left ventricular hypertrophy patients noted, 30 patients with left ventricular dysfunction were noted, 47 patients with mitral valve prolapse, 27 patients with atrial septal defects, 39 patients with Wolf-Parkinson-White, 21patients with ideopathic dilated cardiomyopathy were discovered. Screening electrocardiography was helpful for Wolf-Parkinson-White identification, while echocardiogram was most helpful for detection of the above other defects. Screening EKG only identified 45% of those patients with myocardial disease (per above) with the modified Seattle Screening and ESC screening criteria.

Conclusion
Screening echocardiogram adds value for screening athletes under 35 years at risk for sudden cardiac death. Consideration of cost-effective echo screening should be considered as part of routine screening.
P4459The influence of the polymorphism BUD13-ZNF259 rs964184 on coronary disease according to age
Authors: Pereira A , Mendonca M , Sousa J A , Mendonca F , Neto M , Rodrigues R , Sousa A C , Freitas A I , Henriques E , Rodrigues M , Ornelas I , Drumond A , Palma Dos Reis R 
Published: October 2019

Abstract

A recent GWAS study found a significant association between the BUD13-ZNF259 rs964184 polymorphism, dyslipidemia and the onset of coronary disease (CAD). This variant encoding zinc finger protein (ZPR1) interacts with the receptor tyrosine kinase at cellular level, increasing oxidative stress, inflammatory response and atherogenesis. There are no studies of the effect of this variant on the Portuguese population.

Objective
Investigate the association of BUD13-ZNF259 rs964184 with dyslipidemia and its impact on CAD risk. Evaluate its impact in different age groups of our population.

Methods
A case-control study was performed with 3050 subjects (1619 coronary patients with 53.3±8 years; 78.9% male and 1431 controls with 52.8±8 years; 76.6% male) from the GENEMACOR study population. Traditional risk factors (smoking, dyslipidemia, diabetes, family history, hypertension, body mass index, alcohol consumption, physical inactivity) and others considered new, such as creatinine clearance, pulse wave velocity, homocysteine, fibrinogen, lipoprotein (a), APOB and PCR (hs) were investigated. BUD13-ZNF259 variant was genotyped and analyzed using the dominant model (CG + GG vs. CC). Bivariate and multivariate analyzes (logistic regression) were used to estimate the ORs and 95% CI, after adjusting for potential confounding factors, in 3 different age groups (<45; 45–55; >55).

Results
BUD13-ZNF259 polymorphism presented an independent and significant risk of CAD (OR=1.58; 95% CI: 1.07–2.32; p=0.019) only in the group of young coronary patients <45 years (n=482 patients), as well as dyslipidemia (OR=2.04; 95% CI: 1.26–3.31; p=0.003). After binary logistic regression entering with the interaction between dyslipidemia and the dominant model ZNF259 (CG + GG vs. CC), we verified an association with CAD risk (OR= 1.78; 95% CI: 1.08–2.95; p=0.025).

Conclusion
BUD13-ZNF259 rs964184 variant showed a significant risk for the onset of CAD in the young population (<45 years). The impact of the interaction of ZPR1 protein with tyrosine kinase (Syk) at the cellular level seems to be more relevant in young patients. This aspect may represent a possible prophylactic and therapeutic target, especially in coronary disease in young people.
P4463The pineal hormone melatonin inhibits doxorubicin-induced mitochondrial dysfunction and apoptosis in cardiomyocytes
Authors: Kasi Ganeshan T , Bell J D , Chong N W 
Published: October 2019

Abstract

Background
Heart failure (HF) is a major end-point of cardiovascular diseases (CVD). The pathogenesis of HF is mostly unresolved but involves metabolic alterations. Treatment of animals and cardiomyocytes with β-adrenergic receptor agonists induces HF. Mitochondrial dysfunction and HF are common complications of anticancer drugs such as doxorubicin (DOX). Melatonin synthesis dramatically decreases with age and in patients with CVD.

Purpose
The aim of this study was to investigate whether DOX-induced cardiac dysfunction can be attenuated by melatonin.

Methods
The Seahorse XF analyser was utilised (with the XFp Cell Energy Phenotype kit) to measure oxygen consumption rate [OCR; oxidative phosphorylation (OXPHOS)] and extracellular acidification rate (ECAR; glycolysis) in living rat cardiomyocyte-derived H9c2 cell line. Mono-layers of cells were treated with cardiotoxic drugs [isoproterenol (ISO, 100μM) or DOX (0.1μM)] for 24hr with and without melatonin co-treatment (MEL, 1μM). Cyan ADP flow cytometry was used to examine the anti-apoptotic properties of MEL (1μM) on DOX-treatment (0.5μM, 24hr). Data are given as mean±SEM (n=separate experiments) and analysis was performed using ANOVA and two-tail unpaired Student's T-test, as applicable.

Results
Isoproterenol-treatment increased peak OCR of H9c2 cells by ∼30% which was inhibited by MEL [CON, 384±17; ISO, 496±33; ISO+MEL, 412±31pmol/min; n=3 (six replicates); CON vs. ISO, p<0.05; ISO vs. ISO+MEL, p<0.05; CON vs. ISO+MEL, p>0.05]. Doxorubicin-treatment decreased OCR by ∼40% which was reversed by MEL [CON, 934±69; DOX, 554±52; DOX+MEL, 858±97pmol/min; n=3 (six replicates); CON vs. DOX, p<0.05; DOX vs. DOX+MEL, p<0.05; CON vs. DOX+MEL, p>0.05]. ISO and DOX significantly increased (∼30%) and decreased (∼25%) ECAR respectively (n=3, p<0.05) which was not inhibited by MEL. Melatonin alone had no significant effect on OCR and ECAR. Melatonin inhibited DOX-induced apoptosis in H9c2 cells [CON, 6.3±0.8%; DOX, 22±1.8%; DOX+MEL, 11±1.7%, n=4 (two replicates); CON vs. DOX, p<0.001; DOX vs. DOX+MEL, p<0.004; CON vs. DOX+MEL, p>0.05].

Conclusions
ISO and DOX-treatment induced mitochondrial dysfunction in H9c2 cells by alteration of OXPHOS and glycolysis; changes in OXPHOS were prevented by MEL. These data indicate that DOX-induced apoptosis in cardiac cells may be mediated, at least in part, by OXPHOS dysfunction which was attenuated by MEL treatment.
P4466Empagliflozin improves heart function after myocardial infarction in the rat
Authors: Goerg J , Sommerfeld M , Kintscher U , Lauer D , Kulikov A , Ivkin D , Okovityi S , Kaschina E 
Published: October 2019

Abstract

Background
Selective Sodium-glucose cotransporter 2 (SGLT2) inhibition with Empagliflozin reduced progression of left ventricular dysfunction and improved tolerance of physical exercise in heart failure by normoglycemic rats. Here, we hypothesized that Empagliflozin prevents cardiac dysfunction after myocardial infarction (MI).

Purpose
This study aimed to investigate whether Empagliflozin protects the heart in the early phase after experimental MI in normoglycemic rats.

Methods
MI was induced in Wistar rats via permanent ligation of the left coronary artery. Treatment with Empagliflozin (1 mg/kg/daily per os) was started after MI and continued for 7 days. Sham operated and vehicle treated animals served as controls (n=8). Hemodynamic parameters were measured via transthoracic echocardiography and intracardiac Samba catheter. Glucose concentration was determined in serum and urine. Protein expression of Na+/H+ exchanger isoform-1 (NHE-1), sodium bicarbonate co-transporter (NBC), Sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA), transforming growth factor beta 1 (TGF-beta1), Smad2 in the left ventricle were also studied. Additionally, NHE-1 regulation was investigated in cardiomyocyte cell line H9c2.

Results
Systolic heart function was improved in Empagliflozin treated MI animals compared to vehicle as demonstrated by Global Longitudinal Strain (GLS) (20,9% vs. 16,6%; p<0.05). E/A ratio was decreased by tendency and blood pressure was not affected. Ejection fraction (p<0.05), fractional shortening (p<0.05), stroke volume (p<0.01) were increased in Empagliflozin treated control rats as compared with the sham group. Moreover, application of Empagliflozin (1mg/kg, i.v. bolus) to healthy rats in 30 min increased maximal pressure in the left ventricle as compared with vehicle (110,5±15,3 mmHg vs 79,1±11,9 mmHg; p<0.05). Parallel, dP/dtmax was increased while dP/dtmin was decreased by tendency. Empagliflozin treatment did not affect glucose concentration in serum and urine. Treatment of cardiac H9c2 cells with Empagliflozin (1μM) down-regulated NHE-1 by 27%.

Conclusion
SGLT2 inhibitor Empagliflozin improved systolic function in the early phase post MI independently from glucose regulation. The cardioprotective mechanisms of SGLT2 inhibitors may involve cardiac NHE-1 exchanger inhibition.