bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gender-related nutritional risk differences in hospitalized patients after primary angioplasty for ST-segment myocardial infarction. Prognostic implications
Authors: Silva-Obregon A , Arroyo-Espliguero R , Viana-Llamas M.C , Estrella-Alonso A , Marian-Crespo C , Saboya-Sanchez S , Uribe-Heredia G , Tirado-Fernandez M.A , Eguileor-Marin Z , Ruiz De Santaquiteria-Torres V , Arriero-Fernandez N , Toran-Martinez C , Castillo-Sandoval A , Perez-Sanchez A , Garcia-Magallon B 
Published: November 2020

Abstract

Background
The prevalence of undernutrition among hospitalized patients is common and it has been associated to worse clinical outcomes, especially in heart failure and coronary artery disease patients. Female gender has been associated with major adverse events after a ST-segment myocardial infarction (STEMI).

Purpose
Assess the relationship between gender-based differences in nutritional status and one-year all-cause mortality among hospitalized patients after a primary angioplasty (PA) for STEMI.

Methods
Cohort of 321 consecutive patients (64.4 years [54.3–75.2]; 22.4% women) admitted to our general ICU after a PA for STEMI between November-2013 and February-2017. NRI was calculated as 1.519 × serum albumin (g/L) + 41.7 × (actual body weight [kg] / ideal weight [kg]). Patients were dichotomized in no to mild (NRI ≥97.5) and moderate to severe nutritional risk (NRI &lt;97.5). The Clinical Frailty Scale (CFS) was used to assess biological frailty. Analyses were made using crosstab tables with Pearson's chi-squared and likelihood-ratio goodness-of-fit tests. Cramér's V test or Kendall rank correlation coefficient were used to measure the degree of association between variables.

Results
Gender distribution among nutritional risk categories showed a significant degree of association (value 0.251; P=0.017) between female gender and moderate to severe NRI (55.7% women vs. 34.9% men, P=0.002) (Figure 1), independently of frailty (P=0.172). Women had significantly greater one-year mortality rate than men (20.8% vs. 5.2%: OR 4.78, 95% confidence interval [CI], 2.15–10.60, P&lt;0.001). Combination of moderate to high nutritional risk (NRI &lt;97.5) and biological vulnerability (CFS ≥4) significantly increased one-year mortality rate in women (53.3% in women vs. 26.7% in men; P&lt;0.001).

Conclusion
Among STEMI patients undergoing PA, women had a greater nutritional risk than men, regardless of biological frailty, and a greater one-year mortality rate. Undernutrition may be a risk factor implicated in the worse clinical outcome of female gender after STEMI.
Figure 1. Gender distribution among NRI categories

Funding Acknowledgement
Type of funding source: None
Cardiac remodeling in ambitious endurance-trained amateur athletes older than 50 years
Authors: Dalos D , Dachs T , Gatterer C , Schneider M , Binder T , Bonderman D , Hengstenberg C , Panzer S , Aschauer S 
Published: November 2020

Abstract

Background
Data on cardiac remodeling in athletes are conflicting and rarely available in veteran athletes.

Purpose
Therefore, in this study we aimed to define echocardiographic features of healthy endurance athletes older than 50 years.

Methods
We included probands aged &gt;50 years, who have performed endurance sports at 70% of their maximum heart rate for at least 1 hour 3 times per week over the previous 5 years.

Results
Between November 2018 and May 2019, 69 probands were recruited. Median age was 57 years (IQR 52–64) and 26% were female. Groups were formed according to the median training time of 6 hours per week: (A) 45 probands with ≥6 hours (IQR 6–10) and (B) 24 probands with &lt;6 hours (IQR 3.5–5). Age, sex and body mass index were similar. Group A demonstrated slightly smaller right atrial and left atrial (LA) diameters when compared to probands in B (53mm (IQR 49–55) vs. 53mm (IQR 51–58), p=0.045, and 52mm (IQR 49–55) vs. 53mm (IQR 52–58), p=0.039, respectively) and showed preserved diastolic function (p=0.026) with lower E/E' ratio (7 (IQR 6–9) vs. 9 (IQR 7–10), p=0.039). Interventricular septal thickness and relative wall thickness ratio were similar.
Global right and left ventricular (LV) strain were similar, but LA reservoir strain was higher in group A than in B (27% (IQR 22–34) vs. 20% (IQR 15–29), p=0.016).

Conclusion
Endurance training in healthy athletes older than 50 years does not result in relevant chamber dilatation or LV hypertrophy and a weekly training duration of ≥6 hours seems beneficial to preserve diastolic function associated with an increased LA reservoir function.

Funding Acknowledgement
Type of funding source: None
Obstructive sleep apnoe and cardiovascular, heart failure and mortality outcomes with empagliflozin versus placebo in the EMPA-REG OUTCOME trial
Authors: Yaggi H.K , Eliasson B , Kasai T , Marx N , Zinman B , Inzucchi S.E , Wanner C , Zwiener I , Wojeck B , Neeland I , Johansen O 
Published: November 2020

Abstract

Background/Introduction
Obstructive sleep apnoe (OSA) and type 2 diabetes (T2D) occurs more frequently in persons with obesity, and both OSA and T2D are associated with metabolic disturbances that increases the risk for cardiovascular disease (CVD). In EMPA-REG OUTCOME, a randomized placebo-controlled outcome trial involving 7020 patients with T2D and CVD, the sodium glucose co-transporter (SGLT)-2 inhibitor empagliflozin reduced HbA1c, systolic blood pressure, waist circumference, and weight, and also reduced the risk of 3-point major adverse CV events (3P- MACE) by 14%, CV death by 38% and hospitalization for heart failure (HHF) by 35%.

Purpose
We investigated incidence rates of CV, HHF, and mortality outcomes in patients with or without OSA at baseline, and the treatment effect of empagliflozin, in EMPA-REG OUTCOME.

Methods
The trial included patients from 42 countries with T2D (with HbA1c 7.0–9.0% for drug-naïve patients and 7.0–10.0% for those on stable glucose-lowering therapy), established CVD, and estimated glomerular filtration rate &gt;30 mL/min/1.73 m2. Patients were randomised (1:1:1) to receive empagliflozin 10 mg, empagliflozin 25 mg, or placebo once daily in addition to standard of care. All CV outcomes were independently adjudicated and events were pooled for the 10 and 25mg doses. In this post-hoc analysis, OSA were assessed based on investigator reports using MedDRA 18.0 and incidence rates for outcomes were reported by adjusted event-rates per 100 patient-years. Analysis of effects on outcomes were performed using Cox regression models with multivariable adjustments.

Results
Of 7020 patients with T2D and CVD, OSA was reported in 391 (5.6% [placebo 5.4%; pooled empagliflozin doses 5.7%]. Compared with patients without OSA at baseline, those with OSA were more frequent males (82.9% vs 70.8%), living in region North-America (63.2% vs 17.3%), and had more obesity (BMI ≥35 kg/m2: 55.2% vs 18.2%) and more coronary artery disease (88.0 vs 74.9%). Over a median 3.1 years, individuals with OSA at baseline relative to those without OSA in the placebo group, experienced 1.3–2.0 fold higher event rates for 3P-MACE (OSA vs no OSA: 6.49 vs 4.27/100-patient-year), CV death (2.57 vs 1.99), HHF (2.71 vs 1.38) and all-cause mortality (4.29 vs 2.78). Empagliflozin improved CV, HHF, and mortality outcomes regardless of presence of OSA at baseline (p-for interactions &gt;0.05 [Figure 1]).

Conclusions
In this post-hoc exploratory analysis, patients with OSA had higher frequency of events for 3P-MACE, HHF and mortality. The cardio-protective effects of empagliflozin was consistent in those with and without OSA at baseline.
Figure 1. Sleep apnea and empagliflozin

Funding Acknowledgement
Type of funding source: Private company. Main funding source(s): Boehringer Ingelheim and Eli Lilly Diabetes Alliance
An absolute risk-guided approach to cardiovascular risk management within a chest pain clinic: the ARCPAC randomized trial
Authors: Black J.A , Campbell J , Sharman J , Nelson M , Parker S , Hamilton G , Marwick T 
Published: November 2020

Abstract

Background
The majority of patients attending chest pain clinics are found not to have a cardiac cause of their symptoms, but have a high burden of cardiovascular risk factors that may be opportunistically addressed. Absolute risk calculators are recommended to guide risk factor management, although it is uncertain to what extent these calculations may assist with patient engagement in risk factor modification.

Purpose
We sought to determine the usefulness of a proactive, absolute risk-based approach, to guide opportunistic cardiovascular risk factor management within a chest pain clinic.

Methods
This was a prospective, open-label, blinded-endpoint study in 192 enhanced risk (estimated 5-year risk ≥8%, based on Australian Absolute Risk Calculator) patients presenting to a tertiary hospital chest pain clinic. Patients were randomized to best practice usual care, or intervention with development of a proactive cardiovascular risk management strategy framed around a discussion of the individual's absolute risk. Patients found to have a cardiac cause of symptoms were excluded as they constitute a secondary prevention population. Primary outcome was 5-year absolute cardiovascular risk score at minimum 12 months follow up. Secondary outcomes were individual modifiable risk factors (lipid profile, blood pressure, smoking status).

Results
192 people entered the study; 100 in the intervention arm and 92 in usual care. There was no statistical difference between the two groups' baseline sociodemographic and clinical variables. The intervention group showed greater reduction in 5-year absolute risk scores (difference −2.77; p&lt;0.001), and more favourable individual risk factors, although only smoking status and LDL cholesterol reached statistical significance (table).

Conclusion
An absolute risk-guided proactive risk factor management strategy employed opportunistically in a chest pain clinic significantly improves 5-year cardiovascular risk scores.

Funding Acknowledgement
Type of funding source: Foundation. Main funding source(s): Tasmanian Community Fund
Comparison of two recent ceramide-based coronary risk prediction scores: CERT and CERT-2
Authors: Leiherer A , Muendlein A , Saely C.H , Laaksonen R , Laaperi M , Vonbank A , Fraunberger P , Drexel H 
Published: November 2020

Abstract

The Coronary Event Risk Test (CERT) is a validated cardiovascular risk predictor that uses circulating ceramide concentrations to allocate patients into one of four risk categories. This test has recently been updated (CERT-2), now additionally including phosphatidylcholine concentrations.
The purpose of this study was to investigate the power of CERT and CERT-2 to predict cardiovascular mortality in patients with cardiovascular disease (CVD).
We investigated a cohort of 999 patients with established CVD.
Overall, comparing survival curves (figure) for over 12 years of follow up and the predictive power of survival models using net reclassification improvement (NRI), CERT-2 was the best predictor of cardiovascular mortality, surpassing CERT (NRI=0.456; p=0.01) and also the 2019 ESC-SCORE (NRI=0.163; p=0.04). Patients in the highest risk category of CERT as compared to the lowest category had a HR of 3.63 [2.09–6.30] for cardiovascular death; for CERT-2 the corresponding HR was 6.02 [2.47–14.64]. Among patients with T2DM (n=322), the HR for cardiovascular death was 3.00 [1.44–6.23] using CERT and 7.06 [1.64–30.50] using CERT-2; the corresponding HRs among non-diabetic subjects were 2.99 [1.20–7.46] and 3.43 [1.03–11.43], respectively.
We conclude that both, CERT and CERT-2 scores are powerful predictors of cardiovascular mortality in CVD patients, especially in those patients with T2D. Performance is even higher with CERT-2.

Funding Acknowledgement
Type of funding source: None
Longitudinal obesity exposure over two decades is associated with subclinical myocardial injury: the Nord-Trondelag Health Study
Authors: Lyngbakken M.N , Rosjo H , Hveem K , Omland T 
Published: November 2020

Abstract

Background
Obesity is associated with subclinical myocardial injury as quantified by concentrations of cardiac troponin, but whether excess weight history is associated with increased cardiac troponin I (cTnI) remains unclear. We aimed to explore the association of obesity with cTnI using different indices of cumulative obesity exposure.

Methods
We analyzed cTnI with a high-sensitivity assay in 14,157 participants with follow-up over two decades in the prospective observational Nord-Trøndelag Health (HUNT) Study at study visit 4 (2017–2019). All subjects were free from known cardiovascular disease at baseline, and we excluded subjects with BMI &lt;18.5 kg/m2. BMI was assessed at study visit 2 (1995–1997), 3 (2006–2008) and 4, and we categorized participants as normal weight (BMI &lt;25), overweight (BMI ≥25 to &lt;30) and obesity (BMI ≥30). At each study visit, BMI was designated a score of 0 (normal weight), 1 (overweight) or 2 (obesity), totaling a score from 0 to 6. Cumulative obesity exposure was calculated as average BMI above 25 kg/m2 between visits multiplied by the time between visits (excess BMI years, kg/m2 × years).

Results
Median age at visit 4 was 64.1 (range 40.9 to 101.5) years and 60% were women. Concentrations of cTnI were detectable in 77.2% of study participants, and were median 2.2 (1.3 to 3.9) ng/L. There was a linear increase in cTnI with increasing BMI score (p for trend &lt;0.001) and increasing BMI score was associated with increased risk of high cTnI (p for trend &lt;0.001; Table 1). For every 100 excess BMI years, there was a 15.6 (95% CI, 13.0 to 18.2) % increase in cTnI at study visit 4 (Figure 1).

Conclusion
Cumulative obesity exposure is associated with a linear increase in cTnI, a highly sensitive index of subclinical myocardial injury, reflecting the detrimental effect of long standing obesity on cardiovascular health.
Figure 1. BMI years and cTnI

Funding Acknowledgement
Type of funding source: Public Institution(s). Main funding source(s): South-Eastern Norway Regional Health Authority
Stroke and myocardial infarction prevention with GLP1 analogues in high or very-high cardiovascular risk diabetic patients
Authors: Cazorla-Morallon D , Cordero A , Pomares Varo A , Torroba Balmori G , Moreno Garcia M.J , Martinez Rey-Ranal E , Bertomeu-Gonzalez V , Zuazola P 
Published: November 2020

Abstract

Background
Patients with established cardiovascular disease have an increased risk of stroke, even in the absence of atrial fibrillation. Several trials have analysed the effect of glucagon-like peptide-1 receptor (GLP1) analogues on cardiovascular events in patients with high cardiovascular disease.

Methods
We performed a metanalysis with all randomized clinical trial that compared a GLP1 analogue vs. placebo. Primary endpoint was stroke incidence, including ischemic and haemorrhagic aetiology, assessed by fixed-effect model.

Results
We identified 7 trials that compared a GLP analogue (albiglutide, dulaglutide, exenatide, liraglutide, lixinatide or semaglutide). A total of 56,004 patients were included in the analysis, 27977 treated with a GLP1 analogue. Mean age of the patients was 63.9 (2.1) years, 25,398 (45.4%) patients had cardiovascular disease.
A total of 1,568 strokes were reported, 711 in patients receiving a GLP analogue and 857 in control arm; treatment with a GLP1 analogue reduced the incidence of stroke by 147% (RR: 0.83, 95% CI 0.75–0.92; p&lt;0.001). No heterogeneity between trials was observed (p=0.835). Globally, treatment with GPL1 analogues reduced the incidence of stroke or myocardial infarction by 11% (RR: 0.89, 95% CI 0.84–0.94; p&lt;0.01)
A total of 3,192 cases of myocardial infarction were reported: 1,524 in patients treated with GLP1 analogues and 1,668 with placebo. Treatment with GLP1 analogues reduce the incidence of myocardial infarction by 8% (RR: 0.92, 95% CI 0.86–0.98; p=0.010)

Conclusions
Treatment with a GLP1 analogue reduced the incidence of stroke by 17% and myocardial infarction by 8%, in different trials involving high or very-high risk patients with diabetes.
Forest plot: stroke and MI

Funding Acknowledgement
Type of funding source: None
Lp (a) &gt;50 mg/dl predicts atherosclerotic cardiovascular events in patients with heterozygous familial hypercholesterolemia who achieved LDL-C &lt;2.6 mmol/l
Authors: Funabashi S , Kataoka Y , Hori M , Ogura M , Matsuki K , Doi T , Noguchi T , Harada-Shiba M 
Published: November 2020

Abstract

Introduction
Lipoprotein (a) [Lp (a)] is a plasma lipoprotein which exhibits atherogenic properties. Lp(a) ≥50 mg/dl has been recently shown to associate with a risk of atherosclerotic cardiovascular diseases (ASCVD) in patients with heterozygous familial hypercholesterolemia (HeFH). While current guideline recommends lowering LDL-C as a first-line therapeutic approach in HeFH subjects, it remains to be fully determined whether an elevated level of Lp(a) confers additional ASCVD risks in HeFH patients who achieved a lower LDL-C level.

Purpose
To investigate cardiovascular outcomes in HeFH subjects with a lower LDL-C but an elevated Lp(a) levels.

Methods
182 HeFH patients with on-treatment LDL-C &lt;2.6 mmol/l under lipid-lowering therapies were analyzed. Clinical characteristics and MACE (= a composite of all-cause death, ACS, stroke, PAD and coronary revascularization) were compared in HeFH subjects with Lp(a) ≥ vs. &lt;50 mg/dl.

Results
The averaged LDL-C and Lp (a) levels were 1.9 mmol/l and 26.8 mg/dl, respectively. 19.2% of study subjects exhibited Lp(a)≥50 mg/dl. HeFH patients with Lp(a) ≥50 mg/dl were more likely to be older and have a history of hypertension, but these comparisons did not meet statistical significance. There was no significant difference in on-treatment LDL-C, HDL-C and Triglyceride level (Table). However, during the observational period (median=4.7 years), there was a 2.7-fold (95% CI, 1.41–5.02; p=0.004) greater likelihood of experiencing MACE in subjects with Lp(a) ≥50 mg/dl (picture). Even after adjusting clinical demographics, Lp(a) ≥50 mg/dl remained an independent predictor for the occurrence of MACE (hazard ratio=2.53, 95% CI: 1.29–4.82, p&lt;0.001).

Conclusions
Despite achieving on-treatment LDL-C &lt;2.6 mmol/l, an elevated risk of MACE was observed in HeFH patients with Lp(a) ≥50 mg/dl. Our findings suggest an increased level of Lp(a) as a risk stratification marker and a potential therapeutic target in patients with HeFH.
Clinical outcome

Funding Acknowledgement
Type of funding source: None
Effect of bempedoic acid on uric acid and gout in 3621 patients with hypercholesterolemia: pooled analyses from phase 3 trials
Authors: Ray K.K , Bakris G.L , Banach M , Catapano A , Duell P.B , Mancini G.B.J , Bloedon L , Feng A , Gotto Jr A.M 
Published: November 2020

Abstract

Background
Bempedoic acid (BA), an oral ATP-citrate lyase inhibitor, significantly lowers low-density lipoprotein cholesterol levels in patients with hypercholesterolemia. In clinical trials of BA, small mean increases in uric acid have been reported. BA weakly inhibits organic anion transporter 2 (OAT2) in vitro, which may account for small elevations in serum uric acid.

Purpose
To assess uric acid levels and incidence of gout with BA treatment.

Methods
Data were pooled from 4 randomized (2:1), double-blind studies of BA (180 mg daily) vs placebo for 12 weeks to 52 weeks in patients with hypercholesterolemia on stable background lipid-lowering therapy. Safety assessments included adverse events of special interest (elevation in uric acid levels, gout) and laboratory assessments.

Results
A total of 2424 patients treated with BA and 1197 patients on placebo were included in this analysis. Mean (SD) baseline uric acid levels were 6.0 (1.4) mg/dL for both groups. History of gout was reported by 5.2% (127/2424) and 5.8% (69/1197) in the BA and placebo groups, respectively. At week 12, mean (SD) serum uric acid levels (% change from baseline) increased from baseline with BA treatment by 0.82 (0.97) mg/dL (14.8%) vs –0.02 (0.82) mg/dL (0.67%) for placebo. Elevations in serum uric acid levels typically occurred within the first 4 weeks of treatment, remained stable during treatment, and returned to baseline after treatment discontinuation. Gout was reported in 1.4% (BA) and 0.4% (placebo) of patients, and hyperuricemia was reported in 1.7% (BA) and 0.6% (placebo) of patients. Other potential clinical consequences of elevated uric acid levels (eg, events associated with nephrolithiasis), were similar between groups (0.7% vs 0.8%). In both groups, patients who reported gout during the studies were more likely to have a medical history of gout or elevated baseline uric acid levels (Table). Few patients discontinued treatment due to gout (n=1, &lt;0.1% [BA]) or uric acid increases (n=2, &lt;0.1% [BA]).

Conclusion
Mean increases in uric acid levels were small, remained stable while patients continued to receive treatment, were infrequently associated with AEs, and were reversible on discontinuation of BA

Funding Acknowledgement
Type of funding source: Private company. Main funding source(s): Esperion Therapeutics funded the research for this study and provided writing support for this abstract. Medical writing assistance was provided by Agnella Izzo Matic, PhD, CMPP, and Kelly M Cameron, PhD, CMPP, of JB Ashtin.
The association between statin pre-treatment and LDL Levels on the rate of STEMI presentation: data from the ACS Israeli Survey (ACSIS) 2008–2018
Authors: Dadon Z , Moriel M , Samuel T.Y , Steinmetz Y , Asher E , Iakobishvili Z , Glikson M , Gottlieb S 
Published: November 2020

Abstract

Background
ST-elevation myocardial infarction (STEMI) mostly occurs as a result of vulnerable coronary artery plaque rupture. Constituting hypolipidemic and pleiotropic effects, statins stabilize coronary artery plaque and may prevent STEMI events.

Purpose
To determine the association between statin pre-treatment and its intensity, low-density-lipoprotein cholesterol (LDL-C) levels and presentation of patients with an ACS (STEMI vs. NSTEMI/unstable angina [UAP]).

Methods
Data was drawn from the Acute Coronary Syndrome Israeli Survey (ACSIS), a biennial prospective survey of ACS patients hospitalized in all CCU/Cardiology departments during 2008–2018. The rate of STEMI vs NSTEMI/UAP at the time of presentation was calculated by LDL-C levels on admission, stratified to 5 subgroups (&lt;50, 50–69, 70–100, 101–130 and &gt;130 mg/dl) and the use of statins, including statin intensity prior to the index ACS event.

Results
Among 5,103 patients, 875 (17%) were pre-treated with high intensity statin (HIST), 1,389 (27%) with low intensity statin (LIST), and 2,839 (56%) were statin naive patients. Statin-pre-treated patients were older, more likely to suffer from co-morbidities and cardiovascular diseases and were more often pre-treated with anti-platelets.
The proportion of patients presenting with STEMI vs. NSTEMI/UAP was significantly lower among HIST vs. LIST vs. statin naive patients (31.0%, 37.8%, 54.0%, respectively, p for trend &lt;0.001). At each LDL-C level, the proportion of STEMI was significantly lower among HIST vs. LIST vs. statin naive patients. Multivariate analysis adjusting for pertinent variables including propensity score for statin use, revealed that HIST was independently associated with lower STEMI presentation, but LDL-C&lt;70 and LIST were not.

Conclusions
Among patients admitted with ACS, pre-treatment with high intensity statin but not LDL-C level, was independently associated with a lower probability of presenting with STEMI.

Funding Acknowledgement
Type of funding source: None