bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of high platelet reactivity on left ventricular remodeling in patients with acute coronary syndrome
Authors: Tsuji M , Kuroda K , Saito E , Kawamura K , Ono T , Tokioka K , Ohe T , Kawai Y 
Published: October 2021

Abstract

Background/Introduction
Previous studies demonstrated that high platelet reactivity (HPR) predicts future cardiovascular death and coronary events in patients undergoing percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS). However, few studies have focused on the impact of HPR on left ventricular remodeling (LVR) and each echocardiographic parameter.

Purpose
The purpose of this study was to investigate the impact of HPR in ACS patients on LVR and changes in echocardiographic volume indexes and LV ejection fraction.

Methods
This is a retrospective cohort study of prospectively collected data in a single center that enrolled patients who underwent emergency PCI for ACS including STEMI and NSTEMI with prasugrel loading. The primary outcome of the study was LVR associated with HPR. Secondary endpoints were changes in indexed LVESV, LVEDV, LVEF, E/e' and LAVI between baseline and follow-up. The P2Y12 reaction unit (PRU) value in response to prasugrel was assessed by the VerifyNow P2Y12 assay. Blood samples were collected once per procedure immediately after PCI. LVR index was calculated as the relative change in LVEDV observed at follow-up compared with baseline. LVR was defined as a relative increase in LVEDV ≥20%, measured at follow-up visit compared with the baseline value before discharge.

Results
A total of 196 ACS patients who underwent emergency PCI between January 2016 and July 2020 were enrolled in the study. The mean age of the study population was 69.9 years, and 76.0% were male. On echocardiography at follow up visit of mean duration of 7.0±4.0 months, LVR was found in 38 patients (19.4%). The optimal cutoff for PRU associated with increased LVR assessed by receiver-operating characteristic curve analysis was 245.5 (AUC: 0.656; 95% CI: 0.564 to 0.749; p=0.003). On the basis of this cutoff, HPR was found in 82 patients (42.1%) and the prevalence of LVR was significantly higher in the HPR group compared to the non-HPR group (30.5% vs. 11.4%; p=0.001). Multiple Cox regression analysis showed that HPR was an independent predictor of LVR (OR 4.22, 95% CI 1.83–9.71, p=0.001). In addition, Δ% EDV and Δ% ESV increased in the HPR group, and decreased in the non-HPR group with significant differences (5.8±32.6% vs. −8.0±26.2% in Δ% EDV; p=0.002, 2.0±37.5% vs. −13.3±33.0% in Δ% ESV; p=0.004, respectively). Δ%EF, Δ%E/e', Δ%LAVI were numerically improved in the non-HPR group compared with the HPR group, but this difference did not reach statistical significance.

Conclusion
In patients with ACS, HPR defined as PRU ≥246 immediately after emergency PCI was an independent predictor of LVR in the chronic phase.

Funding Acknowledgement
Type of funding sources: None. Predictors of the presence of LVRChanges (Δ%) of LVEDV and LVESV
Sacubitril/Valsartan in heart failure with reduced ejection fraction: clinical and echocardiographic insights from a real world population
Authors: Valli F , Bursi F , Santangelo G , Toriello F , Rusconi I , Mondellini G , Vella A.M , Faggiano A , Persampieri S , Carugo S , Guazzi M 
Published: October 2021

Abstract

Background
Following the PARADIGM trial, some studies have identified cardiac remodeling as major background for hard end point benefits of Sacubitril/Valsartan (S/V), but few adopted a well described definition in the literature.

Purpose
We aimed at a comprehensive evaluation of the effects of S/V on echo-derived measures of cardiac remodeling along with clinical and laboratory data over a medium-term follow-up pointing to a real-world HFrEF population.

Methods
This is a prospective observational study of HFrEF patients on optimal medical therapy (OMT) initiated with S/V at Heart Failure Clinic of our institute (January 2017-January 2020). In 62 HFrEF, echocardiographic, laboratory and clinical data were collected at baseline and over 10 (Q1-Q3 8–13) months after S/V initiation. Mean age was 68±12 years, 79% men. Left ventricular reverse remodeling (LVRR) was defined as: 1) an absolute increase in LVEF ≥10 points or a LVEF ≥50% at follow-up and 2) a relative decrease in indexed left ventricular end-diastolic diameter of at least 10% or an indexed left ventricular end-diastolic diameter ≤33 mm/m2.

Results
Compared to baseline, S/V promoted a significant improvement of LV ejection fraction (LVEF, from 30% to 37%; p&lt;0,0001) with an absolute median increase in LVEF of 8 points. Parallel significant reductions in left ventricular and atrial volumes, lower mitral regurgitation degree and a better diastolic dysfunction along with clinical improvement (NYHA class and NT-proBNP values) were observed at follow up. sPAP (systolic Pulmonary Arterial Pressure) was significantly decreased at follow-up evaluation (37 mmHg vs 31 mmHg p=0,005) (Table 1). Overall, LVRR as defined above was observed in 30% of patients. Younger age (64 vs 74 years, p=0,007), a shorter duration of the disease (7 vs 23 months, p=0,009), and non ischaemic etiology (79% vs 33% p=0,003), along with a smaller baseline LAESVi (Left Atrial End Systolic Volume, 41 vs 48 ml/m2 p=0,012) were more common in patients with LVRR. sPAP and Right Ventricular (RV) function estimated by tricuspid annular plane systolic excursion (TAPSE) were significantly better in LVRR patients along with TAPSE/sPAP ratio (Table 2).

Conclusions
Our data point to a remarkable medium-term reverse remodeling effect by S/V in HFrEF. Findings reinforce the concept that the main benefits of S/V on hard end-points are mediated by its cardiac-related effects. Both a left and right reverse remodeling occur in HFrEF patients who start S/V in the most adaptable phase of the disease supporting an early administration.

Funding Acknowledgement
Type of funding sources: None.
Deformation imaging by strain in chronic heart failure over sacubitril/valsartan: a multicenter echocardiographic registry (DISCOVER) ARNI
Authors: Mandoli G.E , Pastore M.C , Giannoni A , Benfari G , Dini F.L , Correale M , Carluccio E , Guaricci A.I , Citro R , Novo G , Pasquini A , Degiovanni A , Santoro C , Malagoli A , Cameli M 
Published: October 2021

Abstract

Background
Sacubitril/valsartan changed the treatment of heart failure with reduced ejection fraction (HFrEF), due to the positive effects morbidity and mortality partly mediated by left ventricular reverse remodeling (LVRR). The aim of this multicenter study was to identify echocardiographic predictors of LVRR after sacubitril/valsartan administration.

Methods
Patients with HFrEF requiring therapy with sacubitril/valsartan from 13 Italian centers were included. Echocardiographic indexes including speckle tracking echocardiography (STE) were used to predict LVRR (defined as LV end-systolic volume reduction and ejection fraction [LVEF] improvement &gt;10% at follow-up) at 6 months follow-up as the primary endpoint. Changes in symptoms (NYHA class) and neurohormonal activations (N-terminal-pro-brain natriuretic peptide [NTproBNP]) were also evaluated as secondary endpoints. Patients with poor acoustic windows and missing data were excluded.

Results
The final population consisted of 341 patients (mean age: 65±10 years; 18% female, median LVEF 30% [interquartile range:25; 34]. At 6 months follow-up, cardiac dimensions and function, including left heart STE parameters, improved (Table 1). Moreover, 82 (24%) patients showed early complete response (LVRR and LVEF ≥35%), 55 (16%) early incomplete response (LVRR and LVEF &lt;35%), 204 (60%) no response (no LVRR and LVEF &lt;35%) after 6 months of sacubitril/valsartan. Among patients with ischemic etiology, 68% (108) did not develop LV RR. Age, sex, general characteristics, baseline NYHA class and NT-pro BNP did not significantly differ between the groups.Conversely, baseline LV dimensions and LVEF showed significant differences between the groups (p&lt;0.0001). Also, STE parameters were considerably better in group 1 compared to group 2 and 3 both at baseline and follow-up. Non-ischemic etiology, a lower left atrial volume index and a higher global longitudinal strain were all independent predictors of LVRR at multivariable logistic analysis (all p&lt;0.01). With ROC and spline curves, LV GLS &gt;−9.3% showed a good accuracy in predicting LV RR (Figure 1). LA strain was the best predictor of positive changes in NYHA class and NT-proBNP (all p&lt;0.05).

Conclusions
STE parameters at baseline could be useful to predict LVRR and early clinical response to sacubitril-valsartan, and thus could be used as a guide for treatment in patients with HFrEF.

Funding Acknowledgement
Type of funding sources: None. Table 1Figure 1
Patterns of left ventricular recovery in patients with heart failure with mid-range ejection fraction
Authors: Chen H.H.L , Lee C , Dhamoon K , Bhat A , Gan G.C.H , Tan T.C 
Published: October 2021

Abstract

Background
Heart failure with mid-range ejection fraction (HFmEF) represents a new classification of heart failure with intermediate clinical characteristics to those with HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). A proportion of HFmEF is attributed to atrio-ventricular dyssynchrony from atrial fibrillation (AF) as opposed to a primary cardiomyopathy with intrinsic cardiac myocyte dysfunction.

Purpose
We aim to compare the rate of left ventricular ejection fraction (LVEF) recovery in those with AF-mediated cardiomyopathy compared to those with primary myocyte dysfunction.

Methods
Consecutive patients with stable non-ischaemic cardiomyopathy with LVEF 40–49% on transthoracic echocardiography (TTE) were recruited from our institution's heart failure clinic and followed for 18 months. Patients with ischaemic, valvular or congenital heart disease, incomplete follow-up or poor quality TTE images were excluded. Eligible patients were separated into two groups: AF-mediated (n=44); and primary myocyte dysfunction (n=116).

Results
A total of 160 patients (62.1±16.4 years, 62% men) were included. There was no significant difference in age (p=0.06) and gender (p=0.59). Comorbid AF was higher in those with AF-mediated HFmEF (100 vs 28.4%; p&lt;0.01), otherwise no significant differences in clinical history was found between groups. AF-mediated HFmEF had lower rates of cardiac-specific beta-blocker use (15.9 vs 47.4%; p&lt;0.01). Baseline TTE showed similar LVEF and LV global longitudinal strain. On log-rank analysis there was no significant difference in all-cause death (p=0.75), or HF-related hospitalisation (p=0.14), however, higher rates of LVEF recovery were observed in the AF-mediated HFmEF group (p&lt;0.01). See figure 1.

Conclusion
There were higher rates of LVEF recovery in those with AF-mediated HFmEF compared to those with a primary myocardial disorder despite lower rates of cardiac-specific beta-blocker use. This did not translate to improvements in intermediate-term survival or HF related hospitalisation. These findings provide insight into the natural history of the disorder and its clinical phenotype.

Funding Acknowledgement
Type of funding sources: None. Figure 1. Rate of LVEF Recovery
Differences in long-term all-cause and cardiovascular mortality according to heart failure aetiology in ambulatory patients
Authors: Spitaleri G , Cediel G , Santiago-Vacas E , Codina P , Domingo M , Zamora E , Santesmases J , Diez-Quevedo C , Troya M , Boldo M , Altimir S , Alonso N , Rivas C , Lupon J , Bayes-Genis A 
Published: October 2021

Abstract

Background
Heart failure (HF) is the final stage of many cardiac disorders. Mortality in heart HF remains challenging despite improvement in outcomes proved in clinical trials in HF with reduced ejection fraction and it can be influenced by the aetiology of HF.

Purpose
To assess differences in long-term mortality (up to 18 years) in a real-life cohort of HF outpatients according to the aetiology of HF.

Methods
Consecutive patients with HF admitted at the HF Clinic from August 2001 to September 2019 were included. Follow-up was closed at 30.9.2020. HF aetiology was divided into ischemic heart disease (IHD), dilated cardiomyopathy (CM) –including non-compaction CM–, hypertensive CM, alcohol-derived CM, drug-derived CM, valvular disease, hypertrophic CM and others. For the present analysis, this latter group was excluded due to the big heterogeneity and limited number of patients in each subtype of aetiology. All-cause death and cardiovascular death were the primary end-points. Fine & Gray method for competing risk was used for cardiovascular mortality analysis.

Results
Out of 2387 patients included (age 66.5±12.5 years, 71.3% men, LVEF 35.4%±14.2, mainly in NYHA class II [65.5%] and III [26.5%]), 1317 deaths were recorded (731 from cardiovascular cause) during a maximum follow-up of 18 years (median 4.1 years [IQR 2–7.8] for the total cohort, 5.3 years [IQR 2.6–9.7] for survivors). Figure 1 shows Cox regression multivariable analysis for all-cause death and cardiovascular mortality. Considering IHD aetiology as reference, only dilated CM showed significantly lower risk of all-cause death, and only drug-induced CM showed higher risk of all-cause death. However, when cardiovascular mortality was considered almost all aetiologies showed significant lower risk of cardiovascular death than IHD. Figure 2 shows adjusted survival curves (A) and adjusted incidence curves of cardiovascular death (B) based on HF aetiology.

Conclusions
After adjusting for multiple prognostic factors among the studied HF aetiologies, dilated CM and drug-related CM showed the lowest and the highest risk of all-cause death, respectively. Patients with IHD showed the highest adjusted risk of cardiovascular death.

Funding Acknowledgement
Type of funding sources: None.
Cardiorenal syndrome and death risk in patients with heart failure or chronic kidney disease: an unmet cardiorenal need?
Authors: Taveira Gomes T , Santos Araujo C , Valente F , Bernardo F , Seabra Carvalho D , Bodegard J , Gavina C 
Published: October 2021

Abstract

Introduction
Heart failure (HF) and chronic kidney disease (CKD) have interlinked pathophysiological pathways and patients having both conditions simultaneously are defined as having cardiorenal syndrome (CRS).

Purpose
To estimate the risk of CRS in patients with initial presentation of HF (without prior CKD) or CKD (without prior HF) compared to mean age overall population in a real-world clinical setting. Also, to estimate the risk of all-cause death, cardiovascular (CV) death and non-fatal major CV events (MACE) in patients with HF, CKD and CRS compared to the mean-age overall population.

Methods
Clinical database analysis of a single primary and secondary healthcare institution from 2008–2019. We defined 4 incident cohorts: Control - patients at age 75; HF - HF patients without prior CKD; CKD - CKD patients without prior HF; CRS - patients with HF and CKD. Patients were indexed at the date of first event and followed one year. We defined HF as either: i) Ejection Fraction (EF)≤40% and NT-proBNP≥200pg/mL (≥600pg/mL if atrial fibrillation (AF)) OR BNP≥100pg/mL (≥125pg/mL if AF); ii) EF&gt;40% in the presence of structural cardiac abnormalities. We defined CKD as eGFR≤60mL/min using EPI-CKD formula. All definitions were constructed using laboratory-level data complemented with episode-level data. Hazard ratios (HR) and 95% confidence intervals were estimated using Cox regression models adjusted for age, sex, age-sex interaction, prior history of hypertension, myocardial infarction, stroke, peripheral artery disease and type 2 diabetes.

Results
We identified 3973 patients with HF, 13990 with CKD, 6784 with CRS and 16182 controls. Patients were in general 75–77 years old. The majority were females and were well treated with CV risk reducing drugs (Table 1). All-cause death risk was 4.7 (4.1–5.2) for HF and 4.9 (4.5–5.4) for CKD. CV death risk was 8.6 (6.8–10.8) for HF and 8.7 (7.1–10.6) for CKD. Non-fatal MACE risk was 7.4 (6.3–8.7) for HF, 4.6 (4.0–5.3) for CKD, and 7.1 (6.1–8.3) for CRS. CRS was associated with the highest risks of all-cause and CV death when compared with the control group- 7.1 (6.4–7.9) and 13.7 (11.7–17.0), respectively (Figure 1). More than half of events occurred in the first 90 days of follow-up for all outcomes.

Conclusions
Cardiorenal disease (HF or CKD) was associated with very high short-term risk (1 year) of developing CRS or death. Consecutively, patients with established CRS had the highest risk of dying. These results demonstrate serious cardiorenal risks in a real-world setting, supporting an urgent need for improved primary and secondary prevention of cardiorenal disease and cardiorenal syndrome.

Funding Acknowledgement
Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): AstraZeneca Produtos Farmacêuticos, Lda. Table 1. Baseline characteristicsFigure 1. Outcomes for CKD, HF and CRS
Long-term evolution of estimated glomerular filtration rate in patients with type 2 diabetes and heart failure
Authors: Escabia C , Codina Verdaguer P , Buchaca D , Spitaleri G , Domingo M , Santiago-Vacas E , Cediel G , Zamora E , Alonso N , Troya M.I , Santesmases J , Crespo E , Nunez J , Lupon J , Bayes-Genis A 
Published: October 2021

Abstract

Background
Limited data are available on the very long-term trajectory of glomerular filtration rate (GFR) in patients with chronic heart failure (HF) and type 2 diabetes mellitus (T2D).

Purpose
To prospectively assess dynamic trajectories of GFR estimated by CKD-EPI in a real-life cohort of HF patients based on the presence or absence of T2D over a 14-year follow-up.

Methods
In a prospective observational registry of real-life HF outpatients, estimated GFR (eGFR) was calculated by CKD-EPI at baseline and on a structured schedule every 3 months up to 14 years. We included in the analysis only eGFR values that were assessed at scheduled visits, discarding urgent renal function assessments. Loess (locally weighted error sum of squares) curves were plotted for the subgroups according to baseline T2D up to 14 years of follow-up. Loess curves are useful to observe a trend or relationship on nonlinear data observed over time.

Results
2386 patients were consecutively included from August 2001 to December 2018. 43.2% of the patients had a history of T2D. Mean age was 67.0±12.6 years, 28.9% were women and 71.0% had HF with reduced ejection fraction (EF&lt;40%). 25080 eGFR values were included in the analysis with a median of 8 values per patient [IQR 4–15] and a range between 1 and 47.
Diabetic patients had a worse baseline eGFR and presented a persistent decline over time. On the contrary non-diabetic patients presented an early decrease, mid-term improvement and a late progressive decline (Figure 1).

Conclusions
eGFR long-term trajectories in diabetic and non-diabetic patients with chronic HF were significantly different.

Funding Acknowledgement
Type of funding sources: None. eGFR evolution according to baseline T2D
Alcohol consumption in young men and risk of heart failure and all-cause mortality- a cohort study
Authors: Habtemichael L.H , Djekic D , Rosengren A.R , Schaufelberger M.S , Aberg M.A , Lindgren M.L , Aberg D.A , Robertson J.R 
Published: October 2021

Abstract

Aim
Wesought to study the association of alcohol consumption with the long-term risk of heart failure and all-cause mortality among adolescent men.

Method
We included 50 460 men (mean age 18.4 years; SD 0.72) that underwent enlistment for military service during 1968–1969. During this period, alcohol consumption was assessed with questionnaires as part of the enlistment protocol. Questionnaire data was transformed to grams of 100% ethanol/week and categorized as light (1–100 g/week), moderate (101–250 g/week), and high (&gt;250 g/week). Follow-up was done through linkage to the nationwide Swedish patient- and cause of death registries. Risk of heart failure and all-cause mortality during follow-up was calculated with cox proportional hazard models, adjusted for age, conscription year, test centre, body mass index, systolic and diastolic blood pressure, parental education, intelligence quotient, cardiorespiratory fitness and muscle strength, and baseline comorbidities (diabetes mellitus and hypertension).

Results
During a median follow-up of 51 years, there were 803 incidentheart failure events (mean age at diagnosis, 61 years) and 6254 deaths (mean age: 55 years). Compared with non-drinkers (0 g/week), the adjusted hazard ratios (HR) for light, moderate and high alcohol consumption were 2.34 (1.24–4.40), 2.38 (1.22–4.68), 5.60 (2.68–11.69) for incident heart failure (Figure 1, model 4)and 1.27 (1.04–1.54), 1.66 (1.35–2.05), 2.25 (1.74–2.91) for all-cause mortality,respectively.

Conclusion
Alcohol consumption in adolescence is strongly associated with heart failure and all-cause mortality in adulthood. Our results suggests that even light alcohol consumption in adolescence is associated with higher long-term risk of heart failure and mortality.

Funding Acknowledgement
Type of funding sources: None. Figure 1. *Model 1 adjusted for age at conscription, conscription year, test center, body mass index and baseline comorbidities (diabetes mellitus and hypertension). †Model 2 as model 1 but additionally adjusted for systolic and diastolic blood pressure at baseline. ‡Model 3 as model 2 but additionally adjusted for parental education. #Model 4 as model 3 but additionally adjusted for intelligence quotient, cardiorespiratory fitness and muscle strength.