bluuebunny/crossref_metadata_2025_split huggingface dataset:
P860Adding clinical risk scores to troponin-based rule-out algorithms improves identification of patients at high risk for coronary revascularization within 6 weeks: the WESTCOR study
Authors: Steiro O , Tjora H , Langorgen J , Omland T , Bjorneklett R , Nygard O , Renstrom R , Skadberg O , Bonarjee V , Lindahl B , Vikenes K , Aakre K 
Published: October 2019

Abstract

Background
The ESC 0/3-h and High-STEACS study algorithms using high-sensitive troponin assays have proven effective in ruling out NSTEMI, but the safety of out-of-hospital follow-up of ruled out patients is disputable. Clinical risk scores may help to identify patients who develop major adverse cardiac events (MACE) defined as NSTEMI, death or coronary lesions in need of acute or elective revascularization within six weeks after admittance.

Purpose
Assess the ability of the ESC and High-STEACS study algorithms alone and in combination with clinical risk scores to identify MACE in unselected patients presenting with chest pain.

Methods
985 patients (mean 63 years, 61% male) with suspected NSTE-ACS were consecutively included from Sept. 2015 to Feb. 2017. Serum samples were collected at 0, 3 and 8–12 hours and hs-cTnT and hs-cTnI were measured. The final diagnosis was adjudicated by two independent cardiologists. The troponin-based algorithms where compared to nine clinical risk scores, HEART, CARE, GRACE, T-MACS, TIMI, EDACS, sEDACS, Goldman and Geleijnse.

Results
The prevalence of NSTEMI during index hospitalization was 13%. The ESC 0/3-h and High-STEACS algorithms missed 3 events of NSTEMI with excellent NPV of 99.5 and 99.6. Rule-out patients with normal ECGs, GRACE score <140 and no residual pain had a prevalence of MACE within 6 weeks of 9% using both algorithms. The most frequent event was non-acute revascularization due to unstable angina pectoris. Three of ten clinical risk scores had higher accuracy than the ESC 0/3-h algorithm for identification of MACE: HEART (AUC 0.84), CARE (AUC 0.79) and T-MACS (AUC 0.76). Combining the ESC 0/3-h rule-out algorithm and HEART≤3 had the best AUC of 0.85, missing only 12 (3%) MACE.
Troponin-based algorithms and HEART True pos. True neg. False pos. False neg. NPV PPV Sens. Spes. Prop. low-risk AUC Troponin-based algorithms, endpoint NSTEMI ESC 0/3h TnT 118 628 196 3 99.5 37.6 97.5 76.2 66.8 0.87 High-STEACS TnI 118 715 109 3 99.6 52.0 97.5 86.8 76.0 0.92 Troponin-based algorithms, endpoint MACE ESC 0/3h TnT 143 577 171 54 91.4 45.5 72.6 77.1 66.8 0.75 High-STEACS TnI 130 651 97 67 90.7 57.3 66.0 87.0 76.0 0.77 Troponin-based algorithms combined with HEART score, endpoint MACE ESC 0/3h HEART 3 185 414 334 12 97.2 35.7 94.1 55.4 44.6 0.85 High-STEACS HEART 3 186 411 337 11 97.4 35.6 94.7 55.0 44.7 0.85
Causes of MACE

Conclusion
The ESC 0/3-h and High-STEACS algorithms identify almost all patients with low risk of NSTEMI, who are candidates for none or out-of-hospital follow-up. However, 9% of ruled out patients have MACE within 6 weeks. The combination of ESC algorithm and clinical risk scores markedly reduce the number of ruled out patients with MACE.
P898Association of acroparesthesias and angiokeratomas with the alpha-galactosidase A gene polymorphisms in females with hypertrophic cardiomyopathy
Authors: Poliakova A A , Gudkova A Y A 
Published: October 2019

Abstract

Introduction
Clinical implications of different single nucleotide polymorphisms (SNPs) in the alpha-galactosidase A gene (α-GLA) as potential cause of symptoms and organ manifestations similarly to those seen in Fabry disease (FD) remain unclear.

Purpose
To study the prevalence of FD among patients with hypertrophic cardiomyopathy (HCM), as well as to evaluate the impact of polymorphic variants of the α-GLA gene on extracardiac manifestations in females with HCM.

Methods
The study included 321 patients with left ventricular hypertrophy ≥15 mm. 24 of the 321 patients (males (n=15) and females (n=9)) presented with HCM phenotype and extracardiac features suggestive of FD: acroparesthesias and pain in hands and feet, stroke at a young age, angiokeratomas, kidney damage (microalbuminuria, proteinuria, decreased glomerular filtration rate), suspicion for X-linked inheritance. This patients carried out screening for FD. A combined enzymatic and genetic strategy was used, measuring the activity of α-D-galactosidase A by tandem mass spectrometry (ESI-MS/MS) and genotyping the α-GLA (in females) in dried filter-paper blood spot samples.

Results
We haven't identified any pathogenic genetic variants in the α-GLA gene. However, in three patients with HCM, the two intronic SNPs within the α-GAL gene (c.640–16A>G [rs2071397] and c.1000–22C>T [rs2071228]) were identified.
Patient no. 1, a 64-year-old female, was admitted to our clinic for the diagnosis of obstructive HCM. She also had a transient 2:1 second degree atrioventricular block, an Adams-Stokes attack, angiokeratomas and left median cerebral artery lacunar stroke in middle age. In case no. 2, a 75-year-old female, were verified obstructive HCM, a 1st degree atrioventricular block, paroxysms of nonsustained ventricular tachycardia, acroparesthesia, pain in hands and angiokeratomas. In patient no. 3, a 41-year-old female, were established combined phenotypes (nonobstructive hypertrophic + restrictive), acroparesthesia, pain in hands and angiokeratomas.

Conclusions
In females with HCM, the intronic SNPs (rs2071397 and rs2071228) in the α-GLA gene can be associated with angiokeratomas and acroparesthesias.
P905Association of ionized serum magnesium with progression of aortic valve calcification
Authors: Mary A , Issa H , Boullier A , Henaut L , Avondo C , Brazier M , Mentaverri R , Tribouilloy C , Messika-Zeitoun D , Kamel S 
Published: October 2019

Abstract

Background
Calcific aortic valve disease (CAVD) is the most common heart valve disease among adults. It is a progressive disease whose final step leads to severe aortic stenosis (AS). Pharmacotherapeutic strategies aimed to limit the progression of valve leaflet calcification could be beneficial to slow-down the CAVD progression and to preserve left ventricular function. Several recent clinical studies demonstrated that lower serum magnesium (Mg) level is associated with vascular calcification. Whether serum magnesium is a determinant of aortic calcific stenosis progression remains unkwown.

Methods
In an ongoing prospective cohort of AS patients (COFRASA/GENERAC) we studied the association between serum Mg with the aortic valve calcification prevalence and progression. Serum Mg was measured at baseline in both its ionized (iMg) and total (tMg) forms. AS stenosis severity was evaluated at baseline and yearly thereafter using mean pressure gradient (MPG), the aortic valve area indexed to body surface (AVAi) assessed by echocardiography and the degree of aortic valve calcification (AVC) assessed by computed tomography. Annual progression was calculated as: (final measurement − baseline measurement)/follow-up duration.

Results
We enrolled 356 patients (73.1±10 years, 73% men), the mean follow-up duration was 2.5±2 years. There was a highly significant correlation between iMg and t Mg concentrations values (r=0.85, p<0.0001). Approximately 37% and 25% of patients have respectively iMg values ≤0.45 mmol/L (normal range 0.45–0.60 mmol/L) and t Mg ≤0.80 mmol/L (normal range 0.80–0.95 mmol/L). At baseline, lower i Mg and t Mg were significantly associated with sex, diabètes, lower heamoglobin and hypertension but not with AVC neither with MPG or AVAi. After mean follow-up of 2.5±2 years, the annual mean Log AVC progression was significantly greater (p=0.01) in patients with values of iMg ≤0.45 mmol/L (2,04±0.73) as compared to patients with iMg >0,45 mmol/L (1.78±0.94). Annual Mean MGP and AVAi also progressed greater in patients with low iMg but without reaching a significant level. Similar association was not found with tMg. In multivariate analysis, iMg remained significantly associated with the progression of AVC (odds ratio per 0.1 mmol/L increment [95% confidence interval] = 0.36 [0.15–0.83]; p=0.015) independently of age, tMg, glucose, type 2 diabetes, Tobacco use, baseline AVC, MPG and AVAi.

Conclusion
In a prospective cohort of asymptomatic patients with a wide range of AS severity, low serum ionized Mg but not low total Mg was independently associated with AVC progression.

Acknowledgement/Funding
ANR -RHU-STOPAS
P908Prognostic value of energy loss index in patients with low gradient severe aortic stenosis and preserved ejection fraction
Authors: Altes A , Ringle Griguer A , Bohbot Y , Bouchot O , Delelis F , Castel A L , Guerbaai R A , Ennezat P V , Graux P , Tribouilloy C , Marechaux S 
Published: October 2019

Abstract

Background
Assessment of pressure recovery adjusted indexed aortic valve area (AVAi) – energy loss index (ELI) – has been shown of prognostic interest for patients with asymptomatic and/or mild aortic stenosis (AS), but limited data are available in the setting of low gradient aortic stenosis (LG-AS).

Purpose
We hypothesized that among these patients with LG-AS, reclassification of AS severity as moderate by ELI may help to identify a subgroup of patients with moderate AS.

Methods
379 patients with low gradient severe AS (defined by AVAi ≤0.6 cm2/m2 and mean aortic pressure gradient (MPG) <40 mmHg) and preserved left ventricular ejection fraction (LVEF ≥50%) were prospectively included. Reclassification as moderate AS by ELI was defined as AVAi ≤0.6 cm2 /m2 but an ELI >0.6 cm2/m2. Clinical and echocardiographic features of patients reclassified by ELI were studied. Clinical outcomes were all-cause and cardiac mortality.

Results
148 patients (39%) were reclassified as moderate AS by ELI. By multivariable logistic regression analysis, patients being reclassified as moderate AS by ELI were associated with increased stroke volume index (SVi), absence of documented coronary artery disease and decreased body surface area, left indexed ventricular mass (all p<0.05). During a median follow-up of 34 months (30–38 months), 119 patients died, 52 of them from cardiac causes. Three-year survival free from all-cause or cardiac death were 76±4%, 96±2% for patients with moderate AS by ELI and 71±3%, 84±3% for patients with severe AS by ELI (p=0.178 and p=0.013, respectively). After adjustment for variables of prognostic interest including aortic valve replacement as a time-dependent covariable, there was a significant reduction of risk of cardiac mortality in patients with moderate AS by ELI (adjusted HR 0.44 [95% CI, 0.23–0.85]; p=0.014) but not for all-cause mortality (adjusted HR 0.85 [95% CI, 0.58–1.25]; p=0.403)

Conclusion
In patients with low gradient “severe” AS and preserved ejection fraction, calculation of ELI permits to reclassify almost 40% of patients as having moderate AS. Patients reclassified as moderate AS by ELI had a reduction of risk of cardiac mortality during follow-up but not for all-cause mortality. Calculation of ELI may be useful for decision making in AS patients with discordant grading and preserved ejection fraction.

Acknowledgement/Funding
Local funding
P913What can we expect after valve-in-valve procedures in failed transcatheter aortic valves?
Authors: Goppel G , Ruge H , Erlebach M , Deutsch O , Ziegelmueller J , Krane M , Lange R 
Published: October 2019

Abstract

Background/Purpose
With the growing use of transcatheter aortic valve replacement (TAVR), we need to determine if repeat TAVR (TAV-in-TAV) is comparable or even superior to surgical aortic valve replacement followed by TAVR (TAV-in-SAV). Although TAV-in-SAV procedures were shown to provide an almost complete sealing of paravalvular leakage at the expense of elevated gradients, data for TAV-in-TAV are lacking. Hence, we compared echocardiographic and clinical outcome in all TAV-in-TAV and TAV-in-SAV procedures in our institution between Oct. 2007 and July 2017.

Methods
130 consecutive valve-in-valve patients out of 2351 TAVR-patients were identified. 24 patients were excluded. Patient data were analysed from our prospectively collected, institutional database. 93% underwent routine out-patient follow-up at 12 months.

Results
75 TAV-in-SAV (75±8 years, male 60%; STS score 5.2±4.0%) and 31 TAV-in-TAV patients (78±8 years, male 65%; STS score 4.6±2.8%) formed the final study population. The type of TAV was similarly distributed in both groups (self-/balloon-expandable valves [%] 57/43 vs. 61/39) with transfemoral being the most frequent access site (68% vs. 87%). The mode of prosthesis failure was mainly stenosis in the TAV-in-SAV group (77%), whereas it was mainly intraoperative paravalvular regurgitation (90%) in the TAV-in-TAV group. 10% TAV-in-TAV patients (78±10 years, 33% male, STS score 5.1±1.5%) underwent redo-TAVR for prosthesis-degeneration after a mean time of 2614±862 days. The TAV-in-TAV group (90% single session vs. 10% staged: mean gradient 10±4 mmHg vs. 15±3 mmHg, p=0.096; aortic valve area 1.62±0.36 cm2 vs. 1.45±0.18 cm2, p=0.240) showed lower gradients and larger aortic valve areas (Table 1). No major intraprocedural complications occurred in either group. 30-day mortality was 0%.
Table 1 75 TAV-in-SAV discharge 31 TAV-in-TAV discharge p-value 69 TAV-in-SAV 12mFU 30 TAV-in-TAV 12mFU p-value AVA (cm2) * 1.18±0.32 1.61±0.35 <0.001† 1.21±0.36 1.63±0.43 <0.001† Peak Gradient (mmHg) 33±14 23±8 <0.001† 31±14 21±8 <0.001† Mean Gradient (mmHg) 19±8 12±5 <0.001† 18±9 11±4 <0.001† AR (0–3)** 0.4±0.5 0.8±0.7 0.003† 0.4±0.5 0.8±0.6 0.001† LV ejection fraction (%) 49±12 49±16 0.970 54±12 50±10 0.081 *AVA = Aortic valve area; **AR = Aortic regurgitation. 0 = none, 1 = mild, 2 = moderate, 3 = severe. †p<0,05 significant.

Conclusion
Indications for TAV-in-TAV differ from those for TAV-in-SAV. TAV-in-TAV results in significantly lower gradients and larger aortic valve areas with no relevant aortic regurgitation. Accordingly, failed TAV valves may be treated with TAV-in-TAV in the future.
P926Comparative safety and effectiveness of vitamin K antagonist and direct oral anticoagulants in patients with atrial fibrillation undergoing transcatheter aortic valve implantation
Authors: Butt J H , De Backer O , Olesen J B , Havers-Borgersen E , Gislason G H , Torp-Pedersen C , Sondergaard L , Kober L , Fosbol E L 
Published: October 2019

Abstract

Background
Data on the comparative safety and effectiveness of direct oral anticoagulants (DOACs) and vitamin K antagonists (VKAs) in patients with atrial fibrillation (AF) undergoing transcatheter aortic valve implantation (TAVI) are sparse.

Purpose
To examine the risk of thromboembolism, bleeding, and all-cause mortality in patients treated with DOACs versus VKAs.

Methods
Danish nationwide registries were used to identify all patients undergoing TAVI (2011–2016) with a history of AF and who were treated with oral anticoagulants. The risk of outcomes in patients treated with DOACs versus VKAs were examined by the Aalen-Johansen estimator and cause-specific Cox regression models.

Results
The study population comprised 762 patients (median age 82 [interquartile range 77–85], 52.9% men), of whom 216 (28.3%) and 546 (71.7%) patients were treated with DOACs and VKAs, respectively. The DOAC group was characterized by a higher prevalence of previous thromboembolism and a lower prevalence of chronic kidney disease compared with the VKA group. The distribution of age, sex, CHA2DS2-VASc and HAS-BLED score, and concomitant antiplatelet therapy was similar between groups. Compared with VKA, treatment with DOACs was not associated with a significantly different 3-year absolute risk of thromboembolism (9.5% [95% confidence interval [CI], 4.7%-16.2%] versus 7.7% [95% CI, 5.3%-10.8%] in the DOAC and VKA group, respectively), bleeding (5.3% [95% CI, 2.4%-10.0%] versus 6.3% [95% CI, 4.1%-9.0%]), and all-cause mortality (32.6% [95% CI, 21.9%-43.7%] versus 33.3% [95% CI, 28.3%-38.5%]). In adjusted analyses, treatment with DOACs, as compared with VKA treatment, was not associated with a significantly different risk of thromboembolism (hazard ratio [HR], 1.25 [95% CI, 0.61–2.57]), bleeding (HR, 1.22 [95% CI, 0.54–2.75]), and all-cause mortality (HR, 0.90 [95% CI, 0.60–1.35]).

Conclusions
In patients with atrial fibrillation undergoing TAVI, treatment with DOACs was not associated with a significantly different risk of thromboembolism, bleeding, and all-cause mortality compared with treatment with VKA.

Acknowledgement/Funding
None
P936Impact of left ventricular ejection fraction in patients with peripheral artery disease: from I-PAD registry
Authors: Fujimori K , Nagae A , Miura T , Katoh T , Hirabayashi M , Kashiwagi D , Yokota D , Yanagisawa T , Sakai T , Senda K , Saigusa T , Ebisawa S , Okada A , Motoki H , Kuwahara K 
Published: October 2019

Abstract

Introduction
In patients with peripheral artery disease (PAD) it is known that CVD is one of prognostic factors. But, it is unclear whether left ventricular ejection fraction (LVEF) affects prognosis of PAD patients. So we investigated that LVEF affects prognosis of PAD patients.

Methods
From July 2015 to July 2016, 371 consecutive PAD patients who performed endovascular treatment (EVT) were enrolled in I-PAD registry. We could conduct follow up survey about 337 (age 73.8±9.6, men 72.4%) patients and divided two groups according to their LVEF (group with LVEF≤40%, n=18, group without LVEF≤40%, n=319). The primary end point was major adverse limb events (MALE: TLR, TVR, major amputations) and secondary end point was all-cause death.

Results
The median follow-up period was 13.6±5.7 months. The 18 months MALE and all-cause death rate were significantly higher in the group with low LVEF than group without low LVEF (61.1% vs 21.6% p<0.001, 44.4% vs 11.6% p<0.001).

Conclusion
LVEF was significantly associated with MALE and all-cause death in patients with PAD.
P950Synergistic impact of renal failure and left ventricular dysfunction on short- and long-term mortality in patients with STEMI undergoing primary PCI
Authors: Pavlovic A S , Milasinovic D , Mehmedbegovic Z , Dedovic V , Jelic D , Zaharijev S , Zobenica V , Zivkovic I , Dudic J , Vukcevic V , Asanin M , Stankovic G 
Published: October 2019

Abstract

Background
Impaired left ventricular function (LV) and renal failure (RF) have both been separately associated with increased risk of mortality in ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).

Purpose
Our aim was to comparatively evaluate the relative impact of LV dysfunction and renal failure (RF) on the risk of mortality in primary PCI-treated STEMI patients.

Methods
5878 patients admitted for primary PCI during 2009–2015, from a prospectively kept, electronic registry of a high-volume catheterization laboratory, were included in the analysis. LV dysfunction was defined as EF<40%, and RF as estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 according to Cockcroft-Gault formula. Adjusted Cox regression models were used to assess 30-day and 3-year mortality hazard, with patients with EF≥40% and normal renal function serving as the reference group.

Results
RF was documented in 17.1% (n=1006), whereas 36.5% had LV dysfunction (n=2141). LV dysfunction and RF were separately associated with increased crude mortality rates, whereas the concurrence of both resulted in the highest mortality rate at 30 days (0.7% if no RF and normal EF vs. 5.4% if RF alone vs. 3.9% if EF<40% alone vs. 12.6% if both RF and EF<40%; p<0.001), and at 3 years (5.7% if no RF and normal EF vs. 29.0% if RF alone vs. 19.0% if EF<40% alone vs. 47.4% if both RF and EF<40%; p<0.001). After multivariable adjustment for other significant mortality predictors, such as age, previous stroke, diabetes, hyperlipidemia, anemia and Killip≥2, RF and LV dysfunction were associated with a comparable increase in mortality risk at 30 days (HR=4.1 and HR=3.7, respectively, p<0.001 for both) and at 3 years (HR=2.8 and HR=2.7, respectively, p<0.001 for both). Importantly, the combined presence of RF and low EF was independently associated with a marked increase in both 30- day (HR=6.5, 95% CI 3.7–11.4, p<0.001), and 3-year mortality (HR=4.3, 95% CI 3.3–5.6, p<0.001).
Kaplan Meier cumulative mortality curves

Conclusion
Apart from each being independently associated with an increased risk of mortality, the concurrence of renal failure and LV dysfunction had a synergistic negative impact on the prognosis of primary PCI-treated STEMI patients
P958Outcomes in nonagenarians with myocardial infarction who activate the primary PCI pathway
Authors: Meah M N U M , Joseph T J , Ding W Y D , Shaw M S , Hasleton J H , Palmer N D P , Velavan P V , Aggarwal S K A 
Published: October 2019

Abstract

Introduction
Current guidelines recommend immediate revascularisation in patients with ST elevation myocardial infarction (STEMI). However it remains unclear whether PPCI reduces mortality in nonagenarians. We aimed to compare mortality in nonagenarians, presenting via the PPCI pathway, who were managed medically (MM) versus those who underwent PCI.

Methods
Electronic records of every nonagenarian who presented as a PPCI activation between 2013–2018 were reviewed. Patients were divided into those who had PCI and those MM. Standard univariate and Kaplan Meier survival analyses were performed. We compared outcomes to an age and sex matched cohort using life tables from the Office for National Statistics (ONS).

Results
There were 157 nonagenarians presenting via the PPCI pathway, of which 111 were “true” myocardial infarction. Table 1 summarises baseline variables and comorbidities. The cohorts were generally well matched. Both groups had similar BCIS PCI 30-day mortality risk scores. The commonest reason to treat medically was presentation 12 hours after symptom onset. There was a trend towards increased 30-day mortality in the MM group. Kaplan Meier analysis (Figure 1) show the survival curves diverge immediately and reach statistical significance at 3 years. Compared to a matched population from ONS life tables, outcomes are worse in MM.
Table 1.S Admission variables & results PCI Group (n=42) Medically Managed Group (n=69) P-value Age 92 (91, 94) 93 (91, 95) 0.22 Female 21 (50.0%) 45 (65.2%) 0.11 Left ventricular failure (EF <45%) 27 (64.3%) 46 (66.6%) >0.99 Cardiogenic shock (Systolic BP <90mmHg) 4 (9.5%) 6 (8.7%) >0.99 Hx of hypertension 24 (57.1%) 45 (65.2%) 0.39 Hx of diabetes 5 (11.9%) 18 (26.1%) 0.07 Hx of chronic kidney disease 12 (28.6%) 25 (36.2%) 0.41 Hx of previous stroke 8 (19.1%) 15 (21.7%) 0.73 Hx of atrial fibrillation 1 (2.4%) 16 (23.2%) 0.003 Presented as non-STEMI 1 (2.4%) 12 (17.4%) 0.017 Presented as completed STEMI 2 (4.8%) 30 (43.5%) <0.001 BCIS PCI 30-day mortality risk 15.7 (14.3, 23.6) 17.5 (15.3, 22.3) 0.17 30-day mortality 10 (23.8%) 28 (40.6%) 0.07
Figure 1. Kaplan Meier Chart

Conclusions
Long term survival even in nonagenarians is significantly improved by timely PPCI when compared with medical management.