bluuebunny/crossref_metadata_2025 huggingface dataset:
2372Causes of death and effect of co-morbidities on mortality in young patients with heart failure. Data from the Swedish Heart Failure, Cause of Death and National Patient Registers
Authors: Basic C , Rosengren A , Dahlstrom U , Edner M , Zverkova Sandstrom T , Schaufelberger M
Published: October 2019

Background

The last two decades incidence and prevalence of heart failure (HF) among young patients have increased in Sweden. Up to the beginning of the 21st century mortality in patients with HF has decreased but causes of death and the effects of co-morbidity on mortality in young patients with HF are not well studied.

Purpose

To address causes of death and the effect of co-morbidity at baseline on mortality during the last decade in young patients with HF.

Methods

The Swedish Heart Failure Register (SwedeHF,) a nationwide quality register, was introduced in Sweden in 2003. All hospital discharge diagnoses are recorded in the National Patient Register (NPR) and deaths are registered in the Cause of Death Register. All patients ≥18 and <55 years with a HF diagnosis in SwedeHF were included and linked to the Cause of Death Register and NPR with the personal identification number. ICD 10-codes for all comorbidities and principal cause of death were identified during the observation period from 2003 to 2016. Besides, comorbidity and mortality data were compared with age and sex matched controls from the general population, database from Statistics Sweden (SCB).

Results

We identified 3752 (6.2%) patients <55 years from the total SwedeHF population (n=60,962) and added 7573 age and sex matched controls. There were 971 (25.9%) women and 2781 (74.1%) men mean age 44.9 (8.4) and 46.4 (7.3) years respectively. Among the young 604 (16.1%) patients died vs. 162 (2.2%) among matched controls (p<0.001) during the observation period. Principal cause of death was HF in 2.7% of the young patients (in men 3% vs. 1.4% in women (p=0.221)), other cardiovascular diseases 48.7% (27.7% in men vs. 20% in women (p=0.05)), congenital heart disease 4% (3% in men vs. 6.9% in women (p=0.077)), cancer 12.9% (9.6% in men vs. 23.6% in women (p=0.003)), neurologic disease 4.5% (5.4% in men vs. 1.4% in women (p=0.028)) suicide 0.8% (0.7% in men vs 1.4% in women (p=0.47)) and other causes 15.1% (15.9% in men vs 12.5% in women (p=0.179)) vs. 0, 26.5%, 1.2%, 32.7%, 1.2%, 9.9% and 18.5% in matched controls (all p<0.0001). The effect of co-morbidity at baseline on mortality in young patients with HF is presented in Figure 1.

Effect of co-morbidity on mortality

Conclusion

Compared to matched controls young patients with HF had worse survival. Almost one quarter of women with HF had cancer as a principal cause of death. Men with AF, obesity and depression at baseline had higher risk to die than women. Women with HF and hypertension, PAH or kidney disease at baseline had higher risk to die than men with HF and the same co-morbidities.

Acknowledgement/Funding

Swedish state under the agreement concerning research and education of doctors, The Swedish Heart and Lung Foundation, Västra Götaland Region grants
2410Oncologic radiotherapy-induced implantable cardioverter-defibrillator malfunctions: a real-time, in-vitro evaluation
Authors: Di Girolamo E , Faustino M , Furia N , Appignani M , Marini M , Genovesi D , Di Carlo C , Delana A , Barbareschi A , Falco M D
Published: October 2019

Background

Direct exposure of implantable cardioverter-defibrillators (ICDs) during radiotherapy is still considered not recommended, or even unsafe, by manufacturers and guidelines. The effects of photon beams on ICDs are unpredictable, depending on multiple factors, and malfunctions may occur during exposure.

Purpose

To evaluate transient ICD malfunctions by direct exposure to doses up to 10 Gy during low-energy radiotherapy, 33 contemporary wireless-enabled ICDs, with at least 4 months to elective replacement indicator (E.R.I.) were evaluated in a realtime in-vitro session.

Methods

All ICDs had baseline interrogation. Single chamber ICDs were programmed in the VVI/40 mode and dual or triple chamber ICDs were programmed in the DDD/40 mode. Rate response function and antitachycardia therapies were disabled, with the ventricular tachycardia (VT)/ventricular fibrillation (VF) detection windows still active. A centering computed tomography was performed to build the corresponding treatment plan and the ICDs were blinded randomized to receive either 2, 5 or 10 Gy exposure by a low photon-energy linear accelerator (6MV) in a homemade water phantom (600 MU/min). The effective dose received by the ICDs was assessed by an in-vivo dosimetry. During radiotherapy, the devices were observed in a real-time session using manufacturer specific programmer, and ICD function (pacing, sensing, programmed parameters, detection) was recorder by the video camera in the bunker throughout the entire photon exposure. All ICDs had an interrogation session immediately after exposure.

Results

During radiotherapy course, almost all ICDs (90.9%) recorded major or minor transient electromagnetic interferences. On detail, 13 ICDs (39.4%) reported atrial and/or ventricular oversensing, with base-rate-pacing inhibition and VT/VF detection. 16 ICDs (48.5%) recorded non clinically relevant noise, and no detections were observed. Only 4 ICDs (12.1%) reported neither transient malfunction nor minor noise, withstanding direct radiation exposure. At immediate post-exposure interrogation, the ICDs that recorded major real-time malfunctions had VT/VF detections stored in the device memory. In none of the ICDs spontaneous changes in parameter settings were reported. Malfunctions occurred regardless of either 2, 5 or 10 Gy photon beam exposure.

Conclusions

Transient electromagnetic interferences were observed in most of the contemporary ICDs during radiotherapy course, regardeless of photon dose. To avoid potentially life-threatening ICD malfunctions such as pacing inhibition or inappropriate shock delivery, magnet application on the pocket site or reprogramming devices in the asynchronous mode are still suggested in ICD patients ongoing even low energy radiotherapy exposure.

Acknowledgement/Funding

None
2417Elevated interleukin-6 and interleukin-18 concentrations predict residual inflammatory risk both before and after interleukin-1beta inhibition with canakinumab
Authors: Ridker P M , MacFadyen J , Thuren T , Libby P
Published: October 2019

Background

The Canakinumab Antiinflammatory Thrombosis Outcomes Study (CANTOS) established that targeting inflammation with interleukin-1b (IL-1b) inhibition can significantly reduce cardiovascular event rates in the absence of beneficial effects on cholesterol. Yet, CANTOS participants treated with both statins and canakinumab remain at considerable risk. Both interleukin-6 (IL-6, a central signaling cytokine) or interleukin-18 (IL-18, which like IL-1b requires the NLRP3 inflammasome for activation) may contribute to the recurrent events that occur even on canakinumab therapy, and thus represent novel targets for treating atherothrombosis.

Purpose

To assess the impact of canakinumab therapy on plasma levels of IL-6 and IL-18, and to assess the potential contributions of IL-6 and IL-18 to residual inflammatory risk both before and after treatment with canakinumab.

Methods

Plasma samples from 3,381 stable post-myocardial infarction patients assigned to active IL-1b inhibition within CANTOS underwent measurement of IL-6 and IL-18 both before and after initiation of canakinumab. All participants were followed over a 3.7 year period for major adverse cardiovascular events (MACE) and all-cause mortality.

Results

When compared to placebo, canakinumab significantly reduced IL-6 levels in a dose-dependent manner yielding placebo-subtracted median percent reductions in IL-6 at 3 months of 24.8, 36.3, and 43.2 percent for the 50mg, 150mg, and 300mg doses, respectively (all p-values <0.001). In marked contrast, no dose of canakinumab significantly altered IL-18 levels measured at 3 months (all effects less than 1 percent, all p-values >0.05). Yet, despite these differential plasma effects, both baseline and on-treatment levels of IL-6 and IL-18 associated with rates of future cardiovascular events and with all-cause mortality. For example, for MACE, each tertile increase in IL-6 measured 3 months after canakinumab initiation associated with a 42 percent increase in risk (95% CI 26–59%, P<0.0001) while each tertile increase in IL-18 measured 3 months after canakinumab initiation associated with a 15 percent increase in risk (95% CI 3–29% P=0.015). Similar effects were observed for MACE-plus, cardiovascular death, and all-cause mortality.

Conclusions

These randomized trial biomarker analyses from CANTOS demonstrate that interleukin-1b inhibition with canakinumab significantly reduces plasma levels of IL-6 but not IL-18, yet that there remains substantial residual inflammatory risk related to both IL-6 and IL-18. As such, our data support further pharmacologic development of potential anti-cytokine therapies for atherothrombosis that simultaneously inhibit IL-1b and IL-18 (such as NLRP3 inhibitors) as well as agents that directly target IL-6 signaling.

Acknowledgement/Funding

Novartis
P1217Zirconium-89 labelled probe for molecular imaging of inflammation in experimental atherosclerosis
Authors: Ahmed M , Tegnebratt T , Tran T , Damberg P , Bone D , Lu L , Gistera A , Tarnawski L , Hedin U , Eriksson P , Holmin S , Gustafsson B , Caidahl K
Published: October 2019

Background

Early detection of inflamed atherosclerotic lesions by molecular imaging might improve risk assessment beyond that of vascular stenosis and plaque morphology imaging, and improve the clinical management of high-risk patients.

Purpose

To target the key features of unstable atherosclerotic lesions, we studied the feasibility of our radiotracer, based on modified human serum albumin (HSA), to identify inflamed atherosclerotic lesions by in vivo molecular imaging.

Methods

We applied a maleylated HSA (Mal-HSA) probe, recognised by scavenger receptors on macrophages, in an experimental in vivo imaging study of atherosclerosis. Mal-HSA was coupled with a positron-emittingmetal ion, Zirconium-89 (89Zr). The targeting potential of this probe was evaluated and compared with unspecific 89Zr-HSA and 18F-FDG in a mouse model of atherosclerosis (Apoe−/−, n=22) and compared with wild-type (WT) mice (C57BL/6, n=21) as controls. Radiotracer accumulation in the aortic arch was analysed in vivo by the fusion of positron emission tomography–magnetic resonance imaging (PET-MRI), radiotracer bio-distribution was measured ex vivo by gamma counter, and plaque uptake was evaluated by phosphor imaging (PI) autoradiography (ARG).

Results

PET-MRI, gamma counter measurements, and PI-ARG showed the accumulation of 89Zr-Mal-HSA in the atherosclerotic lesions of Apoe−/− mice. The maximum standardised uptake value (SUVmax) for 89Zr-Mal-HSA at 16 and 20 weeks were 26% and 20% higher (P<0.05) in Apoe−/− mice than control WT mice, whereas no difference in SUVmax was found for 18F-FDG in the same animals. 89Zr-Mal-HSA uptake in the aorta as evaluated by gamma counter 48 h post-injection was 32% higher (P<0.01) for Apoe−/− mice compared to WT mice, and the aorta-to-blood ratio was 10-fold higher (P<0.001) for 89Zr-Mal-HSA compared with unspecific 89Zr-HSA. HSA probes were mainly distributed to the liver, spleen, kidneys, bone and lymph nodes. The PI-ARG results corroborated the PET and gamma counter measurements, showing higher accumulation of 89Zr-Mal-HSA in the aortas of Apoe−/− mice compared to WT mice; 9.4±1.4 vs 0.8±0.3% (P<0.001).

Conclusions

The modified HSA-based radiotracer showed in vivo targeting of inflamed atherosclerotic lesions of mouse aorta, which could also be verified ex vivo. 89Zr-Mal-HSA seems to be a promising diagnostic tool for the identification of vascular inflammation. Further methodological studies are needed to verify its applicability for detecting rupture-prone plaques.

Acknowledgement/Funding

Swedish Research Council (22036); the Swedish HLF (20150423, 20170669); ALF (20150517, 447561, 726481); Söderberg Foundations, VINNOVA and KI
P1221Effect of transcatheter aortic valve implantation on cardiac sympathetic nervous function assessed by 123I-metaiodobenzylguanidine scintigraphy in patients with severe aortic stenosis
Authors: Kadoya Y , Zen K , Tamaki N , Ito N , Kuwabara K , Yamano M , Yamano T , Nakamura T , Yaku H , Matoba S
Published: October 2019

Background

Cardiac sympathetic nervous (CSN) function assessed by 123I-metaiodobenzylguanidine (MIBG) scintigraphy is associated with poor prognosis in patients with heart failure.

Purpose

The aim of this study was to investigate the effects of transcatheter aortic valve implantation (TAVI) on CSN function in patients with severe aortic stenosis (AS) using MIBG scintigraphy.

Methods

This was a single-center prospective observational study that enrolled patients between July 2017 and July 2018. Among 77 registered patients who scheduled to undergo TAVI, 35 patients (7 men; mean age: 87 years) were evaluated. The MIBG scintigraphy was performed at baseline and 6 months after TAVI procedure to evaluate the heart-mediastinum ratio (H/M) and washout rate (WR). The MIBG parameter changes were compared with B-type natriuretic peptide (BNP) levels and echocardiographic parameters, including aortic valve area (AVA), peak velocity (Vmax), mean pressure gradient (PG), and left ventricular ejection fraction (LVEF).

Results

All patients successfully underwent TAVI with improved BNP level (388±341 pg/mL vs. 167±118 pg/mL, p<0.001). The AVA, Vmax, mean PG and LVEF improved after TAVI (0.6±0.2 cm2 vs. 1.6±0.5 cm2, p<0.001; 4.6±0.8 m/s vs. 2.1±0.3 m/s, p<0.001; 54±20 mmHg vs. 9±3 mmHg, p<0.001; 58±11% vs. 63±9%, p=0.01, respectively). In the MIBG imaging, the delayed H/M significantly increased (2.5±0.6 vs. 2.6±0.7, p=0.03), and the WR decreased (32±8% vs. 29±8%, p=0.047) after TAVI. There was a correlation between the changes in the MIBG parameters and the change in mean PG from baseline to 6 months (delayed H/M: r=0.391, p=0.02; WR: r=0.347, p=0.04). Multivariate logistic regression analysis showed that baseline mean PG was an independent predictor of improved both delayed H/M and WR (odds ratio=1.062; 95% confidence interval: 1.009–1.137; p=0.042).

Conclusions

TAVI can improve the CSN function in patients with AS. Such CSN improvement was related with hemodynamic changes.

Acknowledgement/Funding

None
P1228Impact of history of vascular disease on lipoprotein(a) associations with cardiovascular outcomes: a Mendelian randomisation study in 283,658 UK Biobank participants
Authors: Stiby A , Clarke R , Parish S , Hopewell J C
Published: October 2019

Background

Mendelian randomisation (MR) studies have been widely used to assess the causal relevance of risk factors for disease and to elucidate the likely effects of novel drug targets. MR studies have confirmed the causal relevance of lipoprotein(a) [Lp(a)] for risk of coronary heart disease (CHD), but the impact of prior vascular disease on these associations remains unclear, and is potentially important when testing the effects of Lp(a) lowering therapies.

Purpose

To examine the associations of LPA variants, as a proxy for Lp(a) levels, with risk of CHD, ischaemic stroke and peripheral vascular disease (PVD), by history of vascular disease in UK Biobank (UKB).

Methods

An LPA genotype score was constructed in 283,658 unrelated white British UKB participants, using 2 SNPs (rs3798220 and rs10455872) previously shown to be independently associated with, and explain ∼40% of the variance in, Lp(a) levels. The LPA score was tested for association with hospitalisation for CHD (n=23,165), presumed ischaemic stroke (n=2,579) and PVD (n=3,780) using Cox PH models. Estimated hazard ratios (per LPA variant) for cardiovascular outcomes are reported both overall and by history of vascular disease (CHD, ischaemic stroke or PVD) at baseline.

Results

As observed in previous studies, LPA was associated with a higher risk of CHD (Hazard ratio [HR] 1.27 per LPA variant; 95% CI: 1.24–1.31). However, the effect was substantially attenuated in participants with versus without prior vascular disease (p-interaction = 3x10–5; Figure). The effect of the LPA score on PVD was comparable to that for CHD (p-heterogeneity = 0.25), whilst the effect on ischaemic stroke was significantly weaker than that for CHD (p-heterogeneity = 6x10–3). As for CHD, the effects of the LPA score on both ischaemic stroke and PVD were weaker in those with versus those without prior vascular disease. Furthermore, the heterogeneity between the effects on cardiovascular outcomes was more extreme when stratified by history of CHD.

Conclusions

This MR study shows that the effects of LPA on risk of CHD, ischaemic stroke and PVD are weaker in individuals with a history of vascular disease, perhaps reflecting the effects of medications used in this setting. Therefore, MR studies in the general population may overestimate the anticipated effects of Lp(a)-lowering therapies in randomised trials, which are typically conducted in individuals with prior vascular disease.

Acknowledgement/Funding

British Heart Foundation
P1239His-bundle pacing in CHF-patients with narrow QRS and chronic AF using dual-chamber ICD
Authors: Slawuta A , Boczar K , Zabek A , Ciesielski A , Hiczkiewicz J , Vijayaraman P , Malecka B , Gajek J
Published: October 2019

The heart rate regularization is crucial for proper treatment of patients with atrial fibrillation and congestive heart failure. The standard resynchronization can be applied, but in patients with narrow QRS this procedure is of no use.

The aim of our study is to assess the efficacy of direct His-bundle pacing in patients with congestive heart failure and chronic atrial fibrillation using dual chamber ICD implanted for prevention of sudden cardiac death.

Methods

The study population included 78 patients with CHF and chronic AF: group A - 56 pts treated with direct His-bundle pacing using atrial port of dual chamber ICD and group B - 22 patients implanted with single chamber ICD as recommended by the guidelines. The patients in group B constituting clinical controls were derived from the Heart Failure Outpatients Clinic with established clinical status and pharmacotherapy.

Results

The demographic data, clinical characteristics and echocardiography measurements at baseline and during follow-up were presented in the table:

Table 1 Group A Group B P value Age (years) 69.7±6.9 66.7±11.3 n.s. Sex (% of male sex) 84.0 86.4 n.s. Ventricular pacing (%) – 46.3±31.2 – His-bundle pacing (%) 81.7±9.2 – – pre post pre post pre vs. post LVEDD (mm) 66.9±4.9 59.9±4.7 64.8±8.0 64.7±8.1 <0.01 n.s. EF (%) 29.6±3.8 43.6±5.9 28.1±6.1 28.8±7.3 <0.01 n.s. NYHA class 2.7±0.6 1.4±0.6 2.5±0.6 2.0±0.2 <0.05 n.s. B-blocker dose (metoprolol equivalent dose) 104.6±41.6 214.3±82.6 78.3±56.6 103.1±49.2 <0.001 <0.05

During 12-months of follow-up the mean values of NYHA functional class, EF and LV dimensions did not change in group B but significantly improved in group A. The physiological His-bundle based pacing enabled optimal beta-blocker dosing. The studied groups had no tachyarrhythmia at baseline so the presumable atrial fibrillation-related harm depends on the rhythm irregularity.

Conclusions

His-bundle-based pacing in CHF-chronic AF patients contributes to significant echocardiographic and clinical improvement. Standard single-chamber ICD implantation in CHF-chronic AF patients yields only SCD prevention without influence on remodeling process. The CHF-patients with narrow QRS and chronic AF benefit from substantially higher beta-blockade which can be instituted in His-bundle pacing group.
P1254Stroke severity and subsequent mortality are worse with atrial fibrillation than in patients without atrial fibrillation
Authors: Vinding N E , Kristensen S L , Roerth R , Butt J H , Oestergaard L , Olesen J B , Torp-Pedersen C , Gislason G , Koeber L , Fosboel E L
Published: October 2019

Background

Data on stroke severity and prognosis in patients with AF are lacking and contemporary knowledge thereon could help identify preventive strategies.

Purpose

To investigate stroke severity among patients with and without AF, and secondly determine in-hospital and 1-year mortality in the two groups.

Methods

Using the nationwide Danish Stroke Registry we identified patients with first-time stroke (1 January 2005–31 December 2016). Patients with prior or new AF were matched 1:1 by sex, age, and calendar-year with patients with no history of AF. Stroke severity on admission was determined by the Scandinavian Stroke Scale (SSS) (0–29 points indicates very severe to severe stroke, 30–58 points indicates moderate to mild stroke) based on eye movements, paralysis and level of consciousness. The Kaplan-Meier estimator was used to calculate cumulative risk of death in AF patients versus non-AF patients. Risk of 1-year mortality was evaluated in an adjusted multivariable Cox-proportional hazard model.

Results

We identified 90,042 patients with first-time stroke; 16,186 (18.0%) had prior or new AF, and were included in the study, and matched with patients without AF. The median age was 80 years (p25-p75: 72–86 years) and 52.2% were females. AF patients had a higher comorbidity burden and more severe strokes compared with non-AF patients (median SSS 44 (p25-p75: 25–54) vs. 49 (p25-p75: 36–56), P value <0.0001) and higher proportion with very severe to severe stroke (SSS 0–29) (29.7% versus 19.1%, P value <0.0001). In-hospital mortality was higher among AF-patients versus non-AF patients (11.3% vs 7.8%, P value <0.0001). Crude 1-year cumulative risk of death was higher among AF-patients versus non-AF patients (32.3%,95% CI: 31.6%-33.1% vs. 22.9%, 95% CI: 22.2%-23.6%, P value <0.0001) (Figure 1), and this difference remained significant after adjustment (hazard ratio 1.34, 95% CI 1.28–1.40, P value <0.0001).

Conclusion

In a nationwide contemporary stroke registry cohort, AF was associated with adverse stroke severity compared with stroke patients without AF. In-hospital mortality and 1-year mortality was higher among AF patients compared with non-AF patients.

Acknowledgement/Funding

This study was supported by an internal grant from Department of Cardiology, Copenhagen University Hospital, Rigshospitalet, Denmark
P1473Global work efficiency 3 months after ST-segment elevation myocardial infarction: prevalence and characteristics of patients with reduced global work efficiency
Authors: Lustosa R , Van Der Bijl P , El-Mahdiui M , Montero-Cabezas J , V Kostyukevich M , Ajmone Marsan N , J Bax J , Delgado V
Published: October 2019

Background

Global work efficiency (GWE) is an index of left ventricular function derived from echocardiographic speckle tracking derived strain-pressure loops. GWE is calculated as constructive work divided by the sum of constructive and wasted work and expressed as a percentage. The prevalence of reduced GWE after ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) is unknown.

Aims

To assess GWE in STEMI patients 3 months after the index admission and report on the prevalence and characteristics of patients with impaired GWE.

Methods and results

This retrospective study included 150 patients (111 men, mean age: 60±10 years) with STEMI. They were divided into GWE normal and GWE reduced groups, based on reference values from the EACVI NORRE study. Reduced GWE was observed in 23% of patients. Those with reduced GWE had significantly higher values of CK [3033.62 U/L (±2003.47) vs. 1308.47 U/L (±1309.07); P<0.001] and troponin T [8.43 μg/L (±6.73) vs. 3.49 μg/L (±4.36); P<0.001)] at baseline, as well as significantly higher left ventricular end-diastolic volume [112 ml (±32) vs. 90 ml (±30); P<0.001] and left ventricular end-systolic volume [62 ml (±21) vs. 39 ml (±17); P<0.001] and significantly lower values of left ventricular ejection fraction [46% (±8) vs. 59% (±8); P<0.001] and impaired global longitudinal strain [−13.03% (±2.54) vs. −18.04% (±2.75); P<0.001] at 3 months (Table 1).

Table 1. Patient characteristics GWE normal (N=116) GWE reduced (N=34) P value Age (years) 60 (±10) 58 (±11) 0.224 HR (bpm) 69 (±13) 74 (± 13) 0.063 SBP (mmHg) 138 (±17) 138 (±21) 0.920 DBP (mmHg) 81 (±12) 84 (±15) 0.214 Maximum CK value at baseline (U/L) 1308.47 (±1309.07) 3033.62 (±2003.47) <0.001 Maximum Troponin at baseline (μg/L) 3.49 (±4.36) 8.43 (±6.73) <0.001 Left ventricular end-systolic volume (ml) 39 (±17) 62 (±21) <0.001 Left ventricular end-diastolic volume (ml) 90 (±30) 112 (±32) <0.001 LVEF (%) 59 (±8) 46 (±8) <0.001 GLS (%) −18.04 (±2.75) −13.03 (±2.54) <0.001

Conclusions

Almost one fourth of STEMI patients treated with primary PCI have impaired GWE at 3 months follow-up. Patients with reduced GWE had larger myocardial damage than those with preserved GWE at 3 months.
P1507Role of adjuvant carotid ultrasound in women undergoing stress echocardiography for the assessment of suspected angina with no previous history of coronary artery disease
Authors: Gurunathan S , Shanmuganathan M , Hampson R , Khattar R , Senior R
Published: October 2019

Introduction

Traditional risk assessment tools classify the majority of women at low risk despite cardiovascular disease remaining the leading cause of death in women. Additionally conventional stress testing techniques have poor predictive value in women, due to unique pathophysiological mechanisms causing ischaemia in women, and the lower prevalence of obstructive CAD. The study sought to evaluate the role of adjuvant carotid ultrasound (CU) in women attending for stress echocardiography (SE).

Methods and results

415 women (Mean age 62±10 years, 28% Diabetes Mellitus, Mean BMI 28) attending for SE prospectively underwent CU, to assess Carotid Intima-media thickness (CIMT) and the presence of plaque.

47 women (11%) had inducible wall motion abnormalities, and carotid disease (CD) was present in 46% (Carotid plaque in 41%, 15% CIMT >75th percentile). Women with CD were older (65 vs 58 years, p<0.0001), more likely to have Diabetes (41% vs 21%, p=0.0001) and hypertension (67% vs 36%, p<0.01), and had higher pretest probability of CAD (59% vs 41%, p<0.0001). 40% of women classified as low Framingham, were found to have evidence of CD. Conversely, only 40% of women classified as high Framingham risk, had CD.

The positive predictive value of SE for flow-limiting CAD was 51%, but the presence of carotid plaque improved this to 71% (p<0.01). Of all clinical and test parameters, carotid plaque (p=0.001) and SE result (p=0.01) were the only independent predictors of >70% angiographic.

Conclusion

CU significantly improves the accuracy of SE alone for identifying flow-limiting disease on coronary angiography. Non-invasive assessment of subclinical atherosclerosis using CU offers an individualized disease-guided approach in women, where conventional scoring systems offer modest risk stratification.
P1539Aortic pulse wave velocity measured by an oscillometric device independently predicts all-cause mortality in a cohort of 4146 subjects
Authors: Lenkey Z , Illyes M , Kahan T , Boutouyrie P , Laurent S , Molnar F T , Schillaci G A , Viigimaa M , Cziraki A
Published: October 2019

Objectives

Assessment of carotid-femoral pulse wave velocity by applanation tonometry independently predicts all-cause and cardiovascular mortality. However, there has been a need for a simpler, user-independent measurement with a validated device, that is applicable even in the primary care setting.

Methods and subjects

4146 subjects (49% men) aged 35–75 years were measured in multiple centers in Hungary. Subjects visited the outpatient department of these centers on their own initiative. The measurement of aortic pulse wave velocity (PWVao) with Arteriograph was performed in addition to taking past medical history, physical examination and laboratory tests. The mean follow-up time of the study was 5.5 years. The number of events (all cause mortality) were provided by the Hungarian National Health Insurance Fund. Cox regression analyses were used to identify predictive factors for this endpoint.

Results

The mean age of the study population was 53 years, brachial systolic and diastolic blood pressure were 137±20 and 82±11 mmHg, and heart rate was 70±10 1/min. The mean value of SCORE was 3 in this large cohort. 410 subjects had a registered cerebro-or cardiovascular event before the measurement, the number of smokers was 656 (16%), 1974 subjects were treated with at least one anti-hypertensive drug (48%), while the number of subjects on lipid-lowering, antidiabetic or antiplatelet medication were 807 (19%), 352 (8%) and 398 (17%), respectively. There were 116 fatal events during a mean follow-up of 5.5 years. According to the Cox regression, PWVao is a significant and independent predictor of all cause-mortality and in univariate analysis, a 1.0 m/s increase in PWVao was associated with HR 1.7 [1.47–1.98; p<0.001], for this endpoint.

Conclusion

Aortic pulse wave velocity measured by an invasively validated, simple, oscillometric device predicted all-cause mortality in a large cohort of relatively young subjects of the general population that may improve risk stratification even in the everyday clinical practice or primary care setting.
P1543Causes of death in patients with myocardial infarction, and non-ischemic myocardial injury
Authors: Kadesjo E , Roos A , Siddiqui A J , Sartipy U , Holzmann M J
Published: October 2019

Background

Information about causes of death in patients with non-ischemic acute and chronic myocardial injury is limited.

Purpose

To explore causes of death, mortality rates and risks of cardiovascular and non-cardiovascular causes of death in patients with type 1 MI (T1MI), type 2 MI (T2MI), and acute and chronic myocardial injury compared with patients without myocardial injury.

Methods

From a cohort of 39,558 patients who visited the ED at our University Hospital during 2011–2014 and who had high-sensitivity cardiac troponin T (hs-cTnT) levels measured, we identified 3,853 patients with hs-cTnT levels above the 99th percentile value and categorised them into the following groups: i) T1MI, ii) T2MI, iii) acute and iv) chronic myocardial injury. Among these we included all patients who died during follow-up. Causes of death were obtained from the Swedish Cause-of-Death register. All deaths among patients without myocardial injury (n=819) from the same cohort were used for comparison. We calculated incidence rates of cause-specific deaths in the different groups and used logistic regression to estimate odds ratios (OR) with 95% confidence intervals (CIs) adjusted for age and sex for different causes of death, using patients without myocardial injury as referent.

Results

2,285 patients died during follow-up at a mean age of 76 (±13) years of whom 46% were female. Patients without myocardial injury died at a younger age (mean 70 years) compared with patients in the groups with myocardial injury (mean 79–82 years). The proportion of cardiovascular (CV) deaths were considerably higher in patients with T1MI (48%), T2MI (39%), acute (43%), and chronic (45%) myocardial injury compared with patients with no myocardial injury (25%). 42% of patients without myocardial injury died from cancer, compared with 18% to 24% among patients with different myocardial injury. Age- and sex-adjusted incidence rates for CV-death were similar for T1MI, T2MI and acute myocardial injury (27 per 100 person-years), slightly lower in patients with chronic myocardial injury (22 per 100 person-years) and almost half in patients with no myocardial injury (14 per 100 person-years). The adjusted ORs with 95% CIs for CV death were highest in patients with T1MI (1.99, 1.48–2.69) and acute myocardial injury (1.72, 1.29–2.11), while only marginally lower in patients with T2MI and chronic myocardial injury (1.43, (0.94–2.16), and 1.65, (1.29–2.11) respectively).

Conclusions

Patients with T1MI and acute or chronic myocardial injury have similar risks to die from cardiovascular causes. Patients without myocardial injury died younger and the proportions of cancer-related deaths were twice as high as in the groups with myocardial injury. Proportions and risks of CV-death among patients with T2MI were higher than in patients without myocardial injury, but lower than in patients with T1MI and acute or chronic myocardial injury.

Acknowledgement/Funding

None
P1563CHA2DS2-VASc score predicts mortality and readmission in octogenarian patients with non-ST-segment elevation myocardial infarction
Authors: Vera Sainz A , Diez Villanueva P , Ariza Sole A , Formiga F , Martinez Selles M , Alegre O , Sanchis J , Marin F , Vidan M , Lopez Palop R , Abu Assi E , Bueno H , Alfonso F
Published: October 2019

Background

CHA2DS2-VASc Score is widely used to predict thromboembolic risk in patients with Atrial Fibrillation (AF). We ought to study if this score predicts outcomes in elderly patients with Non ST-segment Elevation Myocardial Infarction (NSTEMI).

Methods

The multicenter LONGEVO-SCA prospective registry included 532 unselected patients with NSTEMI aged ≥80 years. Data to calculate CHA2DS2-VASc Score were available in 523 patients (98.3%). They were classified according to CHA2DS2-VASc Score: group 1 (score 0–4), and 2 (5–9). We studied outcomes in terms of mortality or readmission at 6 months follow-up.

Results

A total of 266 patients (51%) had a high CHA2DS2-VASc Score (group 2). They were more often women, with more cardiovascular risk factors like hypertension or diabetes mellitus, and history of previous stroke and cardiovascular disease and heart failure (all, p=0.001). Geriatric syndromes (Barthel Index, Lawton Brody, cognitive impairment and frailty) and Charlson index were worse in this group (all, p=0.001). They had poorer clinical status on admission, with worse Killip class and lower left ventricle ejection fraction (all, p=0.001), and developed new onset AF more often during admission (12.4% vs. 6.6%, p=0,024). At six months follow-up, patients in group 2 had higher reinfarction, all cause mortality, and mortality or readmission rates (all, p=0.001). (Table) A CHA2DS2-VASc Score >4 predicted mortality (HR 2,60 [95% CI 1,48–4,55], p<0,001) (Figure 1) and was associated with mortality or readmission at 6 months (HR 2.07 [CI 95% 1.51–2.84], p<0.001).

CHADS VASC2 0–4 (n=257) CHADS >4 (n=266) p Geriatric syndromes   Barthel Index 94 (13) 85 (22) 0.001   Lawton brody 6.2 (2) 4.9 (3) 0.001   Charlson Index 1.5 (1) 3.3 (2) 0.001 Cognitive impairment 0.001   No 201 (79.1) 155 (58.7)   Mild 49 (19.3) 100 (37.9)   Severe 4 (1.6) 9 (3.4) Nutritional risk (MNA-SF*) 122 (48) 149 (57.1) 0.040 Frailty (FRAIL scale) 0.001   Non-frail 111 (43.2) 69 (25.9)   Prefrail 102 (39.7) 101 (38)   Frail 44 (17.1) 96 (36.1) Outcomes at 6 months   Reinfarction 26 (6.9) 16 (13.9) 0.018   Mortality or readmission 111 (28.9) 60 (50.4) 0.001   All cause mortality 38 (9.9) 24 (20.2) 0.003

Conclusions

A CHA2DS2-VASc sore>4 is present in half of octogenarians with NSTEMI and is associated with a poor outcome.
P1566Identification of the cardiovascular threshold limit for serum uric acid. Analysis from a general Italian population
Authors: Virdis A , Casiglia E , Masi S , Desideri G , Tikhonoff V , Muiesan M L , Grassi G , Borghi C
Published: October 2019

Background

Serum uric acid (SUA) is increasingly recognised as an important predictor of cardiovascular disease (CVD) and total mortality. However, the levels of SUA that discriminate across the different strata of risk for CVD and total mortality remain unknown, complicating the identification of subjects at high or low mortality risk for SUA in clinical practice.

Purpose

In this study we used a large Italian population comprising >3ehz748.0326 subjects to assess the threshold of SUA that increases the risk of total and CVD mortality.

Methods

The URic Acid Right for heArt Health (URRAH) study is a regional-basis multicentre cohort study which collected data from prospective studies and databases from different hypertension centres, including subjects with at least one measure of SUA and a follow-up of about 20 years. Total mortality was defined as mortality for any causes, cardiovascular mortality as death due to fatal myocardial infraction, stroke or heart failure. Multivariate dichotomic logistic and Cox regression models were used to confirm the relationship between SUA and mortality status both from cardiovascular and any causes, while ROC curves were used to identify the threshold of SUA that better discriminated people at higher or lower mortality risk.

Results

A total of 22.275 subjects had SUA and mortality information. Logistic regression identified a direct and strong association between SUA and an increased risk of total (OR 1.176, 95% CI 1.127–1.227) and CVD (OR 1.147, 95% CI 1.093–1.203) mortality, independently of other CVD risk factors (age, BMI, LDL cholesterol, diagnosis of diabetes, hypertension, chronic kidney disease, alcohol consumption and smoking). Cox models confirmed the presence of an independent association between SUA and any causes (HR 1.123, 95% CI 1.090–1.567) and CVD (HR 1.124, 95% CI 1.081–1.169) mortality. ROC curve analysis identified a cut-off value od SUA [(4.79 mg/dL (95% CI 4.7–5.4 mg/dl)] able to discriminate total mortality status, and a different one [(5.60 mg/dL (95% CI 5.09–5.89 mg/dl)] able to identify CVD mortality status. Multivariate Cox analysis adjusted for confounders confirmed that subjects with SUA >4.79 mg/dl had a significantly higher total mortality (HR 1.293, 95% CI 1.181–1.416) compared to those with SUA <4.79 mg/dl, independently of covariables. Similarly, subjects with SUA >5.60 mg/dl had a significantly higher CVD mortality (HR 1.428, 95% CI 1.273–1.600) than those with SUA <5.60 mg/dl after adjustment for the same confounders.

Conclusion

Levels of SUA that increase the risk of total and CVD mortality are significantly lower than those commonly used for the definition of hyperuricemia in clinical practice. Our data provide the first large evidence of a level of “cardiovascular” SUA that might be used in clinical practice to identify subjects at greater risk of total and CVD mortality.
P1573Chemotherapy-induced vasotoxicity in patients undergoing therapy for breast cancer
Authors: Anastasiou M , Antonopoulos A S , Oikonomou E , Zagouri F , Siasos G , Vogiatzi G , Tsalamandris S , Mistakidi C V , Psaltopoulou T , Bamias A , Dimopoulos M , Tousoulis D
Published: October 2019

Background

Cardiotoxicity is a well-known adverse effect of anthracycline and HER-2 monoclonal antibodies, however the vascular effects of these agents remain less-well studied.

Purpose

To explore the effects of breast chemotherapy on vascular function.

Methods

A total of 57 female patients undergoing breast diagnosed with breast cancer and scheduled for anthracycline-based and HER-2 chemotherapy were included in this study. At baseline, at 3, 6 and 12 months, patients underwent assessment of cardiac function by transthoracic echocardiography, endothelial function assessment by brachial flow mediated dilation (FMD) and assessment of arterial stiffness by carotid-radial pulse wave velocity (PWV) and augmentation index (Aix).

Results

There was a significant decrease in left ventricular ejection fraction (LVEF) overtime compared to baseline (A). This was paralleled by a significant decrease in brachial FMD at 6 months (B) and a significant increase in PWV compared to baseline (C). There was no significant change in Aix compared to baseline levels (D). Chemotherapy-induced cardiotoxicity (expressed by the change in LVEF) was not associated with either the change in FMD or PWV at 6 months.

Conclusions

Breast chemotherapy-induced cardiotoxicity is paralleled by vasotoxicity, which is manifested as endothelial dysfunction and increased arterial stiffness. Systemic vasotoxicity is not directly related to cardiotoxicity, suggesting that monitoring of both cardiac and vascular function could be useful in identifying early signs of cardiovascular toxicity.
P1577Incidence, etiologies and predictors of 30-day readmission after percutaneous coronary intervention in end-stage renal disease patients; Analysis from national readmission database
Authors: Hassan H , Krittanawong C , Jazner S , Rangaswami J , Bozorgnia B , Amanullah A
Published: October 2019

Background

End stage renal disease (ESRD) is a known risk factor for coronary artery disease (CAD). The association of ESRD with short-term readmissions after percutaneous coronary intervention (PCI) has not been well studied.

Purpose

This study aims to examine he 30-day readmission rate, predictors of readmission and etiologies of readmission in ESRD patients after PCI.

Methods and results

The Healthcare Cost and Utilization Project National Readmission Database encompassing 722 US hospitals was used to identify index PCI cases in ESRD patients ≥18 years old. Hierarchical regression analyses were used to examine the factors associated with risk of 30-day readmission and higher cumulative costs.

Results

We evaluated 96,869 hospitalized patients who survived to discharge after PCI from January through November 2014 and analyzed unplanned readmissions over 30 days after discharge. A total of 11,624 patients (12%) were readmitted within 30 days. Among the readmitted patients, majority of readmissions were due to non-cardiac causes. Nineteen percent had congestive heart failure (HF), 11% had PCI, 2% had coronary artery bypass surgery, and 1.5% died during the readmission. Acute respiratory failure (21%) and infections (14%) compromised majority of non-cardiac causes. Predictors of increased readmissions were female sex (odds ratio (OR) 1.09, 95% confidence interval (CI) 1.01- 1.0, p<0.001), infections (OR 2.06, 95% CI 1.44–2.4, p<0.001), diabetes (OR 1.91, 95% CI 1.07–2.63, P<0.001), chronic lung disease (OR 3.16, 95% CI 2.11–4.2, p<0.001), chronic liver disease (OR 1.96, 95% CI 1.1–2.23, p<0.001), acute HF (OR 1.17, 95% CI 1.12–1.22, p<0.001) and anemia (OR 1.09, 95% CI 1.06–1.13, p<0.001).

Conclusion

ESRD patients are at high risk of 30-day readmissions after PCI. Although majority of patients are readmitted with non-cardiac causes, HF and repeat PCI were the most common cardiac etiologies of readmissions. Female sex, infections, chronic liver and lung diseases are independently associated with high risk of 30-day readmission in ESRD patients after PCI.

Acknowledgement/Funding

None
P1581Early blood pressure reduction by intravenous vasodilators associates with acute kidney injury in patients with hypertensive acute decompensated heart failure
Authors: Arao Y , Sawamura A , Nakatochi M , Oishi H , Kato H , Yamaguchi S , Haga T , Kuwayama T , Yokoi T , Hiraiwa H , Kondo T , Morimoto R , Okumura T , Murohara T
Published: October 2019

Background

In patients with hypertensive acute decompensated heart failure (ADHF), intravenous vasodilators are commonly used. However, little is known about optimal use in blood pressure (BP) management to avoid acute kidney injury (AKI).

Purpose

To investigate the association between systolic BP (SBP) changes in first 6 h and incidence of AKI within 48 h in patients with hypertensive ADHF.

Methods

Post-hoc analysis was performed on a prospectively enrolled cohort. We investigated 245 patients with ADHF and SBP >140 mmHg on arrival (mean age, 76 years; 40% female). We defined “SBP-fall” as maximum percent reduction in SBP 6h after intravenous treatment. AKI was defined as serum creatinine (SCr) ≥0.3 mg/dL, or urine output <0.5 mL/kg/h at 48 h.

Results

Mean SBP, SBP-fall and SCr level at arrival were 180 mmHg, 29.4%, and 1.21 mg/dL, respectively. Sixty-six patients experienced AKI. There were no significant differences in age, NYHA functional class, SBP and SCr at admission between AKI and Non-AKI group. AKI group had the greater SBP-fall compared with Non-AKI (36.7%versus 27.2%, p≤0.0001). Logistic regression analyses revealed that SBP-fall had an independent predictor of AKI (Table). In addition, SBP-fall had positive association with the number of concomitant used intravenous vasodilators in first 6 h (Figure).

Logistic regression analyses for AKI Univariate Multivariate AUC OR 95% CI P OR 95% CI P Ages, years, per 10 years 1.04 0.82–1.33 0.17 0.75 SBP at arrival, per 10 mmHg 1.01 0.93–1.11 0.77 SBP-fall, per 10% 1.49 1.22–1.81 <0.001 1.54 1.24–1.91 <0.001 HR, per 10 beat/min 1.12 1.00–1.25 0.049 1.07 0.95–1.21 0.28 COPD 2.95 1.06–8.21 0.04 3.06 0.99–9.43 0.054 SCr, per 1 mg/dL 1.40 0.83–2.37 0.21 Furosemide i.v. 1.12 0.42–2.95 0.82 Carperitide 3.22 1.69–6.13 0.0002 4.39 2.16–8.93 <0.001 NTG/ISDN i.v. 0.97 0.54–1.74 0.92 CCB i.v. 1.86 0.76–4.53 0.18 OR, odds ratio; CI, confidence interval; AUC, area under the curve; SBP, systolic blood pressure; COPD, chronic obstructive pulmonary disease; SCr, serum creatinine; i.v., intravenous; NTG, nitroglycerin; ISDN, isosorbide dinitrate; CCB, calcium channel blocker.

SBP-fall odds ration for AKI

Conclusion

In the first 6h of management for hypertensive ADHF patients, aggressive SBP reduction by the combination use of vasodilator agents predicted the incidence of AKI.
P1588Beta-blocker therapy and risk of dementia: a population-based prospective study
Authors: Holm H , Ricci F , Di Martino G , Bachus E , Nilsson E D , Ballerini P , Melander O , Hansson O , Nagga K , Magnusson M , Fedorowski A
Published: October 2019

Introduction

Cerebral side effects have long been recognized as complications to beta-blocker treatment. However, evidence of a longitudinal relationship between the use of beta-blockers and incident dementiais still controversial.

Objective

To evaluate the longitudinal relationship between use of beta-blockers, as a class, and incident risk of all-cause dementia, vascular dementia, Alzheimer and mixed dementia.

Methods

From the prospective, population-based, Malmö Preventive Project, 18,063 individuals (mean age 68.2, males 63.4%) were included at baseline and followed for 84,506 person-years. Patients with prevalent cerebrovascular disease and dementia were excluded. In order to weight the risk of incident dementia associated with beta-blocker consumption, we performed propensity score matching analysis, resulting in 3,720 matched pairs of beta-blocker users and non-users at baseline, and multivariable Cox proportional-hazardsregression.

Results

Overall, 122 study participants (1.6%) were diagnosed with dementia over the course of follow-up. Use of beta-blockers was independently associated with increased risk of developing vascular dementia, regardless of confounding factors (HR: 1.72, 95% CI 1.01–3.78; p=0.048). Conversely, treatment with BB was not associated with increased risk of all-cause, Alzheimer and mixed dementia (HR: 1.15; 95% CI 0.80–1.66; p=0.44; HR: 0.85; 95% CI 0.48–1.54; P=0.59 and HR: 1.35; 95% CI 0.56–3.27; p=0.50, respectively).

Conclusions and relevance

We observed that use of beta-blockers, as a class, is associated with increased longitudinal risk of vascular dementia in the general elderly population, regardless of cardiovascular risk factors, prevalent or incident history of atrial fibrillation, stroke, coronary events and heart failure. Further studies are needed to confirm our findings in the general population and to explore the mechanisms underlying the relationship between use of beta-blockers and increased risk of vascular dementia.