bluuebunny/crossref_metadata_2025_split huggingface dataset:
P5278Myocardial abnormalities in people living with Human Immunodeficiency Virus (PLWH) detected using cardiovascular magnetic resonance (CMR)
Authors: Manmathan G P R , Kotecha T , Chacko L , Brown J , Little C , Knight D , Kinloch S , Barber T , Johnson M A , Burns F , Fontana M A , Rakhit R D 
Published: October 2019

Abstract

Background
Antiretroviral therapy (ART) has dramatically improved the prognosis in PLWH with survival nearing that of HIV negative people. PLWH may develop significant comorbidities as they age including cardiovascular disease (CVD) such as myocardial infarction, sudden cardiac death, heart failure, as well as subclinical evidence of myocardial inflammation. Overall, ART treated patients are at an increased CVD risk with some studies quoting a 2.2 fold relative risk.

Aim
To assess the incidence of functional, structural and tissue characterisation changes in PLWH using CMR with multiparametric mapping

Methods
39 PLWH (34 men, mean age 55.8±10.9, mean duration of HIV 17.8±9.29 years) and 29 healthy volunteers (20 men, mean age 45.1±8.3) underwent CMR with late gadolinium enhancement (LGE) imaging, T1 and T2 mapping.

Results
Of PLWH, only 7 scans (18%) were normal. LV ejection fraction was significantly lower and LV mass significantly higher compared to controls. Native T1, a marker of diffuse fibrosis or increased myocardial water content was no different between the groups. T2, a more specific marker of myocardial oedema, was elevated in PLWH. Sixteen PLWH (41%) had evidence of LGE including 8 with an ischaemic pattern (7 sub-endocardial and one transmural) and 8 with a non-ischaemic pattern (5 with mid-wall enhancement and 3 with RV insertion point LGE. No controls had evidence of LGE.
Student t-Test: PLWH versus controls PLWH (n=39) Control (n=29) P-value LVEF (%) 59±15 67±5 <0.01 iLVM 79±24 56±13 <0.01 Native T1 (ms) 1021±52 1001±41 0.116 T2 (ms) 48±2 46±2 <0.05 LGE 16 (41%) 0 (0%) <0.001 LVEF (%) = Left Ventricular Ejection Fraction; iLVM = Indexed Left Ventricular Mass (g/m2); LGE = Late Gadolinium Enhancement.

Conclusion
This study identifies a number of cardiac changes associated with HIV and prolonged treatment with ART. The elevated LV mass may be associated with hypertension, commonly found in PLWH. The elevated myocardial T2 compared to controls may be due to chronic inflammation associated to prolonged HIV exposure. There was no evidence of diffuse fibrosis but focal areas of non-ischaemic scar were a common finding which may relate to previous myocarditis or HIV-related cardiomyopathy. A fifth of PLWH also had evidence of previous myocardial infarction.
We propose to image asymptomatic PLWH to further classify, diagnose and treat a vulnerable group of patients who are now described as having a normal life expectancy.
P5282Comparison of cardiovascular magnetic resonance ejection fraction and left ventricular volumes by long axis feature tracking strain analysis versus standard short axis stack contour tracing
Authors: Vasquez M , Puntmann V , Nagel E 
Published: October 2019

Abstract

Introduction
Cardiovascular magnetic resonance (CMR) feature tracking (FT) is based on the recognition of endocardial features obtained during standard CMR cine imaging to be tracked and followed throughout the cardiac cycle. Global longitudinal strain (GLS) has been proposed as a superior measure for diagnosis and prognosis than ejection fraction (EF). However, EF remains an important primary parameter to describe cardiac function. A rapid determination of GLS based on three long axis views (LAX) allows for a simultaneous calculation of EF without additional imaging or post-processing promising a significant reduction of scan and post-processing time.

Purpose
The purpose of this work is to compare the LV volumes and EF obtained during assessment of GLS based on CMR feature tracking with standard analysis of a short axis (SAX) stack used as the reference standard.

Methods
75 consecutive patients underwent a routine clinical scan obtaining a full SAX stack as well as 3 standard LAX views using either 3-Tesla or 1,5-Tesla clinical scanners. We determined LV volumes and EF based on the reference standard as well as feature tracking analysis with additional GLS. A p value <0.01 was considered statistically significant.

Results
Mean EF was 45.9% using standard SAX (range, 13%-72%) and 51.1% using triplanar feature tracking (r=0.950; p<0.0001, figure 1A). Bland-Altman analysis showed a systematic bias of 5,27%; without proportional bias (figure 1B). End-diastolic volumes (r=0,975; p<0.0001) and end-systolic volumes (r=0.985; p<0.0001) demonstrated similar results. Mean GLS was −17.3% (range: −30,7% to −3,3%) and was significantly correlated with standard EF (r=−0,884; p<0.0001). Classification of EF into categories: reduced, mid-range or preserved (<40%, 40–49%, ≥50%) remain unchanged in 79% of patients when using EF by feature tracking analysis. Twelve of 16 reclassifications occurred in the mid-range category.
Figure 1

Conclusion
There is a good correlation between EF obtained by rapid post-processing of GLS with EF based on a full SAX stack resulting in an identical categorization in 79% of patients. Reduction of EF within the mid-range might be best assesses by the standard SAX stack.
P5316Birthweight, childhood growth patterns and left ventricular structure at midlife: Northern Finland 1966 Birth Cohort Study
Authors: Korpela N , Kaikkonen K , Auvinen J , Tulppo M P , Junttila J , Perkiomaki J , Jarvelin M.-R , Huikuri H V , Kiviniemi A M 
Published: October 2019

Abstract

Background
Higher cardiac left ventricular (LV) mass (LVM) has independently been associated with cardiovascular risk and mortality. Changes in LV structure have been observed in children with obesity. However, information about the long-term influence of early growth on LV structure is limited.

Purpose
To explore the associations between early growth patterns, specifically birth weight, age and body mass index (BMI) at infant BMI peak and at childhood BMI rebound, and LV structure at midlife.

Methods
At the age of 46, a sample of the participants of the Northern Finland Birth Cohort 1966 took part in follow-up examinations. A randomly selected subpopulation was enrolled to echocardiographic examinations (n=1124). BMI at various ages in childhood was calculated from frequent anthropometric measurements collected from child welfare clinical records. Age and BMI at BMI peak (n=541, mean age 9.0 months) and at BMI rebound (n=657, mean age 5.8 years) were derived from random effect models.

Results
Birth weight (n=1124), BMI at BMI peak and at BMI rebound were directly associated with LVM (beta [standardized]: 0.171, 0.186 and 0.223, respectively, p<0.001 for all) and LVM index (LVMI) (beta: 0.146, 0.120 and 0.120, respectively, p<0.01 for all) at midlife. All the associations, except that between BMI at BMI peak and LVMI, remained significant after adjustments for gender, adult blood pressure, heart rate, antihypertensive medications, heart diseases and diabetes (p<0.05 for all). Significant interaction between gender and age at BMI rebound was observed in LVMI. Age at BMI rebound was inversely associated with LVMI in both genders, the association being stronger in males (beta: −0.212, p<0.001) compared to females (beta: −0.117, p=0.025) and independent of potential confounders. There were direct univariate associations of birth weight and BMI at BMI peak and rebound with LV relative wall thickness (p=0.009–0.019), which were largely explained by potential confounders. However, the association of birth weight with LV relative wall thickness retained its significance even after relevant adjustments (beta: 0.097, p=0.001). After additional adjustments for adult BMI, only associations of birth weight and BMI at BMI peak with LVM remained significant, which, however, did not remain significant after additional adjustment for adult height.

Conclusions
This study shows that birth weight and early growth patterns are associated with LV structure at midlife, which is largely explained by adult BMI. Therefore, the relationship between early growth patterns to LV structure in the adulthood may be largely explained by their strong tracking to obesity and related cardiovascular risk factors at midlife and to some extent by normal somatic growth.
P5323HDL-C and all-cause mortality in a high-risk population: impact of LDL-C
Authors: Dhindsa D , Sandesara P B , Liu C , Topel M , Mehta A , Allard-Ratick M , Sperling L , Quyyumi A 
Published: October 2019

Abstract

Background
Previous studies have shown increased cardiovascular (CV) risk with both high (>60mg/dl) and low concentrations of high-density lipoprotein cholesterol (HDL-C). The effect of elevated HDL-C levels (>60mg/dL) at differing LDL-C concentrations on outcomes is unknown.

Purpose
To study the relationship between elevated HDL-C levels (>60mg/dl) in relation to LDL-C concentration (greater vs less than 70mg/dL) and adverse CV outcomes in an at-risk population.

Methods
Participants included 5,746 individuals (mean age 63.3±12.4 years, 35% female, 23% African American) enrolled in the cardiovascular biobank. Individuals were stratified by HDL-C categories (<30, 31–40, 41–50, 51–60 and ≥60 mg/dL) and LDL-C categories (≥70 and <70 mg/dL). A Cox proportional hazards model was used to examine the association between HDL-C and adverse outcomes, with HDL-C 41–50 mg/dL as the reference group. All models were adjusted for age, race, sex, body mass index, hypertension, smoking, triglycerides, heart failure history, myocardial infarction (MI) history, diabetes, angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker use, beta blocker use, statin use, aspirin use, estimated glomerular filtration rate, obstructive coronary artery disease.

Results
Over a median follow-up of 6.2 years (25th-75th percentiles = 3.3–8.0 years), a total of 286 MIs, 691 CV deaths and 1,093 all-cause deaths occurred. Individuals with HDL-C ≥60 mg/dL (n=632) had an increased risk of all-cause mortality with an LDL-C ≥70mgdL (HR 1.59; 95% CI=1.10–2.29, p=0.013) after adjustment for the aforementioned variables. This association was not statistically significant with LDL-C <70mg/dL (HR 1.16; 95% CI 0.60–1.21, p=0.66). There was no statistically significant difference for CV death or MI at elevated HDL-C in either group.

Conclusion
Elevated HDL-C levels is associated with increased all-cause mortality with an LDL-C ≥70mg/dL, though does not appear to be associated with worse outcomes when LDL-C is <70mg/dL.
P5326Effect of evolocumab on lipoprotein(a) levels: results across 15 studies
Authors: Toth P P , Jones S R , Monsalvo M L , Elliott-Davey M , Lopez J A G , Banach M 
Published: October 2019

Abstract

Background/Introduction
Elevated levels of lipoprotein(a) (Lp[a]) have been associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD). Elevated Lp(a) is relatively refractory to lifestyle change and pharmacologic intervention.

Purpose
To examine the effect of evolocumab on Lp(a) in a range of clinical trial populations, including hypercholesterolaemia/mixed dyslipidaemia, statin-intolerance, diabetes mellitus, and heterozygous familial hypercholesterolaemia (HeFH) at different timepoints up to 5 years.

Methods
Fifteen phase 2 and phase 3 double-blind and open-label extension studies, with a minimum 12 weeks duration that used approved doses of evolocumab (140 mg every 2 weeks [Q2W] or 420 mg once monthly [QM]) were included in this analysis. Studies were pooled on the basis of patient population, duration, and comparator groups (of which the MENDEL-1, -2, GAUSS-1, -2, and LAPLACE-2 atorvastatin cohort studies employed ezetimibe comparators). The effect of evolocumab on percent change from baseline in Lp(a) was examined.

Results
In short-term studies, evolocumab led to a median percent change in Lp(a) from baseline to week 12 of −21.2% to −33.3% overall (Table). Results were similar for both evolocumab doses with median percent change ranging from −22.0% to −38.2% for 140 mg Q2W and −20.0% to −33.3% for 420 mg QM. In long-term studies (1 to 5 years), percent change in Lp(a) ranged from −23.8% to −33.3%.
Patient populations Percent change from baseline in Lp(a), median (Q1, Q3), % Ezetimibe comparator trials Placebo comparator trials Evolocumab Ezetimibe Evolocumab Placebo 12-week studies   Hypercholesterolaemia/mixed dyslipidaemia (YUKAWA-1, -2, LAPLACE-TIMI-57, LAPLACE-2, MENDEL-1, -2) −22.0 (−39.4, 0.0), n=760 0.0 (−11.8, 14.6), n=387 −26.3 (−44.7, −5.0), n=1838 0.0 (−10.4, 15.4), n=1179   Statin intolerance (GAUSS-1, -2) −23.1 (−42.0, −3.3), n=223 0.0 (−16.7, 3.6), n=126 – –   HeFH (RUTHERFORD-1, -2) – – −21.2 (−38.1, −7.0), n=263 0.0 (−4.2, 15.3), n=150   Type 2 diabetes (BANTING, BERSON) – – −33.3 (−55.6, −16.7), n=833 0.0 (−16.2, 16.7), n=425 Long-term studies   1-Year (DESCARTES) – – −28.4 (−49.2, −6.0), n=535 −5.5 (−20.5, 0.9), n=272   2-Year (OSLER-2)†‡ −23.8 (−44.4, 0.0), n=3077 – – –   5-Year (OSLER-1)† −33.3 (−51.3, −11.1), n=941 – – – †All patients received evolocumab in the OSLER studies. ‡OSLER-2 was a 3-year study; however, only 2-year data were available for Lp(a).

Conclusion
Evolocumab reduces Lp(a) in a variety of patient populations at 12 weeks with sustained lowering over 5 years.

Acknowledgement/Funding
Amgen Inc.
P5327Are we being able to meet current guidelines LDL-cholesterol goals in very high risk patients? How many of them could benefit of PSCK9 inhibition by the FOURIER/ODYSSEY and NICE criteria?
Authors: El Andere T , Soto J A T , Moreira I S , Wamser M N , Freitas H C , Almeida M P C , Goncalves R M , Zatz H P , Araujo D B , Sulzbach M L , Bertolami A , Faludi A A 
Published: October 2019

Abstract

Background/Introduction
With increasing evidence of LDL-cholesterol (LDL-c) lowering and a subsequent reduction in cardiovascular events, guidelines of different parts of the world aim for lower LDL-c goals by risk stratification. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition has been able to reduce up to 60% LDL-c levels, with further reduction in cardiovascular outcomes.

Purpose
Our aim was to evaluate the proportion of very high risk patients in a tertiary cardiology center that met LDL-c goal of less than 50mg/dL proposed by the Brazilian Society of Cardiology (BSC) guidelines. Furthermore, we assessed the number of patients that were receiving adequate statin intensity therapy and could benefit from PCSK9 inhibition by the FOURIER/ODYSSEY and by the National Institute for Health and Care Excellence (NICE) criteria.

Methods
We screened 2180 consecutive patients from March, 2018 to February, 2019 for cardiovascular risk factors, cholesterol and glycemic levels, and current medical therapy at use. Patients were stratified by level of risk, and compliance to recommended statin therapy was evaluated. We then analyzed how many of the very high risk patients, that were in use of high intensity statin therapy, met the inclusion LDL-c levels of the FOURIER/ODYSSEY trials (≥70mg/dL) and the NICE recommendations (≥140mg/dL) for the introduction of PCSK9 inhibitors.

Results
Of the 2180 patients enrolled to our study, 1225 (56.2%) patients were at very high cardiovascular risk level. Of these patients, 136 (11.1%) met LDL-c BSC guideline levels. Using the LDL-c target of 70mg/dL, an additional 320 (26.1%) patients were below target range. When analyzing statin therapy at use, 913 (74,5%) were receiving adequate statin therapy. Of the very high risk patients in adequate statin treatment, 617 (65.9%) by the FOURIER/ODYSSEY criteria and 88 (9.4%) patients by the NICE criteria would benefit from PCSK9 inhibitors.

Conclusions
With lower LDL-c goals, achievement of optimal LDL-c levels is now a challenge for current clinical practice. Even though many patients are receiving adequate guideline-based statin therapy, difficulty remains in achieving optimal treatment, especially in the higher risk stratum. These patients would benefit from PCSK9 inhibition, being the NICE criteria, a more cost-effective strategy, still applicable in a substantial portion of our patients.
P5329Montreal score and coronary artery calcification in the prediction of cardiovascular event in patients with familial hypercholesterolemia
Authors: Miname M , Bittencourt M S B , Jannes C E J , Pereira A C P , Krieger J E K , Santos R D S 
Published: October 2019

Abstract

Introduction
Familial hypercholesterolemia (FH) is characterized by elevated levels of LDL-C and early cardiovascular disease (CVD). However, the risk of CVD in HF is variable. The Montreal score was designed to stratify cardiovascular risk in the FH population. Coronary calcium score (CAC) is a tool that can be used to optimize CVD risk assessment in FH.

Purpose
The objective of this study is to evaluate whether CAC is superior to the Montreal score in cardiovascular risk discrimination in FH.

Methods
We Included 206 patients with molecular diagnosis of FH (36.4% men, mean age 45±14 years, mean baseline LDL-C: 269±70 mg/dL). All patients underwent CAC and were treated with maximum tolerated statin therapy. We evaluated cardiovascular risk factors and calculated Montreal score as prior publication. Cox regression analysis was performed to test the association of CAC with the incidence of cardiovascular events. CAC was transformed into LogCAC + 1 to optimize the distribution of the CAC as previously described. Area under the ROC curve was calculated for Montreal score and CAC.

Results
Patients were followed by a median of 3.7 years (interquartile range: 2.7 to 6.8 years). Mean Montreal score was 22±8, median of 22. CAC was positive in 105 individuals (51%) and 15 CVD events (7.2%) had occurred. Montreal score above the median was associated with CAC (OR: 8.36, 95% CI: 4.47–15.62, p<0.001), and there was a gradient of increase in the Montreal score with CAC increase (mean Montreal score for CAC = 0, CAC 1–100, CAC>100: 17±7, 23±7, 30±4, p<0.001). Univariate analysis showed that the following variables were associated with CVD occurrence: male gender, family history of early coronary disease, corneal arcus, HDL-c (protective), logCAC + 1 and Montreal score. Multivariate analysis was performed: model 1 with Montreal score and logCAC + 1, only logCAC + 1 was associated with the occurrence of CVD (RR: 3.886; 95% CI: 2.112–7.148, p<0.001). Model 2 with family history of early coronary disease, corneal arcus, logCAC + 1 and Montreal score, only the latter was not associated with the occurrence of CVD. CAC presents greater area under the ROC curve for CVD event discrimination compared to the Montreal score: 0.839 versus 0.685, p=0.0074.

Conclusion
The Montreal score is associated with CAC in FH, however CAC is superior than this clinical score in predicting the occurrence of CVD in FH.
P5330Evaluating lipid-lowering and anti-atherogenic effect of injectable curcumin in a rabbit model of atherosclerosis
Authors: Momtazi-Borojeni A A , Banach M , Majeed M , Sahebkar A 
Published: October 2019

Abstract

Background and purpose
The present study was aimed to evaluate lipid-lowering and anti-atherogenic effect of an intravenous (IV) curcumin in the rabbit fed high cholesterol diet (HCD).

Methods
New Zealand white male rabbits (4–6 months old, n=25, weight 2.286±0.256 kg)were fed on a normal chow enriched with 0.5% (w/w) cholesterol for 5 weeks. Atherosclerotic rabbits were randomly divided into three group, including a control group receiving intravenous (IV) injection of saline buffer, two treatment groups receiving IV injection of curcumin at two different dosages, 1and 10 mg/kg/week, for 4 weeks. Blood samples were collected from fasted rabbits at pre- (week 5) and post-treatment (week 11) points for analysis of serum lipid levels, including low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), triglyceride (TG), and total cholesterol (TC). Aortic arch atherosclerotic lesions were assessed using hematoxylin and eosin (H&E) staining.

Results
To evaluate curcumin's effects on the hyperlipidemic states and atherosclerosis plaque, HCD-fed rabbits were weekly treated with the injectable curcumin at the low (1mg/kg/week) and high (10 mg/kg/week) doses by 4 weeks. At week 4 in compared with the control group, low-dose curcumin could reduce serum levels of LDL-c, HDL-c, TG, and TC by −6.22% ±1.77, −35.24% ±12.49, −29.84% ±10.14, −14.19% ±5.19, respectively. In the case of high-dose curcumin, serum levels of LDL-c, HDL-c, TG, and TC were changed by −44.36%±3.24, 14.05% ±6.39, −25.92% ±5.57, −56.59% ±10.22, respectively, when compared with the control group at week 4. Low-dose curcumin after 4 weeks' treatment could reduce serum levels LDL-c, HDL-c, TG, and TC up to 103±28 mg/dL, 18.33±4.66 mg/dL, 97.5±31 mg/dL, and 356.5±19.5 mg/dL, respectively, when compared with the base line levels (week 0). High-dose curcumin after 4 weeks' treatment could decrease serum levels of LDL-c, HDL-c, TG, HDL-c, and TC up to 207±17.04 mg/dL, 15.5±0.5 mg/dL, 333±40 mg/dL, and 514.5±22.23 mg/dL, respectively (Figure). H&E staining declared that atherosclerotic lesion grades were significantly lower in the curcumin-treated groups than the control group.
Changes of lipids in rabbits on curcumin

Conclusions
The injectable curcumin at the low (1mg/kg) and high (10 mg/kg) could significantly improve dyslipidemia and alleviate atherosclerotic lesion in HCD-induced atherosclerotic rabbits.