bluuebunny/crossref_metadata_2025_split huggingface dataset:
1108Effectiveness of nursing counseling for patients with cardiovascular risk factors: controlled clinical trial with a 24 months post-intervention follow-up
Authors: Salazar A , Vilchez-Barboza V , Saez K , Paravic T 
Published: October 2019

Abstract

Objective
To establish the effect after 24 months of a face-to-face and telephone nursing counseling intervention, aimed at controlling cardiovascular risk factors (hypertension, dyslipidemia and overweight) and improving health-related quality of life (HRQoL) in patients of the cardiovascular health program of family health centers of Concepciόn, Chile.

Methods
Randomized controlled clinical trial with a 24 months post-intervention follow-up. 120 patients with cardiovascular risk factors under the cardiovascular health program were recruited from 6 family health centers and randomized into a control group (60) and an intervention group (60). The intervention group received the regular care in addition to face-to-face and telephone nursing counseling. Baseline measurements were taken and also at the end of the intervention (7 months). Participants returned then after 12 and 24 months for follow-up evaluations. A total of 109 subjects completed the intervention at 7 months and 45 returned at 24 months. During follow-up evaluations both groups continued to receive regular care given in the health centers. The measurements consisted of HRQoL (physical and mental health), systolic blood pressure (SBP) and diastolic blood pressure (DBP), body mass index (BMI), abdominal circumference (AC), total cholesterol (TC), low density lipoproteins (LDL-Chol), high density lipoprotein (HDL-Chol), atherogenicity index (LDL/HDL), cardiovascular risk factor (TC/HDL), 10-year coronary risk. Ethical requirements were considered and statistical analysis was carried out using MANCOVA and d-Cohen repeated measurements.

Results
The analysis of the effects of the intervention in the 24-month follow-up showed that subjects in the intervention group only maintained significant improvement of AC over time (F=3.18; p=0.03), compared to the control group.

Conclusion
Although participants in the intervention group only maintained the AC improvement over time, this can be regarded as an indirect indicator of the presence of intra-abdominal fat that makes it possible to predict and classify the risk of cardiovascular disease. Long-term follow-up studies are required to investigate behaviors and mechanisms that contribute to maintaining improvements in this indicator. Additionally, future research should include reinforcement activities, either face-to-face or by telephone, to help maintain the positive results of interventions.

Acknowledgement/Funding
Universidad de Concepciόn 214.082.049-1.0
1181Role of rho-mdia1 signaling to maintain cardiac function in response to pressure overload in mice
Authors: Abe I , Terabayashi T , Teshima Y , Ishii Y , Miyoshi M , Kira S , Kondo H , Saito S , Yufu K , Takahashi N , Ishizaki T 
Published: October 2019

Abstract

Background
Cardiac hypertrophy is a compensatory response to pressure overload that leads to heart failure. Recent studies have shown that Rho signaling has crucial regulatory roles in actin cytoskeleton rearrangement during cardiac hypertrophic responses. Rho is rapidly activated in response to pressure overload, but the mechanisms by which Rho and its downstream proteins control actin dynamics during hypertrophic responses remain unclear.

Objective
To identify the essential roles of mDia1 (Rho-effector molecule) in pressure overload-induced ventricular hypertrophy.

Methods and results
Male wild-type (WT) and mDia1-knockout (mDia1KO) mice (10–12 weeks old) were subjected to transverse aortic constriction (TAC) or a sham operation. The heart weight/tibia length ratio, cardiomyocyte cross-sectional area, left ventricular wall thickness, and expression of hypertrophy-specific genes were significantly decreased in mDia1KO mice 3 weeks after TAC, and the mortality rate was higher at 12 weeks. Echocardiography and the pressure-volume loop indicated that mDia1 deletion increased the severity of heart failure 8 weeks after TAC. Microarray gene expression profiling showed that the induction of immediate early genes due to the TAC operation was significantly lower in mDia1KO mice than WT mice, as was the activation of extracellular signal-regulated kinase (ERK) and focal adhesion kinase (FAK). We examined the role of mDia1 in neonatal rat ventricular cardiomyocytes (NRVMs) exposed to mechanical stress. The siRNA-mediated silencing of mDia1 attenuated stretch-induced ERK and FAK phosphorylation, and gene expression of c-fos. Importantly, loss of mDia1 suppressed an increase in the F/G-actin ratio in response to pressure overload in the mice. In addition, increases in nuclear myocardin-related transcription factors (MRTFs) and serum response factor (SRF) were perturbed in response to pressure overload in mDia1KO mice and to mechanical stretch in mDia1 depleted NRVMs.

Conclusions
Rho-mDia1, through actin dynamics, plays critical roles in pressure overload-induced hypertrophy by regulating ERK and FAK phosphorylation and the transcriptional activity of MRTF-SRF.
1199Reduction in blood pressure following renal denervation for patients with differing baseline cardiovascular risk
Authors: Mahfoud F , Mancia G , Schmieder R , Narkiewicz K , Ruilope L , Schlaich M , Williams B , Fahy M , Bohm M 
Published: October 2019

Abstract

Background
Lowering blood pressure (BP) reduces clinical events. Renal denervation (RDN) is under investigation for treatment of uncontrolled hypertension and might represent a particularly attractive option for patients with high cardiovascular (CV) risk. To evaluate this proposal, it is important to determine whether baseline CV risk impacts the efficacy of RDN in lowering BP.

Purpose
We evaluated whether BP changes after RDN were dependent on baseline CV risk.

Methods
AHA/ACC Atherosclerosis CV Disease (ASCVD) risk score was calculated for patients in the Global Symplicity Registry (GSR; NCT01534299), a global registry of RDN in patients with uncontrolled hypertension, using baseline office systolic BP, total/HDL cholesterol measurements, diabetic and smoking status, gender, age, and number of baseline anti-hypertensive medications. Patients were separated into 3 groups based on ASCVD risk scores: <10%, ≥10% and <20% and ≥20%. Baseline demographics and 24-hour systolic BP changes at 6 months and 1, 2 and 3 years were compared between groups, as well as rates of adverse events at 3 years.

Results
Individual ASCVD risk scores were calculated for 1,434 patients in GSR. The median ASCVD risk score was 19.4% and 403 patients had a risk score of <10%, 326 a risk score of ≥10 and <20%, and 705 a risk score ≥20%. Patients with ASCVD risk score ≥20% had a higher baseline office systolic BP, were significantly older, and had higher rates of prior myocardial infarction and/or diabetes (all p<0.0001 compared to patients with lower risk scores). RDN reduced BP similarly across all groups of patients. Changes in 24-hour systolic BP at 6 months and 1, 2 and 3 years are shown in Figure 1. Adverse events at 3 years are shown in Table 1.
Adverse events at 3 years ASCVD risk score <10% ASCVD risk score ≥10% & <20% ASCVD risk score ≥20% p-value (N=265) (N=224) (N=468) Death 3 (1.1) 5 (2.2) 41 (8.8) <0.0001 Cardiovascular death 3 (1.1) 2 (0.9) 23 (4.9) 0.0017 Myocardial infarction 6 (2.3) 6 (2.7) 11 (2.4) 0.9513 Stroke 8 (3.0) 9 (4.0) 24 (5.1) 0.3894 Hospitalization for new onset heart failure 4 (1.5) 7 (3.1) 26 (5.6) 0.0194 Values are proportions reported as n (%).

Conclusions
BP changes after RDN were similar for patients with varying baseline ASCVD risk scores, suggesting uniform BP-lowering efficacy of RDN regardless of patients' baseline CV risk. The impact of baseline risk on clinical event reduction by RDN-induced BP reduction will need to be evaluated in further studies.

Acknowledgement/Funding
The Global SYMPLICITY Registry is funded by Medtronic.
1410Clinical predictors of NT-proBNP response to early initiation of sacubitril/valsartan after hospitalisation for decompensated heart failure: An analysis of the TRANSITION study
Authors: Pascual-Figal D , Bao W , Senni M , Wachter R , Behlolavek J , Chakrabarti A , Noe A , Schwende H , Butylin D , Prescott M 
Published: October 2019

Abstract

Background
NT-proBNP has diagnostic and prognostic value in patients with heart failure (HF). Compared with enalapril, sacubitril/valsartan (S/V) significantly reduced NT-proBNP within 1 week (wk) of administration and reduced HF re-hospitalisation in patients with acute decompensated HF (ADHF) in PIONEER-HF. Identification of predictors of NT-proBNP reduction with S/V could aid prognostication following hospitalisation.

Methods
TRANSITION (NCT02661217) is an open label study in stabilised ADHF patients with HFrEF that compared S/V initiation pre- versus post-discharge (within 2 wk of discharge). Baseline NT-proBNP was measured at randomisation in both S/V groups (n=950). Clinical predictors of favourable response of NT-proBNP to S/V therapy (defined as reduction to <1000 pg/ml or >30% reduction vs. baseline) were studied at discharge, 4 wk and 10 wk post-randomisation.

Results
Median NT-proBNP at randomisation was similar in patients with S/V started pre- and post-discharge (1919 vs 1659 pg/ml). In patients receiving S/V in-hospital, NT-proBNP was reduced by 28% at discharge, compared to a 3% reduction in patients receiving optimised standard of care (between group p<0.001). A favorable response was reached in 46% vs 18% patients at discharge, 46% vs 42% at 4 weeks and 51% vs 48% at 10 weeks in pre- vs post-discharge groups. (Figure 1). Predictors of favourable NT-proBNP response to S/V at discharge were hypertension and shorter time from admission to first S/V dose. At 4 wk after randomisation, NT-proBNP was reduced similarly in patients started on S/V pre- and post-discharge. When the two S/V initiation groups were combined, predictors of favorable NT-proBNP response at 4 wk were higher initial dose of S/V (≥49/51 mg b.i.d.), higher baseline levels of NT-proBNP, de novo HF hospitalisation, ACEI/ARB naïve, lower baseline creatinine, no atrial fibrillation (AFib), no prior myocardial infarction (MI). A further reduction in NT-proBNP was seen at 10 wk post-randomisation in patients started on S/V pre- and post-discharge (38% vs 34%, between group p=0.250). Predictors of favourable NT-proBNP response to S/V were similar at 4 wk and 10 wk post-randomisation.

Conclusion
In-hospital initiation of sacubitril/valsartan shortly after stabilisation was associated with a prompt improvement of NT-proBNP already at discharge, whereas higher baseline levels of NT-proBNP, higher starting dose, absence of AFib and MI history, de novo HF and ACEI/ARB naïve status were associated with favourable NT-proBNP response in the vulnerable phase after discharge.

Acknowledgement/Funding
The TRANSITION study was funded by Novartis
1411The effect of eplerenone on fibrosis in hypertrophic cardiomyopathy. A randomised controlled trial assessed using cardiopulmonary exercise testing and cardiovascular magnetic resonance
Authors: Bhatti Y J , O'hanlon R , Ismail T F , Pennell D , Vassiliou V , Prasad S 
Published: October 2019

Abstract

Background
Recent studies have implicated aldosterone, a hormone of the renin-angiotensin-aldosterone system to cardiac hypertrophy, and cardiac and vascular fibrosis in cardiomyopathy. High levels of circulating aldosterone have been shown to cause myocardial and aortic fibrosis in animal models. In humans, high aldosterone concentrations have been associated with endothelial dysfunction, myocardial infarction, left ventricular hypertrophy and death. Aldosterone antagonism with spironolactone or eplerenone reverses the process of fibrosis in animal models.

Purpose
Left ventricular dysfunction due to hypertrophic cardiomyopathy (HCM) is a disorder associated with an increased risk of morbidity and premature mortality. An important pathological feature seen in cardiomyopathy is the development of fibrosis and its association with functional impairment and arrhythmia, including predisposition to sudden cardiac death. This trial observes the effect of eplerenone on myocardial fibrosis and exercise tolerance in patients with HCM.

Methods
42 patients were recruited into a double-blinded, placebo-controlled randomised study. Each patient had an established diagnosis of HCM without exclusion criteria (figure 1). 2 patients withdrew before enrolment. Enrolled patients were established on maximally tolerated doses of standard drugs used in the treatment of HCM and the doses of these drugs remained unchanged in the 2 months preceding enrolment to the trial. Patients were randomised to receive a maximal dose of 50mg eplerenone (n=21) or placebo (n=19). The patients underwent cardiopulmonary exercise testing and cardiovascular magnetic resonance (CMR) scan at baseline and 52 week follow up.

Results
At 52 weeks follow up there was no difference between placebo and treatment groups in peak oxygen consumption (−1.05 vs 0.63, p=0.32), anaerobic threshold (0.4 vs 1.45, p=0.31) or ventilatory efficiency slope (−0.77 vs 1.76, p=0.065). In addition, there was no significant difference observed in LV mass or fibrosis as assessed by CMR.
Inclusion and Exclusion Criteria

Conclusion
In the first randomised controlled trial using eplerenone in humans with HCM, we report no effect of treatment after 52 weeks on exercise capacity compared with placebo. In addition, we report no effect of treatment on the presence of fibrosis detected by CMR. Interpretation of these results are limited by small sample size and further studies will require a multi-centre recruitment process. The data presented here support the feasibility of eplerenone treatment in patients with HCM and provide statistical power calculation for future trials.
1440Anti-inflammatory adipokine, omentin, attenuates angiotensin II-induced abdominal aortic aneurysm formation in apolipoprotein-E knockout mice
Authors: Fang L , Ohashi K , Otaka N , Kawanishi H , Takikawa T , Murohara T , Ouchi N 
Published: October 2019

Abstract

Background
Abdominal aortic aneurysm (AAA) is an increasing and life-threatening disease. Obesity is associated with an increased risk of AAA. Omentin is a circulating adipokine, which is downregulated by obesity. Recently we have demonstrated that omentin is an anti-inflammatory adipokine that prevents the development of atherosclerosis in apolipoprotein-E knockout (apoE-KO) mice. Here we examined whether omentin could modulate angiotensin II-induced AAA formation in apoE-KO mice.

Methods and results
To overexpress human omentin in apoE-KO mice, apoE-KO mice were crossed with transgenic mice expressing the human omentin gene in fat tissue under the control of AP2 promoter (OMT-Tg mice). Circulating levels of human omentin in apoE-KO/OMT-Tg mice were approximately threefold higher than those in healthy human subjects, whereas human omentin was undetectable in apoE-KO mice. There were no differences in body weight, blood pressure and heart rate between apoE-KO/OMT-Tg and apoE-KO mice. We also subjected apoE-KO/OMT-Tg and apoE-KO mice at 24 weeks of age to continuous angiotensin II-infusion by using osmotic mini pumps for 4 weeks, which is a widely-accepted model of experimental AAA. ApoE-KO/OMT-Tg mice exhibited a lower incidence of AAA formation and a reduced maximal diameter of AAA determined by direct measurement and ultrasound imaging as compared with apo-E KO mice. In histological analyses with van Gieson staining, apoE-KO/OMT-Tg mice showed attenuated disruption of medial elastic fibers in response to angiotensin II compared with apo-E KO mice. ApoE-KO/OMT-Tg mice also displayed reduced mRNA levels of matrix metalloproteinase (MMP) 2 and MMP9 as well as pro-inflammation genes including interleukin (IL)-6 in aortic walls compared with apo-E KO mice. Treatment of human monocyte-derived macrophages with human omentin protein attenuated LPS-stimulated expression of MMP9, TNF-α and IL-6. Omentin treatment also reduced LPS-induced activation of MMP9 in cultured media of human macrophages as evaluated by gelatinolytic zymography. Omentin treatment increased phosphorylation levels of Akt in human macrophages. The suppressive effects of omentin on inflammatory response in macrophages were reversed by treatment with LY294002, which is an inhibitor of PI3 kinase/Akt signaling.

Conclusion
These data suggest that omentin acts as an adipokine that can attenuate angiotensin II-induced development of AAA through suppression of MMP activation and inflammatory response in the vascular wall.
2130The patient in clinical research: disposable guinea pig or involved actor?
Authors: Cosmi D , Mariottoni B , Cosmi F 
Published: October 2019

Abstract

Background
The request for informed consent to join a clinical trial often creates mistrust and hesitation in the patient who should be enrolled.

Methods
In the last ten years of cardiovascular clinical research we asked an informed consent to 2,586 patients. 59% agreed to join clinical trials, 40% refused. The 1% initially accepted and then withdrew the consent. We asked all the patients who refused the consent to answer a brief interview about the reasons for rejection. Patients who refused to join clinical trials were relatively young (mean age 62±5) and had a high level of education; 619 (60%) had a high school diploma or a degree.

Results
Of 1031 patients, 629 (61%), accepted to answer the interview; 176 (28%) answered they refused on relatives', friends' or other doctors' advices, or after Internet searches; 157 (25%) answered they didn't agree about how the trials were carried out (double blind control procedure, use of placebo, ecc); 126 (20%) didn't trust official medicine. 63 (10%) couldn't guarantee their presence at the controls. 69 (11%) didn't want to undergo additional medical examinations. 31 (5%) had previous bad research experiences (feeling like a guinea pig, ecc). 7 (about 1%) refused for other reasons.
Table 1. Acceptance or refusal to join cardiological intervention or observational clinical trials in the last 10 years Informed consent Immediately after reading and Principal Investigator's explanation After discussion with family, GP or Internet searches Total Accepted 914 (35%) 608 (24%) 1522 (29%) Initially accepted with subsequent withdrawal before randomization 1 (0.03%) 30 (1.2%) 31 (1%) Initially accepted with subsequent withdrawal after randomization 0 2 (0.07%) 2 (0.07%) Refused 151 (6%) 880 (34%) 1.031 (40%) Total 1.066 (41%) 1.520 (59%) 2.586 (100%)

Conclusions
Recruitment into clinical research studies is still a major challenge; patients are not fully aware of the importance of participation in clinical research studies for the development and implementation of medical advances. Paradoxically, people who refuse to participate in a trial are young and have a high level of education. Researcher's duty is to involve the patient in the trial and clarify the benefits of join the research.
2154Apolipoprotein B/apolipoprotein A-I ratio is comparable with C-reactive protein in predicting cancer mortality: results from two multi-ethnic US populations
Authors: Mazidi M , Mikhailidis D P , Katsiki N , Sniderman A , Banach M 
Published: October 2019

Abstract

Background
There is a lack of evidence regarding the link between apolipoproteins and cancer mortality.

Purpose
By using two nationally representative samples of US adults, we prospectively evaluated the associations between apolipoprotein B (apoB) levels and apoB/apolipoprotein A-I (apoA-I) ratio with cancer mortality. We also examined the role of C-reactive protein (CRP) in these associations.

Method
Adults aged ≥20 years, enrolled in the Third National Health and Nutrition Examination Survey (NHANES-III, 1988–1994) and continuous NHANES (2005–2010), and followed up to December 31st 2011, were included in the present analysis. Multiple Cox regressionswere applied to evaluate the associations between the variables of interest and cancer mortality.

Results
Overall, 7,695 participants were included (mean age: 49.2 years; 50.4% men, median follow-up: 19.1 years). In the fully adjusted (for age, gender, race, poverty to income ratio, educational status, body mass index, alcohol and dietary intake, smoking, dyslipidemia, hypertension and diabetes) model, participants in the highest quartile (Q4) of apoB/apoA-I had a significantly greater risk for cancer mortality [hazard ratio (HR): 1.40, 95% confidence interval (CI): 1.25–1.93] compared with those in the first quartile (Q1) (Figure). In the same model, a positive and significant association between apoB levels and fatal cancer was observed for individuals in the Q3 (HR: 1.12, 95% CI: 1.09–1.16) and Q4 (HR: 1.17, 95% CI: 1.09–1.25) compared with those in the Q1. When CRP levels were added in the analysis, the apoB/apoA-I ratio, but not apoB levels, remained significantly related to cancer mortality (Q4= HR: 1.17, 95% CI 1.09–1.25). In contrast, CRP levels were not able to predict cancer death after correction for apoB/apoA-I ratio.
Cancer death and quartiles of ApoB/ApoA1

Conclusions
In a large representative sample of the US adult population, the apoB/apoA-I ratio and apoB levels significantly predicted cancer mortality, independently of several cardiometabolic risk factors. The predictive value of apoB/apoA-I, but not apoB levels, remained significant after taking into account CRP, whereas CRP was not associated with cancer mortality after adjustment for apoB/apoA-I ratio. If further evidence supports our findings, apoA-I and apoB measurements could be considered in general health-care policies.

Acknowledgement/Funding
None
2209Oxygen therapy in suspected acute myocardial infarction and concurrent chronic obstructive pulmonary disease: a prespecified subgroup analysis from the DETO2X-AMI trial
Authors: Andell P , James S K , Ostlund O , Yndigegn T , Sparv D , Pernow J , Jernberg T , Lindahl B , Herlitz J , Erlinge D , Hofmann R 
Published: October 2019

Abstract

Background
The DETermination of the role of Oxygen in suspected Acute Myocardial Infarction (DETO2X-AMI) trial did not find any benefit of oxygen therapy compared to ambient air in normoxemic patients with suspected acute myocardial infarction (AMI). Patients with chronic obstructive pulmonary disease (COPD) may both benefit and be harmed by supplemental oxygen. Thus, we evaluated the effect of routine oxygen therapy compared to ambient air in normoxemic COPD patients with suspected AMI.

Methods and results
A total of 6629 patients with suspected AMI were randomized in the DETO2X-AMI trial to oxygen or ambient air. In the oxygen group (n=3311) and the ambient air group (n=3318), 155 and 141 patients, respectively, had COPD (prevalence of 4.5%). Patients with COPD were older, had more comorbid conditions and experienced a two-fold higher risk of death at one year (COPD: 32/296 [10.8%] vs. non-COPD 302/6333 [4.8%]). Oxygen therapy compared to ambient air was not associated with improved outcomes at 365 days (COPD: all-cause mortality HR 0.99 [95% CI 0.50–1.99, interaction-p=0.96]; cardiovascular death HR 0.80 [0.32–2.04, interaction-p=0.59]; rehospitalization with AMI or death HR 1.27 [0.71–2.28, interaction-p=0.46]; hospitalization for heart failure or death HR 1.08 [0.61–1.91, interaction-p=0.77]); there were no significant treatment-by-COPD interactions.
Outcome

Conclusions
Although COPD patients had twice the mortality rate compared to non-COPD patients, this prespecified subgroup analysis from the DETO2X-AMI trial on oxygen therapy versus ambient air in normoxemic COPD patients with suspected AMI revealed no evidence for benefit of routine oxygen therapy consistent with the main trial's findings.