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Circulation - recientes

American Heart Association’s Call to Action for Payment and Delivery System Reform [AHA Policy Statement]
14/8/2017
Vincent J. Bufalino, Scott A. Berkowitz, Timothy J. Gardner, Ileana L. Pina, Madeleine Konig
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The healthcare system is undergoing a transition from paying for volume to paying for value. Clinicians, as well as public and private payers, are beginning to implement alternative delivery and payment models, such as the patient-centered medical home, accountable care organizations, and bundled payment arrangements. Implementation of these new models will necessitate delivery system transformation and will actively involve all fields of medical care, in particular medicine and surgery. This call to action, on behalf of the American Heart Association’s Expert Panel on Payment and Delivery System Reform, serves to offer support and direction for further involvement by the American Heart Association. In doing so, it (1) provides baseline review and definition of the present models and some of the early results of these delivery models, including outcomes; (2) initiates a conversation within the American Heart Association on the impact of payment and delivery system reform, as well as how the American Heart Association should engage in the interest of patients; (3) issues a call to action to our organization and to cardiovascular and stroke health professionals across the country to become educated about these models so to as to understand their impact on patient care; and (4) asks the government and other funding agencies, including the American Heart Association, to begin supporting and prioritizing meaningful research endeavors to further evaluate these models.

Reflections of the Editor–in–Chief [Editor’s Page]
14/8/2017
Joseph A. Hill
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Charting Our Future Together [Perspective]
14/8/2017
Gary H. Gibbons
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Particulate Matter Exposure and Stress Hormone Levels [Original Research Article]
14/8/2017
Huichu Li, Jing Cai, Renjie Chen, Zhuohui Zhao, Zhekang Ying, Lin Wang, Jianmin Chen, Ke Hao, Patrick L. Kinney, Honglei Chen, Haidong Kan
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Background:Exposure to ambient particulate matter (PM) is associated with a number of adverse health outcomes, but potential mechanisms are largely unknown. Metabolomics represents a powerful approach to study global metabolic changes in response to environmental exposures. We therefore conducted this study to investigate changes in serum metabolites in response to the reduction of PM exposure among healthy college students.Methods:We conducted a randomized, double-blind crossover trial in 55 healthy college students in Shanghai, China. Real and sham air purifiers were placed in participants’ dormitories in random order for 9 days with a 12-day washout period. Serum metabolites were quantified by using gas chromatography-mass spectrometry and ultrahigh performance liquid chromatography-mass spectrometry. Between-treatment differences in metabolites were examined using orthogonal partial least square-discriminant analysis and mixed-effect models. Secondary outcomes include blood pressure, corticotropin-releasing hormone, adrenocorticotropic hormone, insulin resistance, and biomarkers of oxidative stress and inflammation.Results:The average personal exposure to PMs with aerodynamic diameters ≤2.5 μm was 24.3 μg/m3 during the real purification and 53.1 μg/m3 during the sham purification. Metabolomics analysis showed that higher exposure to PMs with aerodynamic diameters ≤2.5 μm led to significant increases in cortisol, cortisone, epinephrine, and norepinephrine. Between-treatment differences were also observed for glucose, amino acids, fatty acids, and lipids. We found significantly higher blood pressure, hormones, insulin resistance, and biomarkers of oxidative stress and inflammation among individuals exposed to higher PMs with aerodynamic diameters ≤2.5 μm.Conclusions:This study suggests that higher PM may induce metabolic alterations that are consistent with activations of the hypothalamus-pituitary-adrenal and sympathetic-adrenal-medullary axes, adding potential mechanistic insights into the adverse health outcomes associated with PM. Furthermore, our study demonstrated short-term reductions in stress hormone following indoor air purification.Clinical Trial Registration:URL: http://www.clinicaltrials.gov. Unique identifier: NCT02712333.

“Stressed” About Air Pollution [Editorials]
14/8/2017
Robert D. Brook, Sanjay Rajagopalan
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Predictors and Association With Clinical Outcomes of the Changes in Exercise Capacity After Transcatheter Aortic Valve Replacement [Original Research Article]
14/8/2017
Omar Abdul–Jawad Altisent, Rishi Puri, Ander Regueiro, Chekrallah Chamandi, Tania Rodriguez–Gabella, Maria del Trigo, Francisco Campelo–Parada, Thomas Couture, Josep Ramon Marsal, Melanie Cote, Jean–Michel Paradis, Robert DeLarochelliere, Daniel Doyle, Siamak Mohammadi, Eric Dumont, Josep Rodes–Cabau
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Background:At present, there are no objective data specifically examining the clinical impact of variations in exercise capacity post–transcatheter aortic valve replacement (TAVR). We describe the changes in exercise capacity between baseline and 6 months post-TAVR, and ascertain factors associated with and clinical implications of a lack of improvement in exercise capacity post-TAVR.Methods:A total of 305 patients (mean age, 79±9 years; 44% men; Society of Thoracic Surgeons predicted risk mortality score, 6.7±4.2%) undergoing TAVR completed both baseline and follow-up exercise capacity assessments at 6 months post-TAVR. Exercise capacity was evaluated by the 6-minute walk test (6MWT). Clinical outcomes were compared between patients displaying greater than (n=152; improving group) versus less than (n=153; nonimproving group) the median percentage change in distance walked between baseline and 6-month follow-up examinations. The primary outcome measure was clinical event rates, measured from the 6-month post-TAVR period onward. Further dichotomization according to baseline 6MWT distance (less than versus more than median walking distance, or slow walker versus fast walker) was also assessed.Results:The mean overall distances walked pre- and post-TAVR (6 months post-TAVR) were 204±119 and 263±116 m, respectively (Δ6MWT=60±106 m), with 219 (72%) patients demonstrating an increase in their walking distance (median percentage increase of the entire population was 20% [interquartile range, 0%–80%]). Factors independently correlated with reduced exercise capacity improvement included a range of baseline clinical characteristics (older age, female sex, chronic obstructive pulmonary disease; P<0.05 for all), periprocedural major or life-threatening bleeding (P=0.009) and new-onset anemia at 6 months post-TAVR (P=0.009). Failure to improve the 6MWT distance by at least 20% was independently associated with all-cause mortality (P=0.002) and cardiovascular death or rehospitalization for cardiovascular causes (P=0.001). Baseline slow walkers who were able to improve the 6MWT distance presented with significantly better outcomes than nonimprovers (P=0.01 for all-cause mortality; P=0.001 for cardiovascular end point).Conclusions:Approximately one-third of patients undergoing TAVR did not improve their exercise capacity postprocedure. The lack of functional improvement post-TAVR was predicted by a mix of baseline and periprocedural factors translating into poorer clinical outcomes. These results suggest that systematically implementing exercise capacity assessment pre- and post-TAVR may help to improve patient risk stratification.

Walking as a Window to Risk and Resiliency [Editorials]
14/8/2017
Karen P. Alexander
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Potent Thrombolytic Effect of N-Acetylcysteine on Arterial Thrombi [Original Research Article]
14/8/2017
Sara Martinez de Lizarrondo, Clement Gakuba, Bradley A. Herbig, Yohann Repesse, Carine Ali, Cecile V. Denis, Peter J. Lenting, Emmanuel Touze, Scott L. Diamond, Denis Vivien, Maxime Gauberti
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Background:Platelet cross-linking during arterial thrombosis involves von Willebrand Factor (VWF) multimers. Therefore, proteolysis of VWF appears promising to disaggregate platelet-rich thrombi and restore vessel patency in acute thrombotic disorders such as ischemic stroke, acute coronary syndrome, or acute limb ischemia. N-Acetylcysteine (NAC, a clinically approved mucolytic drug) can reduce intrachain disulfide bonds in large polymeric proteins. In the present study, we postulated that NAC might cleave the VWF multimers inside occlusive thrombi, thereby leading to their dissolution and arterial recanalization.Methods:Experimental models of thrombotic stroke induced by either intra-arterial thrombin injection or ferric chloride application followed by measurement of cerebral blood flow using a combination of laser Doppler flowmetry and MRI were performed to uncover the effects of NAC on arterial thrombi. To investigate the effect of NAC on larger vessels, we also performed ferric chloride–induced carotid artery thrombosis. In vitro experiments were performed to study the molecular bases of NAC thrombolytic effect, including platelet aggregometry, platelet-rich thrombi lysis assays, thromboelastography (ROTEM), and high-shear VWF string formation using microfluidic devices. We also investigated the putative prohemorrhagic effect of NAC in a mouse model of intracranial hemorrhage induced by in situ collagenase type VII injection.Results:We demonstrated that intravenous NAC administration promotes lysis of arterial thrombi that are resistant to conventional approaches such as recombinant tissue-type plasminogen activator, direct thrombin inhibitors, and antiplatelet treatments. Through in vitro and in vivo experiments, we provide evidence that the molecular target underlying the thrombolytic effects of NAC is principally the VWF that cross-link platelets in arterial thrombi. Coadministration of NAC and a nonpeptidic GpIIb/IIIa inhibitor further improved its thrombolytic efficacy, essentially by accelerating thrombus dissolution and preventing rethrombosis. Thus, in a new large-vessel thromboembolic stroke model in mice, this cotreatment significantly improved ischemic lesion size and neurological outcome. It is important to note that NAC did not worsen hemorrhagic stroke outcome, suggesting that it exerts thrombolytic effects without significantly impairing normal hemostasis.Conclusions:We provide evidence that NAC is an effective and safe alternative to currently available antithrombotic agents to restore vessel patency after arterial occlusion.

Thrombolytic Potential of N-Acetylcysteine [Editorials]
14/8/2017
David Lillicrap
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Plasminogen Activator Inhibitor Type I Controls Cardiomyocyte Transforming Growth Factor-{beta} and Cardiac Fibrosis [Original Research Article]
14/8/2017
Panagiotis Flevaris, Sadiya S. Khan, Mesut Eren, Adam J. T. Schuldt, Sanjiv J. Shah, Daniel C. Lee, Sweta Gupta, Amy D. Shapiro, Paul W. Burridge, Asish K. Ghosh, Douglas E. Vaughan
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Background:Fibrosis is the pathological consequence of stress-induced tissue remodeling and matrix accumulation. Increased levels of plasminogen activator inhibitor type I (PAI-1) have been shown to promote fibrosis in multiple organ systems. Paradoxically, homozygous genetic deficiency of PAI-1 is associated with spontaneous age-dependent, cardiac-selective fibrosis in mice. We have identified a novel PAI-1-dependent mechanism that regulates cardiomyocyte-derived fibrogenic signals and cardiac transcriptional pathways during injury.Methods:Cardiac fibrosis in subjects with homozygous mutation in SERPINE-1 was evaluated with late gadolinium-enhanced cardiac magnetic resonance imaging. A murine cardiac injury model was performed by subcutaneous infusion of either saline or Angiotensin II by osmotic minipumps. We evaluated blood pressure, cardiac function (by echocardiography), fibrosis (with Masson Trichrome staining), and apoptosis (with TUNEL staining), and we performed transcriptome analysis (with RNA sequencing). We further evaluated fibrotic signaling in isolated murine primary ventricular myocytes.Results:Cardiac fibrosis was detected in 2 otherwise healthy humans with complete PAI-1 deficiency because of a homozygous frameshift mutation in SERPINE-1. In addition to its suppressive role during spontaneous cardiac fibrosis in multiple species, we hypothesized that PAI-1 also regulates fibrosis during cardiac injury. Treatment of young PAI-1−/− mice with Angiotensin II induced extensive hypertrophy and fibrotic cardiomyopathy, with increased cardiac apoptosis and both reactive and replacement fibrosis. Although Angiotensin II-induced hypertension was blunted in PAI-1−/− mice, cardiac hypertrophy was accelerated. Furthermore, ventricular myocytes were found to be an important source of cardiac transforming growth factor-β (TGF-β) and PAI-1 regulated TGF-β synthesis by cardiomyocytes in vitro as well as in vivo during cardiac injury. Transcriptome analysis of ventricular RNA after Angiotensin II treatment confirmed that PAI-1 deficiency significantly enhanced multiple TGF-β signaling elements and transcriptional targets, including genes for extracellular matrix components, mediators of extracellular matrix remodeling, matricellular proteins, and cardiac integrins compared with wild-type mice.Conclusions:PAI-1 is an essential repressor of cardiac fibrosis in mammals. We define a novel cardiomyocyte-specific regulatory mechanism for TGF-β production by PAI-1, which explains the paradoxical effect of PAI-1 deficiency in promoting cardiac-selective fibrosis. Thus, PAI-1 is a molecular switch that controls the cardiac TGF-β axis and its early transcriptional effects that lead to myocardial fibrosis.

Cardiomyocyte Regeneration [Consensus Report]
14/8/2017
Thomas Eschenhagen, Roberto Bolli, Thomas Braun, Loren J. Field, Bernd K. Fleischmann, Jonas Frisen, Mauro Giacca, Joshua M. Hare, Steven Houser, Richard T. Lee, Eduardo Marban, James F. Martin, Jeffery D. Molkentin, Charles E. Murry, Paul R. Riley, Pilar Ruiz–Lozano, Hesham A. Sadek, Mark A. Sussman, Joseph A. Hill
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Eleventh Oriental Congress of Cardiology [Highlights From Major Meetings]
14/8/2017
Junbo Ge
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From the Literature [Cardiology News]
14/8/2017
Tracy Hampton
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Acute Coronary Syndrome [ECG Challenges]
14/8/2017
Miguel Fiol–Sala, Antonio Bayes de Luna
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Letter by Rowshani et al Regarding Article, “Gene Expression Profiling for the Identification and Classification of Antibody-Mediated Heart Reȷection” [Correspondence]
14/8/2017
Aȷda T. Rowshani, Kadir Caliskan, Jan H. von der Thusen
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Letter by Moayedi et al Regarding Article, “Gene Expression Profiling for the Identification and Classification of Antibody-Mediated Heart Reȷection” [Correspondence]
14/8/2017
Yasbanoo Moayedi, Juan Duero Posada, Mosaad Alhussein, Heather Joan Ross
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Response by Loupy et al to Letters Regarding Article, “Gene Expression Profiling for the Identification and Classification of Antibody-Mediated Heart Reȷection” [Correspondence]
14/8/2017
Alexandre Loupy, Luis Hidalgo, Jean Paul Duong, Patrick Bruneval, Xavier Jouven, Philip F. Halloran
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2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America [ACC/AHA/HFSA Focused Update]
7/8/2017
Clyde W. Yancy, Mariell Jessup, Biykem Bozkurt, Javed Butler, Donald E. Casey, Jr, Monica M. Colvin, Mark H. Drazner, Gerasimos S. Filippatos, Gregg C. Fonarow, Michael M. Givertz, Steven M. Hollenberg, JoAnn Lindenfeld, Frederick A. Masoudi, Patrick E. McBride, Pamela N. Peterson, Lynne Warner Stevenson, Cheryl Westlake
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Medical Podcasting and Circulation on the Run [Perspective]
7/8/2017
Carolyn S.P. Lam, Karen Barry, Amit Khera
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Day-to-Day Blood Pressure Variability and Risk of Dementia in a General Japanese Elderly Population [Original Research Article]
7/8/2017
Emi Oishi, Tomoyuki Ohara, Satoko Sakata, Masayo Fukuhara, Jun Hata, Daigo Yoshida, Mao Shibata, Toshio Ohtsubo, Takanari Kitazono, Yutaka Kiyohara, Toshiharu Ninomiya
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Background:Several observational studies have reported that higher visit-to-visit blood pressure variability is a risk factor for cognitive impairment and dementia. However, no studies have investigated the association of day-to-day blood pressure variability assessed by home blood pressure measurement with the development of dementia.Methods:A total of 1674 community-dwelling Japanese elderly without dementia, ≥60 years of age, were followed up for 5 years (2007–2012). Home blood pressure was measured 3 times every morning for a median of 28 days. Day-to-day systolic (SBP) and diastolic blood pressure variabilities, calculated as coefficients of variation (CoV) of home SBP and diastolic blood pressure, were categorized into quartiles. The hazard ratios and their 95% confidence intervals of the CoV levels of home blood pressure on the development of all-cause dementia, vascular dementia (VaD), and Alzheimer disease (AD) were computed with a Cox proportional hazards model.Results:During the follow-up, 194 subjects developed all-cause dementia; of these, 47 had VaD and 134 had AD. The age- and sex-adjusted incidences of all-cause dementia, VaD, and AD increased significantly with increasing CoV levels of home SBP (all P for trend <0.05). These associations remained unchanged after adjustment for potential confounding factors, including home SBP. Compared with subjects in the first quartile of CoV levels of home SBP, the risks of the development of all-cause dementia, VaD, and AD were significantly higher in those in the fourth quartile (hazard ratio=2.27, 95% confidence interval=1.45–3.55, P<0.001 for all-cause dementia; hazard ratio=2.79, 95% confidence interval=1.04–7.51, P=0.03 for VaD; hazard ratio=2.22, 95% confidence interval=1.31–3.75, P<0.001 for AD). Similar associations were observed for CoV levels of home diastolic blood pressure. Meanwhile, home SBP levels were significantly associated with the risk of VaD but not with the risks of all-cause dementia and AD. There was no interaction between home SBP levels and CoV levels of home SBP on the risk of each subtype of dementia.Conclusions:Our findings suggest that increased day-to-day blood pressure variability is, independently of average home blood pressure, a significant risk factor for the development of all-cause dementia, VaD, and AD in the general elderly Japanese population.







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