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Circulation - recientes
Recommendations for the Use of Mechanical Circulatory Support: Ambulatory and Community Patient Care: A Scientific Statement From the American Heart Association [AHA Scientific Statements]19/6/2017
Jennifer L. Cook, Monica Colvin, Gary S. Francis, Kathleen L. Grady, Timothy M. Hoffman, Mariell Jessup, Ranjit John, Michael S. Kiernan, Judith E. Mitchell, Francis D. Pagani, Michael Petty, Pasala Ravichandran, Joseph G. Rogers, Marc J. Semigran, J. Matthew Toole
2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [AHA/ACC Guideline]19/6/2017
Rick A. Nishimura, Catherine M. Otto, Robert O. Bonow, Blase A. Carabello, John P. Erwin III, Lee A. Fleisher, Hani Jneid, Michael J. Mack, Christopher J. McLeod, Patrick T. O’Gara, Vera H. Rigolin, Thoralf M. Sundt III, Annemarie Thompson
Letter by Barakat et al Regarding Article, “Implantable Cardioverter-Defibrillator for Nonischemic Cardiomyopathy: An Updated Meta-Analysis” [Correspondence]19/6/2017
Amr F. Barakat, Marwan Saad, Islam Y. Elgendy
Letter by Nery et al Regarding Article, “Implantable Cardioverter-Defibrillator for Nonischemic Cardiomyopathy: An Updated Meta-Analysis” [Correspondence]19/6/2017
Pablo B. Nery, Krystina B. Lewis, David H. Birnie
Response by Golwala et al to Letter Regarding Article, “Implantable Cardioverter-Defibrillator for Nonischemic Cardiomyopathy: An Updated Meta-Analysis” [Correspondence]19/6/2017
Harsh Golwala, Navkaranbir Singh Bajaj, Garima Arora, Pankaj Arora
Letter by Freeman and Freeman Regarding Article, “Sex Differences in Faculty Rank Among Academic Cardiologists in the United States” [Correspondence]19/6/2017
Michelle L. Freeman, William D. Freeman
It Is Time to End the Dualistic Short Versus Long Duration of Dual Antiplatelet Therapy Debates [Perspective]19/6/2017
Glenn N. Levine, Eric R. Bates
Optimizing a Drone Network to Deliver Automated External DefibrillatorsClinical Perspective [Original Research Article]19/6/2017
Justin J. Boutilier, Steven C. Brooks, Alyf Janmohamed, Adam Byers, Jason E. Buick, Cathy Zhan, Angela P. Schoellig, Sheldon Cheskes, Laurie J. Morrison, Timothy C. Y. Chan
Background:Public access defibrillation programs can improve survival after out-of-hospital cardiac arrest, but automated external defibrillators (AEDs) are rarely available for bystander use at the scene. Drones are an emerging technology that can deliver an AED to the scene of an out-of-hospital cardiac arrest for bystander use. We hypothesize that a drone network designed with the aid of a mathematical model combining both optimization and queuing can reduce the time to AED arrival.Methods:We applied our model to 53 702 out-of-hospital cardiac arrests that occurred in the 8 regions of the Toronto Regional RescuNET between January 1, 2006, and December 31, 2014. Our primary analysis quantified the drone network size required to deliver an AED 1, 2, or 3 minutes faster than historical median 911 response times for each region independently. A secondary analysis quantified the reduction in drone resources required if RescuNET was treated as a large coordinated region.Results:The region-specific analysis determined that 81 bases and 100 drones would be required to deliver an AED ahead of median 911 response times by 3 minutes. In the most urban region, the 90th percentile of the AED arrival time was reduced by 6 minutes and 43 seconds relative to historical 911 response times in the region. In the most rural region, the 90th percentile was reduced by 10 minutes and 34 seconds. A single coordinated drone network across all regions required 39.5% fewer bases and 30.0% fewer drones to achieve similar AED delivery times.Conclusions:An optimized drone network designed with the aid of a novel mathematical model can substantially reduce the AED delivery time to an out-of-hospital cardiac arrest event.
Daniel B. Mark, Steen M. Hansen, Monique L. Starks, Mary L. Cummings
Thresholds for Ambulatory Blood Pressure Among African Americans in the Jackson Heart StudyClinical Perspective [Original Research Article]19/6/2017
Joseph Ravenell, Daichi Shimbo, John N. Booth III, Daniel F. Sarpong, Charles Agyemang, Danielle L. Beatty Moody, Marwah Abdalla, Tanya M. Spruill, Amanda J. Shallcross, Adam P. Bress, Paul Muntner, Gbenga Ogedegbe
Background:Ambulatory blood pressure (BP) monitoring is the reference standard for out-of-clinic BP measurement. Thresholds for identifying ambulatory hypertension (daytime systolic BP [SBP]/diastolic BP [DBP] ≥135/85 mm Hg, 24-hour SBP/DBP ≥130/80 mm Hg, and nighttime SBP/DBP ≥120/70 mm Hg) have been derived from European, Asian, and South American populations. We determined BP thresholds for ambulatory hypertension in a US population-based sample of African American adults.Methods:We analyzed data from the Jackson Heart Study, a population-based cohort study comprised exclusively of African American adults (n=5306). Analyses were restricted to 1016 participants who completed ambulatory BP monitoring at baseline in 2000 to 2004. Mean SBP and DBP levels were calculated for daytime (10:00 am–8:00 pm), 24-hour (all available readings), and nighttime (midnight–6:00 am) periods, separately. Daytime, 24-hour, and nighttime BP thresholds for ambulatory hypertension were identified using regression- and outcome-derived approaches. The composite of a cardiovascular disease or an all-cause mortality event was used in the outcome-derived approach. For this latter approach, BP thresholds were identified only for SBP because clinic DBP was not associated with the outcome. Analyses were stratified by antihypertensive medication use.Results:Among participants not taking antihypertensive medication, the regression-derived thresholds for daytime, 24-hour, and nighttime SBP/DBP corresponding to clinic SBP/DBP of 140/90 mm Hg were 134/85 mm Hg, 130/81 mm Hg, and 123/73 mm Hg, respectively. The outcome-derived thresholds for daytime, 24-hour, and nighttime SBP corresponding to a clinic SBP ≥140 mm Hg were 138 mm Hg, 134 mm Hg, and 129 mm Hg, respectively. Among participants taking antihypertensive medication, the regression-derived thresholds for daytime, 24-hour, and nighttime SBP/DBP corresponding to clinic SBP/DBP of 140/90 mm Hg were 135/85 mm Hg, 133/82 mm Hg, and 128/76 mm Hg, respectively. The corresponding outcome-derived thresholds for daytime, 24-hour, and nighttime SBP were 140 mm Hg, 137 mm Hg, and 133 mm Hg, respectively, among those taking antihypertensive medication.Conclusions:On the basis of the outcome-derived approach for SBP and regression-derived approach for DBP, the following definitions for daytime, 24-hour, and nighttime hypertension corresponding to clinic SBP/DBP ≥140/90 mm Hg are proposed for African American adults: daytime SBP/DBP ≥140/85 mm Hg, 24-hour SBP/DBP ≥135/80 mm Hg, and nighttime SBP/DBP ≥130/75 mm Hg, respectively.
George S. Stergiou, Angeliki Ntineri, Anastasios Kollias
Prospective Study of Adenosine on Atrioventricular Nodal Conduction in Pediatric and Young Adult Patients After Heart TransplantationClinical Perspective [Original Research Article]19/6/2017
Jonathan N. Flyer, Warren A. Zuckerman, Marc E. Richmond, Brett R. Anderson, Tamar G. Mendelsberg, Jennie M. McAllister, Leonardo Liberman, Linda J. Addonizio, Eric S. Silver
Background:Supraventricular tachycardia is common after heart transplantation. Adenosine, the standard therapy for treating supraventricular tachycardia in children and adults without transplantation, is relatively contraindicated after transplantation because of a presumed risk of prolonged atrioventricular block in denervated hearts. This study tested whether adenosine caused prolonged asystole after transplantation and if it was effective in blocking atrioventricular nodal conduction in these patients.Methods:This was a single-center prospective clinical study including healthy heart transplant recipients 6 months to 25 years of age presenting for routine cardiac catheterization during 2015 to 2016. After catheterization, a transvenous pacing catheter was placed and adenosine was given following a dose-escalation protocol until atrioventricular block was achieved. The incidence of clinically significant asystole (≥12 seconds after adenosine) was quantified. The effects of patient characteristics on adenosine dose required to produce atrioventricular block and duration of effect were also measured.Results:Eighty patients completed adenosine testing. No patient (0%; 95% confidence interval, 0–3) required rescue ventricular pacing. Atrioventricular block was observed in 77 patients (96%; 95% confidence interval, 89–99). The median longest atrioventricular block was 1.9 seconds (interquartile range, 1.4–3.2 seconds), with a mean duration of adenosine effect of 4.3±2.0 seconds. No patient characteristic significantly predicted the adenosine dose to produce atrioventricular block or duration of effect. Results were similar across patient weight categories.Conclusions:Adenosine induces atrioventricular block in healthy pediatric and young adult heart transplant recipients with minimal risk when low initial doses are used (25 μg/kg; 1.5 mg if ≥60 kg) and therapy is gradually escalated.Clinical Trial Registration:URL: http://www.clinicaltrials.gov. Unique identifier: NCT02462941.
Cholesterol Efflux Capacity, High-Density Lipoprotein Particle Number, and Incident Cardiovascular EventsClinical Perspective [Original Research Article]19/6/2017
Amit V. Khera, Olga V. Demler, Steven J. Adelman, Heidi L. Collins, Robert J. Glynn, Paul M Ridker, Daniel J. Rader, Samia Mora
Background:Recent failures of drugs that raised high-density lipoprotein (HDL) cholesterol levels to reduce cardiovascular events in clinical trials have led to increased interest in alternative indices of HDL quality, such as cholesterol efflux capacity, and HDL quantity, such as HDL particle number. However, no studies have directly compared these metrics in a contemporary population that includes potent statin therapy and low low-density lipoprotein cholesterol.Methods:HDL cholesterol levels, apolipoprotein A-I, cholesterol efflux capacity, and HDL particle number were assessed at baseline and 12 months in a nested case-control study of the JUPITER trial (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin), a randomized primary prevention trial that compared rosuvastatin treatment to placebo in individuals with normal low-density lipoprotein cholesterol but increased C-reactive protein levels. In total, 314 cases of incident cardiovascular disease (CVD) (myocardial infarction, unstable angina, arterial revascularization, stroke, or cardiovascular death) were compared to age- and gender-matched controls. Conditional logistic regression models adjusting for risk factors evaluated associations between HDL-related biomarkers and incident CVD.Results:Cholesterol efflux capacity was moderately correlated with HDL cholesterol, apolipoprotein A-I, and HDL particle number (Spearman r= 0.39, 0.48, and 0.39 respectively; P<0.001). Baseline HDL particle number was inversely associated with incident CVD (adjusted odds ratio per SD increment [OR/SD], 0.69; 95% confidence interval [CI], 0.56–0.86; P<0.001), whereas no significant association was found for baseline cholesterol efflux capacity (OR/SD, 0.89; 95% CI, 0.72–1.10; P=0.28), HDL cholesterol (OR/SD, 0.82; 95% CI, 0.66–1.02; P=0.08), or apolipoprotein A-I (OR/SD, 0.83; 95% CI, 0.67–1.03; P=0.08). Twelve months of rosuvastatin (20 mg/day) did not change cholesterol efflux capacity (average percentage change −1.5%, 95% CI, −13.3 to +10.2; P=0.80), but increased HDL cholesterol (+7.7%), apolipoprotein A-I (+4.3%), and HDL particle number (+5.2%). On-statin cholesterol efflux capacity was inversely associated with incident CVD (OR/SD, 0.62; 95% CI, 0.42–0.92; P=0.02), although HDL particle number again emerged as the strongest predictor (OR/SD, 0.51; 95% CI, 0.33–0.77; P<0.001).Conclusions:In JUPITER, cholesterol efflux capacity was associated with incident CVD in individuals on potent statin therapy but not at baseline. For both baseline and on-statin analyses, HDL particle number was the strongest of 4 HDL-related biomarkers as an inverse predictor of incident events and biomarker of residual risk.Clinical Trial Registration:URL: http://www.clinicaltrials.gov. Unique identifier: NCT00239681.
SOX17 Regulates Conversion of Human Fibroblasts Into Endothelial Cells and Erythroblasts by Dedifferentiation Into CD34+ Progenitor CellsClinical Perspective [Original Research Article]19/6/2017
Lianghui Zhang, Ankit Jambusaria, Zhigang Hong, Glenn Marsboom, Peter T. Toth, Brittney-Shea Herbert, Asrar B. Malik, Jalees Rehman
Background:The mechanisms underlying the dedifferentiation and lineage conversion of adult human fibroblasts into functional endothelial cells have not yet been fully defined. Furthermore, it is not known whether fibroblast dedifferentiation recapitulates the generation of multipotent progenitors during embryonic development, which give rise to endothelial and hematopoietic cell lineages. Here we established the role of the developmental transcription factor SOX17 in regulating the bilineage conversion of fibroblasts by the generation of intermediate progenitors.Methods:CD34+ progenitors were generated after the dedifferentiation of human adult dermal fibroblasts by overexpression of pluripotency transcription factors. Sorted CD34+ cells were transdifferentiated into induced endothelial cells and induced erythroblasts using lineage-specific growth factors. The therapeutic potential of the generated cells was assessed in an experimental model of myocardial infarction.Results:Induced endothelial cells expressed specific endothelial cell surface markers and also exhibited the capacity for cell proliferation and neovascularization. Induced erythroblasts expressed erythroid surface markers and formed erythroid colonies. Endothelial lineage conversion was dependent on the upregulation of the developmental transcription factor SOX17, whereas suppression of SOX17 instead directed the cells toward an erythroid fate. Implantation of these human bipotential CD34+ progenitors into nonobese diabetic/severe combined immunodeficiency (NOD-SCID) mice resulted in the formation of microvessels derived from human fibroblasts perfused with mouse and human erythrocytes. Endothelial cells generated from human fibroblasts also showed upregulation of telomerase. Cell implantation markedly improved vascularity and cardiac function after myocardial infarction without any evidence of teratoma formation.Conclusions:Dedifferentiation of fibroblasts to intermediate CD34+ progenitors gives rise to endothelial cells and erythroblasts in a SOX17-dependent manner. These findings identify the intermediate CD34+ progenitor state as a critical bifurcation point, which can be tuned to generate functional blood vessels or erythrocytes and salvage ischemic tissue.
P2X7 Deficiency Blocks Lesional Inflammasome Activity and Ameliorates Atherosclerosis in MiceClinical Perspective [Original Research Article]19/6/2017
Peter Stachon, Adrian Heidenreich, Julian Merz, Ingo Hilgendorf, Dennis Wolf, Florian Willecke, Sunaina von Garlen, Philipp Albrecht, Carmen Hardtner, Nicolas Ehrat, Natalie Hoppe, Jochen Reinohl, Constantin von zur Muhlen, Christoph Bode, Marco Idzko, Andreas Zirlik
Background:Extracellular adenosine triphosphate (ATP) binds as a danger signal to purinergic receptor P2X7 and promotes inflammasome assembly and interleukin-1β expression. We hypothesized a functional role of the signal axis ATP–P2X7 in inflammasome activation and the chronic inflammation driving atherosclerosis.Methods:P2X7-competent and P2X7-deficient macrophages were isolated and stimulated with lipopolysaccharide, ATP, or both. To assess whether P2X7 may have a role in atherosclerosis, P2X7 expression was analyzed in aortic arches from low density lipoprotein receptor-/- mice consuming a high-cholesterol or chow diet. P2X7+/+ and P2X7−/− low density lipoprotein receptor−/− mice were fed a high-cholesterol diet to investigate the functional role of P2X7 knockout in atherosclerosis. Human plaques were derived from carotid endarterectomy and stained against P2X7.Results:Lipopolysaccharide or ATP stimulation alone did not activate caspase 1 in isolated macrophages. However, priming with lipopolysaccharide, followed by stimulation with ATP, led to an activation of caspase 1 and interleukin-1β in P2X7-competent macrophages. In contrast, P2X7-deficient macrophages showed no activation of caspase 1 after sequential stimulation while still expressing a basal amount of interleukin-1β. P2X7 receptor was higher expressed in murine atherosclerotic lesions, particularly by lesional macrophages. After 16 weeks of a high-cholesterol diet, P2X7-deficient mice showed smaller atherosclerotic lesions than P2X7-competent mice (0.162 cm2±0.023 [n=9], P2X7−/− low density lipoprotein receptor−/− : 0.084 cm2±0.01 [n=11], P=0.004) with a reduced amount of lesional macrophages. In accord with our in vitro findings, lesional caspase 1 activity was abolished in P2X7−/− mice. In addition, intravital microscopy revealed reduced leukocyte rolling and adhesion in P2X7-deficient mice. Last, we observe increased P2X7 expression in human atherosclerotic lesions, suggesting that our findings in mice are relevant for human disease.Conclusions:P2X7 deficiency resolved plaque inflammation by inhibition of lesional inflammasome activation and reduced experimental atherosclerosis. Therefore, P2X7 represents an interesting potential new target to combat atherosclerosis.
A Structured Review of Antithrombotic Therapy in Peripheral Artery Disease With a Focus on Revascularization [In Depth]19/6/2017
Connie N. Hess, Lars Norgren, Gary M. Ansel, Warren H. Capell, John P. Fletcher, F. Gerry R. Fowkes, Anders Gottsater, Kerry Hitos, Michael R. Jaff, Joakim Nordanstig, William R. Hiatt
Peripheral artery disease affects >200 million people worldwide and is associated with significant limb and cardiovascular morbidity and mortality. Limb revascularization is recommended to improve function and quality of life for symptomatic patients with peripheral artery disease with intermittent claudication who have not responded to medical treatment. For patients with critical limb ischemia, the goals of revascularization are to relieve pain, help wound healing, and prevent limb loss. The baseline risk of cardiovascular and limb-related events demonstrated among patients with stable peripheral artery disease is elevated after revascularization and related to atherothrombosis and restenosis. Both of these processes involve platelet activation and the coagulation cascade, forming the basis for the use of antiplatelet and anticoagulant therapies to optimize procedural success and reduce postprocedural cardiovascular risk. Unfortunately, few high-quality, randomized data to support use of these therapies after peripheral artery disease revascularization exist, and much of the rationale for the use of antiplatelet agents after endovascular peripheral revascularization is extrapolated from percutaneous coronary intervention literature. Consequently, guideline recommendations for antithrombotic therapy after lower limb revascularization are inconsistent and not always evidence-based. In this context, the purpose of this structured review is to assess the available randomized data for antithrombotic therapy after peripheral arterial revascularization, with a focus on clinical trial design issues that may affect interpretation of study results, and highlight areas that require further investigation.
Coverage and Cardioprotective Benefits of PCSK9 Take Center Stage at the American College of Cardiology Meeting [Cardiology News]19/6/2017
Bridget M. Kuehn
Jimmy Robert, Clement Derkenne, Daniel Jost, Jean–Pierre Tourtier
Geoffrey Allan Rubin, Lauren Tal Grinspan, Jonathan Ginns
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