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Circulation - recientes

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association [AHA Scientific Statements]
16/10/2017
Sean van Diepen, Jason N. Katz, Nancy M. Albert, Timothy D. Henry, Alice K. Jacobs, Navin K. Kapur, Ahmet Kilic, Venu Menon, E. Magnus Ohman, Nancy K. Sweitzer, Holger Thiele, Jeffrey B. Washam, Mauricio G. Cohen
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Cardiogenic shock is a high-acuity, potentially complex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated with multisystem organ failure. Despite improving survival in recent years, patient morbidity and mortality remain high, and there are few evidence-based therapeutic interventions known to clearly improve patient outcomes. This scientific statement on cardiogenic shock summarizes the epidemiology, pathophysiology, causes, and outcomes of cardiogenic shock; reviews contemporary best medical, surgical, mechanical circulatory support, and palliative care practices; advocates for the development of regionalized systems of care; and outlines future research priorities.

Correction to 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [Correction]
16/10/2017
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Correction to: 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [Correction]
16/10/2017
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The Ethics of Conducting Clinical Trials With Sodium-Glucose Cotransporter-2 Inhibitors in Heart Failure [Perspective]
16/10/2017
Javed Butler, Stefan D. Anker
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Efficacy and Safety of a Pharmaco-Invasive Strategy With Half-Dose Alteplase Versus Primary Angioplasty in ST-Segment-Elevation Myocardial Infarction [Original Research Article]
16/10/2017
Jun Pu, Song Ding, Heng Ge, Yaling Han, Jinchen Guo, Rong Lin, Xi Su, Heng Zhang, Lianglong Chen, Ben He
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Background:Timely primary percutaneous coronary intervention (PPCI) cannot be offered to all patients with ST-segment–elevation myocardial infarction (STEMI). Pharmaco-invasive (PhI) strategy has been proposed as a valuable alternative for eligible patients with STEMI. We conducted a randomized study to compare the efficacy and safety of a PhI strategy with half-dose fibrinolytic regimen versus PPCI in patients with STEMI.Methods:The EARLY-MYO trial (Early Routine Catheterization After Alteplase Fibrinolysis Versus Primary PCI in Acute ST-Segment–Elevation Myocardial Infarction) was an investigator-initiated, prospective, multicenter, randomized, noninferiority trial comparing a PhI strategy with half-dose alteplase versus PPCI in patients with STEMI 18 to 75 years of age presenting ≤6 hours after symptom onset but with an expected PCI-related delay. The primary end point of the study was complete epicardial and myocardial reperfusion after PCI, defined as thrombolysis in myocardial infarction flow grade 3, thrombolysis in myocardial infarction myocardial perfusion grade 3, and ST-segment resolution ≥70%. We also measured infarct size and left ventricular ejection fraction with cardiac magnetic resonance and recorded 30-day clinical and safety outcomes.Results:A total of 344 patients from 7 centers were randomized to PhI (n=171) or PPCI (n=173). PhI was noninferior (and even superior) to PPCI for the primary end point (34.2% versus 22.8%, P noninferiority<0.05, Psuperiority=0.022), with no significant differences in the frequency of the individual components of the combined end point: thrombolysis in myocardial infarction flow 3 (91.3% versus 89.2%, P=0.580), thrombolysis in myocardial infarction myocardial perfusion grade 3 (65.8% versus 62.9%, P=0.730), and ST-segment resolution ≥70% (50.9% versus 45.5%, P=0.377). Infarct size (23.3%±11.3% versus 25.8%±13.7%, P=0.101) and left ventricular ejection fraction (52.2%±11.0% versus 51.4%±12.0%, P=0.562) were similar in both groups. No significant differences occurred in 30-day rates of total death (0.6% versus 1.2%, P=1.0), reinfarction (0.6% versus 0.6%, P=1.0), heart failure (13.5% versus 16.2%, P=0.545), major bleeding events (0.6% versus 0%, P=0.497), or intracranial hemorrhage (0% versus 0%), but minor bleeding (26.9% versus 11.0%, P<0.001) was observed more often in the PhI group.Conclusions:For patients with STEMI presenting ≤6 hours after symptom onset and with an expected PCI-related delay, a PhI strategy with half-dose alteplase and timely PCI offers more complete epicardial and myocardial reperfusion when compared with PPCI. Adequately powered trials with this reperfusion strategy to assess clinical and safety outcomes are warranted.Clinical Trial Registration:URL: https://www.clinicaltrials.gov. Unique identifier: NCT01930682.

Recalibrating Reperfusion Waypoints [Editorials]
16/10/2017
Paul W. Armstrong, Robert C. Welsh
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Experimental Modeling Supports a Role for MyBP-HL as a Novel Myofilament Component in Arrhythmia and Dilated Cardiomyopathy [Original Research Article]
16/10/2017
David Y. Barefield, Megan J. Puckelwartz, Ellis Y. Kim, Lisa D. Wilsbacher, Andy H. Vo, Emily A. Waters, Judy U. Earley, Michele Hadhazy, Lisa Dellefave-Castillo, Lorenzo L. Pesce, Elizabeth M. McNally
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Background:Cardiomyopathy and arrhythmias are under significant genetic influence. Here, we studied a family with dilated cardiomyopathy and associated conduction system disease in whom prior clinical cardiac gene panel testing was unrevealing.Methods:Whole-genome sequencing and induced pluripotent stem cells were used to examine a family with dilated cardiomyopathy and atrial and ventricular arrhythmias. We also characterized a mouse model with heterozygous and homozygous deletion of Mybphl.Results:Whole-genome sequencing identified a premature stop codon, R255X, in the MYBPHL gene encoding MyBP-HL (myosin-binding protein-H like), a novel member of the myosin-binding protein family. MYBPHL was found to have high atrial expression with low ventricular expression. We determined that MyBP-HL protein was myofilament associated in the atria, and truncated MyBP-HL protein failed to incorporate into the myofilament. Human cell modeling demonstrated reduced expression from the mutant MYBPHL allele. Echocardiography of Mybphl heterozygous and null mouse hearts exhibited a 36% reduction in fractional shortening and an increased diastolic ventricular chamber size. Atria weight normalized to total heart weight was significantly increased in Mybphl heterozygous and null mice. Using a reporter system, we detected robust expression of Mybphl in the atria, and in discrete puncta throughout the right ventricular wall and septum, as well. Telemetric electrocardiogram recordings in Mybphl mice revealed cardiac conduction system abnormalities with aberrant atrioventricular conduction and an increased rate of arrhythmia in heterozygous and null mice.Conclusions:The findings of reduced ventricular function and conduction system defects in Mybphl mice support that MYBPHL truncations may increase risk for human arrhythmias and cardiomyopathy.

Closing the Genotype-Phenotype Loop for Precision Medicine [Editorials]
16/10/2017
Calum A. MacRae, Christine E. Seidman
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Direct Comparison of Cardiac Myosin-Binding Protein C With Cardiac Troponins for the Early Diagnosis of Acute Myocardial Infarction [Original Research Article]
16/10/2017
Thomas E. Kaier, Raphael Twerenbold, Christian Puelacher, Jack Marȷot, Nazia Imambaccus, Jasper Boeddinghaus, Thomas Nestelberger, Patrick Badertscher, Zaid Sabti, Maria Rubini Gimenez, Karin Wildi, Petra Hillinger, Karin Grimm, Sarah Loeffel, Samyut Shrestha, Dayana Flores Widmer, Janosch Cupa, Nikola Kozhuharov, Oscar Miro, F. Javier Martin–Sanchez, Beata Morawiec, Katharina Rentsch, Jens Lohrmann, Wanda Kloos, Stefan Osswald, Tobias Reichlin, Ekkehard Weber, Michael Marber, Christian Mueller
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Background:Cardiac myosin-binding protein C (cMyC) is a cardiac-restricted protein that is more abundant than cardiac troponins (cTn) and is released more rapidly after acute myocardial infarction (AMI). We evaluated cMyC as an adjunct or alternative to cTn in the early diagnosis of AMI.Methods:Unselected patients (N=1954) presenting to the emergency department with symptoms suggestive of AMI, concentrations of cMyC, and high-sensitivity (hs) and standard-sensitivity cTn were measured at presentation. The final diagnosis of AMI was independently adjudicated using all available clinical and biochemical information without knowledge of cMyC. The prognostic end point was long-term mortality.Results:Final diagnosis was AMI in 340 patients (17%). Concentrations of cMyC at presentation were significantly higher in those with versus without AMI (median, 237 ng/L versus 13 ng/L, P<0.001). Discriminatory power for AMI, as quantified by the area under the receiver-operating characteristic curve (AUC), was comparable for cMyC (AUC, 0.924), hs-cTnT (AUC, 0.927), and hs-cTnI (AUC, 0.922) and superior to cTnI measured by a contemporary sensitivity assay (AUC, 0.909). The combination of cMyC with hs-cTnT or standard-sensitivity cTnI (but not hs-cTnI) led to an increase in AUC to 0.931 (P<0.0001) and 0.926 (P=0.003), respectively. Use of cMyC more accurately classified patients with a single blood test into rule-out or rule-in categories: Net Reclassification Improvement +0.149 versus hs-cTnT, +0.235 versus hs-cTnI (P<0.001). In early presenters (chest pain <3 h), the improvement in rule-in/rule-out classification with cMyC was larger compared with hs-cTnT (Net Reclassification Improvement +0.256) and hs-cTnI (Net Reclassification Improvement +0.308; both P<0.001). Comparing the C statistics, cMyC was superior to hs-cTnI and standard sensitivity cTnI (P<0.05 for both) and similar to hs-cTnT at predicting death at 3 years.Conclusions:cMyC at presentation provides discriminatory power comparable to hs-cTnT and hs-cTnI in the diagnosis of AMI and may perform favorably in patients presenting early after symptom onset.Clinical Trial Registration:URL: https://www.clinicaltrials.gov. Unique identifier: NCT00470587.

In Vivo Functional Selection Identifies Cardiotrophin-1 as a Cardiac Engraftment Factor for Mesenchymal Stromal Cells [Original Research Article]
16/10/2017
Francesca Bortolotti, Giulia Ruozi, Antonella Falcione, Sara Doimo, Matteo Dal Ferro, Pierluigi Lesizza, Lorena Zentilin, Lawrence Banks, Serena Zacchigna, Mauro Giacca
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Background:Transplantation of cells into the infarcted heart has significant potential to improve myocardial recovery; however, low efficacy of cell engraftment still limits therapeutic benefit. Here, we describe a method for the unbiased, in vivo selection of cytokines that improve mesenchymal stromal cell engraftment into the heart both in normal conditions and after myocardial infarction.Methods:An arrayed library of 80 secreted factors, including most of the currently known interleukins and chemokines, were individually cloned into adeno-associated viral vectors. Pools from this library were then used for the batch transduction of bone marrow–derived mesenchymal stromal cells ex vivo, followed by intramyocardial cell administration in normal and infarcted mice. Three weeks after injection, vector genomes were recovered from the few persisting cells and identified by sequencing DNA barcodes uniquely labeling each of the tested cytokines.Results:The most effective molecule identified by this competitive engraftment screening was cardiotrophin-1, a member of the interleukin-6 family. Intracardiac injection of mesenchymal stromal cells transiently preconditioned with cardiotrophin-1 preserved cardiac function and reduced infarct size, parallel to the persistence of the transplanted cells in the healing hearts for at least 2 months after injection. Engraftment of cardiotrophin-1–treated mesenchymal stromal cells was consequent to signal transducer and activator of transcription 3–mediated activation of the focal adhesion kinase and its associated focal adhesion complex and the consequent acquisition of adhesive properties by the cells.Conclusions:These results support the feasibility of selecting molecules in vivo for their functional properties with adeno-associated viral vector libraries and identify cardiotrophin-1 as a powerful cytokine promoting cell engraftment and thus improving cell therapy of the infarcted myocardium.

FunSel [Editorials]
16/10/2017
James E. Hudson, Enzo R. Porrello
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Epigenome-Wide Association Study Identifies Cardiac Gene Patterning and a Novel Class of Biomarkers for Heart Failure [Original Research Article]
16/10/2017
Benjamin Meder, Jan Haas, Farbod Sedaghat-Hamedani, Elham Kayvanpour, Karen Frese, Alan Lai, Rouven Nietsch, Christina Scheiner, Stefan Mester, Diana Martins Bordalo, Ali Amr, Carsten Dietrich, Dietmar Pils, Dominik Siede, Hauke Hund, Andrea Bauer, Daniel Benjamin Holzer, Arjang Ruhparwar, Matthias Mueller-Hennessen, Dieter Weichenhan, Christoph Plass, Tanja Weis, Johannes Backs, Maximilian Wuerstle, Andreas Keller, Hugo A. Katus, Andreas E. Posch
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Background:Biochemical DNA modification resembles a crucial regulatory layer among genetic information, environmental factors, and the transcriptome. To identify epigenetic susceptibility regions and novel biomarkers linked to myocardial dysfunction and heart failure, we performed the first multi-omics study in myocardial tissue and blood of patients with dilated cardiomyopathy and controls.Methods:Infinium human methylation 450 was used for high-density epigenome-wide mapping of DNA methylation in left-ventricular biopsies and whole peripheral blood of living probands. RNA deep sequencing was performed on the same samples in parallel. Whole-genome sequencing of all patients allowed exclusion of promiscuous genotype-induced methylation calls.Results:In the screening stage, we detected 59 epigenetic loci that are significantly associated with dilated cardiomyopathy (false discovery corrected P≤0.05), with 3 of them reaching epigenome-wide significance at P≤5×10−8. Twenty-seven (46%) of these loci could be replicated in independent cohorts, underlining the role of epigenetic regulation of key cardiac transcription regulators. Using a staged multi-omics study design, we link a subset of 517 epigenetic loci with dilated cardiomyopathy and cardiac gene expression. Furthermore, we identified distinct epigenetic methylation patterns that are conserved across tissues, rendering these CpGs novel epigenetic biomarkers for heart failure.Conclusions:The present study provides to our knowledge the first epigenome-wide association study in living patients with heart failure using a multi-omics approach.

DNA Methylation and Human Heart Failure [Editorials]
16/10/2017
Christoph D. Rau, Thomas M. Vondriska
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Activation and Inhibition of Sodium-Hydrogen Exchanger Is a Mechanism That Links the Pathophysiology and Treatment of Diabetes Mellitus With That of Heart Failure [In Depth]
16/10/2017
Milton Packer
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The mechanisms underlying the progression of diabetes mellitus and heart failure are closely intertwined, such that worsening of one condition is frequently accompanied by worsening of the other; the degree of clinical acceleration is marked when the 2 coexist. Activation of the sodium-hydrogen exchanger in the heart and vasculature (NHE1 isoform) and the kidneys (NHE3 isoform) may serve as a common mechanism that links both disorders and may underlie their interplay. Insulin insensitivity and adipokine abnormalities (the hallmarks of type 2 diabetes mellitus) are characteristic features of heart failure; conversely, neurohormonal systems activated in heart failure (norepinephrine, angiotensin II, aldosterone, and neprilysin) impair insulin sensitivity and contribute to microvascular disease in diabetes mellitus. Each of these neurohormonal derangements may act through increased activity of both NHE1 and NHE3. Drugs used to treat diabetes mellitus may favorably affect the pathophysiological mechanisms of heart failure by inhibiting either or both NHE isoforms, and drugs used to treat heart failure may have beneficial effects on glucose tolerance and the complications of diabetes mellitus by interfering with the actions of NHE1 and NHE3. The efficacy of NHE inhibitors on the risk of cardiovascular events may be enhanced when heart failure and glucose intolerance coexist and may be attenuated when drugs with NHE inhibitory actions are given concomitantly. Therefore, the sodium-hydrogen exchanger may play a central role in the interplay of diabetes mellitus and heart failure, contribute to the physiological and clinical progression of both diseases, and explain certain drug–drug and drug–disease interactions that have been reported in large-scale randomized clinical trials.

Increases in Natriuretic Peptides Precede Heart Failure Hospitalization in Patients With a Recent Coronary Event and Type 2 Diabetes Mellitus [Research Letter]
16/10/2017
Emil Wolsk, Brian Claggett, Rafael Diaz, Kenneth Dickstein, Hertzel C. Gerstein, Lars Kober, Francesca C. Lawson, Eldrin F. Lewis, Aldo P. Maggioni, John J. V. McMurray, Jeffrey L. Probstfield, Matthew C. Riddle, Scott D. Solomon, Jean–Claude Tardif, Marc A. Pfeffer
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Letter by Musso et al Regarding Article, “Cardiac Outcomes After Ischemic Stroke or Transient Ischemic Attack: Effects of Pioglitazone in Patients With Insulin Resistance Without Diabetes Mellitus” [Correspondence]
16/10/2017
Giovanni Musso, Maurizio Cassader, Roberto Gambino
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Letter by Jin-Shan and Xue-Bin Regarding Article, “Cardiac Outcomes After Ischemic Stroke or Transient Ischemic Attack: Effects of Pioglitazone in Patients With Insulin Resistance Without Diabetes Mellitus” [Correspondence]
16/10/2017
He Jin-Shan, Li Xue-Bin
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Response by Young et al to Letters Regarding Article, “Cardiac Outcomes After Ischemic Stroke or Transient Ischemic Attack: Effects of Pioglitazone in Patients With Insulin Resistance Without Diabetes Mellitus” [Correspondence]
16/10/2017
Lawrence H. Young, Catherine M. Viscoli, Silvio E. Inzucchi, Walter N. Kernan
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Who Would Be Branded With Failure? [On My Mind]
9/10/2017
Lynne Warner Stevenson
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Prolonged, Uninterrupted Sedentary Behavior and Glycemic Biomarkers Among US Hispanic/Latino Adults [Original Research Article]
9/10/2017
Keith M. Diaz, Jeff Goldsmith, Heather Greenlee, Garrett Strizich, Qibin Qi, Yasmin Mossavar-Rahmani, Denise C. Vidot, Christina Buelna, Carrie E. Brintz, Tali Elfassy, Linda C. Gallo, Martha L. Daviglus, Daniela Sotres-Alvarez, Robert C. Kaplan
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Background:Excessive sedentary time is ubiquitous in developed nations and is associated with deleterious health outcomes. Few studies have examined whether the manner in which sedentary time is accrued (in short or long bouts) carries any clinical relevance. The purpose of this study was to examine the association of prolonged, uninterrupted sedentary behavior with glycemic biomarkers in a cohort of US Hispanic/Latino adults.Methods:We studied 12 083 participants from the HCHS/SOL (Hispanic Community Health Study/Study of Latinos), a population-based study of Hispanic/Latino adults 18 to 74 years of age. Homeostatic model assessment of insulin resistance and glycosylated hemoglobin were measured from a fasting blood sample, and 2-hour glucose was measured after an oral glucose tolerance test. Sedentary time was objectively measured with a hip-mounted accelerometer. Prolonged, uninterrupted sedentariness was expressed as mean sedentary bout length.Results:After adjustment for potential confounders and moderate to vigorous physical activity, longer sedentary bout duration was dose-dependently associated with increased homeostatic model assessment of insulin resistance (P for trend<0.001) and 2-hour glucose levels (P for trend=0.015). These associations were not independent of total sedentary time; however, a significant interaction between sedentary bout duration and total sedentary time was observed. Evaluation of the joint association of total sedentary time and sedentary bout duration showed that participants in the upper quartile for both sedentary characteristics (ie, high total sedentary time and high sedentary bout duration) had the highest levels of homeostatic model assessment of insulin resistance (P<0.001 versus low group for both sedentary characteristics) and 2-hour glucose (P=0.002 versus low group for both sedentary characteristics). High total sedentary time or high sedentary bout duration alone were not associated with differences in any glycemic biomarkers.Conclusions:Accruing sedentary time in prolonged, uninterrupted bouts may be deleteriously associated with biomarkers of glucose regulation.







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