The metabolic syndrome has received increased attention in the past few years. This statement from the American Heart Association (AHA) and the National Heart, Lung, and Blood Institute (NHLBI) is intended to provide up-to-date guidance for professionals on the diagnosis and management of the metabolic syndrome in adults.

The metabolic syndrome is a constellation of interrelated risk factors of metabolic origin— metabolic risk factors —that appear to directly promote the development of atherosclerotic cardiovascular disease (ASCVD).1 Patients with the metabolic syndrome also are at increased risk for developing type 2 diabetes mellitus. Another set of conditions, the underlying risk factors , give rise to the metabolic risk factors. In the past few years, several expert groups have attempted to set forth simple diagnostic criteria to be used in clinical practice to identify patients who manifest the multiple components of the metabolic syndrome. These criteria have varied somewhat in specific elements, but in general they include a combination of both underlying and metabolic risk factors.

The most widely recognized of the metabolic risk factors are atherogenic dyslipidemia, elevated blood pressure, and elevated plasma glucose. Individuals with these characteristics commonly manifest a prothrombotic state and a pro-inflammatory state as well. Atherogenic dyslipidemia consists of an aggregation of lipoprotein abnormalities including elevated serum triglyceride and apolipoprotein B (apoB), increased small LDL particles, and a reduced level of HDL cholesterol (HDL-C). The metabolic syndrome is often referred to as if it were a discrete entity with a single cause. Available data suggest that it truly is a syndrome, ie, a grouping of ASCVD risk factors, but one that probably has more than one cause. Regardless of cause, the syndrome identifies individuals at an elevated risk for ASCVD. The magnitude of the increased risk can vary according to which components of the syndrome are …

https://www.lipidcenter.com/pdf/metabolic.pdf

Diagnosis and Management of the Metabolic Syndrome An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement

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It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced in the detection, management,

/pdf/acc-aha-2006-guidelines-for-the-management-of-patients-with-27qfh9fc7i.pdf

ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease

WRITING GROUP MEMBERS Emelia J. Benjamin, MD, SCM, FAHA Michael J. Blaha, MD, MPH Stephanie E. Chiuve, ScD Mary Cushman, MD, MSc, FAHA Sandeep R. Das, MD, MPH, FAHA Rajat Deo, MD, MTR Sarah D. de Ferranti, MD, MPH James Floyd, MD, MS Myriam Fornage, PhD, FAHA Cathleen Gillespie, MS Carmen R. Isasi, MD, PhD, FAHA Monik C. Jiménez, ScD, SM Lori Chaffin Jordan, MD, PhD Suzanne E. Judd, PhD Daniel Lackland, DrPH, FAHA Judith H. Lichtman, PhD, MPH, FAHA Lynda Lisabeth, PhD, MPH, FAHA Simin Liu, MD, ScD, FAHA Chris T. Longenecker, MD Rachel H. Mackey, PhD, MPH, FAHA Kunihiro Matsushita, MD, PhD, FAHA Dariush Mozaffarian, MD, DrPH, FAHA Michael E. Mussolino, PhD, FAHA Khurram Nasir, MD, MPH, FAHA Robert W. Neumar, MD, PhD, FAHA Latha Palaniappan, MD, MS, FAHA Dilip K. Pandey, MBBS, MS, PhD, FAHA Ravi R. Thiagarajan, MD, MPH Mathew J. Reeves, PhD Matthew Ritchey, PT, DPT, OCS, MPH Carlos J. Rodriguez, MD, MPH, FAHA Gregory A. Roth, MD, MPH Wayne D. Rosamond, PhD, FAHA Comilla Sasson, MD, PhD, FAHA Amytis Towfighi, MD Connie W. Tsao, MD, MPH Melanie B. Turner, MPH Salim S. Virani, MD, PhD, FAHA Jenifer H. Voeks, PhD Joshua Z. Willey, MD, MS John T. Wilkins, MD Jason HY. Wu, MSc, PhD, FAHA Heather M. Alger, PhD Sally S. Wong, PhD, RD, CDN, FAHA Paul Muntner, PhD, MHSc On behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart Disease and Stroke Statistics—2017 Update

Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association

Author(s): Writing Group Members; Mozaffarian, Dariush; Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; Das, Sandeep R; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Isasi, Carmen R; Jimenez, Monik C; Judd, Suzanne E; Kissela, Brett M; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Magid, David J; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Muntner, Paul; Mussolino, Michael E; Nasir, Khurram; Neumar, Robert W; Nichol, Graham; Palaniappan, Latha; Pandey, Dilip K; Reeves, Mathew J; Rodriguez, Carlos J; Rosamond, Wayne; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Woo, Daniel; Yeh, Robert W; Turner, Melanie B; American Heart Association Statistics Committee; Stroke Statistics Subcommittee

Heart Disease and Stroke Statistics—2016 Update: A Report From the American Heart Association

Appendix I: List of Statistical Fact Sheets. URL: http://www.americanheart.org/presenter.jhtml?identifier=2007

We wish to thank Drs Brian Eigel and Michael Wolz for their valuable comments and contributions. We would like to acknowledge Tim Anderson and Tom Schneider for their editorial contributions and Karen Modesitt for her administrative assistance.

Disclosures 



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# Summary {#article-title-2}

Each year, the American Heart Association, in conjunction with the Centers for Disease Control and Prevention, the National Institutes of Health, and other government agencies, brings together the most up-to-date statistics on heart disease, stroke, other vascular diseases, and their risk factors and presents them in its Heart Disease and Stroke Statistical Update. The Statistical Update is a valuable resource for researchers, clinicians, healthcare policy makers, media professionals, the lay public, and many others who seek the best national data available on disease …

Heart Disease and Stroke Statistics—2010 Update A Report From the American Heart Association

Critical Care Medicine www.ccmjournal.org 1199 REFERENCES 1. Idris AH, Roberts LJ 2nd, Caruso L, et al: Oxidant injury occurs rapidly after cardiac arrest, cardiopulmonary resuscitation, and reperfusion. Crit Care Med 2005; 33:2043–2048 2. Geppert A, Zorn G, Karth GD, et al: Soluble selectins and the systemic inflammatory response syndrome after successful cardiopulmonary resuscitation. Crit Care Med 2000; 28:2360–2365 3. Trzeciak S, Jones AE, Kilgannon JH, et al: Significance of arterial hypotension after resuscitation from cardiac arrest. Crit Care Med 2009; 37:2895–2903; quiz 2904 4. Hypothermia after Cardiac Arrest Study Group: Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346:549–556 5. Bernard SA, Gray TW, Buist MD, et al: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002; 346:557–563 6. Perman SM, Ellenberg JH, Grossestreuer AV, et al: Shorter time to target temperature is associated with poor neurologic outcome in post-arrest patients treated with targeted temperature management. Resuscitation 2015; 88:114–119 7. Uber AJ, Perman SM, Cocchi MN, et al: Increased Heat Generation in Postcardiac Arrest Patients During Targeted Temperature Management Is Associated With Better Outcomes. Crit Care Med 2018; 46:1133–1138 8. Choi HA, Ko SB, Presciutti M, et al: Prevention of shivering during therapeutic temperature modulation: The Columbia anti-shivering protocol. Neurocrit Care 2011; 14:389–394 9. Kilgannon JH, Roberts BW, Jones AE, et al: Arterial blood pressure and neurologic outcome after resuscitation from cardiac arrest*. Crit Care Med 2014; 42:2083–2091 10. Roberts BW, Kilgannon JH, Chansky ME, et al: Association between postresuscitation partial pressure of arterial carbon dioxide and neurological outcome in patients with post-cardiac arrest syndrome. Circulation 2013; 127:2107–2113 11. Roberts BW, Kilgannon JH, Hunter BR, et al: Association between early hyperoxia exposure after resuscitation from cardiac arrest and neurological disability: A prospective multi-center protocol-directed cohort study. Circulation 2018 Feb 1. [Epub ahead of print] 12. Sundgreen C, Larsen FS, Herzog TM, et al: Autoregulation of cerebral blood flow in patients resuscitated from cardiac arrest. Stroke 2001; 32:128–132 13. Scaravilli V, Bonacina D, Citerio G: Rewarming: Facts and myths from the systemic perspective. Crit Care 2012; 16(Suppl 2):A25 14. Geocadin RG, Murthy SB: Prognostication following cardiac arrest: Do we have our patients’ safety in mind?*. Crit Care Med 2014; 42:1959–1961 15. Oddo M, Friberg H: Neuroprognostication after cardiac arrest in the light of targeted temperature management. Curr Opin Crit Care 2017; 23:244–250

Working Memory Training: A Promising Intervention?


 Introduction:
 Standard of care (SOC) anticoagulation for thromboembolism (TE) prevention in patients <18 years old with cardiac disease includes low molecular weight heparins or vitamin K antagonists. Limited data exist comparing direct oral anticoagulants as edoxaban with conventional anticoagulants in this population.
 
 
 Hypothesis:
 Edoxaban is at least as safe as the current standard-of-care (low molecular weight heparins and/or vitamin K antagonists) with regard to the incidence of major and clinically relevant nonmajor bleeding in pediatric patients with cardiac diseases at risk of thromboembolism.
 
 
 Methods:
 We performed a phase 3, multinational, prospective, randomized, open-label, blinded-endpoint trial in patients <18 years old with cardiac disease (ENNOBLE-ATE, NCT00687882). Children were randomized 2:1 to age- and weight-based oral edoxaban once-daily versus SOC for 3 months (main study). Randomization was stratified by concomitant use of aspirin and by underlying disease groups, as follow: history of Fontan procedure; Kawasaki disease; heart failure; other. Both groups continued in an extension with edoxaban through 1 year. The primary endpoint was adjudicated International Society on Thrombosis and Haemostasis defined clinically-relevant bleeding (CRB). The main secondary endpoint was a composite of symptomatic TE and asymptomatic intracardiac thrombosis.
 
 
 Results:
 We randomized 168 children from May 2018 to September 2021. The CRB event rates were similar between groups during the main period. One subject per group experienced a nonmajor CRB. Treatment-emergent adverse events occurred in 46.8% (51/109) with edoxaban and 41.4% (24/58) with SOC. One SOC subject experienced 2 TE events (DVT with PE). In 152 subjects continuing in the extension, one CRB event (0.7%; trauma related) and 4 TEs occurred (2.8%; 2 strokes and 2 coronary artery thromboses and/or myocardial infarctions).
 
 
 Conclusion:
 Bleeding and TE occurred rarely for both groups and during the extension,suggesting that edoxaban is safe and effective for TE prevention in this population. Once daily edoxaban may provide advantage for children considering difficulties with enoxaparin injections and food and drug interactions with warfarin.


Abstract 11530: Edoxaban For Pediatric Patients With Cardiac Diseases: A Randomized, Open Label, Multicenter Study

Blood glucose level and early neurologic recovery after cardiac surgery with circulatory arrest in infants

Frequency domain near infrared spectroscopy (FD-NIRS) and diffuse correlation spectroscopy (DCS) can provide noninvasive means to study cerebral hemodynamics in neonates with congenital heart disease (CHD). Using these advanced optical technologies, our preliminary data shows that neonates with CHD have lower cerebral oxygen metabolism than healthy neonates.

Jane W. Newburger

Papers

Working Memory Training: A Promising Intervention?

Abstract 11530: Edoxaban For Pediatric Patients With Cardiac Diseases: A Randomized, Open Label, Multicenter Study

Blood glucose level and early neurologic recovery after cardiac surgery with circulatory arrest in infants

Lower Cerebral Oxygen Metabolism In Neonates With Congenital Heart Disease As Compared To Healthy Neonates

Evaluation of the Bioavailability of Sarpicillin, the Methoxymethyl Ester of Hetacillin, in Humans