2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.

ACC/AHA
: American College of Cardiology/American Heart Association
ACCF/AHA
: American College of Cardiology Foundation/American Heart Association
ACE
: angiotensin-converting enzyme
ACEI
: angiotensin-converting enzyme inhibitor
ACS
: acute coronary syndrome
AF
: atrial fibrillation

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2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

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

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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

The so-called congenital long QT syndrome (LQTS) is an inherited arrhythmia syndrome predisposing to life-threatening ventricular arrhythmias and sudden death. It is caused by prolongation of the repolarization phase of the cardiac action potential, which may manifest as lengthening of the heart rate-corrected QT interval (QTc) on the surface electrocardiogram (ECG). This chapter reviews the clinical presentation of LQTS, its diagnosis, and principles of management in the context of recent clinical advances and molecular genetics, with a focus on the most common forms of LQTS – LQT1, LQT2, and LQT3.

Long QT Syndrome

There have been remarkable advances in our knowledge of the underlying heritability of cardiac arrhythmias. Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, progressive cardiac conduction disease and the short QT syndrome comprise the inherited arrhythmia syndromes (IASs). Pathogenic variants in cardiac ion channel and calcium handling protein genes lead to these conditions, usually in the absence of overt structural cardiac disease. Diagnosis is contingent on the ECG phenotype but genetic testing may help to confirm the diagnosis and provide information on the mechanism of arrhythmogenesis that may guide treatment and provide prognostic information in relation to the risk of sudden arrhythmic death. Clinical genetic testing uses ‘panels’ of genes that are the likely culprits for the IASs being investigated. An International Consortium (Clinical Genome Resource) has curated gene panels based on genetic and experimental evidence of causation of inherited conditions and that have a role in clinical genetic testing. A ‘single gene’ or monogenic basis for IASs exists but in future, missing heritability and incomplete penetrance will be uncovered by association of common variants through genome-wide association studies. Novel rare variants will also be detected through whole-genome sequencing. The formulation of polygenic risk scores will likely help to predict phenotypic expression and response to treatments/risk stratification and move genetic testing very much to the fore of the diagnostic process.

Cardiogenetics: the role of genetic testing for inherited arrhythmia syndromes and sudden death

We read with interest the recent paper by Colivicchi et al., whichreported on the clinical presentation, diagnostic work-up and long-term outcome of a consecutive series of elite athletes (n=33) with recurrent exercise-related syncope (ERS).1

The athletes were referred to the authors' syncope clinic after 12-lead ECG and transthoracic echocardiography. The only structural heart disease detected was mitral valve prolapse with mild mitralregurgitation in two individuals. Subsequently, Holter monitoring, exercise testing, electro-encephalography, electrophysiological testing and head-up tilt testing were performed, although the numbers of each investigation performed was not stated. Most of the athletes (66%) had a positive …

Elite athletes with recurrent ERS.

Early Repolarisation in Athletes

INTRODUCTION Before ablation, predicting the site of origin (SOO) of outflow tract ventricular arrhythmia (OTVA), can inform patient consent and facilitate appropriate procedural planning. We set out to determine if OTVA variability can accurately predict SOO. METHODS Consecutive patients with a clear SOO identified at OTVA ablation had their prior 24-h ambulatory ECGs retrospectively analysed (derivation cohort). Percentage ventricular ectopic (VE) burden, hourly VE values, episodes of trigeminy/bigeminy, and the variability in these parameters were evaluated for their ability to distinguish right from left-sided SOO. Effective parameters were then prospectively tested on a validation cohort of consecutive patients undergoing their first OTVA ablation. RESULTS High VE variability (coefficient of variation ≥0.7) and the presence of any hour with <50 VE, were found to accurately predict RVOT SOO in a derivation cohort of 40 patients. In a validation cohort of 29 patients, the correct SOO was prospectively identified in 23/29 patients (79.3%) using CoV, and 26/29 patients (89.7%) using VE < 50. Including current ECG algorithms, VE < 50 had the highest Youden Index (78), the highest positive predictive value (95.0%) and the highest negative predictive value (77.8%). CONCLUSION VE variability and the presence of a single hour where VE < 50 can be used to accurately predict SOO in patients with OTVA. Accuracy of these parameters compares favorably to existing ECG algorithms.

Elijah R. Behr

Papers

Long QT Syndrome

Cardiogenetics: the role of genetic testing for inherited arrhythmia syndromes and sudden death

Elite athletes with recurrent ERS.

Early Repolarisation in Athletes

Hourly Variability in Outflow Tract Ectopy as a Predictor of its Site of Origin