Rationale and Design of the Personalized Therapy Study: Evaluating Real-World Performance of Two Automated Defibrillation Therapy Algorithms.

Background: Barriers to maximizing patient benefit with implantable defibrillation devices include limited ability to tailor antitachycardia pacing (ATP) therapy in real-time and identify patients at risk of heart failure (HF) events early on. The Personalized Therapy study aims to evaluate the performance of two algorithms, intrinsic ATP (iATP) and TriageHF, to address these barriers in routine clinical practice.

Methods And Results: The Personalized Therapy Study was designed as a prospective, multicenter, post-market registry study expected to enroll approximately 2,200 patients meeting the following criteria: (1) implanted with a study-eligible device regardless of procedure type; (2) Medtronic CareLink® Network enrolled; (3) TriageHF enabled within CareLink and High Risk Alert notifications turned ON; and (4) iATP enabled.

The importance of early evaluation after cardiac resynchronization therapy to redefine response: Pooled individual patient analysis from 5 prospective studies.

Background: Cardiac resynchronization therapy (CRT) reduces mortality and improves outcomes in appropriately selected patients with heart failure (HF); however, response may vary.

Objective: We sought to correlate 6-month CRT response assessed by clinical composite score (CCS) and left ventricular end-systolic volume index (LVESVi) with longer-term mortality and HF-related hospitalizations.

Methods: Individual patient data from 5 prospective CRT studies-Multicenter InSync Randomized Clinical Evaluation (MIRACLE), Multicenter InSync ICD Randomized Clinical Evaluation (MIRACLE ICD), InSync III Marquis, predictors of response to cardiac resynchronization therapy (PROSPECT), and Adaptive CRT-were pooled.

Real-world behavior of CRT pacing using the AdaptivCRT algorithm on patient outcomes: Effect on mortality and atrial fibrillation incidence.

Background: The AdaptivCRT (aCRT) algorithm continuously adjusts cardiac resynchronization therapy (CRT) according to intrinsic atrioventricular conduction, providing synchronized left ventricular pacing in patients with normal PR interval and adaptive BiV pacing in patients with prolonged PR interval. Previous analyses demonstrated an association between aCRT and clinical benefit. We evaluated the incidence of patient mortality and atrial fibrillation (AF) with aCRT compared with standard CRT in a real-world population.

Elevated Myocardial Extracellular Volume Fraction in Duchenne Muscular Dystrophy.

Duchenne muscular dystrophy (DMD) is a genetic, X-linked recessive disease with an associated cardiomyopathy characterized by myocardial fibrosis leading to heart failure, arrhythmias, and death. Earlier detection and treatment of cardiac involvement in DMD hold potential to improve outcomes. Cardiovascular magnetic resonance (CMR) extracellular volume (ECV) quantification using T1 mapping is a histologically validated, non-invasive marker of diffuse fibrosis.

Comparison of right and left ventricular function and size in Duchenne muscular dystrophy.

Introduction: Right ventricular (RV) size and function in Duchenne muscular dystrophy (DMD) have not been well described. Using cardiac magnetic resonance (CMR) imaging we describe the relationship of RV and left ventricular (LV) size and function in a large DMD cohort.

Methods: Latest CMR scans of 272 patients consecutively seen at a single tertiary referral center (2011-2014) with skeletal muscle biopsy confirmed DMD were included.

Myocardial fibrosis burden predicts left ventricular ejection fraction and is associated with age and steroid treatment duration in duchenne muscular dystrophy.

Background: Patients with Duchenne muscular dystrophy exhibit progressive cardiac and skeletal muscle dysfunction. Based on prior data, cardiac dysfunction in Duchenne muscular dystrophy patients may be influenced by myocardial fibrosis and steroid therapy. We examined the longitudinal relationship of myocardial fibrosis and ventricular dysfunction using cardiac magnetic resonance in a large Duchenne muscular dystrophy cohort.

Dystrophin genotype-cardiac phenotype correlations in Duchenne and Becker muscular dystrophies using cardiac magnetic resonance imaging.

Duchenne and Becker muscular dystrophies are caused by mutations in dystrophin. Cardiac manifestations vary broadly, making prognosis difficult. Current dystrophin genotype-cardiac phenotype correlations are limited.

The relationship between cardiac resynchronization therapy and diastolic function.

Cardiac resynchronization therapy (CRT) improves measures of systolic function and clinical status. However, its effect on diastolic function is not well established. Commonly used parameters of diastolic function are measured from echocardiography, using pulse wave and tissue Doppler technologies, as well as timing and deformation data.

Effect of automated, point-of-care electronic medical record screening for appropriate implantable device use in heart failure patients.

The authors evaluated the effects of an electronic health record (EHR)-based real-time screening of outpatients for potential defibrillator therapy on practice metrics. Based on ejection fraction (EF) ≤ 35% and absence of a defibrillator, the physicians were prompted for an action: electrophysiology consultation, EF evaluation, or "not indicated." Although the number of patients screened remained stable at nearly 6000 per month, consultations and echocardiograms peaked early but returned to a low steady state by 10 months.

Patterns of left ventricular remodeling in patients with Duchenne Muscular Dystrophy: a cardiac MRI study of ventricular geometry, global function, and strain.

The cardiac disease ubiquitously associated in Duchenne Muscular Dystrophy (DMD) has traditionally been considered a progressive dilated cardiomyopathy (DCM). However, left ventricular (LV) dilatation as measured with cardiac MRI has not been a consistent finding in this population, even as circumferential strain (ε(cc)) declines with advancing disease. We hypothesized that a distinct pattern of changes in LV geometry, during the course of ε(cc) decline, distinguishes DMD associated heart disease from DCM.