Risk Stratification in Arrhythmic Right Ventricular Cardiomyopathy Without Implantable Cardioverter-Defibrillators.

Objectives: The primary objective of this study is risk stratification of patients with arrhythmic right ventricular cardiomyopathy (ARVC).

Background: There is a need to identify those who need an automatic implantable defibrillator (ICD) to prevent sudden death.

Methods: This is an analysis of 88 patients with ARVC from three centers who were not treated with an ICD.

Mimicking the cardiac cycle in intact cardiomyocytes using diastolic and systolic force clamps; measuring power output.

Aims: A single isolated cardiomyocyte is the smallest functional unit of the heart. Yet, all single isolated cardiomyocyte experiments have been limited by the lack of proper methods that could reproduce a physiological cardiac cycle. We aimed to investigate the contractile properties of a single cardiomyocyte that correctly mimic the cardiac cycle.

AlluraClarity Radiation Dose-Reduction Technology in the Hybrid Operating Room During Endovascular Aneurysm Repair.

Purpose: To evaluate the effect of radiation dose reduction with the Allura ClarityIQ image processing technology for fixed C-arms in comparison with a mobile C-arm and an Allura fixed C-arm without ClarityIQ technology during endovascular aneurysm repair (EVAR) procedures.

Methods: Radiation dose data from 85 patients (mean age 74.2±7.

Routinely analyzed leukocyte characteristics improve prediction of mortality after coronary angiography.

Background: Inflammation and leukocyte infiltration are hallmarks of atherosclerosis. Clinically routine hematology analyzers mostly perform an entire differential blood count by default, irrespective of the requested parameter. We hypothesize that these normally unreported leukocyte characteristics associate with coronary artery disease (CAD) severity and can improve prediction of mortality in coronary angiography patients.

BLT1 antagonist LSN2792613 reduces infarct size in a mouse model of myocardial ischaemia-reperfusion injury.

Aims: Restoration of coronary blood flow is crucial in the treatment of acute myocardial infarction. Reperfusion, however, induces ischaemia-reperfusion (IR) injury, which further deteriorates myocardial function. The innate immune system plays an important role in this process, mediating rapid influx of immune cells into the reperfused myocardium.

Trans-ancestry genome-wide association study identifies 12 genetic loci influencing blood pressure and implicates a role for DNA methylation.

We carried out a trans-ancestry genome-wide association and replication study of blood pressure phenotypes among up to 320,251 individuals of East Asian, European and South Asian ancestry. We find genetic variants at 12 new loci to be associated with blood pressure (P = 3.9 × 10(-11) to 5.

Women Undergoing Coronary Angiography for Myocardial Infarction or Who Present With Multivessel Disease Have a Poorer Prognosis Than Men.

Background: Coronary artery disease affects both men and women. In this study, we examine sex-specific differences in occurrence of major adverse cardiovascular events (MACEs) after coronary angiography.

Methods: We analyzed data from the coronary angiography cohort Utrecht Coronary Biobank (n = 1283 men, 480 women).

Approach to family screening in arrhythmogenic right ventricular dysplasia/cardiomyopathy.

Aims: A combination of variable expression, age-related penetrance, and unpredictable arrhythmic events complicates management of relatives of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) patients. We aimed to (i) determine predictors of ARVD/C diagnosis and (ii) optimize arrhythmic risk stratification among first-degree relatives of ARVD/C patients.

Methods And Results: Detailed phenotypic and outcome data of 274 first-degree relatives (46% male; 36.

Liver X receptor activation enhances CVB3 viral replication during myocarditis by stimulating lipogenesis.

Aims: Viral myocarditis (VM) is severe cardiac inflammation that can result in sudden death or congestive heart failure in previously healthy adults, with no effective therapy. Liver X receptor (LXR) agonists have both anti-inflammatory and lipid-lowering properties. This study investigates whether LXR agonist T0901317 may modulate viral replication and cardiac inflammation during VM.

Targets for therapy in sarcomeric cardiomyopathies.

To date, no compounds or interventions exist that treat or prevent sarcomeric cardiomyopathies. Established therapies currently improve the outcome, but novel therapies may be able to more fundamentally affect the disease process and course. Investigations of the pathomechanisms are generating molecular insights that can be useful for the design of novel specific drugs suitable for clinical use.

Research priorities in sarcomeric cardiomyopathies.

The clinical variability in patients with sarcomeric cardiomyopathies is striking: a mutation causes cardiomyopathy in one individual, while the identical mutation is harmless in a family member. Moreover, the clinical phenotype varies ranging from asymmetric hypertrophy to severe dilatation of the heart. Identification of a single phenotype-associated disease mechanism would facilitate the design of targeted treatments for patient groups with different clinical phenotypes.

Faster cross-bridge detachment and increased tension cost in human hypertrophic cardiomyopathy with the R403Q MYH7 mutation.

The first mutation associated with hypertrophic cardiomyopathy (HCM) is the R403Q mutation in the gene encoding β-myosin heavy chain (β-MyHC). R403Q locates in the globular head of myosin (S1), responsible for interaction with actin, and thus motor function of myosin. Increased cross-bridge relaxation kinetics caused by the R403Q mutation might underlie increased energetic cost of tension generation; however, direct evidence is absent.

Gene-specific increase in the energetic cost of contraction in hypertrophic cardiomyopathy caused by thick filament mutations.

Aims: Disease mechanisms regarding hypertrophic cardiomyopathy (HCM) are largely unknown and disease onset varies. Sarcomere mutations might induce energy depletion for which until now there is no direct evidence at sarcomere level in human HCM. This study investigated if mutations in genes encoding myosin-binding protein C (MYBPC3) and myosin heavy chain (MYH7) underlie changes in the energetic cost of contraction in the development of human HCM disease.

NVVC/NHJ Durrer prizes 2013.

At the annual Spring Congress of the NVVC, the Durrer prizes were awarded to the authors of two of the best original/review articles published in the year 2013, one paper being more basically oriented and one paper being more clinically oriented. This annual tradition has existed since the year 2006.