Genetic variation in the alternative splicing regulator RBM20 is associated with dilated cardiomyopathy.

Background: Dilated cardiomyopathy (DCM) is a leading cause of heart failure and death. The etiology of DCM is genetically heterogeneous.

Objectives: We sought to define the prevalence of mutations in the RNA splicing protein RBM20 in a large cohort with DCM and to determine whether genetic variation in RBM20 is associated with clinical outcomes.

Targeting device therapy: genomics of sudden death.

This article discusses the development and use of genomic predictors to define the population at risk for sudden cardiac death, which is usually defined as death from cardiac causes within an hour of symptom onset. The identification of genetic predictors of sudden death in heart failure is in its earliest stages. Mutations in ion channels have been shown to cause inherited forms of sudden death; there is, however, little evidence that mutations or rare single nucleotide polymorphisms (SNPs) in those genes are important causes of the common forms of sudden death.

Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage.

Background And Purpose: Cardiac injury persistence after aneurysmal subarachnoid hemorrhage (aSAH) is not well described. We hypothesized that post-aSAH cardiac injury, detected by elevated cardiac troponin I (cTnI), is related to aSAH severity and associated with electrocardiographic and structural echocardiographic abnormalities that are persistent.

Methods: Prospective longitudinal study was conducted of patients with aSAH with Fisher grade >or=2 and/or Hunt/Hess grade >or=3.

Ventricular arrhythmia risk after subarachnoid hemorrhage.

Introduction: Cardiac morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH) are attributable to myocardial injury, decreased ventricular function, and ventricular arrhythmia (VA). Our objective was to test the relationships between QTc prolongation, VA, and survival after SAH.

Methods: In 200 subjects with acute aneurysmal SAH, electrocardiograms, echocardiograms, and telemetry were evaluated.

Relation of elevation in cardiac troponin I to clinical severity, cardiac dysfunction, and pulmonary congestion in patients with subarachnoid hemorrhage.

An increase in cardiac troponin I (cTnI) occurs often after aneurysmal subarachnoid hemorrhage (SAH), but its significance is not well understood. One hundred three patients with SAH were prospectively evaluated in the SAHMII Study to determine the relations of cTnI to clinical severity, systolic and diastolic cardiac function, pulmonary congestion, and length of intensive care unit stay. Echocardiographic ejection fraction, wall motion score, mitral inflow early diastolic (E) and mitral annular early (E') velocities were assessed.