Obstructive Sleep Apnea in Heart Failure: Review of Prevalence, Treatment with Continuous Positive Airway Pressure, and Prognosis.

Obstructive sleep apnea is a sleep-related breathing disorder that has a major impact on cardiovascular function. It has been associated with hypertension, coronary artery disease, cardiac arrhythmias, sudden cardiac death, and heart failure. This review focuses on the relationship between obstructive sleep apnea and heart failure with either reduced or preserved ejection fraction.

Heart failure performance measures: do they have an impact on 30-day readmission rates?

Congestive heart failure (CHF) accounts for more health care costs than any other diagnosis. Readmissions contribute to this expenditure. The authors evaluated the relationship between adherence to performance metrics and 30-day readmissions.

Comparison of the 2006 and 2010 cardiac CT appropriateness criteria in a real-world setting.

Background: Coronary CT angiography (CCTA) is a relatively new technique whose role has yet to be fully defined. The initial appropriateness criteria (AC) guidelines published in 2006 have already been revised. There is paucity of data on the effect of the AC on the use of CCTA at academic centers and none for the private sector.

Comparative effectiveness analysis of anticoagulant strategies in a large observational database of percutaneous coronary interventions.

Background: Percutaneous coronary intervention (PCI) is the most commonly used procedure for coronary revascularization. There are multiple adjuvant anticoagulation strategies available. In this era of cost containment, we performed a comparative effectiveness analysis of clinical outcomes and cost of the major anticoagulant strategies across all types of PCI procedures in a large observational database.

The relationship between childhood trauma and borderline personality symptomatology in a consecutive sample of cardiac stress test patients.

Objective: In this study, we examined relationships between five types of childhood trauma and two measures of borderline personality symptomatology in a non-psychiatric clinical population in order to assess a potential association between these variables in a non-psychiatric-treatment-seeking population.

Method: Using a cross-sectional sample and a survey approach in 250 consecutive patients presenting for cardiac stress testing, we explored self-reported histories of five types of childhood trauma (i.e.

Prevalence and self-reported medical history of overweight in a cardiac stress testing population.

Objectives: To determine the prevalence of overweight in a cardiac stress testing population, and the percentage of subjects who indicate a history of overweight.

Methods: A total of 251 consecutive subjects presenting for cardiac stress testing in a 450-bed community hospital from June to September 2010 were asked to complete a survey booklet. The survey included all patients presenting for stress testing, regardless of indication.

Multiple interactions between the alpha 2C- and beta1-adrenergic receptors influence heart failure survival.

Background: Persistent stimulation of cardiac beta1-adrenergic receptors by endogenous norepinephrine promotes heart failure progression. Polymorphisms of this gene are known to alter receptor function or expression, as are polymorphisms of the alpha 2C-adrenergic receptor, which regulates norepinephrine release from cardiac presynaptic nerves. The purpose of this study was to investigate possible synergistic effects of polymorphisms of these two intronless genes (ADRB1 and ADRA2C, respectively) on the risk of death/transplant in heart failure patients.

A GRK5 polymorphism that inhibits beta-adrenergic receptor signaling is protective in heart failure.

Beta-adrenergic receptor (betaAR) blockade is a standard therapy for cardiac failure and ischemia. G protein-coupled receptor kinases (GRKs) desensitize betaARs, suggesting that genetic GRK variants might modify outcomes in these syndromes. Re-sequencing of GRK2 and GRK5 revealed a nonsynonymous polymorphism of GRK5, common in African Americans, in which leucine is substituted for glutamine at position 41.

Inhibition of ischemic cardiomyocyte apoptosis through targeted ablation of Bnip3 restrains postinfarction remodeling in mice.

Following myocardial infarction, nonischemic myocyte death results in infarct expansion, myocardial loss, and ventricular dysfunction. Here, we demonstrate that a specific proapoptotic gene, Bnip3, minimizes ventricular remodeling in the mouse, despite having no effect on early or late infarct size. We evaluated the effects of ablating Bnip3 on cardiomyocyte death, infarct size, and ventricular remodeling after surgical ischemia/reperfusion (IR) injury in mice.

A functional polymorphism of the Galphaq (GNAQ) gene is associated with accelerated mortality in African-American heart failure.

Galphaq, encoded by the human GNAQ gene, is an effector subunit of the Gq heterotrimeric G-protein and the convergence point for signaling of multiple Gq-coupled neurohormonal receptors. To identify naturally occurring mutations that could modify GNAQ transcription, we examined genomic DNA isolated from 355 normal subjects for genetic variants in transcription factor binding motifs. Of seven variants identified, the most common was a GC to TT dinucleotide substitution at -694/-695 (allele frequency of 0.

Quantitative left ventricular systolic function: from chamber to myocardium.

One of the most common indications for obtaining a Doppler echocardiographic study is to ascertain left ventricular (LV) systolic function. There are many ways in which LV function can be determined, but an important assumption that is often overlooked is that every measure that we commonly use is only a surrogate marker of LV function due to the fact that it is impossible to characterize the complex geometric and volumetric function of the ventricle (or myocyte) in a single number. Stated in another way, there is no one perfect measure of LV function.

Mediating ERK 1/2 signaling rescues congenital heart defects in a mouse model of Noonan syndrome.

Noonan syndrome (NS) is an autosomal dominant disorder characterized by a wide spectrum of defects, which most frequently include proportionate short stature, craniofacial anomalies, and congenital heart disease (CHD). NS is the most common nonchromosomal cause of CHD, and 80%-90% of NS patients have cardiac involvement. Mutations within the protein tyrosine phosphatase Src homology region 2, phosphatase 2 (SHP2) are responsible for approximately 50% of the cases of NS with cardiac involvement.

Impact of Preoperative 64-Slice CT Scanning on Mini-Maze Atrial Fibrillation Surgery.

Background: : Multidetector computed tomography (MDCT) is emerging as a powerful noninvasive diagnostic tool. The appropriate role of this technique in the preoperative evaluation of cardiovascular disease has yet to be fully defined. Atrial fibrillation is the most common sustained cardiac arrhythmia, and novel minimally invasive surgical techniques have been developed to treat this condition by electrically isolating the pulmonary veins.

Cardiomyocyte degeneration with calpain deficiency reveals a critical role in protein homeostasis.

Regulating the balance between synthesis and proteasomal degradation of cellular proteins is essential for tissue growth and maintenance, but the critical pathways regulating protein ubiquitination and degradation are incompletely defined. Although participation of calpain calcium-activated proteases in post-necrotic myocardial autolysis is well characterized, their importance in homeostatic turnover of normal cardiac tissue is controversial. Hence, we evaluated the consequences of physiologic calpain (calcium-activated protease) activity in cultured cardiomyocytes and unstressed mouse hearts.

STAT-3 activation is necessary for ischemic preconditioning in hypertrophied myocardium.

The JAK-STAT pathway is activated in the early and late phases of ischemic preconditioning (IPC) in normal myocardium. The role of this pathway and the efficacy of IPC in hypertrophied hearts remain largely unknown. We hypothesized that phosphorylated STAT-3 (pSTAT-3) is necessary for effective IPC in pressure-overload hypertrophy.

The presence of Lys27 instead of Asn27 in human phospholamban promotes sarcoplasmic reticulum Ca2+-ATPase superinhibition and cardiac remodeling.

Background: Phospholamban (PLN) is an inhibitor of the Ca2+ affinity of sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2). The amino acid sequence of PLN is highly conserved, and although all species contain asparagine (Asn), human PLN is unique in containing lysine (Lys) at amino acid 27.

Methods And Results: Human PLN was introduced in the null background.

Sarcoplasmic reticulum adenosine triphosphatase overexpression in the L-type Ca2+ channel mouse results in cardiomyopathy and Ca2+ -induced arrhythmogenesis.

Background: Overexpression of the L-type voltage-dependent calcium channel alpha(1C)-subunit (L-VDCC OE) in transgenic mice results in adaptive hypertrophy followed by a maladaptive phase associated with a decrease in sarcoplasmic reticulum adenosine triphosphatase (SERCA)2a expression at 8 to 10 months of age. Overexpressing SERCA to manipulate calcium (Ca(2+)) cycling and prevent pathologic phenotypes in some models of heart failure has been proven to be a promising genetic strategy.

Objective: In this study we investigated whether genetic manipulation that increases Ca(2+) uptake into the sarcoplasmic reticulum by overexpressing SERCA1a (skeletal muscle specific) into the L-VDCC OE background could restore or further deteriorate Ca(2+) cycling, contractile dysfunction, and electrical remodeling in the heart failure phenotype.

Cardiac myosin-binding protein-C phosphorylation and cardiac function.

The role of cardiac myosin binding protein-C (cMyBP-C) phosphorylation in cardiac physiology or pathophysiology is unclear. To investigate the status of cMyBP-C phosphorylation in vivo, we determined its phosphorylation state in stressed and unstressed mouse hearts. cMyBP-C phosphorylation is significantly decreased during the development of heart failure or pathologic hypertrophy.

Murine echocardiography: a practical approach for phenotyping genetically manipulated and surgically modeled mice.

There have now been literally hundreds of genetically manipulated mouse models developed during the past decade of cardiac research. Echocardiography is considered an extremely important tool to noninvasively assess and serially follow the phenotype of genetically and surgically altered mice. This review describes in detail the technical considerations, various routinely used methods to assess cardiac function, and some emerging techniques in the assessment of cardiac function in experimental mouse models of cardiac disease.

Proapoptotic effects of caspase-1/interleukin-converting enzyme dominate in myocardial ischemia.

Caspase-1/interleukin-converting enzyme (ICE) is a cysteine protease traditionally considered to have importance as an inflammatory mediator, but not as an apoptotic effector. Because of the dual functions of this caspase, the pathophysiological impact of its reported upregulation in hypertrophy and heart failure is not known. Here, the consequences of increased myocardial expression of procaspase-1 were examined on the normal and ischemically injured heart.

Physiological growth synergizes with pathological genes in experimental cardiomyopathy.

Hundreds of signaling molecules have been assigned critical roles in the pathogenesis of myocardial hypertrophy and heart failure based on cardiac phenotypes from alpha-myosin heavy chain-directed overexpression mice. Because permanent ventricular transgene expression in this system begins during a period of rapid physiological neonatal growth, resulting phenotypes are the combined consequences of transgene effects and normal trophic influences. We used temporally-defined forced gene expression to investigate synergy between postnatal physiological cardiac growth and two functionally divergent cardiomyopathic genes.

Evolution of the mdx mouse cardiomyopathy: physiological and morphological findings.

Heart failure is a major cause of death in boys with Duchenne muscular dystrophy. In order to determine if the cardiac function of the mdx mouse is similarly disturbed, we performed murine echocardiograms and left heart catheterization studies, along with morphometric analysis of cardiac fibrosis. Serial echocardiograms in mdx mice revealed the evolution from normal cardiac function in young mice to a dilated cardiomyopathy in adult mice.