scholarly journals Induction of Ankrd1 in Dilated Cardiomyopathy Correlates with the Heart Failure Progression

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Julius Bogomolovas ◽  
Kathrin Brohm ◽  
Jelena Čelutkienė ◽  
Giedrė Balčiūnaitė ◽  
Daiva Bironaitė ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Cardiac Remodeling ◽  
Expression Patterns ◽  
Clinical Manifestations ◽  
Left Ventricular ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Expression Levels ◽  
Potential Marker ◽  
End Stage

Progression of idiopathic dilated cardiomyopathy (IDCM) is marked with extensive left ventricular remodeling whose clinical manifestations and molecular basis are poorly understood. We aimed to evaluate the clinical potential of titin ligands in monitoring progression of cardiac remodeling associated with end-stage IDCM. Expression patterns of 8 mechanoptotic machinery-associated titin ligands (ANKRD1,ANKRD2,TRIM63,TRIM55,NBR1,MLP,FHL2, andTCAP) were quantitated in endomyocardial biopsies from 25 patients with advanced IDCM. When comparing NYHA disease stages, elevatedANKRD1expression levels marked transition from NYHA < IV to NYHA IV.ANKRD1expression levels closely correlated with systolic strain depression and short E wave deceleration time, as determined by echocardiography. On molecular level, myocardialANKRD1and serum adiponectin correlated with lowBAX/BCL-2ratios, indicative of antiapoptotic tissue propensity observed during the worsening of heart failure. ANKRD1 is a potential marker for cardiac remodeling and disease progression in IDCM.ANKRD1expression correlated with reduced cardiac contractility and compliance. The association ofANKRD1with antiapoptotic response suggests its role as myocyte survival factor during late stage heart disease, warranting further studies on ANKRD1 during end-stage heart failure.

Surgical therapy for heart failure

2018 ◽  
pp. 157-174
Author(s):  
Stephen Westaby
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Acute Coronary Syndromes ◽  
Symptomatic Relief ◽  
Left Ventricular ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Coronary Syndromes ◽  
Artery Disease ◽  
End Stage ◽  
Age Range

Congestive heart failure affects 23 million people worldwide, and is the final pathway for many diseases that affect the myocardium. Successful intervention in acute coronary syndromes together with improved management of idiopathic dilated cardiomyopathy and dysrhythmia provide an ever-increasing number of advanced heart failure patients spread over a wide age range. In Western countries, coronary artery disease is responsible for about 70% of patients with idiopathic dilated cardiomyopathy and valvular heart disease accounting for 15%. Since 10% of patients older than 65 years suffer systolic left ventricular dysfunction, the numbers with heart failure will double within the next 25 years. For end-stage patients, cardiac transplantation provides the benchmark for increased longevity and symptomatic relief. However, the vast majority of patients are over 65 years of age or are referred with established comorbidity, which precludes transplantation.

scholarly journals Gene expression of adrenomedullin in failing myocardium: comparison to atrial natriuretic peptide

2002 ◽  
Vol 92 (3) ◽  
pp. 1058-1063 ◽  
Author(s):  
Anselm T. Bäumer ◽  
Christina Schumann ◽  
Bodo Cremers ◽  
Gabi Itter ◽  
Wolfgang Linz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Normal Subjects ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Human Myocardium ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Left Ventricular Myocardium ◽  
End Stage ◽  
Atrial Natriuretic

The expression of adrenomedullin (AM) and atrial natriuretic factor (ANF) were investigated in the myocardium of a rat model of chronic ischemic heart failure (CHF) compared with sham-operated controls. In addition, human myocardium of patients with end-stage heart failure due to idiopathic dilated cardiomyopathy compared with myocardium of normal subjects (NF) was studied. In CHF, similar AM levels but increased ANF expression were observed in left ventricular myocardium, as assessed by semiquantitative PCR. Functional experiments with freshly excised papillary muscles showed no influence of AM on myocardial contractility. In NF human myocardium, the expression of AM mRNA was threefold higher in atrial compared with ventricular tissue. In analogy, ANF mRNA was increased by ∼15-fold in atrial tissue. In dilated cardiomyopathy, the expression of AM was significantly increased in right and left ventricles compared with NF. In parallel, ventricular ANF expression was enhanced.

Abstract 20178: Short Chain Acyl-CoA Intermediates in the Failing Heart: Further Evidence of an Energy Starved State

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Nathaniel Snyder ◽  
Kenneth C Bedi ◽  
Ali Javaheri ◽  
Clementina Mesaros ◽  
Ken Margulies ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular ◽  
Short Chain ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Orthotopic Heart Transplantation ◽  
Potential Marker ◽  
Lipid Species ◽  
Chain Acyl ◽  
End Stage Heart Failure ◽  
End Stage

Introduction: Several studies have implicated energetic deficits in chronic heart failure. Recently, our group has described a state of myocardial substrate deficiency across a broad spectrum of lipid species in non-diabetic end-stage heart failure. We hypothesized that lipid substrate depletion in end-stage heart failure would be associated with dysregulation of short chain acyl-CoA intermediates implicated in important metabolic pathways. Methods: Left ventricular samples were obtained at the time of orthotopic heart transplantation for failing cases with idiopathic dilated cardiomyopathy (DCM) n=16, and brain-dead organ donors without a history of heart failure (NF) n=18. Samples were snap frozen at -80°C for further analysis with liquid chromatography in tandem mass spec LC MS/MS. Stable isotope labeled essential nutrient in cell culture (SILEC) internal standards for acyl-CoAs were generated using 13 C 3 15 N 1 pantotheonate in Hepa1c1c7 cells. Results: In the myocardium of failing as compared to NF, we identified a significant decrease in Succinyl-CoA (Avg 10.5 versus 17.7 pmol/mg, p = 0.004 ), Propionyl-CoA (0.9 versus 1.8 pmol/mg, p=0.004) and a concomitant increase in β-hydroxybutyryl -CoA (BHB-CoA Avg 0.57 versus 0.29 pmol/mg, p =0.008 ). The ratio of myocardial Succinyl-CoA to Acetyl-CoA, a potential marker of tricarboxylic acid cycling, is significantly decreased in end-stage heart failure ( 0.84 versus 1.93, p= 0.005 ). The figure depicts the levels of myocardial acyl-CoA species in the non-diabetic cohort. Conclusion: We have identified important differences in myocardial acyl CoA species—an increase in the ketogenic BHB-CoA and decreased Succinyl-CoA and Propionyl-CoA in end-stage human heart failure. These data, along with the recently identified state of myocardial lipodeficiency, are strongly supporting the concept of a bio-energetic deficit in end-stage heart failure.

Sign in / Sign up

Export Citation Format

Share Document