scholarly journals Expression of the adipokine adiponectin is higher in the left ventricular myocardium than in epicardial adipose tissue in human end-stage heart failure and correlates with cardiac index

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P4156-P4156
Author(s):  
J. Mlynarova ◽  
M. Hulman ◽  
V. Hudec ◽  
E. Demesova ◽  
P. Musil ◽  
...  
Keyword(s):  
Heart Failure ◽  
Adipose Tissue ◽  
Cardiac Index ◽  
Epicardial Adipose Tissue ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
End Stage Heart Failure ◽  
End Stage

Deloading of the Left Ventricle by Ventricular Assist Device Normalizes Increased Expression of Endothelin ET A Receptors But Not Endothelin-Converting Enzyme-1 in Patients With End-Stage Heart Failure

Circulation ◽  
2000 ◽  
Vol 102 (suppl_3) ◽  
Author(s):  
Henning Morawietz ◽  
Marten Szibor ◽  
Winfried Goettsch ◽  
Babett Bartling ◽  
Matthias Barton ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Transplantation ◽  
Ace Inhibitor ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Converting Enzyme ◽  
Ventricular Assist ◽  
End Stage Heart Failure ◽  
End Stage

Background —Ventricular assist devices (VAD) are implanted in patients with end-stage heart failure for bridging the time until heart transplantation, resulting in hemodynamic unloading of the failing heart, improved cardiac contractile and mitochondrial function, and reversal of cardiac hypertrophy. It is unknown whether VAD unloading may affect the cardiac endothelin (ET) system, which has been proposed as one of the putative pathomechanisms of heart failure. Methods and Results —With the use of standard-calibrated, competitive reverse-transcription–polymerase chain reaction mRNA expression of components of the ET system was analyzed in left ventricular myocardium from nonfailing donor hearts, from failing hearts without and with ACE inhibitor therapy, and from patients with end-stage heart failure at the time of VAD implantation and 103±15 days after VAD implantation during removal with subsequent heart transplantation. ET receptor A (ET A ) was markedly upregulated in failing human myocardium. This increased ET A expression was not affected by ACE inhibitor treatment but was normalized by VAD unloading. ET A expression before or after VAD implantation did not correlate with duration of VAD implantation or suppression of Pro-ANP mRNA. ET B mRNA expression was unaffected by heart failure or VAD. In contrast, increased ET-converting enzyme-1 mRNA and ET-1 peptide levels in failing myocardium were partially normalized by ACE inhibition but not by VAD unloading. Conclusions —We conclude that VAD implantation normalizes ET A expression in failing human left ventricular myocardium, probably as the result of the beneficial effects of VAD unloading.

Validation of reference genes in human epicardial adipose tissue and left ventricular myocardium in heart failure

Biologia ◽  
2019 ◽  
Vol 74 (12) ◽  
pp. 1687-1698
Author(s):  
Jana Mlynarova ◽  
Andrea Gazova ◽  
Peter Musil ◽  
Andrea Raganová ◽  
Ondrej Sprusansky ◽  
...  
Keyword(s):  
Heart Failure ◽  
Adipose Tissue ◽  
Reference Genes ◽  
Epicardial Adipose Tissue ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium

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.

scholarly journals Left ventricular systolic function decreases in lamin a/c cardiomyopathy wihout concomitant ventricular dilatation

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
ES Eystein Skjolsvik ◽  
OL Oyvind Haugen Lie ◽  
MC Monica Chivulescu ◽  
MR Margareth Ribe ◽  
AIC Anna Isotta Castrini ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular ◽  
University Hospital ◽  
Lv Function ◽  
Lamin A ◽  
Age Related ◽  
End Stage Heart Failure ◽  
Lv Volumes ◽  
End Stage

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): This work was supported by the Norwegian Research Council [203489/030] onbehalf Department of Cardiology, Research group for genetic cardiac diseases and sudden cardiac death, Oslo University Hospital, Rikshospitalet, Oslo, Norwa Background Lamin A/C disease is an inheritable cardiomyopathy characterized by conduction abnormalities, ventricular arrhythmias and end stage heart failure with complete age-related penetrance. Purpose To assess left ventricular structural and functional progression in patients with lamin A/C cardiomyopathy. Methods We included and followed consecutive lamin A/C genotype positive patients with clinical examination and echocardiography at every visit. We evaluated progression of left- ventricular size and function by mixed model statistics. Results We included 101 consecutive lamin A/C genotype positive patients (age 44 [29-54] years, 39% probands, 51%female) with 576 echocardiographic exams during 4.9 (IQR 2.5-8.1) years of follow-up. LV ejection fraction (LVEF) declined from 50 ± 12% to 47 ± 13%, p < 0.001 (rate -0.5%/year). LV end diastolic volumes (LVEDV) remained stationary with no significant dilatation in the total population (136 ± 45ml to 138 ± 43ml, p = 0.60), (Figure). In the subgroup of patients >58 years, we observed a decline in LV volumes 148, SE 9 ml to 140, SE 9 ml p < 0.001 (rate -2.7 ml/year) towards end stage heart failure. Conclusions LVEF deteriorated, while LV size remained unchanged during 4.9 years of follow-up in patients with lamin A/C cardiomyopathy. In patients <58 years, we observed a reduction in LV volumes. These findings represent loss of LV function without the necessary compensatory dilation to preserve stroke volume indicating high risk of decompensated end stage heart failure in lamin A/C. Abstract Figure.

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