Myocardial length-force relationship in end stage dilated cardiomyopathy and normal human myocardium: analysis of intact and skinned left ventricular trabeculae obtained during 11 heart transplantations

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.

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Surgical therapy for heart failure

Core Concepts in Cardiac Surgery ◽

10.1093/med/9780198735465.003.0009 ◽

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.

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The Role of Cardiac T-Cadherin in the Indicating Heart Failure Severity of Patients with Non-Ischemic Dilated Cardiomyopathy

Medicina ◽

10.3390/medicina56010027 ◽

2020 ◽

Vol 56 (1) ◽

pp. 27

Author(s):

Vaida Baltrūnienė ◽

Ieva Rinkūnaitė ◽

Julius Bogomolovas ◽

Daiva Bironaitė ◽

Ieva Kažukauskienė ◽

...

Keyword(s):

Heart Failure ◽

Dilated Cardiomyopathy ◽

Experimental Studies ◽

Left Ventricular ◽

Human Myocardium ◽

Enzyme Linked Immunosorbent Assay ◽

Cox Regression Analysis ◽

Non Ischemic Dilated Cardiomyopathy ◽

The Mean

Background and objectives: T-cadherin (T-cad) is one of the adiponectin receptors abundantly expressed in the heart and blood vessels. Experimental studies show that T-cad sequesters adiponectin in cardiovascular tissues and is critical for adiponectin-mediated cardio-protection. However, there are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Materials and Methods: 29 patients with chronic NI-DCM and advanced HF were enrolled. Patients underwent regular laboratory investigations, echocardiography, coronary angiography, and right heart catheterization. TNF-α and IL6 in serum were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, endomyocardial biopsies were obtained, and the levels of T-cad were assessed by ELISA and CD3, CD45Ro, CD68, and CD4- immunohistochemically. Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean PCWP < 19 mmHg. Patients were followed-up for 5 years. The study outcome was composite: left ventricular assist device implantation, heart transplantation, or death from cardiovascular causes. Results: T-cad shows an inverse correlation with the mean PCWP (rho = −0.397, p = 0.037). There is a tendency towards a lower T-cad concentration in patients with more severe HF, as indicated by the mean PCWP > 19 mmHg compared to those with mean PCWP ≤ 19 mmHg (p = 0.058). Cardiac T-cad levels correlate negatively with myocardial CD3 cell count (rho = −0.423, p = 0.028). Conclusions: Univariate Cox regression analysis did not prove T-cad to be an outcome predictor (HR = 1, p = 0.349). However, decreased T-cad levels in human myocardium can be an additional indicator of HF severity. T-cad in human myocardium has an anti-inflammatory role. More studies are needed to extend the role of T-cad in the outcome prediction of patients with NI-DCM.

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Improved Left Ventricular Strain and Dyssynchrony After Pulmonary Artery Banding in an Infant with End-Stage Dilated Cardiomyopathy: Insights from Three-Dimensional Speckle Tracking

Pediatric Cardiology ◽

10.1007/s00246-019-02138-8 ◽

2019 ◽

Vol 40 (6) ◽

pp. 1317-1319

Author(s):

Yu-Hsuan Liu ◽

Yih-Sharng Chen ◽

Ming-Tai Lin ◽

Chun-An Chen

Keyword(s):

Pulmonary Artery ◽

Dilated Cardiomyopathy ◽

Speckle Tracking ◽

Three Dimensional ◽

Left Ventricular ◽

Pulmonary Artery Banding ◽

Left Ventricular Strain ◽

End Stage

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Decrease Tyrosine Phosphorylation of Stat3 in Human Myocardium with End-Stage Congestive Heart Failure

Microscopy and Microanalysis ◽

10.1017/s1431927600035479 ◽

2000 ◽

Vol 6 (S2) ◽

pp. 596-597

Author(s):

C. Wei ◽

J. S. McLaughlin

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Protein Expression ◽

Cardiac Tissue ◽

Normal Subjects ◽

Human Myocardium ◽

Stat3 Phosphorylation ◽

Normal Human ◽

Human Cardiac Tissue ◽

End Stage

Recent study demonstrated that decrease signal transducer and activator of transcription-3 (STAT3) phosphorylation and increase apoptosis might be a critical point in the transition between compensatory cardiac hypertrophy and heart failure. To date, the protein expression of STAT3 in normal and failing human heart remains unclear. Therefore, the current study was designed to investigate the protein expression of STAT3 in human myocardium with end-stage congestive heart failure (CHF) and compared with that in normal human cardiac tissue.Human cardiac atrial tissue was obtained from normal subjects (n=5) and end-stage CHF patients (n=5) during cardiac transplantation. To detect the DNA fragmentation, in situ terminal deoxymucleotidyl transferase dUTP nick end labeling (TUNEL) was performed. An average of 1000 nuclei was analyzed for TUNEL study. STAT3 protein expression and phosphorylation of STAT3 were determined by immunohistochemical staining (IHCS) with total STAT3 and phospho-specific STAT3 antibodies.

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