Feasibility of Distorted Born Iterative Method for Detecting Early Stage of Heart Failure

2020 ◽  
Author(s):  
Semih Dogu ◽  
Egemen Bilgin ◽  
Sulayman Joof ◽  
Mehmet Nuri Akinci
Keyword(s):  
Heart Failure ◽  
Iterative Method ◽  
Early Stage

Abstract 065: Cardiac Fibrosis and Heart Failure Caused by DsRed Tetramers Involves the Induction of Tissue Inhibitor of Metalloproteinase-1

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Tsung-Hsien Chen ◽  
Shan-Wen Liu ◽  
Mei-Ru Chen ◽  
Kurt M Lin
Keyword(s):  
Heart Failure ◽  
Cardiac Fibrosis ◽  
Fluorescent Protein ◽  
Early Stage ◽  
Transglutaminase 2 ◽  
Underlying Mechanism ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Tissue Inhibitor ◽  
Cardiac Tissues ◽  
Cardiac Symptoms

Whereas aggregation of intracellular proteins was linked to the initiation of cardiac myopathy, the sequence of participating events, including myocyte apoptosis, autophagy, necrosis and fibrosis as the underlying mechanisms leading to heart failure, was not clear. Green fluorescent protein (GFP) and its derivatives induced cardiac dysfunction in mice when expressed in high quantity; however, the mechanism underlying the aggregation of fluorescent protein leading to heart failure remains unexplored.We created a transgenic mouse with switchable expression of the GFP monomer or the expression of DsRed, a red fluorescent protein (RFP) tetramer that tends to aggregate into a large protein complex. GFP mice were free of cardiac symptoms; in contrast, RFP mice with homozygous DsRed alleles developed myocyte necrosis, carditis, ventricular hypertrophy and fibrosis, left atrium thrombosis, dilated heart failure and death at the age of approximately five months. The hemizygote mice displayed similar symptoms at a later age. The expression of the microtubule-associated protein 1 light chain 3 cleaved isoform II (LC3 II) and transglutaminase 2, and the expression of many myopathy- and fibrosis-related genes were significantly induced in the hearts of two-month-old RFP mice. Together with the findings of increased autophagosomes, lysosomes and dysfunctional mitochondria, these results suggest a marked induction of myocyte autophagy and fibrosis as the main underlying mechanism of heart failure in RFP mice. Interestingly, apoptosis was not elevated in RFP hearts. One of the most up-regulated genes in the early stage RFP heart was the tissue inhibitor of matrix metalloproteinases type 1 (TIMP-1), corroborating the role of TIMP-1 in cardiac remodeling and anti-apoptotic activity. The heart-origin of the morbidity in RFP mice was confirmed by expressing DsRed tetramers specifically in cardiac tissues, and the same phenotypes as in RFP mice were observed. In summary, in cardiac myocytes under the stress of protein aggregation, strong induction of TIMP-1 and down-regulation of MMP activity may play a significant role in enhancing the synthesis of extracellular matrix, resulting in fibrosis and heart failure.

scholarly journals AUTOREGULATION OF BRAIN CIRCULATION IN PROGRESSING CARDIAC FAILURE AND ITS RELATION TO THE APPEARANCE OF SEIZURE READINESS

2016 ◽  
Vol 15 (2) ◽  
pp. 86-93
Author(s):  
M.L. Mamalyga ◽  
◽  
L.M. Mamalyga ◽  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Failure ◽  
Early Stage ◽  
Brain Circulation ◽  
Brain Disorders ◽  
Compression Tests ◽  
Cardiac Decompensation ◽  
Severe Stage ◽  
Basilar Arteries

On the early stage of cardiac decompensation, the blood flow in common carotid and basilar arteries does not change, however the seizure readiness (SR) of animals increases. The preserved reaction on hypercapnic and compression tests allows us to stipulate that the increased SR is not related to the circulatory brain disorders. Progressive aggravation of cardiac failure (CF) leads to the severe stage of decompensation accompanied by decreased blood flow in common carotid and basilar arteries, as well as increases SR. At the same time the metabolic cascade of autoregulation is areactive and myogenic is significantly decreased. Ineffective operation of heart in different stages of heart failure shows not the same effect or backup possibilities for cerebral hemodynamic autoregulation affecting the formation and aggravation of SR. The increased SR in cardiac failure is not always caused by brain ischemia.

scholarly journals Diagnosis, treatment, and follow-up of heart failure patients by general practitioners: A Delphi consensus statement

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0244485
Author(s):  
Caroline Verhestraeten ◽  
Gijs Weijers ◽  
Daphne Debleu ◽  
Agnieszka Ciarka ◽  
Marc Goethals ◽  
...  
Keyword(s):  
Heart Failure ◽  
General Practitioner ◽  
General Practitioners ◽  
Early Stage ◽  
Blood Analysis ◽  
Care Process ◽  
Delphi Panel ◽  
Delphi Consensus ◽  
Heart Failure Patients

Aims Creation of an algorithm that includes the most important parameters (history, clinical parameters, and anamnesis) that can be linked to heart failure, helping general practitioners in recognizing heart failure in an early stage and in a better follow-up of the patients. Methods and results The algorithm was created using a consensus-based Delphi panel technique with fifteen general practitioners and seven cardiologists from Belgium. The method comprises three iterations with general statements on diagnosis, referral and treatment, and follow-up. Consensus was obtained for the majority of statements related to diagnosis, referral, and follow-up, whereas a lack of consensus was seen for treatment statements. Based on the statements with good and perfect consensus, an algorithm for general practitioners was assembled, helping them in diagnoses and follow-up of heart failure patients. The diagnosis should be based on three essential pillars, i.e. medical history, anamnesis and clinical examination. In case of suspected heart failure, blood analysis, including the measurement of NT-proBNP levels, can already be performed by the general practitioner followed by referral to the cardiologist who is then responsible for proper diagnosis and initiation of treatment. Afterwards, a multidisciplinary health care process between the cardiologist and the general practitioner is crucial with an important role for the general practitioner who has a key role in the up-titration of heart failure medication, down-titration of the dose of diuretics and to assure drug compliance. Conclusions Based on the consensus levels of statements in a Delphi panel setting, an algorithm is created to help general practitioners in the diagnosis and follow-up of heart failure patients.

scholarly journals Characteristics and Outcomes of Women Developing Heart Failure After Early Stage Breast Cancer Chemotherapy: A Population-Based Matched Cohort Study

2021 ◽  
Author(s):  
Husam Abdel-Qadir ◽  
Felicia Tai ◽  
Ruth Croxford ◽  
Peter C. Austin ◽  
Eitan Amir ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Heart Failure ◽  
Early Stage ◽  
Sequential Therapy ◽  
Cardiovascular Death ◽  
Population Based ◽  
Emergency Department Visits ◽  
Early Stage Breast Cancer ◽  
Administrative Databases ◽  
Breast Cancer Chemotherapy

Background: The prognosis of heart failure (HF) after early stage breast cancer (EBC) treatment with anthracyclines or trastuzumab is not well-characterized. Methods: Using administrative databases, women diagnosed with HF after receiving anthracyclines or trastuzumab for EBC in Ontario during 2007 to 2017 (the EBC-HF cohort) were categorized by cardiotoxic exposure (anthracycline alone, trastuzumab alone, sequential therapy with both agents) and matched on age with ≤3 cancer-free HF controls to compare baseline characteristics. To study prognosis after HF onset, we conducted a second match on age plus important HF prognostic factors. The cumulative incidence function was used to describe risk of hospitalization or emergency department visits (hospital presentations) for HF and cardiovascular death. Results: A total of 804 women with EBC developed HF after anthracyclines (n=312), trastuzumab (n=112), or sequential therapy (n=380); they had significantly fewer comorbidities than 2411 age-matched HF controls. After the second match, the anthracycline-HF cohort had a similar 5-year incidence of HF hospital presentations (16.5% [95% CI, 12.0%–21.7%]) as controls (17.1% [95% CI, 14.4%–20.1%]); the 5-year incidence was lower than matched controls for the trastuzumab-HF (9.7% [95% CI, 4.7%–16.9%]; controls 16.4% [95% CI, 12.1%–21.3%]; P =0.03) and sequential-HF cohorts (2.7% [95% CI, 1.4%–4.8%]; controls 10.8% [95% CI, 8.9%–13.0%]; P <0.001). At 5 years, the incidence of cardiovascular death was 2.9% (95% CI, 1.2%–5.9%) in the anthracycline-HF cohort vs. 9.5% (95% CI, 6.9%–12.6%) in controls, and 1.7% (0.6%–3.7%) for women developing HF after trastuzumab vs. 4.3% (95% CI, 3.1–5.8%) for controls. Conclusions: Women developing HF after cardiotoxic EBC chemotherapy have fewer comorbidities than cancer-free women with HF; trastuzumab-treated women who develop HF have better prognosis than matched HF controls.

Abstract 71: STAT3 Affects Myofibrillar Structure and Its Loss May Contribute to Heart Failure in Hypertension

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Fouad Zouein ◽  
Carlos Zgheib ◽  
John Fuseler ◽  
John E Hall ◽  
Mazen Kurdi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Myocytes ◽  
Transcriptional Activity ◽  
Cardiac Myocyte ◽  
Early Stage ◽  
Systolic Dysfunction ◽  
Wild Type ◽  
Patients With Heart Failure ◽  
Protective Proteins ◽  
Fractional Shortening

How hypertension causes heart failure is not known. Since patients with heart failure have reduced cardiac STAT3 and STAT3 KO mice develop heart failure with age, we tested the hypothesis that reduced STAT3 transcriptional activity contributes at an early stage to remodeling that precedes heart failure in hypertension using SA mice with a STAT3 S727A mutation. SA and wild type (WT) mice received angiotensin (A) II (1000 ng/kg/min) or saline (S) for 17 days. Hearts of WT and SA mice had similar levels of STAT3-induced protective proteins Bcl-xL and SOD2, and unlike STAT3 KO mice, cardiac miR-199a levels were not increased in SA mice. AII increased systolic blood pressure measured by telemetry in SA (124 ± 1 to 167 ± 3) and WT (122 ± 3 to 162 ± 3) mice to the same extent. AII increased cardiac levels of cytokines (pg/μg protein) associated with heart failure in both WT and SA mice, but significantly less so (P<0.05) in SA mice; IL-6, 13.6 ± 1.4 vs. 9.1 ± 0.6; TGFβ, 56 ± 4 vs. 38 ± 3 and MCP1 35 ± 2 vs. 22 ± 2. Compared to WT mice, hearts of SA mice showed signs of developing systolic dysfunction with AII as seen by a significant (P<0.05) reduction in ejection fraction (63.7 ± 7.1 to 51.7 ± 6.9) and fractional shortening (34.3 ± 4.9 to 26.4 ± 4.3). AII caused fibrosis in the left ventricle of both WT and SA mice characterized by cardiac myocyte loss and increased % collagen: WT+S, 5.59 ± 0.34; WT+AII, 15.70 ± 1.87; SA+S, 6.70 ± 0.40; SA+AII, 16.50 ± 1.91. In WT+AII mice there was a nonsignificant trend towards a loss of myofibrillar content of cardiac myocytes, but an increase in the mass of the myofibrils (IOD/myofibrillar area). In contrast, cardiac myocytes of SA+AII mice had a significant (P<0.001) % loss in myofibrils (5.71 ± 0.28) compared to SA+S (0.75 ± 0.07), WT+S (0.80 ± 0.06) and WT+AII (1.54 ± 0.10) mice. In addition, the mass of the myofibrils in SA+AII mice (6.01 ± 0.07) was significantly less (P<0.001) than those of SA+S mice (6.46 ± 0.04), although greater than WT+S (4.85 ± 0.06) or WT+AII (5.27 ± 0.08) mice. Our findings reveal that STAT3 transcriptional activity is important for proper morphology of the myofibrils of cardiac myocytes. Loss of STAT3 activity may impair cardiac function in the hypertensive heart due to defective myofibrillar structure and remodeling that may lead to heart failure.

Early Stage Detection of Heart Failure Using Machine Learning Techniques

2021 ◽  
pp. 75-88
Author(s):  
Zulfikar Alom ◽  
Mohammad Abdul Azim ◽  
Zeyar Aung ◽  
Matloob Khushi ◽  
Josip Car ◽  
...  
Keyword(s):  
Machine Learning ◽  
Heart Failure ◽  
Early Stage ◽  
Machine Learning Techniques ◽  
Learning Techniques

Reductions of myocardial Na-K-ATPase activity and ouabain binding sites in heart failure: prevention by nadolol

1993 ◽  
Vol 265 (6) ◽  
pp. H2086-H2093 ◽  
Author(s):  
T. H. Fan ◽  
R. P. Frantz ◽  
H. Elam ◽  
S. Sakamoto ◽  
N. Imai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atpase Activity ◽  
Binding Sites ◽  
Early Stage ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Adrenergic Stimulation ◽  
Ouabain Binding ◽  
Systemic Hemodynamic

To study the changes in myocardial digitalis binding sites in heart failure, we measured myocardial ouabain binding sites, Na-K-adenosinetriphosphatase (ATPase) activity, and ventricular muscle mechanical responses to acetylstrophanthidin in dogs with right-heart failure (RHF) produced by tricuspid avulsion and pulmonary artery constriction. Sham-operated dogs were studied as the control. RHF produced a significant decrease in ouabain binding sites in the right and left ventricular myocardium, which was accompanied by a proportional decrease in Na-K-ATPase activity. However, RHF and sham-operated dogs did not differ in systemic hemodynamic or right ventricular trabeculate muscle isometric contractile responses to acetylstrophanthidin. To determine whether chronic beta-adrenergic stimulation contributed to the development of Na-K-ATPase downregulation, we administered nadolol (40 mg/day) to a separate group of dogs during an early stage of RHF development. Nadolol effectively prevented the reduction of myocardial ouabain binding sites that occurred in RHF. Thus we conclude that myocardial ouabain binding sites and Na-K-ATPase activity are reduced in dogs with experimental heart failure and that these changes probably occur as a result of the attendant heightened sympathetic activity.

Skeletal muscle phosphate metabolism abnormalities in volume-overload experimental heart failure

1994 ◽  
Vol 267 (6) ◽  
pp. H2186-H2192 ◽  
Author(s):  
Z. Chati ◽  
F. Zannad ◽  
C. Michel ◽  
B. Lherbier ◽  
P. M. Mertes ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Early Stage ◽  
Volume Overload ◽  
Significant Rise ◽  
Initial Slope ◽  
Heart Weight ◽  
Resonance Spectroscopy ◽  
Phosphate Metabolism

We studied skeletal muscle phosphate metabolism abnormalities to examine their contribution at an early stage of congestive heart failure (CHF) in rats with aortocaval fistula (ACF) 4 wk after the procedure. In a group of 26 rats (13 with ACF and 13 sham operated), we assessed the degree of CHF. The ACF produced a significant rise in heart weight and plasma atrial natriuretic peptide. In a second group of 26 rats (13 ACF and 13 sham operated), we performed 31P-magnetic resonance spectroscopy in the gastrocnemius muscle during motor activity produced by electrical stimulation. The rate of phosphocreatine depletion, expressed by its initial slope, was higher in the ACF rats compared with controls (0.078 +/- 0.01 vs. 0.041 +/- 0.007; P < 0.03). pH and ATP decreased and phosphodiesters increased in all rats during electrical stimulation, with no difference between ACF rats and controls. The kinetics of phosphocreatine recovery were not different between ACF rats and controls. Together with previous studies, our present results suggest that muscle metabolism abnormalities in CHF may vary according to the experimental model and may be observed early in the course of the disease.

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