The severity of pulmonary lesions in acquired heart defects

2021 ◽  
pp. 8-13
Author(s):  
Marina Leonidovna Kochieva
Keyword(s):  
Heart Failure ◽  
Blood Circulation ◽  
Heart Defects ◽  
Fatal Outcome ◽  
Shortness Of Breath ◽  
Internal Organs ◽  
Pulmonary Lesions ◽  
Valve Insufficiency ◽  
Heart Apparatus ◽  
Structure And Functions

Acquired heart defects are a group of diseases (represented by stenosis, valve insufficiency, combined and concomitant defects), accompanied by a violation of the structure and functions of the valvular heart apparatus and leading to changes in the intracardiac circulation. Against the background of such violations, stagnation occurs not only in the small, but also in the great blood circulation circle, which is manifested by a chronic dry cough, often with an admixture of blood. Compensated heart defects can be hidden, while decompensated ones are manifested by shortness of breath, palpitations, fatigue, pain in the heart, and a tendency to fainting. In such conditions, there is an increase in pressure in the pulmonary artery, which ultimately can cause the development of pulmonary edema. Acquired heart defects are also a serious danger in terms of the development of heart failure, damage to internal organs (in particular, the liver and kidneys), the appearance of ascites, and if the course is unfavorable, the fatal outcome is possible.

Features of the course and diagnosis of heart failure in non-coronary myocardial lesions

1982 ◽  
Vol 63 (5) ◽  
pp. 67-71
Author(s):  
V. E. Anisimov
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Coronary Arteries ◽  
Functional Capacity ◽  
Pulmonary Circulation ◽  
Heart Defects ◽  
Heart Damage ◽  
Valve Insufficiency ◽  
Myocardial Lesions

Heart failure occurs as a result of various diseases, both caused by damage to the coronary arteries (in most cases, atherosclerosis), and not associated with the involvement of the coronary arteries in the process. A decrease in the functional capacity of the myocardium with heart damage is either a consequence of its excessive overload with an increased volume of blood entering the chambers of the heart during diastole, or the result of increased resistance to blood outflow during systole. The first occurs with heart defects with valve insufficiency, and the second occurs in case of obstruction of the blood flow in patients with stenosis of the holes or with hypertension of the large and pulmonary circulation.

scholarly journals Distinct remodeling pattern between pediatric and adult heart failure: a focus on Ca2+ signaling pathway at proteomic level

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Zhang ◽  
U Kuzmanov ◽  
S Urschel ◽  
F Wang ◽  
S Wang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Signaling Pathways ◽  
Myocardial Dysfunction ◽  
Heart Defects ◽  
Systolic Dysfunction ◽  
Cellular Growth ◽  
Reverse Remodeling ◽  
Funding Source ◽  
Course Of Illness ◽  
Reduced Ejection Fraction

Abstract Background Dilated cardiomyopathy (DCM) is among the most common causes leading to end-stage heart failure with reduced ejection fraction (HF-rEF) in adult and pediatric patients. Despite similar phenotypes characterized as systolic dysfunction and eccentric ventricular dilation, pediatric DCM are biologically distinct entities with age- and development-specific features in the heart. Though underlying mechanisms may vary between the two populations, it's largely unexplored with few studies conducted to date. Purpose HF-rEF typically results from impaired myocardial contractility, triggered by defective cellular Ca2+ handling and cytoskeletal remodeling. Hence, we aim to integrate clinical profile and experimental data from human explanted hearts: 1) to unravel the age-dependent disparate Ca2+ signaling pathways; and 2) to identify pediatric-specific HF signatures or potential cures for precision managements. Methods Non-ischemic failing hearts (n=6 adult and n=6 pediatric) were procured immediately after excision via Human Explanted Heart Program. Age-matched adult non-failing control hearts (NFC, n=6) were obtained from deceased donors without cardiovascular history, while pediatric NFC (n=6) were collected from children with congenital heart defects but no primary myocardial dysfunction constituting relatively reasonable controls. Myocardial metabolic and oxidative profile were evaluated spectrophotometrically, and tissue remodeling was assessed immunohistochemically. Global proteomics and phosphoproteomics were performed on a Q-Exactive mass spectrometer, followed by network biology pathway analyses. Expression of screened proteins and kinases was validated by gel electrophoresis. Apoptosis and cellular growth signaling pathways were also incorporated into analysis. Results Both HF groups had remarkably lower LVEF (26.6±10.7% in pediatric vs. 26.5±9.1% in adult DCM) while compared to the NFC (both ≥60%) respectively. Histologically, adult-DCM demonstrated significantly worse fibrosis than pediatric-DCM (p<0.01). It was consistent with excessive reactive oxygen species (ROS) production and perturbed anti-ROS defense noted in adult-DCM, indicative of possible reverse remodeling in the pediatric failing hearts with shorter course of illness till transplant. Mechanistically, NCX1 was elevated with SERCA2 decreased in adult-DCM versus adult-NFC (p<0.05), while both pediatric groups exhibited comparable levels. Reduced p-/t-phospholamban and p-/t-CaMK in adult-DCM, unlike in pediatric-DCM, also illustrated altered phosphorylation patterns. Moreover, GSK-3β and AMPK pathways were inhibited while AKT-473 was activated in adult-DCM. Conclusions Pediatric DCM exhibited less adverse remodeling partially mediated by divergent Ca2+ handling and downstream signaling pathways, illustrating the fundamental differences between adult and pediatric DCM. Our findings may provide a scientific basis for the development of specific therapies for pediatric DCM. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Canadian Institutes for Health Research (CIHR); Heart & Stroke Foundation (HSF)

In Vivo Evaluation of Bioprinted Cardiac Patches Composed of Cardiac-Specific Extracellular Matrix and Progenitor Cells in a Model of Pediatric Heart Failure

2021 ◽  
Author(s):  
Donald Bejleri ◽  
Matthew Robeson ◽  
Milton Brown ◽  
Jervaughn Hunter ◽  
Joshua Maxwell ◽  
...  
Keyword(s):  
Heart Failure ◽  
Extracellular Matrix ◽  
Congenital Heart ◽  
Pediatric Patients ◽  
Heart Defects ◽  
In Vivo Evaluation ◽  
Surgical Methods ◽  
Pediatric Heart Failure ◽  
The Right

Pediatric patients with congenital heart defects (CHD) often present with heart failure from increased load on the right ventricle (RV) due to both surgical methods to treat CHD and the...

Shortness of breath at night and health status in congestive heart failure: Effects of environmental conditions and health-related and dietary factors

2009 ◽  
Vol 109 (2) ◽  
pp. 166-174 ◽  
Author(s):  
Mark S. Goldberg ◽  
Nadia Giannetti ◽  
Richard T. Burnett ◽  
Nancy E. Mayo ◽  
Marie-France Valois ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Health Status ◽  
Environmental Conditions ◽  
Dietary Factors ◽  
Shortness Of Breath ◽  
Health Related

scholarly journals Efficacy and safety of balloon valvuloplasty as a treatment of choice for pulmonary stenosis in children and adolescents

2014 ◽  
Vol 142 (9-10) ◽  
pp. 542-546
Author(s):  
Vojislav Parezanovic ◽  
Milan Djukic ◽  
Sanja Dzelebdzic ◽  
Tamara Ilisic ◽  
Igor Stefanovic ◽  
...  
Keyword(s):  
Congenital Heart ◽  
Pulmonary Valve ◽  
Heart Defects ◽  
Pulmonary Stenosis ◽  
Age Groups ◽  
Balloon Valvuloplasty ◽  
Pulmonary Artery Stenosis ◽  
Pulmonary Valve Insufficiency ◽  
Valve Insufficiency

Introduction. Pulmonary artery stenosis (PS) is a congenital heart defect which occurs in 10% of all congenital heart defects. Pulmonary balloon valvuloplasty (BVP) has been the treatment of choice of PS over the last 30 years. Objective. The purpose of this study was to evaluate the efficacy of this method based on middle-term hospital follow-up, and safety of BVP based on our experience. Methods. The study included 88 patients diagnosed with PS. The patients were divided into three groups based on the severity of the disease. Also, they were divided into two age groups in order to analyze the frequency of complications. Hemodynamic measurements and echocardiography results were recorded before, 24-36 hours after BVP and at the end of follow-up. Results. The studied group involved patients of average age 3.75?4.3 years (20 days to 17 years). Immediately after BVP a significant decrease of pressure gradient across the pulmonary valve (PV) was recorded in all patients; this result was similar in all 3 groups of patients regardless of the severity of stenosis (p<0.001). Complications of BVP occurred most commonly in children up to 12 months of age (ventricular tachycardia 4.5% and supraventricular tachycardia 6.8%). Pulmonary valve insufficiency after dilatation occurred in 6.6% of cases, and was most common in children aged up to 12 months. In 87 (98.9%) patients BVP was a definitive solution, and a significant residual stenosis was not recorded during follow-up. Conclusion. BVP is a safe and effective procedure in the treatment of isolated PS in children, regardless of the severity of stenosis but also regardless of patients? age.

scholarly journals Immune-inflammatory concept of the pathogenesis of chronic heart failure in dogs with dilated cardiomyopathy

2019 ◽  
Vol 12 (9) ◽  
pp. 1491-1498 ◽  
Author(s):  
Yu Vatnikov ◽  
A. Rudenko ◽  
P. Rudenko ◽  
Ev Kulikov ◽  
A. Karamyan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Dilated Cardiomyopathy ◽  
Internal Organs ◽  
Clinically Normal ◽  
Progressive Loss ◽  
Intestinal Dysbiosis ◽  
Immune Mediated ◽  
Functional Classes ◽  
Neurohumoral System

Background: Dilated cardiomyopathy is common in dogs. This form of cardiomyopathy is the main cause of death due to heart disease in dogs. Death can occur suddenly in clinically normal animals as a result of the progression of congestive heart failure (CHF). The pathogenesis of heart failure syndrome in dogs with dilated cardiomyopathy involves activation of the neurohumoral system and immune-mediated inflammation, which leads to further progression of the condition. Heart failure syndrome in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, the involvement of other key internal organs, and intestinal dysbiosis. Aim: This study aimed to determine the immunological and inflammatory mechanisms surrounding the development of heart failure syndrome in dogs with dilated cardiomyopathy. Materials and Methods: The subjects of this study were dogs with a dilated form of cardiomyopathy (n=159), complicated by various functional classes of heart failure syndrome. Evaluation of myocardial remodeling, systolic function, and systemic hemodynamics was performed using EMP-860 Vet and PU-2200V ultrasound scanners according to the standard technique. Electrocardiography was performed with all dogs in right lateral recumbency using the EK1T-04 Midas electrocardiograph (50 mm/s speed and 1 mV gain = 1 cm). Results: In some affected animals, especially in cases of compensated dilated cardiomyopathy, leukocytosis was noted. In patients with dilated cardiomyopathy complicated by heart failure syndrome of various functional classes, the number of neutrophils was significantly increased, and the number of lymphocytes was decreased by 1.9-2.1 times when compared with those in clinically normal animals. In dogs with dilated cardiomyopathy, neutrophilic leukocytosis develops with a simple regenerative shift to the left. The results of immunological studies indicate that dogs with dilated cardiomyopathy develop T lymphocytopenia as compared with clinically normal animals. Conclusion: The central component of heart failure syndrome in dogs with dilated cardiomyopathy is the activation of the neurohumoral system and immune-mediated inflammation. The development of CHF in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, involvement of other key internal organs, and intestinal dysbiosis.

A plain language summary of the EXPLORER-HCM study: mavacamten for obstructive hypertrophic Cardiomyopathy

2021 ◽  
Author(s):  
Cynthia Burstein Waldman ◽  
Anjali Owens
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Hypertrophic Cardiomyopathy ◽  
Well Being ◽  
Daily Activities ◽  
Shortness Of Breath ◽  
Plain Language ◽  
Clinical Trial Registration ◽  
Obstructive Hypertrophic Cardiomyopathy ◽  
Active Substances

Mavacamten is an investigational therapy for the treatment of hypertrophic cardiomyopathy (HCM), a condition where the heart muscle wall thickens, becomes stiff, and makes it harder for the heart to pump blood. In obstructive HCM (sometimes referred to as oHCM or HOCM), the thickened muscle also blocks blood flow from the heart. The EXPLORER-HCM trial compared mavacamten to placebo (a pill with no medicine/active substances) in symptomatic people with obstructive HCM who had exercise limitations and suffered from shortness of breath, tiredness, palpitations, and chest pain. The study showed that mavacamten reduced the obstruction that restricts blood flow and improved people’s symptoms, well-being, and ability to participate in daily activities. Side effects, such as irregular heartbeat, palpitations, rapid heartbeat, and heart failure, were similar for people who received mavacamten or placebo. To read the full Plain Language Summary of this article, click on the View Article button above and download the PDF. Clinical Trial Registration: NCT03470545 ( ClinicalTrials.gov )

The Obstetric Patient for Cardiac Surgery

2019 ◽  
pp. 335-340
Author(s):  
Lauren Powlovich ◽  
Amanda M. Kleiman
Keyword(s):  
Heart Failure ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Cardiac Disease ◽  
Medical Management ◽  
Heart Defects ◽  
Pregnant Patient ◽  
Developed Countries ◽  
Peripartum Hemorrhage ◽  
In Pregnancy

Cardiac disease is the second leading cause of morbidity and mortality in pregnancy behind peripartum hemorrhage. In developed countries, a majority of cardiac disease in pregnancy is secondary to congenital heart defects, whereas in developing countries, mitral stenosis secondary to rheumatic fever prevails as the leading cause of cardiac disease during pregnancy. There is added workload on the heart during pregnancy due to the increased blood volume and cardiac output of the parturient. In patients with preexisting cardiac disease, this added workload may lead to decompensated congestive heart failure. Alternatively, such physiologic changes may unmask an unknown cardiac lesion in an unsuspecting patient. Medical management is always the first-line treatment of the pregnant patient with decompensated heart failure. However, if medical management has failed, cardiac surgery with cardiopulmonary bypass may be necessary. Due to the unique maternal physiology and the presence of not only one but also two patients, anesthesia, cardiac surgery, and cardiopulmonary bypass come with specific challenges, hemodynamic goals, and ethical dilemmas.

scholarly journals HAND1 loss-of-function within the embryonic myocardium reveals survivable congenital cardiac defects and adult heart failure

2019 ◽  
Vol 116 (3) ◽  
pp. 605-618 ◽  
Author(s):  
Beth A Firulli ◽  
Rajani M George ◽  
Jade Harkin ◽  
Kevin P Toolan ◽  
Hongyu Gao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Gene Dosage ◽  
Diastolic Heart Failure ◽  
Heart Defects ◽  
Conduction System ◽  
Cardiac Conduction ◽  
Bhlh Transcription Factor ◽  
Loss Of Function ◽  
Regulatory Pathways ◽  
Morphological Alterations

Abstract Aims To examine the role of the basic Helix-loop-Helix (bHLH) transcription factor HAND1 in embryonic and adult myocardium. Methods and results Hand1 is expressed within the cardiomyocytes of the left ventricle (LV) and myocardial cuff between embryonic days (E) 9.5–13.5. Hand gene dosage plays an important role in ventricular morphology and the contribution of Hand1 to congenital heart defects requires further interrogation. Conditional ablation of Hand1 was carried out using either Nkx2.5 knockin Cre (Nkx2.5Cre) or α-myosin heavy chain Cre (αMhc-Cre) driver. Interrogation of transcriptome data via ingenuity pathway analysis reveals several gene regulatory pathways disrupted including translation and cardiac hypertrophy-related pathways. Embryo and adult hearts were subjected to histological, functional, and molecular analyses. Myocardial deletion of Hand1 results in morphological defects that include cardiac conduction system defects, survivable interventricular septal defects, and abnormal LV papillary muscles (PMs). Resulting Hand1 conditional mutants are born at Mendelian frequencies; but the morphological alterations acquired during cardiac development result in, the mice developing diastolic heart failure. Conclusion Collectively, these data reveal that HAND1 contributes to the morphogenic patterning and maturation of cardiomyocytes during embryogenesis and although survivable, indicates a role for Hand1 within the developing conduction system and PM development.

scholarly journals Predictor of Death in Diarrheal Children Under 5 Years of Age Having Severe Sepsis in an Urban Critical Care Ward in Bangladesh

2019 ◽  
Vol 6 ◽  
pp. 2333794X1986271 ◽  
Author(s):  
Monira Sarmin ◽  
Farzana Afroze ◽  
Sharifuzzaman ◽  
Tahmina Alam ◽  
Nusrat Jahan Shaly ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Septic Shock ◽  
Severe Sepsis ◽  
Early Identification ◽  
Fatal Outcome ◽  
Shortness Of Breath ◽  
Clinical Predictors ◽  
Resource Poor ◽  
Care Ward ◽  
Children Under 5

We aimed to identify clinical predictors of fatal outcome in children under 5 years of age having diarrhea and severe sepsis and treated in the Intensive Care Unit of the Dhaka Hospital of icddr,b from October 2010 through September 2011. Among 191 enrolled children, 70 (37%) died and were considered to be cases, while the remaining 121 (63%) who survived constituted the controls. The cases more often had shortness of breath (SOB), septic shock, dehydrating diarrhea compared with the controls (for all, P < .05). After adjusting for potential confounders using logistic regression analysis, the likelihood of death was higher in children who had septic shock and SOB and lower in children having dehydrating diarrhea (for all, P < .05). Thus, SOB can trigger an early alarm for sepsis recognition; otherwise, these children can end up with fatality from septic shock. In resource-poor settings, early identification of these predictors can alleviate death.

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