Forms Of Heart Disease Research Articles

Abstract 15315: SGLT2 Inhibitor Ertugliflozin Decreases Elevated Intracellular Sodium, Improves Myocardial Energetics and Enhances Function in Metabolic Heart Disease

Background: Sodium-glucose co-transporter 2 (SGLT2) inhibitors are antidiabetic drugs of great interest in cardiology due to their improvement of heart failure outcomes independent of diabetes. As SGLT2 is not expressed in cardiomyocytes, the mechanism of such benefit remains unclear. Elevated myocardial intracellular sodium [Na + ] i has been found in heart failure and SGLT2 inhibition lowers [Na + ] i in isolated cardiomyocytes. Elevated [Na + ] i was shown to decrease mitochondrial calcium via mitochondrial Na/Ca exchanger (NCx MITO ), resulting in decreased mitochondrial ATP synthesis. We have previously shown that mice fed a diet high in fat and sugar (HFHS) develop metabolic heart disease (MHD) characterized by decreased mitochondrial ATP synthesis with decreased phosphocreatine (PCr), worsened diastolic function and contractile reserve. We hypothesize that the SGLT2 inhibitor ertugliflozin (ERTU) decreases the elevated [Na + ] i to improve energetics and contractile function in MHD. Methods and Results: Isolated hearts from mice after 6 months of HFHS vs. control diet (CD), +/- ERTU in the last month, were studied using 31 P and 23 Na NMR spectroscopy to measure PCr/ATP ratio and [Na + ] i , respectively. As expected, HFHS hearts showed lower PCr/ATP, diastolic dysfunction (↑LVEDP) and lack of contractile reserve (↓RPP) during high work protocol compared to CD hearts. Myocardial [Na + ] i was elevated more than 2-fold in HFHS compared to CD. One month of ERTU treatment decreased [Na + ] i and improved energetics and contractile function in HFHS to levels similar to or better than CD. Perfusion with CGP 37157, which inhibits NCx MITO , improved PCr/ATP in HFHS hearts. Conclusion: Lowering of myocardial [Na + ] i by ertugliflozin contributes to improved energetics and function in MHD. These results suggest targeting [Na + ] i as an effective strategy to improve cardiac dysfunction in MHD and other forms of heart disease associated with elevated myocardial [Na + ] i.

Expert System Diagnosing Heart Disease using Bayes' Theorem Method

Heart disease is one of the leading causes of death in Indonesia. The high number of deaths from heart disease is caused by the lack of cardiologists, the lack of public awareness of conducting regular heart health checks and the poor lifestyle of patients. So we need an application that can make it easier for users to detect heart disease early and independently. In this study, the aim is to build an application using the website-based Bayes Theorem method as a tool for diagnosing coronary heart disease. In this application, patients do not have to wait long for treatment by a doctor, but it can be an alternative to anticipate treatment quickly and precisely. How to use this application, the admin inputs questions in the form of symptoms that will be answered by the user, then the system will process all user answers using the Bayes theorem method and the system will issue output in the form of diagnostic results in the form of heart disease and various solutions. This application uses a Web programming language and Php & Mysql as a database. The system that has been built can assist patients in knowing the type of heart disease that is being suffered by the patient and according to the analysis of heart disease experts.

Canine infantile left ventricular noncompaction

BackgroundLeft ventricular noncompaction (LVNC) is a rare form of cardiomyopathy currently described in humans and cats. It consists of a spongy myocardium characterized by prominent trabeculation and deep recesses involving more than 50% of the ventricular thickness. We describe the clinical and pathological features of LVNC combined with tricuspid valve dysplasia, double-orifice tricuspid valve and severe pulmonary stenosis in a puppy. In addition, we briefly review the LVNC causes, pathogenesis, forms and current diagnostic criteria.Case presentationA seven-week-old intact German Shorthaired Pointer-cross male was presented with a poor body condition, exercise intolerance and dyspnea. Clinical exam identified a bilateral systolic murmur (grade IV/VI over the right heart base and grade III/VI over the left heart base). Echocardiography identified tricuspid valve dysplasia, mild mitral regurgitation, and severe pulmonic stenosis with a trans-valvar systolic pressure gradient of 106 mmHg. Left ventricular noncompaction was diagnosed by necropsy and further confirmed histopathologically by the presence of two distinct myocardial layers: an inner noncompacted zone covering more than 50% of ventricular thickness containing prominent trabeculation and deep recesses, and an outer zone of compact myocardium.ConclusionsThis is the first case describing LVNC in a canine patient, supporting the introduction of this form of heart disease as a differential diagnosis for cardiomyopathies in juvenile and adult dogs.

Joint effect of depression and health behaviors or conditions on incident cardiovascular diseases: A Korean population-based cohort study

BackgroundThe precise relationships among depression, risk factors for cardiovascular disease (CVD), and incident CVD remain uncertain. This study examined the joint effect of depression and other CVD risk factors on the incidence of CVD. MethodsWe conducted a prospective cohort study using South Korea's National Health Insurance Service-National Sample Cohort (NHIS-NSC). To estimate incident CVD, 199,544 participants without CVD diagnosed with depression between 2003 and 2005 were followed through 2013. The clinician's diagnosis used measurements for depression, CVD risk factors, and CVD. ResultsControlling for other CVD risk factors, depressed individuals had a higher risk for ischemic heart disease (AHR, 1.01; 99%%CI, 1.01–1.50) and other forms of heart disease likely related to atherosclerosis (AHR, 1.43; 99%%CI, 1.13–1.82). There were no statistically significant interactions between depression and CVD risk factors. However, when depression was comorbid with overweight or diabetes, there was a higher risk for incident ischemic heart disease, as compared to depression or CVD risk factors alone. For other forms of heart disease likely related to atherosclerosis, the coexistence of depression and physical inactivity or overweight showed a similar pattern to that shown in ischemic heart disease. LimitationsThe severity of depression was not reported for depressed patients, and our dataset provided a limited number of covariates. Also, the self-reported health behavior data may be biased. ConclusionAs depression could be a significant predictor of incident CVD independently with other CVD risk factors, professionals should recognize and manage depression as a major CVD risk factor.

AB23A Reduces TGF-β1-Induced Human Cardiac Fibroblasts (HCF) Proliferation and Collagen Secretion via MER/ERK1/2/CREB Pathway

Background and Objectives: Myocardial fibrosis is associated with many forms of heart diseases which is characterized by the accumulation of activated cardiac fibroblasts (CFBs) and excess deposition of extracellular matrix (ECM). Natural compounds such as Alisol B 23-acetate has been proved to maintain the activation of ERK1/2, but whether it can affect cardiac fibroblasts by MER/ERK1/2/CREB signaling pathway is still unknown. Methods: The cell was identified with α-SMA protein level detected by immunofluorescence staining method. The cell proliferation was examined by CCK8 assay. Col I and Col III protein levels were examined by western blot and sirius red staining to detect the ECM level. Furthermore, p-MERK, MERK, P-ERK, ERK and CREB were examined by western blot to verify whether Alisol could activate the MERK/ERK1/2/CREB pathway in myocardial fibrosis. Results: CCK8 assay result indicated that Alisol reduced the cell viability of CFBs induced by TGF-β1. In addition, Alisol significantly decreased the ECM deposition of CFBs. Furthermore, Alisol could activate MERK/ERK1/2/CREB signaling pathway. Conclusion: These results verified that Alisol inhibited myocardial fibrosis via MERK/ERK1/2/CREB pathway.

Use of computed radiology as a screening test for the identification of congenital heart disease in dogs

The objectives of this study were to evaluate the accuracy of thoracic radiology as a screening test for congenital heart diseases in dogs, to identify the main contributions and limitations of this modality, and to verify the reproducibility of the evaluations by three observers with different levels of training. An interobserver, observational, retrospective and prospective study was carried out, including ninety dogs: thirty healthy animals, thirty with acquired heart diseases and thirty with congenital heart diseases, which all had thoracic radiographs and a confirmed echocardiographic diagnosis. The cases were separated and randomized by a mediator who did not participate in the reading of the radiographic examinations, and no evaluator had access to the patients' data. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy of each observer were calculated in relation to the correct classification of dogs to groups of normal or acquired and congenital heart diseases, as well as identification of enlargement of the cardiac silhouette and large vessels of dogs with congenital heart diseases. Finally, the Kappa coefficient was obtained between the observers to verify the reproducibility of the radiological evaluations performed. In general, sensitivity, PPV and accuracy were unsatisfactory ( 70%), and the agreement ranged from poor to reasonable (between 0 and 0.39). Although greater accuracy was achieved in the differentiation of healthy dogs from those with acquired and congenital heart diseases by thoracic radiography, when compared to the other studies, the modality was able only to identify healthy patients, and could not differentiate the individuals with different forms of heart disease or define the cardiac malformations. In addition, there was low reproducibility between observers, therefore, this technique should not be used as a sole screening method in dogs with suspected congenital heart diseases.

Precipitating factors leading to decompensation of heart failure in patients attending a tertiary care centre of Nepal

Background and Aims: Heart failure is one of the debilitating conditions in patients with various forms of heart disease. It can have impacts on various aspects of the life of a patient. There have been few studies on the etiological aspects and precipitants of heart failure in the Nepalese population. The aim of our study is to find out the major factors that lead to decompensation of heart failure in patients who already have established heart failure.
 Methods: This study was a single-centre, prospective, observational study conducted in the emergency department of Manmohan Cardiothoracic Vascular and Transplant Centre (MCVTC) from 1st June 2019 to 30th November 2019. Hundred and one patients with established heart failure in the past, who presented again with decompensated heart failure were enrolled.
 Results: The mean age of the patients was 62.81 years (SD=15.92). Factors responsible for acute decompensation of heart failure were identified in 95.0 % of patients included in the study. The most common factor identified was poor compliance with medications and diet and fluid intake (38.6%). Next to it was arrhythmia identified in about 35.6% of cases.Other important factors responsible for decompensation in our study were infection (12.8%), anemia (4.9%) and ischemia (2.9%).
 Conclusion: Preventable and identifiable factors are responsible for the decompensation of heart failure. Most of these factors can be modified with the use of proper patient counseling/patient education, thereby reducing recurrent hospital admissions and economic burden to the patient and the government as well.

A REVIEW: ANGIOGRAPHY AND ANGIOPLASTY

The cardiovascular system refers to the heart, blood vessels and the blood. Blood contains oxygen and other nutrients which your body needs to survive. The body takes these essential nutrients from the blood. Angiography is an imaging test that uses X-rays to view your body's blood vessels. The X-rays provided by an angiography are called angiograms. This test is used to study narrow, blocked, enlarged, or malformed arteries or veins in many parts of your body, including your brain, heart, abdomen, and legs. Angioplasty is a procedure to restore blood flow through the artery. You have angioplasty in a hospital. The doctor threads a thin tube through a blood vessel in the arm or groin up to the involved site in the artery. The tube has a tiny balloon on the end. Cardiovascular disease generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina) or stroke. Other heart conditions, such as those that affect your heart's muscle, valves or rhythm, also are considered forms of heart disease.
 Keyword: cardiovascular system, angiography, angioplasty

Ventricular Arrhythmias

Ventricular arrhythmias are common in all forms of heart disease and are an important cause of cardiac arrest and sudden death. Many ventricular arrhythmias are benign but may serve as a marker for underlying disease or its severity. Others are life threatening. The significance of an arrhythmia is determined by the specific characteristics of the arrhythmia and the associated heart disease, and these features guide evaluation and therapy. This review discusses various mechanisms and types of ventricular arrhythmias and management based on clinical presentation (including patients with symptomatic arrhythmia and increased risk of sudden death without arrhythmia symptoms). Genetic arrhythmia syndromes, such as abnormalities of repolarization and the QT interval, catecholaminergic polymorphic ventricular tachycardia (VT), and inherited cardiomyopathies, are discussed in depth. Under the rubric of management of ventricular arrhythmias, drug therapy for ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs), and catheter ablation for VT are also covered. Tables chart out guideline recommendations for ICD therapy, drugs for the management of ventricular arrhythmias, and indications and contraindications for catheter ablation of ventricular arrhythmias. Electrocardiograms are provided, as well as management algorithms for ventricular arrhythmias based on patient presentation, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection less than or equal to 35% who are candidates for consideration of an ICD for primary prevention of sudden cardiac death. This review contains 5 figures, 8 tables, and 61 references. Keywords: Ventricular arrhythmias, implanted cardioverter-defibrillator (ICD), Ventricular tachycardia (VT), Premature Ventricular Contractions (PVC), Myocardial Infarction (MI), Brugada syndrome, Arrhythmogenic right ventricular cardiomyopathy (ARVC), electrocardiographic (ECG)

Ventricular Arrhythmias

Ventricular arrhythmias are common in all forms of heart disease and are an important cause of cardiac arrest and sudden death. Many ventricular arrhythmias are benign but may serve as a marker for underlying disease or its severity. Others are life threatening. The significance of an arrhythmia is determined by the specific characteristics of the arrhythmia and the associated heart disease, and these features guide evaluation and therapy. This review discusses various mechanisms and types of ventricular arrhythmias and management based on clinical presentation (including patients with symptomatic arrhythmia and increased risk of sudden death without arrhythmia symptoms). Genetic arrhythmia syndromes, such as abnormalities of repolarization and the QT interval, catecholaminergic polymorphic ventricular tachycardia (VT), and inherited cardiomyopathies, are discussed in depth. Under the rubric of management of ventricular arrhythmias, drug therapy for ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs), and catheter ablation for VT are also covered. Tables chart out guideline recommendations for ICD therapy, drugs for the management of ventricular arrhythmias, and indications and contraindications for catheter ablation of ventricular arrhythmias. Electrocardiograms are provided, as well as management algorithms for ventricular arrhythmias based on patient presentation, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection less than or equal to 35% who are candidates for consideration of an ICD for primary prevention of sudden cardiac death. This review contains 5 figures, 8 tables, and 61 references. Keywords: Ventricular arrhythmias, implanted cardioverter-defibrillator (ICD), Ventricular tachycardia (VT), Premature Ventricular Contractions (PVC), Myocardial Infarction (MI), Brugada syndrome, Arrhythmogenic right ventricular cardiomyopathy (ARVC), electrocardiographic (ECG)

Translating Translation to Mechanisms of Cardiac Hypertrophy.

Cardiac hypertrophy in response to chronic pathological stress is a common feature occurring with many forms of heart disease. This pathological hypertrophic growth increases the risk for arrhythmias and subsequent heart failure. While several factors promoting cardiac hypertrophy are known, the molecular mechanisms governing the progression to heart failure are incompletely understood. Recent studies on altered translational regulation during pathological cardiac hypertrophy are contributing to our understanding of disease progression. In this brief review, we describe how the translational machinery is modulated for enhanced global and transcript selective protein synthesis, and how alternative modes of translation contribute to the disease state. Attempts at controlling translational output through targeting of mTOR and its regulatory components are detailed, as well as recently emerging targets for pre-clinical investigation.

Exosomes: From Potential Culprits to New Therapeutic Promise in the Setting of Cardiac Fibrosis.

Fibrosis is a significant global health problem associated with many inflammatory and degenerative diseases affecting multiple organs, individually or simultaneously. Fibrosis develops when extracellular matrix (ECM) remodeling becomes excessive or uncontrolled and is associated with nearly all forms of heart disease. Cardiac fibroblasts and myofibroblasts are the main effectors of ECM deposition and scar formation. The heart is a complex multicellular organ, where the various resident cell types communicate between themselves and with cells of the blood and immune systems. Exosomes, which are small extracellular vesicles, (EVs), contribute to cell-to-cell communication and their pathophysiological relevance and therapeutic potential is emerging. Here, we will critically review the role of endogenous exosomes as possible fibrosis mediators and discuss the possibility of using stem cell-derived and/or engineered exosomes as anti-fibrotic agents.

Role of Transient Receptor Potential Canonical Channels in Heart Physiology and Pathophysiology.

Transient receptor potential canonical (TRPC) channels are involved in the regulation of cardiac function under (patho)physiological conditions and are closely associated with the pathogenesis of cardiac hypertrophy, arrhythmias, and myocardial infarction. Understanding the molecular mechanisms and the regulatory pathway/locus of TRPC channels in related heart diseases will provide potential new concepts for designing novel drugs targeting TRPC channels. We will present the properties and regulation of TRPC channels and their roles in the development of various forms of heart disease. This article provides a brief review on the role of TRPC channels in the regulation of myocardial function as well as how TRPC channels may serve as a therapeutic target in heart failure and cardiac arrhythmias including atrial fibrillation.

Physical Illnesses Before Diagnosed as Schizophrenia: A Nationwide Case-Control Study.

Some physical illnesses are potentially associated with the development of schizophrenia. However, few studies have investigated these associations. Here, we examined physical illnesses and medical utilization patterns existing before patients received a diagnosis of schizophrenia. We enrolled a large representative cohort of the general population in Taiwan (N = 1 000 000) and identified 1969 young patients with a new diagnosis of schizophrenia from January 1, 2000 to December 31, 2013. We conducted a nested case-control study based on risk-set sampling. Each case was age-matched and sex-matched with 4 controls selected from the general population. The case and control groups were compared on the basis of various clinical characteristics. Conditional logistic regression was used to estimate the magnitude of risk associated with newly diagnosed schizophrenia. Within the 1 year before the schizophrenia diagnosis, the cases were most likely to visit the psychiatry department, followed by internal medicine and family medicine departments. According to multivariate analysis, compared with the controls, the cases had substantially higher risk of physical conditions in the prodromal phase, including hypertension (adjusted risk ratio [aRR] = 1.93, P = .001), other forms of heart disease (aRR = 2.07, P < .001), cerebrovascular diseases (aRR = 2.96, P = .001), chronic obstructive pulmonary disease (aRR = 1.50, P = .005), asthma (aRR = 1.76, P = .003), and irritable bowel syndrome (aRR = 2.00, P < .001). A wide range of psychiatric diseases and concomitant use of medications were significantly associated with schizophrenia development. In conclusion, several physical illnesses were identified to be associated with schizophrenia development, indicating that people with these illnesses could be vulnerable to schizophrenia.

Anisotropic conduction in the myocardium due to fibrosis: the effect of texture on wave propagation

Cardiac fibrosis occurs in many forms of heart disease. It is well established that the spatial pattern of fibrosis, its texture, substantially affects the onset of arrhythmia. However, in most modelling studies fibrosis is represented by multiple randomly distributed short obstacles that mimic only one possible texture, diffuse fibrosis. An important characteristic feature of other fibrosis textures, such as interstitial and patchy textures, is that fibrotic inclusions have substantial length, which is suggested to have a pronounced effect on wave propagation. In this paper, we study the effect of the elongation of inexcitable inclusions (obstacles) on wave propagation in a 2D model of cardiac tissue described by the TP06 model for human ventricular cells. We study in detail how the elongation of obstacles affects various characteristics of the waves. We quantify the anisotropy induced by the textures, its dependency on the obstacle length and the effects of the texture on the shape of the propagating wave. Because such anisotropy is a result of zig-zag propagation we show, for the first time, quantification of the effects of geometry and source-sink relationship, on the zig-zag nature of the pathway of electrical conduction. We also study the effect of fibrosis in the case of pre-existing anisotropy and introduce a procedure for scaling of the fibrosis texture. We show that fibrosis can decrease or increase the preexisting anisotropy depending on its scaled texture.

The Roles of Noncardiomyocytes in Cardiac Remodeling.

Cardiac remodeling is a common characteristic of almost all forms of heart disease, including cardiac infarction, valvular diseases, hypertension, arrhythmia, dilated cardiomyopathy and other conditions. It is not merely a simple outcome induced by an increase in the workload of cardiomyocytes (CMs). The remodeling process is accompanied by abnormalities of cardiac structure as well as disturbance of cardiac function, and emerging evidence suggests that a wide range of cells in the heart participate in the initiation and development of cardiac remodeling. Other than CMs, there are numerous noncardiomyocytes (non-CMs) that regulate the process of cardiac remodeling, such as cardiac fibroblasts and immune cells (including macrophages, lymphocytes, neutrophils, and mast cells). In this review, we summarize recent knowledge regarding the definition and significant effects of various non-CMs in the pathogenesis of cardiac remodeling, with a particular emphasis on the involved signaling mechanisms. In addition, we discuss the properties of non-CMs, which serve as targets of many cardiovascular drugs that reduce adverse cardiac remodeling.

Pattern of heart diseases among patients referred to a paediatric cardiology clinic in Sri Lanka, the situation from 2010 to 2012

Background: Epidemiology of cardiac diseases among paediatric population remain largely undocumented in Sri Lanka. The objective of this study was to identify the pattern of heart diseases among patients referred to the Paediatric cardiology clinic at Teaching Hospital Kandy and Sirimavo Bandaranaike Specialized Childrens’ Hospital (SBSCH) Peradeniya. Methods: Demographic, clinical details and echocardiography details of patients referred for cardiac assessment between 1st 2010 to 30th November, 2012 were descriptively analysed. Results: Ten thousand, six hundred and seventy-eight (10678) newly referred patients were evaluated over the study period. Of the study cohort 6582 patients had some form of heart disease. Among them, 5363 (50.2%) had congenital heart diseases (CHDs). The most frequent acyanotic heart disease was Atrial Septal Defect (ASD-3024 patients). Ventricular Septal Defect (VSD) ranked second in frequency (697 patients). The commonest cyanotic CHD was Tetralogy of Fallot (79 patients). There were 1200 patients with acquired heart diseases. The most frequent preventable acquired heart disease was Rheumatic valvular heart disease (80 patients). Conclusions: The commonest CHD among the study cohort was ASD while Tetralogy of Fallot was the commonest cyanotic heart disease. Early identification is important to ensure appropriate interventions and prevent complications.

PREVALENCE OF METABOLIC SYNDROME IN NEWLY DIABETES MELLITUS PATIENTS

Introduction: Diabetes mellitus (DM) is defined or described as a group of metabolic disorders which is characterized by a high blood sugar level over a prolonged period. Metabolic syndrome (MS) is described as insulin resistance, clusters of abnormalities including abdominal obesity, hypertension, hyperglycaemia, increased triglycerides, and decreased high-density lipoprotein cholesterol (HDL-C). For the diagnosis of metabolic syndrome there are different diagnostic criteria. According to WHO modified criteria metabolic syndrome is defined as a presence of diabetes and e”2 of the following: 1) BMI &gt;30 kg/m2 or Waist hip ratio&gt;0.9 for men, &gt;0.85 for women. 2) TG e”150 mg/dl or HDL. 3) BP e”140/90 mm Hg or on medication. According to the studies people having diabetes mellitus, at least 65% were associated metabolic syndrome die of some form of heart disease or stroke. So it is necessary to investigate a newly detected diabetes mellitus for signs of the metabolic syndrome so that complications can be prevented. One of the study showed that in India there is a highest increase in the population with diabetes from 19 million in 1995 to 66.8 million in 2015 and which is predicted to increase to 123.5 million by 2040. The prevalence rate of diabetes in urban areas is about 9% and the prevalence in rural areas has also increased to around 3% of the total population. According to the data of Third National Health and Nutrition Examination Survey (NHANES III) people without metabolic syndrome had the lowest risk for cardiovascular disease (CVD) whereas people with metabolic syndrome had an intermediate level of risk, and those with diabetes had the highest level of risk.&#x0D; Aim: The main aim of this study is to find prevalence of Metabolic Syndrome in newly diagnosis of Diabetes Mellitus. Material and methods: Total 100 patients were included in this study in which 80 were male and 20 were females with recently diagnosis as diabetes mellitus within 6 months prior to the date of presentation. From all the patients detail history was collected and other risk and associated factors. For all the patients detailed clinical examinations, including weight in kg, height in cm, body mass index (BMI) (weight in kg/height in m2) were recorded.&#x0D; Result: Prevalence of metabolic syndrome among 100 study participants was found to be 70.0%. Prevalence of metabolic syndrome was found to be highest in the age group of 35 -45 years (65.4%).The mean value of FBS in the metabolic syndrome group was 178 mg/dl; post prandial blood sugar mean value was 250 mg/dl. Out of cases 100 cases with TG&gt;150, 92 had metabolic syndrome (92%). In this study, 65 % of the cases with the criteria for WC, WC &gt; 90 cm for males and &gt;80 cm for females had metabolic syndrome.&#x0D; Conclusion: Therefore in this study showed that diabetes significantly increases the risk for metabolic syndrome. Low HDL-C and evaluated TGs were seen to be associated with most cases of metabolic syndrome. Diabetic patients with morbid obesity, WC and central obesity have a high association with metabolic syndrome.&#x0D; Keywords: Diabetes Mellitus, Metabolic Syndrome, triglycerides obesity

From the Literature

From the Literature

ST2/IL-33 signaling in cardiac fibrosis

Cardiac fibrosis is a significant global health problem associated with nearly all forms of heart disease. In the heart interstitial fibrosis may be reparative, replacing areas damaged by myocyte loss after acute infarction, or compensative, responding to cardiac overload. However, after injury in chronic cases activated myofibroblasts contribute to the tissue imbalance of the newer molecules associated with cardiac fibrosis, interleukin (IL-33), and suppression of tumorigenicity 2 (ST2). Physiological stretching causes myofibroblasts to release IL-33 which binds the ST2 receptor (ST2L) on the cardiomyocyte membrane, promoting cell survival and integrity. But in chronic conditions, local and neighboring cells can increase the release of IL-33′s decoy, soluble ST2 (sST2), which blocks IL-33/ST2L binding, promoting tissue fibrosis. We review recent studies that have illustrated novel aspects of ST2/IL-33 signaling mediating cardiac fibrosis, and some newer biomolecular targets for the prevention and treatment of maladaptive remodeling.