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UIowa study examines altered gene expression in heart failure

(University of Iowa Health Care) Heart tissue from patients with heart failure exhibits increased levels of Cdk8 protein. Mimicking this increased Cdk8 expression in transgenic mouse hearts alters gene expression in a way that promotes heart failure. When University of Iowa researchers examined the mouse heart cells before a decrease in heart function was detectable, they found over 3,400 genes already expressed with a profile similar to that of human heart muscle cells with dilated cardiomyopathy and heart failure.
Source: EurekAlert! - Medicine and Health - Category: International Medicine & Public Health Source Type: news

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Authors: Schlitt A, Guha M, Noutsias M, Klein HH, Klein HU Abstract Assessment of a permanent risk of life-threatening ventricular arrhythmia in patients with severely reduced left ventricular ejection fraction (LVEF
Source: Herz - Category: Cardiology Tags: Herz Source Type: research
In this study we examined the effects of Ivabradine that inhibited the hyperpolarization-activated cyclic nucleotide-gated channel (HCN channel, also called funny current If), thereby leading to selective heart rate reduction and improved myocardial oxygen supply on the cardiac biomarkers sST2, GDF-15, suPAR and H-FABP in 50 CHF patients at the University Hospital of Jena. Patients were divided into three groups based on the etiology of CHF: dilated cardiomyopathy (DCM, n=20), ischemic cardiomyopathy (ICM, n=20) and hypertensive cardiomyopathy (HCM, n=10). The patients were administered Ivabradine (5 mg, bid for 3 months, ...
Source: Acta Pharmacologica Sinica - Category: Drugs & Pharmacology Authors: Tags: Acta Pharmacol Sin Source Type: research
Background— Mutations in LMNA (lamin A/C), which encodes lamin A and C, typically cause age-dependent cardiac phenotypes, including dilated cardiomyopathy, cardiac conduction disturbance, atrial fibrillation, and malignant ventricular arrhythmias. Although the type of LMNA mutations have been reported to be associated with susceptibility to malignant ventricular arrhythmias, the gene-based risk stratification for cardiac complications remains unexplored. Methods and Results— The multicenter cohort included 77 LMNA mutation carriers from 45 families; cardiac disorders were retrospectively analyzed. The mean age...
Source: Circulation: Cardiovascular Genetics - Category: Cardiology Authors: Tags: Arrhythmias, Sudden Cardiac Death, Genetic, Association Studies, Cardiomyopathy, Heart Failure Original Articles Source Type: research
In this report, we describe epitope mapping analysis of SERCA2a in A/J mice that leads us to make five observations: 1) SERCA2a contains multiple T cell epitopes that induce varying degrees of myocarditis. One epitope, SERCA2a 971-990, induces widespread atrial inflammation without affecting noncardiac tissues; the cardiac abnormalities could be noninvasively captured by echocardiography, electrocardiography, and magnetic resonance microscopy imaging. 2) SERCA2a 971-990-induced disease was associated with the induction of CD4 T cell responses and the epitope preferentially binds MHC class II/IAk rather than IEk By creating...
Source: Journal of Immunology - Category: Allergy & Immunology Authors: Tags: J Immunol Source Type: research
Conclusions -The data show that nicotinamide riboside, the most energy-efficient among NAD precursors, could be useful for treatment of HF notably in the context of DCM, a disease with few therapeutic options. PMID: 29217642 [PubMed - as supplied by publisher]
Source: Circulation - Category: Cardiology Authors: Tags: Circulation Source Type: research
Discussion Dilated cardiomyopathy leads to heart failure which can cause death. So, it is important to know the changes occurring in a heart due to dilated cardiomyopathy for the prognosis and further treatment for the disease. The finding ranges from minimal change to many other variation in the myocytes which is discussed further.
Source: Journal of the Anatomical Society of India - Category: Anatomy Source Type: research
A 90-year-old-man was scheduled for resection for sigmoid colon cancer. He was taking digitalis for chronic heart failure due to dilated cardiomyopathy. His medical history was unclear, but he did not recall undergoing previous internal jugular vein (IJV) catheterization.
Source: Journal of Cardiothoracic and Vascular Anesthesia - Category: Anesthesiology Authors: Tags: Letter to the Editor Source Type: research
Hypertrophic cardiomyopathy (HCM) is an atypical condition in the spectrum of cardiovascular diseases. The medical community instinctively equates cardiac disease with impaired contractile force and reduction in myocardial strength, epitomized by the final common pathway of dilated cardiomyopathy and systolic heart failure. In HCM, clinical evaluation and experimental evidence show the opposite. Whether by direct increase in myosin activity (caused by MHY7 mutations) or a decreased inhibitory effect of myosin binding protein C on myosin itself (caused by MYBPC mutations), HCM-causing gene defects result in myocardial hypercontractility.
Source: International Journal of Cardiology - Category: Cardiology Authors: Tags: Editorial Source Type: research
Conclusions There is high concordance between clinical and pathologic diagnosis, except for sarcoidosis and genetic diseases. Few misclassifications result in disadvantages to patients based on the new allocation system, but rare diseases like sarcoidosis remain problematic. To improve the UNOS database and enhance outcome research, pathology of the explanted hearts should be required post-transplantation. Graphical abstract
Source: JACC: Heart Failure - Category: Cardiology Source Type: research
Authors: Nakamura M, Sunagawa O, Kugai T, Kinugawa K Abstract A 43-year-old man was referred to our hospital in June 2014 because of severe heart failure. He was diagnosed with familial dilated cardiomyopathy and was administered oral tolvaptan and amiodarone for atrial and ventricular tachycardia. Since up-titration of carvedilol had failed and he was dependent on dobutamine, a left ventricular assist device (LVAD) was implanted. Tolvaptan and furosemide were both discontinued after LVAD implantation and he was discharged from the hospital. Thirteen months later, he was hospitalized for lethargy and hyponatremia o...
Source: International Heart Journal - Category: Cardiology Tags: Int Heart J Source Type: research
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