Heart Muscle Injury

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 42 Experts worldwide ranked by ideXlab platform

Pekka Koskinen - One of the best experts on this subject based on the ideXlab platform.

  • Novartis Foundation Symposium 216 - Alcohol and Cardiovascular Diseases - Alcohol, cardiac arrhythmias and sudden death.
    Novartis Foundation Symposium, 2007
    Co-Authors: Markku Kupari, Pekka Koskinen
    Abstract:

    : Studies in experimental animals have shown varying and apparently opposite effects of alcohol on cardiac rhythm and conduction. Given acutely to non-alcoholic animals, ethanol may even have anti-arrhythmic properties whereas chronic administration clearly increases the animals' susceptibility to cardiac arrhythmias. Chronic heavy alcohol use has been incriminated in the genesis of cardiac arrhythmias in humans. The evidence has come from clinical observations, retrospective case-control studies, controlled studies of consecutive admissions for arrhythmias, and prospective epidemiological investigations. Furthermore, electrophysiological studies have shown that acute alcohol administration facilitates the induction of tachyarrhythmias in selected heavy drinkers. The role of alcohol appears particularly conspicuous in idiopathic atrial fibrillation. Occasionally, ventricular tachyarrhythmias have also been provoked by alcohol intake. Several lines of evidence suggest that heavy drinking increases the risk of sudden cardiac death with fatal arrhythmia as the most likely mechanism. According to epidemiological studies this effect appears most prominent in middle-aged men and is only partly explained by confounding traits such as smoking and social class. The basic arrhythmogenic effects of alcohol are still insufficiently delineated. Subclinical Heart Muscle Injury from chronic heavy use may be instrumental in producing patchy delays in conduction. The hyperadrenergic state of drinking and withdrawal may also contribute, as may electrolyte abnormalities, impaired vagal Heart rate control, repolarization abnormalities with prolonged QT intervals and worsening of myocardial ischaemia or sleep apnoea. Most of what we know about alcohol and arrhythmias relates to heavy drinking. The effect of social drinking on clinical arrhythmias in non-alcoholic cardiac patients needs to be addressed further.

Lin Zhe-zhan - One of the best experts on this subject based on the ideXlab platform.

  • Diagnosis and therapy of Hyperthyroid Heart Disease
    Medical Recapitulate, 2020
    Co-Authors: Lin Zhe-zhan
    Abstract:

    Hyperthyroid Heart disease is a series of signs and symptoms of cardiovascular system resulting from metabolic disorder,which caused by the direct or indirect toxic actions of excessive thyroid hormones.Its genensis is associated with age of patient,course of disease,regular therapy or not,Heart dilatation,Heart Muscle Injury,hypopotassaemia and infection.Its clinical manifestation is arrhythmia,Heart dilatation or Heart failure,angina pectoris or myocardial infarction,which are often curative companyed by the controling of hyperthyreosis.

Ruth Williams - One of the best experts on this subject based on the ideXlab platform.

  • The Year’s Successes in Failure Circulation Research Takes a Look at the Key Research Developments of 2009 That Are Providing Hope in the Field of Heart Failure
    Circulation Research, 2010
    Co-Authors: Ruth Williams
    Abstract:

    When the Heart struggles to meet the body’s demand for blood supply, it adapts and grows—a condition known as cardiac hypertrophy. Such growth can occur as a healthy response to altered physiological states, such as pregnancy and regular aerobic exercise, or in response to pathological conditions, such as high blood pressure or Heart Muscle Injury. If pathological conditions persist, hypertrophy can lead to functional degradation of the Heart and, ultimately, to its failure. Researchers strive to identify the molecular pathways that lead to physiological and pathological hypertrophy and to understand what causes hypertrophy to transition into life-threatening Heart failure. This year has seen the emergence of a number of new molecular mediators and microRNAs as key regulators of pathways that lead to hypertrophy. These finding provide cardiologists with a choice selection of targets for future therapies. Here is our pick of the year’s articles. First discovered in the mid 1990s, microRNAs (miRs) are single-stranded RNA molecules of 18 to 25 nucleotides in length that regulate gene expression. In animals, miRs generally bind to complementary sequences in the 3’UTR of a target messenger RNA. This either prevents the transcript from being translated or causes its degradation. In recent years, a number of miRs have been found to be involved in Heart development and disease.1,2 The opening shot that launched Heart-related miR research was fired by Eric Olson and colleagues in 2007. These investigators showed that cardiac-specific miR-208 (the gene for which resides within an intron of the α-myosin heavy chain gene) is required for myocyte hypertrophy and fibrosis.2 Maha Abdellatif (University of Medicine and Dentistry of New Jersey, Newark, NJ) describes how miR-208 and other miRs have provided a much-needed boost to the Heart failure and hypertrophy field. “We had almost stagnated at some point with the signaling molecules …

Li Yushu - One of the best experts on this subject based on the ideXlab platform.

  • GW24-e2299 Effects of serum from patients of atrial fibrillation on chemotaxis of cardiac fibroblasts
    Heart, 2013
    Co-Authors: Duan Kadan, Li Yushu
    Abstract:

    Objectives Atrial fibrillation is a clinically common arrhythmia, which is characterised by atrial fibrosis, myocardial fibroblast is play a important role in fibrosis process. We designed this experiment to investigate the different chemotatic effects of the cardiac fibroblasts to the serum between atrial fibrillation and other control groups, and to predict the relationship between fibrosis followed atrial fibrillation and movemoment behavior of fibroblast. Methods The selected objects was divided into four groups which were controls (SR, n = 16), non-Af atrial arrhythmia (AA, n = 18), paroxysmalAf (Paro-Af, n = 19) and persistent Af (Pers-Af, n = 20), serum were detected; Cardiac fibroblasts were isolated from the ventricles of neonatal Sprague-Dawley rats (1–3days old) and primary cultured with digestion, different speed adherence methods. The cell in 3 to 4 passages were used for transwel lchamber assay to determine the chemotatic effects of the cardiac fibroblasts to the serum between atrial fibrillation and other control groups, which is designed to analysis the cells through the polycarbonate membrane and atrial fibrillation inthe relevance of each group, and to predict the progress of Af. Results Compared with control, the cells that migrated through the polycarbonate membrane were obviously increased in Af groups. The strongest Chemotaxis was induced by the serum from the patients of persistent Atrial fibrillation (pers-Af), the numbers of migrated cells in non-Af atrial arrhythmia(AA) were higher than that in paroxysmal Atrial fibrillation (paro-Af), that in control group was least. The multiple logistic regression analyses show that the migrated cells in the lower surface were related to atrial fibrillation and left atrial diameter. Conclusions 1). The chmotactic effects of the Af serum are obviously higher than that of control serum. The differences of Af serum among each group show that myocardial fibrosis is a chronic, insidious, delayed process. The migration and infiltration of cardiac fibroblast indirectly reflect the presence, severity, extent of the myocardial damage. 2). The changes of migrated cells precede the changes of left atrial diameter (LAD), indicating that the cause of fibrosis is more important, and the positive correlation between Af and left atrial diameter may not directly causality, they are caused by the fibrosis due to the Heart Muscle Injury and the fibrosis is closely related to synchronisation of the atrial contraction. 3). The number of cells migration may be due to inducer that the damaged tissue and cell release.

Michael Przybylski - One of the best experts on this subject based on the ideXlab platform.