Cardiomyopathies: Evolution of pathogenesis concepts and potential for new therapies

Abstract

Cardiomyopathies are defined as diseases of the myocardium with associated structural and functional abnormalities. Knowledge of these pathologies for a long period was not clear in clinical practice due to uncertainties regarding definition, classification and clinical diagnosis. In recent decades, major advances have been made in the understanding of the molecular and genetic issues, pathophysiology, and clinical and radiological assessment of the diseases. Progress has been made also in management of several types of cardiomyopathy. Advances in the understanding of these diseases show that cardiomyopathies represent complex entities. Here, special attention is given to evolution of classification of cardiomyopathies, with the aim of assisting clinicians to look beyond schematic diagnostic labels in order to achieve more specific diagnosis. Knowledge of the genotype of cardiomyopathies has changed the pathophysiological understanding of their etiology and clinical course, and has become more important in clinical practice for diagnosis and prevention of cardiomyopathies. New approaches for clinical and prognostic assessment are provided based on contemporary molecular mechanisms of contribution in the pathogenesis of cardiomyopathies. The genotype-phenotype complex approach for assessment improves the clinical evaluation and management strategies of these pathologies. The review covers also the important role of imaging methods, particularly echocardiography, and cardiac magnetic resonance imaging in the evaluation of different types of cardiomyopathies. In summary, this review provides complex presentation of current state of cardiomyopathies from genetics to management aspects for cardiovascular specialists.

Structures reveal details of small molecule binding to cardiac troponin

“…By far, the most common cause of HFrEF is ischemic cardiomyopathy. However, in the absence of atherosclerotic coronary disease or valvular abnormalities, a wide range of etiologies encompassing infiltrative, infectious, autoimmune, toxic, hormonal, and genetic causes, can give rise to dilated cardiomyopathy (DCM)[2]. Over time, the volume overload that develops in HFrEF causes the heart muscle to further dilate, thin, and scar, making it even more difficult to generate force.…”

Late Gadolinium Enhancement Amount As an Independent Risk Factor for the Incidence of Adverse Cardiovascular Events in Patients with Stage C or D Heart Failure

“…The most common cause of end-stage heart failure includes ischemia-dilated cardiomyopathy (IDCM) and non-ischemia-dilated cardiomyopathy (NIDCM; Sisakian, 2014). Histologically, the main feature of end-stage damaged myocardium, whether ischemic or non-ischemic, is the development of interstitial and replacement fibrosis that varies in severity (Schaper et al, 1991; Yarbrough et al, 2012).…”

Role of augmented transferrin during the retraining for undeveloped left ventricle

“…The failure of the animal model to mimic human TGA 9 makes the mechanism study for PAB very difficult. However, the overloaded LV definitely released or recruited various proteins in the peripheral blood to participate in the process of hypertrophy 10,11. Therefore, we focused on the altered plasma proteins which could mediate the hypertrophy of immature cardiomyocytes.…”