Why is fibrosis of the cardiac muscle serious?

Fibrosis restricts the supply of oxygen and nourishment to the myocardium (2, 3). Myocardial fibrosis causes electrical and structural changes that predispose patients to arrhythmias, heart failure and ischaemia (12).

How does fibrosis affect the heart?

Cardiac fibrosis occurs when fibroblasts are activated to myofibroblasts and produce elevated amounts of ECM proteins that form scar tissue and alter normal degradation of ECM (FIGURE 1). Both processes lead to a buildup of collagen, which impacts both systolic and diastolic function.

What is the treatment for cardiac fibrosis?

Inhibitors of TGF-β Signaling for the Treatment of Cardiac Fibrosis. The renin-angiotensin system (RAS) inhibitors are currently used as standard therapy for HF and have been shown to inhibit activation of fibroblast and differentiation into myofibroblast.

Can cardiac fibrosis causes heart attack?

Cardiovascular disease (CVD), a class of diseases that impact the heart or cardiovascular system, is responsible for 31% of all deaths and remains the leading cause of mortality worldwide [1]. Ischemic heart disease and endomyocardial fibrosis are the primary causes of end-stage heart failure [2].

Is cardiac fibrosis fatal?

Myocardial fibrosis is involved in the progression of LV dilatation and deterioration of the cardiac muscle, leading to pump function failure. Pump function failure, cardiomyocyte separation, and fibrosis itself may induce fatal arrhythmias.

Can Exercise reverse cardiac fibrosis?

High-Intensity Exercise Reduces Cardiac Fibrosis and Hypertrophy but Does Not Restore the Nitroso-Redox Imbalance in Diabetic Cardiomyopathy.

Can cardiac fibrosis be reversed?

Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.

How long can you live with fibrosis?

The average life expectancy of patients with pulmonary fibrosis is three to five years after diagnosis. However, early detection of the disease is key to slowing progression, and conditions such as chronic obstructive pulmonary disease (COPD) or pulmonary arterial hypertension (PAH) can impact disease prognosis.

What triggers fibrosis?

Fibrosis is the end result of chronic inflammatory reactions induced by a variety of stimuli including persistent infections, autoimmune reactions, allergic responses, chemical insults, radiation, and tissue injury.

Can cardiac fibrosis be prevented?

The approaches that inhibit myofibroblast formation have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells using biomaterials.

Can you reverse heart wall thickening?

Treatment. There is no treatment which can reverse the changes of the heart muscle. Treatment aims to ease symptoms if they occur and to prevent complications. If you do not have any symptoms or you only have mild symptoms then you may not need any treatment.

What is the pathophysiology of cardiac fibrosis?

Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis.

What is myocardial fibrosis and how serious is it?

Myocardial fibrosis is a significant global health problem associated with nearly all forms of heart disease.

What is the effect of myocardial infarction on cardiac fibroblasts?

Remodeling of cardiac fibroblasts following myocardial infarction results in increased gap junction intercellular communication. Cardiovasc Pathol. 2010;19:e233–240.

How does fibrosis affect the development of ventricular arrhythmias?

The development of fibrosis is known to disrupt the normal arrangement of myocytes and fibroblasts, and as such, has serious implications in the development of ventricular arrhythmias in patients following an acute myocardial injury.