What is myocardial interstitial fibrosis?
Myocardial interstitial fibrosis (MIF) is a histological hallmark of several cardiac diseases that alter myocardial architecture and function and are associated with progression to heart failure.
What causes interstitial fibrosis of the heart?
Coronary heart disease, aortic stenosis and hypertension are the most frequent causes of myocardial fibrosis (13). Aortic stenosis and hypertension result in pressure overload of the left ventricle where the increased wall stress induces hypertrophy and interstitial fibrosis (2–4).
Is fibrosis of the heart 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.
What happens myocardial fibrosis?
Myocardial fibrosis is an important part of cardiac remodeling that leads to heart failure and death. Myocardial fibrosis results from increased myofibroblast activity and excessive extracellular matrix deposition. Various cells and molecules are involved in this process, providing targets for potential drug therapies.
Can myocardial fibrosis be reversed?
To reverse replacement fibrosis, resorption of fibrous tissue needs to be coupled with robust myocardial regeneration. The latter is currently not feasible in adult human hearts. Reversal of interstitial fibrosis poses several challenges (see text) and may require co-operation of several different cell types (A).
How long can you live with cardiac fibrosis?
Myocardial Fibrosis Predicts 10-Year Survival in Patients Undergoing Aortic Valve Replacement | Circulation: Cardiovascular Imaging.
How is myocardial fibrosis treated?
A new trial suggests that pirfenidone, an approved treatment for idiopathic pulmonary fibrosis, may also reduce myocardial fibrosis in patients with heart failure who have a preserved left ventricular ejection fraction.
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.