Myocardiocyte The cardiac myocyte is the major cell involved in<unk> . Fibroblasts, collagen, the interstitium, and the coronary vessels to a lesser extent, also play a role. A common scenario for<unk>  is after myocardial infarction. There is myocardial necrosis (cell death) and disproportionate thinning of the heart. This thin, weakened area is unable to withstand the pressure and volume load on the heart in the same manner as the other healthy tissue. As a result, there is dilatation of the chamber arising from the infarct region. The initial<unk>  phase after a myocardial infarction results in repair of the necrotic area and myocardial scarring that may, to some extent, be considered beneficial since there is an improvement in or maintenance of LV function and cardiac output. Over time, however, as the heart undergoes ongoing<unk> , it becomes less elliptical and more spherical.<unk>  mass and volume increase, which together adversely affect cardiac function. Eventually, diastolic function, or the heart's ability to relax between contractions may become impaired, further causing decline. After a myocardial infarction (MI), cardiac myocyte death can be triggered by necrosis, apoptosis, or autophagy, leading to thinning of the cardiac wall. The surviving cardiac myocytes either arrange in parallel or in series to each other, contributing to<unk>  dilatation or<unk>  hypertrophy, depending on the loading stress on the<unk>  wall. Besides, reduced expression of V1 myosin and L-type calcium channels on cardiac myocytes are also thought to cause cardiac<unk> . Under normal body conditions, fatty acid accounts for 60 to 90% of the energy supply of the heart. Post MI, as fatty acid oxidation decreases, it leads to reduced energy supply for the cardiac myocytes, accumulation of fatty acids to toxic levels, and dysfunction of mitochondria. These consequences also led to the increase in oxidative stress on the heart, causing the proliferation of fibroblasts, activation of metalloproteinases, and induction of apoptosis, which would be explained below. Besides, inflammatory immune response after MI also contributes to the above changes. Besides, the cardiac interstitium which consisted of largely Type I and Type III collagen fibres are also involved in cardiac<unk> . Cardiac collagen is synthesized by fibroblasts and degraded by metalloproteinases. Fibroblasts are activated post MI, leading to increased collagen synthesis and fibrosis of the heart. Increase expression of MMP1 and MMP9 led to degradation of collagen fibres, and subsequently dilatation of the heart. Several signal pathways such as Angiotensin II, Transforming growth factor beta (TGF-beta), and Endothelin 1 are known to trigger synthesis and degradation of collagen fibres in the heart. Other factors such as high blood pressure, activation of sympathetic system which releases norepinephrine, activation of renin–angiotensin system which releases renin and anti-diuretic hormones are important contributors of cardiac<unk> . However, atrial natriuretic peptide is thought to be cardio-protective.
Ventricular remodeling
Myocardial scarring
Cardiac fibrosis
Pacemaker crosstalk
Myocardial stunning
Cardiomyocyte proliferation
Coronary vasospasm
Ventricular hypertrophy