<unk>  can be both a physiological and pathophysiological process. It becomes pathophysiological (damaging) when there is excessive<unk> . The pathophysiological process mainly occurs through aberrant signalling of the neuroendocrine hormones; angiotensin II, endothelin-1 and the catecholamines (e.g. noradrenaline). Angiotensin-II and endothelin-1 Angiotensin-II and endothelin-1 are hormones that bind to the angiotensin (AT) and endothelin (ET) receptors. These are G-protein coupled receptors that act via internal signalling pathways. Through several intermediates, these pathways directly or indirectly increase reactive oxygen species (ROS) production causing accumulation in myocardial cells. This can subsequently induce necrotic cell death, fibrosis, and mitochondrial dysfunction. This has been demonstrated in animal studies. Protein Kinase C (PKC) is an intermediate molecule in the signalling pathway and mice lacking PKC shown resistance to heart failure compared to mice overexpressing PKC which shown heart dysfunction. Targeting the renin–angiotensin (RAAS) system (using angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers) are a well-recognized clinical approach for reversing maladaptive cardiac<unk>  independently of blood pressure. Catecholamines Catecholamines levels increase due to increased sympathetic nervous system activity. Catecholamines can act on the alpha-adrenergic receptors and beta-adrenergic receptors which are G-protein coupled receptors. This binding initiates the same intracellular signalling pathways as angiotensin and endothelin. There is also activation of cAMP and an increase in intracellular Ca2+ which leads to contractile dysfunction and fibrosis. Others Hormones are not the only cause of<unk> .<unk>  can also be caused by mechanical forces, mTOR pathways, nitric oxide and immune cells. Immune cells can cause<unk>  by inducing inflammation.
Right ventricular hypertrophy
Left ventricular hypertrophy
Right atrial enlargement
Aortic unfolding
types of Cardiomegaly
Ventricular hypertrophy
Atrial enlargement
Left atrial enlargement