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 RVH. Hypertrophy can also be caused by mechanical forces, mTOR pathways, nitric oxide and immune cells. Immune cells can cause hypertrophy by inducing inflammation. Diagnosis
The two main diagnostic tests used to confirm right ventricular hypertrophy are electrocardiography and echocardiography. Electrocardiography
The use of electrocardiogram (ECG) to measure cardiac chamber hypertrophy is well established but since the left ventricular activity is dominant on the ECG a large degree of RVH is often required for any detectable changes. Nonetheless, the ECG is used to assist with the diagnosis of RVH. A post mortem study on 51 adult male patients concluded that anatomical RVH may be diagnosed using one or more of the following ECG criteria:
Right axis deviation of more than (or equal to) 110° (see hexaxial reference figure)
R-wave dominant over S-wave in V1 or V2
S-wave dominant over R-wave in V6However, the American Heart Association recommended the use of additional diagnostic tests to diagnose RVH because no single criteria or set of criteria were considered sufficiently reliable. Echocardiography
Echocardiography can be used to directly visualise right ventricular wall thickness. The preferred technique is the trans-oesophageal approach giving a view of 4 chambers.
Surgery is also a treatment option. In epilepsy surgery (focal resection or hemispherectomy) the part of the brain which creates the abnormal electrical current through the brain must be resected, but the surgery is very complicated and needs to be performed by expert surgeons in epilepsy reference centers. None of these treatments, with the exception of some metabolic disorders with specific treatments available, have shown any efficacy at avoid long-term consequences of the disease. Prognosis
The prognosis is usually poor. Mortality rate is high during early infancy and almost half of the children die by 2 years of age. In the patient with severe phenotype, even when optimal treatment is initiated promptly, the prognosis remains poor. Most of the survivors suffer from psychomotor impairment and develop electroclinical features of other epilepsy syndromes (i.e Lennox- Gastaut syndrome). In patients with reduced phenotype, if there is early treatment initiated the better developmental outcome can be observed. Epidemiology
The prevalence estimates among EME are of <1 / 1 000 000. References


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