This is sometimes called ‘concentric’ hypertrophy.  The symptoms of HCM include shortness of breath due to stiffening and decreased blood filling of the ventricles, exertional chest pain (sometimes known as angina) due to reduced blood flow to the coronary arteries, uncomfortable awareness of the heart beat (palpitations), as well as disruption of the electrical system running through the abnormal heart muscle, lightheadedness, weakness, fainting and sudden cardiac death. Cardiomyopathy UK is registered in England and Wales as a charity, no 1164263.  It is often due to mutations in certain genes involved with making heart muscle proteins. Dr Maite Tome talks about exercise in hypertrophic cardiomyopathy (HCM), Assessing risk in hypertrophic cardiomyopathy by Dr Constantinos O'Mahony, Cardiomyopathy UK Apical hypertrophic cardiomyopathy (ApHCM) is a variant of HCM that is characteristic of focal thickening of the LV apical myocardium only, showing a spade-shaped shadow on LV ventriculogram.1 ApHCM is known to show a favourable prognosis among morphologically classified types of HCM, with …  The first modern description of the disease was by Donald Teare in 1958. , For children with HCM, treatment strategies aim to reduce disease symptoms and lower the risk of sudden death. Thrombolytic agents (e.g., tissue plasminogen activator) have been used with some success to break down an existing aortic thromboembolism, but their cost is high and outcome appears to be no better than giving a cat time (48–72 hours) to break down its own clot. Cardiac magnetic resonance imaging (CMR), considered the gold standard for determining the physical properties of the left ventricular wall, can serve as an alternative screening tool when an echocardiogram provides inconclusive results. An insertion/deletion polymorphism in the gene encoding for angiotensin converting enzyme (ACE) alters the clinical phenotype of the disease. Medications may include the use of beta blockers or disopyramide. Treatment aims to control symptoms and reducecomplications. Familial hypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. In HCM the muscular walls of the heart’s ventricles (lower pumping chambers) become thickened. This means that blood leaks back into the atrium (called mitral regurgitation) which can cause a murmur (sound that can be heard through a stethoscope). It fails to acknowledge the age at which relatives suffered sudden cardiac death, as well as the frequency of the cardiac events. , Shortness of breath is largely due to increased stiffness of the left ventricle (LV), which impairs filling of the ventricles, but also leads to elevated pressure in the left ventricle and left atrium, causing back pressure and interstitial congestion in the lungs. Symptoms are not closely related to the presence or severity of an outflow tract gradient. The following are examples of what might help. Calcium channel blockers – these reduce the force at which the heart contracts and reduce left. For people whose symptoms are not relieved by the above treatments, disopyramide can be considered for further symptom relief. Cardiomyopathy often goes undiagnosed,5 so the numbers can vary.  This results in the heart being less able to pump blood effectively and also may cause electrical conduction problems. Beta blockers are considered first-line agents, as they can slow down the heart rate and decrease the likelihood of ectopic beats.  However, transplantation must occur before the onset of symptoms such as pulmonary vessel hypertension, kidney malfunction, and thromboembolism in order for it to be successful. Symmetrical hypertrophy – the thickening affects the whole of the left ventricle, reducing its volume. The objective of this work was to investigate the effect of hypertrophic cardiomyopathy-linked A8V and E134D mutations in cardiac troponin C (cTnC) on the response of reconstituted thin filaments to calcium upon phosphorylation of cardiac troponin I (cTnI) by protein kinase A. It may block or reduce the blood flow from the left ventricle to the aorta. The cardiac myosin binding protein C mutation identified in Maine Coon cats has not been found in any other breed of cat with HCM, but more recently another myosin binding protein C mutation has been identified in Ragdoll cats with HCM.  For this reason, euthanasia is often a valid consideration. Often, only one part of the heart is thicker than the other parts.  For example, the identification of segmental lateral ventricular hypertrophy cannot be accomplished with echocardiography alone. Some people have minor or even no symptoms.