Symptoms And Treatment Of Hypertrophic Cardiomyopathy Essay

Hypertrophic cardiomyopathy is an inherited autosomal-dominant pattern affecting nearly 1 in 500 people, affecting both men and women equally. Which makes it the most “common genetic heart disease in the United States” [5] Many studies have been done on the causes of this disease. Research has shown the mutations of between 10 to 13 sarcomeric proteins are associated with HCM. Each mutated gene has a different pathological characteristic.

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

As this disease progresses and the workload of the heart is consistently increased, ventricular hypertrophy occurs. At first, the hypertrophied heart muscles will increase contractility, thus increasing cardiac output; however, as hypertrophy of the ventricular myocardial cells continues, it begins to have poor contractility, requires more oxygen to perform, and has poor circulation from the coronary arteries. This can result in heart tissue ischemia and lead into cardiac dysrhythmias (Lewis et al. 2014, 768).

Young children who have hypertrophic cardiomyopathy tend to have no symptoms of their condition until

Systolic heart failure results from the inability of the cardiac muscle to contract effectively from inadequate cardiac output. As the cardiac output drops, compensatory mechanisms to try to restore its function through takes place by ventricular remodeling. During this remodeling phase, the heart begins to develop changes in its size and becomes hypertrophic that results in a decreased ability of the heart to contract, decreased available oxygen, and available ATP. Secondly, this hypertrophic states increases preload that results

HCM happens when the heart muscle enlarges and thickens without an obvious cause. Usually the ventricles, the lower chambers of the heart, and septum thicken. The thickened areas create narrowing or blockages in the ventricles, making it harder for the heart to pump blood; however, in very few instances the heart actually contracts with much greater force causing an obstruction to the blood flow (CMUK, 2015). HCM also can cause stiffness of the ventricles, changes in the mitral valve, and cellular changes in the heart tissue.

Congestive heart failure (CHF) is a condition where the heart is unable to efficiently pump blood to supply the body with adequate blood flow and it can cause fluid to build up in the lungs. There are several disease processes and risk factors that predispose an individual to this condition. CHF can be chronic or acute and life threatening, and most of these patients are in the older adult population. Some symptoms of CHF include fatigue, shortness of breath, edema, and diminished exercise capacity. There are several medical management techniques for this condition including lifestyle modifications, medications and surgical intervention. Below, I will summarize two articles on two different medical treatments for CHF.

As cardiomyopathy progresses, the heart becomes weaker and is less able to pump blood normally. This results in heart failure. There are different types of cardiomyopathy- hypertrophic, dilated, and restrictive. Hypertrophic cardiomyopathy occurs when the heart muscle cells enlarge which causes the thickening of the left ventricular wall. Although the ventricle size stays normal, the thickening makes it harder for the heart to pump blood. In some cases, the septum also thickens and expands to the left ventricle which causes a blockage of blood flow out of the left ventricle. The cause of the disease is unknown but hypertrophic cardiomyopathy is usually caused by changes in the genes in heart muscle proteins. It can also develop due to

Risk for having CAD or established CAD, previous MI or heart failure with decreased ejection fraction and ventricular arrhythmias are the known risk factors for SCD[17, 136]. The estimated incidence rate of SCD in infants, children, adolescents, and young adults is about 1.3 to 8.5 per 100,000 patient/years [137] but it still costs to thousands life per year. Sudden infant death syndrome accounting for approximately 10% of the crib death is believed to be due to cardiac arrhythmia or long QT syndrome [138]. A study suggest that out of 158 deaths of American athletes, 30% were due to hypertrophic cardiomyopathy and 13% due to abnormal blood circulation, 10% due to increased cardiac mass due to cardiomyopathy [139]. Another study suggest 20% death due to CAD and 10% deaths due to right ventricular cardiomyopathy/ dysplasia in young population [140]. Patients suffering from SCD with normal heart or without any cardiac disease history, on autopsy show structural abnormalities. Sudden unexplained deaths are also a major concern in epidemiology of SCD and careful post-mortem and histological examination can play a vital role [17]. In a study with 270 autopsies 55 were found to have structural heart disease and a specific cause for death were found in 180 cases with 65% having CAD, 14% with congenital anomalies and 11% with myocarditis. Left

Heart failure due to a defect in expulsion of blood caused by an abnormality in systolic function, or ventricular contractile dysfunction. (Hart, RHIA, CCS, CCS-P, Stegman, MBA, CCS, and Ford, RHIT, CCS)

Some people die right on the spot from HCM and there were no signs to show of it beforehand. For example, Gerald Grain was an average high school student in Chicago. He died after a routine long-distance run in gym class in September of 1997. He had no previous diagnostics of any heart disease and lived a normal life…until it ended. Robert Seigal, in ‘Sudden Death of Young Athletes”, writes about many more instances when high school athletes die due to normal physical exertion. Instances like that are reasons why heart doctors and general practitioners try to spread the awareness of “low-lying” conditions like HCM. All people should always educate themselves about their own

defects correlating with areas of noncompacted myocardium. Post-mortemfollowup and 90% develop LV dysfunction within a period of 10 years of

Cardiac hypertrophy is the enlargement of the lower, ventricular walls of the heart. Most commonly occurring in the left ventricular side, cardiac hypertrophy can occur on one side or both. Characterized by abnormal heart muscle growth it can be a healthy response to pregnancy or exercise. However, an increase in heart size could also be a sign of hypertension, diabetes, muscular dystrophy, obesity, or cardiomyopathy. Hypertrophy of the heart can be adaptive or maladaptive, therefore the growth may not lead to an increase in cardiac output.

In fact, TTC is not even in the top three most common types of cardiomyopathy. The most common type is hypertrophic cardiomyopathy (or HCM). People with HCM have a heart muscle that is excessively thick and prone to scarring. This process makes the muscle stiff, which causes blood-pumping difficulties. The second most common subgroup is dilated cardiomyopathy (DCM). This occurs when the pumping chambers of the heart enlarge, which makes the muscle thin and weak. Many people with DCM have breathing problems due to the fluid build-up in their lungs. The third most common type of cardiomyopathy is arrhythmogenic right ventricular cardiomyopathy (ARVC), where heart muscle cells are replaced by scar tissue and fat cells. All three of these instances are

This condition can masquerade as an acute myocardial infarction clinically, biochemically, and electrocardiographically; however, its underlying pathophysiology is quite different. A significant portion of these patients have serious complications including cardiogenic shock, heart failure, arrhythmias, cardiogenic shock, and death. The major distinguishing feature that differentiates this syndrome from ischemic cardiomyopathy is the lack of obstructive coronary disease and presence of regional wall motion abnormalities typically extending beyond a single epicardial coronary distribution, making TC a diagnosis of exclusion, after coronary anatomy has been delineated [1].