Cardiac Hypertrophy Research Paper

Dilated Cardiomyopathy (DCM) is a type of heart disease in which the chambers of the heart increase in size and the muscle walls thin; the relative thinness of the heart’s walls, compared to the dilated size of the heart, leads to a weakened ability to pump blood to the rest of the body (3). DCM affects one out of 2500 people each year (4) and is one of the leading causes of heart failure in young adults (5). Diagnosis of this disease is difficult because its symptoms are not severe or debilitating, and diagnosis – taking a biopsy of the heart – is often invasive and risky (2); not as many people are being diagnosed with it as the number of those who have it. This limited sample size inhibits the study of

Myocarditis is a very difficult disease to treat and to properly diagnose. The disease is symptomatic in some patients and asymptomatic in others. Myocarditis is one of the proposed mechanisms of sudden athlete death (SAD). Cardiovascular diseases are the number one cause of morbidity and mortality in western societies. Myocarditis is an inflammatory heart disease that may be caused by different pathogens and triggers; it is gaining increasing importance because of its links to sudden death syndrome in young athlete, and to dilated cardiomyopathy (Yilmaz et al., 2012). There are many proposed causes of sudden athlete death; one of the primary causes is hypertrophic cardiomyopathy (HCM). As with any disease we should investigate all factors influencing its pathology including but not limited to: genetic, cultural, and environmental factors. Hypertrophic cardiomyopathy is a heritable disease that is typically passed down as an autosomal dominant trait; only one copy of the dominant allele is required to display the effected phenotype.

The heart is a muscular organ at the epicenter of the human circulatory system. The adult heart pumps five quarts of blood each minute or nearly 2,000 gallons of blood each day (Arkansas Heart Hospital, 2016). Like any part of the body, the heart is susceptible to disease. Cardiomyopathy also known as “disease of the heart muscle” affects 1 in 500 adults and is the leading source of heart failure and the most common reason for needing a heart transplant (Texas Heart Institute, 2016). One of the rarest forms of cardiomyopathy is termed restrictive cardiomyopathy, accounting for less than 5 % of all cardiac disease (TheHeart.org, 2017). By definition, restrictive cardiomyopathy is a disease of the myocardium characterized by restrictive filling

A significant number of patients with hypertrophic cardiomyopathy do not have any symptoms and will have normal life expectancies, though they should be counseled to avoid particularly strenuous activities or competitive athletics. These patients should also be screened for risk factors for sudden cardiac death. In patients with resting or inducible outflow obstructions, situations that will cause dehydration or vasodilation (such as the use

Hypertrophic cardiomyopathy is a genetic disease that causes the heart muscle to become thickened (Maron, 2015). According to the Mayo Clinic (n.d.), hypertrophic cardiomyopathy is a genetic disorder; however, environmental or lifestyle factors may influence how and when the disease appears in individuals.

Despite the absence of a cure or preventative measures for Hypertrophic Cardiomyopathy, there have been notable advances in both diagnostic techniques and successful treatments available.

Congenital heart diseases (CHD) are defects in the heart that are present from birth and affect 8 in every 1,000 newborns each year (National Heart Lung and Blood Institute, 2011). Hypertrophic cardiomyopathy (HCM) is the most common congenital disease of the heart (O’Hanlon and Pennell, 2009) and the most common cause of sudden cardiac death (SCD) among apparently healthy athletes and younger generations (Maron, 1995; Maron and Maron, 2013). HCM is a condition in which there is abnormal thickening of the myocardium in the left ventricle (LV), also know as left ventricular hypertrophy (LVH), where the heart is not dilated and there is no other systemic or cardiac cause (Maron et al 2003; Maron et al 2006). Although many patients are asymptomatic to HCM, some patient’s will present with, or develop progressive exercise intolerance, heart failure symptoms and SCD (Keren et al 2008).

The patient’s chart did not state which type of cardiomyopathy he had a history of, but there are four types of cardiomyopathies. Dilated cardiomyopathy is when both heart ventricles are dilated and the heart’s pumping function is impaired because the ventricular walls stretch out to very thin widths (Dechant, 2016). Hypertrophic cardiomyopathy is where the walls of the ventricles thicken and grow inwards, and could impair the outflow of blood when the heart contracts (Dechant, 2016). Restrictive cardiomyopathy is when the ventricles stiffen in elasticity, restricting the inflow of blood into the ventricles at rest (Dechant, 2016). Finally, arrhythmogenic right ventricular cardiomyopathy could involve either ventricle and is when the myocardial tissue is replaced by fatty tissue, impairing overall ventricular function (Dechant, 2016).

The third defect is Right Ventricular Hypertrophy, which causes a thicker than normal right ventricle. Right ventricular hypertrophy occurs because the heart pumping action becomes harder creating an increase in the hearts work load. Subsequently, this causes a thicker and more muscular heart muscle. This defect causes also causes a reduction in oxygen flowing to the body. The left side of the heart may be underdeveloped from increased work load on the right side of the heart.

Familial Cardiomyopathies (FC) are a collection of cardiac diseases that vary vastly genetically, and pathologically (1, 2). Hypertrophic cardiomyopathy (HCM) is the most common form of FC (2). HCM is diagnosed often with left ventricular hypertrophy without a noticeable increase in external load and smaller ventricular cavity, but with a preserved ejection fraction (3). That is, the percent of blood leaving the left ventricle (5) does not change. Other pathologies include interstitial fibrosis, thickening of the media in intramural arteries, and myocytes disarray greater than 5%; which is a hallmark of HCM (4). HCM shows variability in its penetrance, from a patient with no symptoms, to having sudden cardiac death (SCD)

Enlarged left heart is when high blood pressure forces your heart to work harder than necessary in order to pump blood to the rest of your body. The left ventricle then thickens or stiffens and is called left ventricular hypertrophy. These changes limit the ventricle's ability to pump blood to your body. This condition increases your risk of heart attack, heart failure and sudden cardiac

Hypertrophic cardiomyopathy is characterized by interventricular septal hypertrophy (in absence of other cardiovascular conditions), causing decrease of left ventricle cavity and potentially leading to outflow obstruction. (1) (6) As a consequence of mutations in several genes encoding for thick and thin filaments which build the cardiac muscle, morphological changes occur leading to tangled, thickened myocardial fibers. It is an important cause of morbidity and mortality. Symptomatology varies a lot, from asymptomatic patients to those with severe cardiac function impairment. Some of the most common symptoms of HCM, which are not specific to this disorder may be: shortness of breath at rest or with exertion, fatigue, chest pain, arrhythmias, dizziness, but not only.

In advanced heart failure (HF), increased arterial elastance and arterio-ventricular uncoupling, excessive sympathetic activation, and extensive abnormalities in the β-adrenoceptors (β-ARs) signalling contributeto cardiac remodelling such as desensitization of cardiac β-ARs, and progression of left ventricular dysfunction (Cohn et al., 2000; Floras, 2002; Kubanek et al., 2013).

Hypertrophic cardiomyopathy (HCM) is one of the most common inherited cardiac disease in humans and

The heart is an exceedingly effective pump with four chambers. The two chambers on the right side get oxygen-poor blood from the body and pump this blood to the lungs, where it gets oxygen. The oxygen-rich blood comes back to the left side of the heart, and the two left chambers pump this oxygenated blood to the rest of the body. The lower (major) pumping chambers, called the ventricles, get blood from the top chambers, the atria, and do the diligent work of pumping the blood to the other parts of the body [1].