Cardiomyopathy In Sports

I observed Dr. André La Gerche, a well-respected sports cardiologist, speak on April 12th for the Mortiz Speaker Series. The series is coordinated by the Nursing College at UTA in order to promote and inform the community on health and wellness. I chose the presentation as it suited my schedule and I’m generally interested in research techniques. Dr. La Gerche described his research on the possible negative health effects for dedicated athletes on their hearts, incorporating an innovative MRI scan while exercise takes place.

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

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).

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The rapid degeneration of myocardial fibers and diffuse inflammation lead to ventricular dilation and hypertrophy which cause atrial enlargement and stasis of blood in the left ventricle (Park, 2008). The enlargement of the remaining heart chambers is mainly due to left ventricular failure, but it may also be secondary to the primary cardiomyopathic process. Dilated cardiomyopathy is associated with both systolic and diastolic dysfunctions, with decreased systolic function being the predominant abnormality (Parker, 2008). This dysfunction leads to decreased contractility and general contractile dysfunction (Parker, 2008). Progressive dilation can lead to significant mitral and tricuspid regurgitation, which may further decrease the cardiac output and increase end-systolic volumes and ventricular wall stress. In turn, this leads to further dilation and myocardial dysfunction (Friedberg, 2008). Dilated cardiomyopathy is the most common type of heart muscle disease in pediatrics (Chow, Ateah, Scott, Ricci, & Kyle, 2013). Dilated cardiomyopathy can be a life threatening condition and can decrease life expectancy if severe damage occurs. Currently, the five-year survival rate for children diagnosed with dilated cardiomyopathy is between forty and eighty percent. The survival rate decreases if they child is diagnosed at five years or older (Friedberg, 2008).

Electrocardiographic changes can include left ventricular hypertrophy with repolarisation changes with T wave inversion and deep Q waves. In family members carrying HCM gene mutations, the electrocardiogram may demonstrate only minor abnormalities. The presence of non-sustained ventricular tachycardia, a risk factor for sudden death, should be tested for by means of Holter monitoring (Maron et al., 2003). At present, the diagnosis of HCM relies on echocardiography revealing symmetric or asymmetric hypertrophy. Secondary causes of hypertrophy, including valvular disease or systemic hypertension, should be excluded. 2D imaging of the left ventricle by echocardiography can confirm the diagnosis in affected patients. The ejection fraction, a measure of left ventricular systolic function, is typically preserved but there is usually evidence of diastolic dysfunction. These can be measured by tissue Doppler ultrasonography, which can show diastolic dysfunction before the development of hypertrophy (Maron, 2002). Histologically, HCM is characterized by cardiac myocyte disarray and fibrosis. Myocyte death and myocardial scarring may be present and coronary arteries may have thickened walls. This pathology can promote ventricular tachycardia and ventricular fibrillation (Maron, 2002).

Should student get screen for heart disease before athletics? Sadly In today’s society, student athletes are dying of heart attacks, at an early age. Which is why student athletes should be required to get screened for heart disease. When the individual gets a screening, they should take both popular diagnostic tests, such as the electrogram (EKG) and the echocardiography (ECHOS). Sudden cardiac arrest (SCA) is the leading cause of death in young athletes (Drezner at al., 2007). SCA in young athletes is not only a concern for the medical community, but also for the community’s at large. SCA occurs when electrical impulses in the heart become rapid or chaotic, which causes the heart to stop beating. Approximately 1 in 220,000 youthful student competitors experience sudden cardiac death (SCD) every year (baggish et al., 2010). Athletes are known to be some of the healthiest people in society, however SCD while being active in sports is odd, its manifestation is universally recorded in the media, caused by the age and health conditions of the athlete. The latest events in many parts of the world show that congestive heart failure of student athletes is still a reality and it keeps challenging experts in cardiology that take care of student athletes (Ferreira et al., 2010). It has come to mind that some easy pre-participation screening, adding a physical, electrocardiograms (ECG/EKG) additionally gathering

Apical hypertrophic cardiomyopathy is a disease that mainly affects the apex of the heart and does not cause any obstruction. [1] These abnormalities in the heart muscle can cause a wide variety of symptoms. As the heart becomes stiff it increases the pressure in the left ventricle which can push blood back into the lungs, causing shortness of breath in exercise. Chest pain can occur as there is not enough oxygen available to the cardiac muscle due to insufficient blood supply. Palpitations and lightheadedness, along with other conditions can occur as a result of HCM. In addition to these discomforting symptoms, the patient may develop an arrhythmias that often goes unnoticed. An arrhythmia takes place as the electrical conduction of the heart is disturbed by the abnormal scattering of myocytes. The two most common arrhythmias are atrial fibrillation causing palpitations, and ventricular tachycardia that can be life threatening causing sudden death. Both conditions can be controlled with medication. [4]

The results demonstrated that the extent of LGE was associated with an increased risk of sudden cardiac death events. The estimated risk of SCD events at 5 years increased incrementally with respect to %LGE, ranging from 4.9% in patients with 10% LGE to 6.9% in patients with 20% LGE. It concluded that extensive LGE measured by contrast-enhanced cardiovascular magnetic resonance (CMR) provided additional information for assessing SCD event risk among HCM patients.

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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.

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.

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

Akashi, K. Nakazawa, M. Sakakibara, F. Miyake, H. Koike, K. Sasaka 2003). Echocardiography with left ventricle pathognomonic wall motion abnormalities such as the base contracting normally but the remaining walls being severely hypokinetic is a key diagnostic feature in takotsubo cardiomyopathy. ECG findings are often confused with those found during an acute anterior wall myocardial infarction because they mimic classic ST-segment elevation, T-wave inversion or QT-interval prolongation (Azzarelli S, Galassi AR, Amico F, Giacoppo M, Argentino V, Tomasello SD, Tamburino C, Fiscella A., 2006), making it difficult to diagnose upon presentation. A coronary angiogram, typically used to evaluate individuals with left ventricular dysfunction, will not reveal any significant blockages. Myocardial enzymes rise only moderately at worst, which may be easily overlooked during diagnosis. Blood tests will show increased white blood cell count, to believe bacterial infections are present although the results will usually be negative.

The literature on the effects of exercise of cardiac output maintains the idea that exercise should affect cardiac output- pulse rate, systolic blood pressure, diastolic blood pressure, QRS-pulse lag, P-T and T-P intervals, because of increased heart rate. For our experiment, we tested this theory by measuring our cardiac output before and after some rigorous exercise. We measured the individual cardiac output and then combined the data to compose a class-wide data average. We compared the results of the experiment to what we expected, which was that exercise does affect our heart. Our data from this experiment supported the notion that exercise does, in fact, change cardiac output.