Cardiac Hypertrophy / Athlete 's Heart

Approximately, 1 of every 500 people is affected with hypertrophic cardiomyopathy, it is important for patients to understand the dynamics of the disease as it could potentially be life threatening. In most cases, the patients quality of life is not affected, but a few will experience symptoms that cause significant discomfort or undetected complications that could lead to sudden cardiac death. With that in mind, it would be beneficial to recognize what it is, specific causes, the steps of diagnoses, and the options for treatment.

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).

Cardiac output adapts throughout a training program. The "American Council on Exercise's Personal Trainer Manual" lists exercise adaptations as increased ventricle size, decreased exercise heart rate and increased stroke volume. Therefore, your heart can maintain a high cardiac output with less effort. Most improvement to cardiac output is contributed to increased stroke volume. Positive adaptations occur in as little as three months of aerobic training.

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).

Cardiac hypertrophy is the enlargement, or thickening, of the heart muscle. After lots of strenuous exercise the heart muscle will increase. If a person does exercise, a thirty minute jog every day, for six months there will be an obvious increase in many other factors but the heart muscles will have grown in size. These changes are reversible when you discontinue aerobic training.

Right ventricular hypertrophy is where the muscle of the right ventricle is thicker than usual and causes the heart to work harder than normal to move blood through the narrowed pulmonary valve.

Long-term hypertension can result in a variety of consequences. These consequences are the result of the heart having to adapt and work harder, i.e. against an increased afterload due to the increased systolic pressure. The heart adapts via hypertrophy of the smooth muscle. Chronic hypertension can also lead to a disruption of the endothelium, thus increasing the

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

Hemodynamic Changes: Contractility is influential in cardiac output and can be compromised due to myocardial infarction, ischemia, cardiomyopathy, and increased cardiac workload, to name a few. Inflammatory, immune, and neurohumoral changes can mediate ventricular remodeling, which will alter myocardial cellular structure resulting in myocardial dilation and further dysfunction of myocyte contractility over time. The decreased contractility will result decreased stroke volume and increased left ventricular end-diastolic volume, which results in dilation of the heart and increased preload. Increased afterload can be caused by increased pulmonary vascular resistance (PVR). This can result from hypertension or aortic valvular disease. The PVR results in resistance to ventricular emptying, increasing the work load of the LV, thus causing hypertrophy of the myocardium. Sustained elevated afterload results in pathologic hypertrophy, caused by angiotensin II and catecholamines. The increase in cardiac muscle mass causes an increase in the heart’s oxygen and energy demands. Thus, more energy from ATP is needed and when demand is greater than supply, cardiac contractility suffers. Ventricular remodeling continues, further

Hypertrophic cardiomyopathy (HCM) is a primary disease of the myocardium (the muscle of the heart) in which a portion of the myocardium ishypertrophied (thickened) without any obvious cause. It is perhaps best known as a leading cause of sudden cardiac death in young athletes.[7] The occurrence of hypertrophic cardiomyopathy is a significant cause of sudden unexpected cardiac death in any age group and as a cause of disabling cardiac symptoms. Younger people are likely to have a more severe form of hypertrophic cardiomyopathy.

Ryan Gillyard is a fifteen-year-old athlete boy who was passionate to play Division I college football. He was a “linebacker” and “running back” in football. He lived in Upper Darby and passed away on April 18, 2015.

While hypertrophic cardiomyopathy often goes undiagnosed, more severe cases will show symptoms. Most cases are not diagnosed because there are no symptoms or because the patient can continue going about life without any significant struggles. It is usually hard to tell if someone has hypertrophic cardiomyopathy just by looking at them. When symptoms do occur, they include the following: shortness of breath and chest pain (especially during exercise), fainting, abnormal heart rhythms (arrythmias), or a heart murmur, which a doctor is able to detect by listening to the heart. It is important for someone with hypertrophic cardiomyopathy to visit a doctor if any of the above symptoms occur frequently, interrupting normal daily routines.

I chose to summarize this review article to understand the reasons behind exercising a patient with hypertrophic cardiomyopathy (HCM). Prior to the reading, my knowledge of stress echos only covered the bases of diagnosing coronary artery disease. This review focuses on the patients subjective complaints and its correlation with sudden death from HCM.

6. Automaticity – ability of heart to beat spontaneously and repetitively without external neurohormonal control. The heart is capable of beating outside the body, given proper laboratory conditions. Automaticity is evidently linked to fluid and electrolyte balance rather than to nervous system control.

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.