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Changes in Cardiac Geometry Due to Hypertrophy

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Changes in Cardiac Geometry Due to Hypertrophy Changes in Cardiac Geometry Due to Hypertrophy By Marta Ellen Pedersen A Master’s Paper Submitted in Partial Fulfillment of The Requirements for the Degree of Master of Science in Clinical Exercise Physiology Dr. Joseph O’ Kroy Date University of Wisconsin-River Falls 2014 Introduction For any given body size, men have larger hearts than women, athletes have larger hearts than nonathletes, and often times, an enlarged heart is a symptom of an underlying disorder that is causing the heart to work harder than normal. This review will emphasize the differences between a pathologically enlarged heart and an athletically enlarged heart. Pathologically induced hypertrophy (myopathy) When heart cells get bigger, (often is the case when heart disease is present) the total heart works less efficiently. Some people suffer from conditions like hypertrophic cardiomyopathy, which includes significant heart muscle enlargement, and can be genetic or caused by high blood pressure. Cardiomyopathy decreases the size of the heart's chambers, reducing blood flow. Hypertrophy, or thickening, of the heart muscle can occur in response to increased stress on the heart. The most common causes of Cardiomyopathy are related to increased blood pressure. The extra work of pumping blood against the increased pressure causes the ventricle to thicken over time, the same way a body muscle increases in mass in response to weightlifting. Cardiomyopathy can occur in both the right and left atrium and the right and left ventricles. Blood travels through the right ventricle to the lungs. If conditions occur that decrease pulmonary circulation, extra stress can be placed on the right ventricle, and can lead to right ventricular myopathy. The most common causes of right ventricular myopathy are diseases that damage the lungs like emphysema and cystic fibrosis. These diseases destroy blood vessels in the lungs, causing increased pressure in the remaining vessels. Conditions that decrease oxygen levels, such as chronic bronchitis and sleep apnea, also lead to right 2 ventricular myopathy. Mild forms of right ventricular myopathy may not show any symptoms at all and in the severe form, patients will experience shortness of breath along with chest pains and pressures. Additionally, the sensation that the heart is beating rapidly and forcefully is also felt. Left ventricular myopathy When the heart has trouble pumping blood, it might start beating more rapidly or at irregular intervals. Drugs like beta-blockers, ACE inhibitors, angiotensin receptor blockers, diuretics, and digoxin may be prescribed. If drugs can not treat the cause, there may be a need to implant a defibrillator or a pacemaker in the patient. The way that the heart pumps blood depends on its shape and contractility. If these changes are due to cardiomyopathy and the thickening of the heart walls, then the heart's left ventricle (LV) will not pump blood as efficiently. This can lead to a reduced ejection fraction which does not allow enough blood to be pumped throughout the body. As the ventricle becomes thicker, it starts to lose its elasticity. Thus, filling during diastole becomes more difficult and depends on atrial systole (26). As a consequence, LV end-diastolic pressure and left atrial pressure increases, resulting in enlargement of the left atrium. Oxygen demand and basal coronary blood flow increases as myocardial myopathy increases. Only with exercise or severe left ventricular hypertrophy (LVH) will subendocardial blood flow be jeopardized, potentially causing myocardial infarction (MI) and fibrosis. Left ventricular hypertrophy is the most common type of hypertrophy seen in both pathologically and athletically enlarged hearts. Pathological left ventricular hypertrophy develops in response to some factors, such as high blood pressure and obesity, which requires the left ventricle to work harder. Left ventricular myopathy usually develops gradually and as the workload increases, the walls of the chamber grow thicker, lose elasticity and 3 eventually may fail to pump with as much force as that of a healthy heart. A person may experience no signs or symptoms, especially during the early stages of the condition. As left ventricular myopathy progresses and complications develop, symptoms such as shortness of breath, chest pain, rapid, fluttering or pounding heartbeats may occur. Left ventricular myopathy changes both the structure and function of the chamber: The enlarged muscle loses elasticity and stiffens, preventing the chamber from filling properly and leading to increased pressure in the heart (29). There are many complications that can occur in those with left ventricular myopathy. These may include an increased inability of the heart to pump enough blood through the body, which is considered heart failure. Left ventricular diastolic function has been studied by use of mechanocardiography, radionuclide techniques, imaging echocardiography, and Doppler velocimetry. Mechanography is the indirect recording of the pulsatile movements of arteries, veins, cardiac apex and pericardium. The changes in contour of these pulsations as well as the measurement of the duration of the various phases during the cardiac cycle can provide information about cardiovascular dynamics and myocardial performance (28). Radionuclide ventriculography provides quantitative measures of biventricular function and regional wall motion. Radionuclide imaging is used for analyzing diastolic function, parametric imaging and uses methods for calculating absolute ventricular volumes. Radionuclide imaging uses a gamma camera to create an image following injection of radioactive material. This test is done to evaluate coronary artery disease (CAD), valvular or congenital cardiac disorders, cardiomyopathy, and other cardiac disorders (24). Echocardiography is the principal method used to diagnose LVH (33). Echocardiography is a complex, noninvasive imaging technique that creates ultrasound images of heart structures and produces accurate assessment of the blood flowing through the heart, using pulsed or continuous wave doppler ultrasound. This allows assessment of both 4 normal and abnormal blood flow through the heart. Color Doppler as well as spectral Doppler is used to visualize any abnormal communications between the left and right side of the heart, any leaking of blood through the valves, and can estimate ejection fraction and how well the valves open and close (3, 34). The use of Stress Echocardiography may also help determine whether any chest pain or associated symptoms are related to heart disease. The electrocardiogram (ECG) can show signs of increased voltage from the heart in individuals with LVH, so this type of test is often used as a screening test to determine if the patient should undergo further testing (30). A 12 lead electrocardiogram showing hypertrophy of the ventricles, will produces QRS complexes that have exaggerated amplitude. With left ventricular hypertrophy, there is a very tall R wave in lead V5, which is the lead over the left ventricle. The second type of test used in determination of ventricular hypertrophy is if the V1 electrode produces a deep S wave. The formula for checking for ventricular hypertrophy is simply to add the depth of the S wave in V1and V2 to the height of the R wave in V5 and 6. If the sum of the two numbers is greater than 35, LVH is present. The determination of the heart’s electrical axis is an important part of the electrocardiogram diagnosis. The direction of the depolarization waves depends on the orientation of the heart during the particular instant of the cardiac cycle being considered. This can be done by observing the voltages of the QRS complex from two different perspectives using two different leads. Lead I provides a horizontal axis (from left arm to right arm). Lead III has an axis of about 120 degrees (from left arm to left leg). Using the recordings from leads I and III, the normal mean electrical axis of the ventricles is about 59 degrees. The axis of the heart shifts toward the hypertrophied ventricle for two reasons: 1. More muscles exist on the hypertrophied side, which allows excess generation of electrical potentials on this side. 2. More time is required for the depolarization to travel to the hypertrophied ventricle. 5 Normal electrical axis is classified as -30 degrees to 90 degrees. Right ventricular hypertrophy is associated with right axis deviation, which is 90 degrees to 180 degrees (19). Right axis deviation may be normal in the young and thin individuals. Right axis deviation is common in taller individuals, because the apex of the heart generally moves lower into the thorax. Other causes of right axis deviation include chronic obstructive pulmonary disease, pulmonary embolism, and Wolf- Parkinson- White syndrome. Left ventricular hypertrophy is associated with left axis deviation, which is classified as 30 degrees to -90 degrees (19). Left ventricular hypertrophy, where the left ventricle is enlarged, generates more electrical activity, so the heart axis is pulled to the left. Left axis deviation is usually not problematic unless there are other diseases present, like a left anterior block. Left axis deviation can be seen in older individuals and those with obesity. In obese people, the diaphragm is often positioned high, pushing the heart upwards and rotating its electrical axis to the left. A study conducted by Peter M. Okin et al. (20) examined gender differences, electrocardiographic voltages, and QRS duration to differences in cardiac dimensions and body size between men and women and gender differences in test performance of ECG criteria for the detection of echocardiographic left ventricular hypertrophy. 389 subjects (112 women and 277 men) were chosen to take part in the study. ECG voltage-duration was calculated as the product of QRS duration and voltages. Some subjects had normal left ventricular mass and some with left ventricular hypertrophy. While men had longer QRS duration, higher Cornell voltage (a calculation method for LVH using an ECG test (RaVL + S-wave amplitude in V(3) [SV(3)]), higher 12-lead sum of QRS voltage, and higher Cornell and 12-lead voltage-duration products than did women (27).
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