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Common Abnormalities of the Heart

by admin — last modified 2011-11-02 09:30

Abnormal Murmurs

Aortic Stenosis

This is stenosis or narrowing of the aortic valve and is detected on exam with a systolic murmur heard in the aortic area. This condition in young people is usually congenital, specially with bicuspid aortic valves and is usually detected during childhood. It can sometimes be caused by rheumatic fever, which is uncommon in the US. It limits the flow of blood out of the heart and may cause symptoms of fatigue, syncope or chest pain. Occasionally it is seen in asymptomatic athletes.

The echocardiogram shows decreased mobility of the aortic valve with a small opening. The valve is often thickened and calcified. Blood flow across the valve is turbulent on color doppler with high velocities across the small orifice. These velocities reflect a large pressure gradient across the valve. The velocity can be measured by doppler and an effective area of the valve can be calculated.

AS with small stenosed opening.

Aortic Regurgitation

The aortic valve leaks blood back into the heart after each contraction as it fails to close completely. It causes a characteristic diastolic decrescendo murmur on examination. It may occur in conjunction with aortic stenosis. It is also occurs commonly after rheumatic fever. Marfans syndrome with an enlarged aortic root can also cause regurgitation.

Echocardiogram shows a large jet of blood leaking back across the valve from the aorta. The breadth of the jet at the aortic orifice gives an idea about the severity.

Blue band is blood leaking back from aortic valve.

Mitral Stenosis

This is a rare lesion and occurs in young people after rheumatic fever. Rarely, it is congenital. In the elderly population it is usually secondary to degenerative disease. It causes exertion shortness of breath, and when severe causes heart failure. The murmur is diastolic with accentuation just before S1.

Echocardiogram shows an enlarged left atrium and thickened poorly mobile mitral valve leaflets with a small opening during diastole. The anterior leaflet assumes a characteristic J shape on opening with doming of the valve. The pulse doppler shows slow exit of blood across the valve. The area can be calculated by the slope of this trace.

Mitral Valve Prolapse

This is a very common abnormality in young people, especially in women. One study in college athletes showed a 21% incidence in women. Occasionally there may be mild mitral regurgitation with the prolapse. The cause is redundant mitral leaflet tissue with myxomatous degeneration. It is a frequent finding in patients with Marfans Syndrome. In the majority of patients the cause is unknown but it appears to be a genetically determined collagen tissue disorder.

It commonly causes a mid to systolic murmur following a mid or late systolic click from the prolapsing mitral valve. The mitral valve on closure prolapses beyond the annulus of the mitral valve into the left atrium on systole. This can be clearly seen on the echocardiogram. Prolapse of other valves may also be evident.

Patients may be asymptomatic or may have palpitations(extra beats) and atypical chest pain. This common condition rarely causes any problems. Antibiotic prophylaxis before dental procedures is recommended in those with severe prolapse or a significant murmur. Occasionally drugs to slow the heart may be used in people who have unbearable palpitations.

MVP.

Mitral Regurgitation

This causes a clearly abnormal murmur at the apex of the heart that lasts throughout contraction. This can be picked up during the physical examination. The valve leaks blood back from the ventricle into the left atrium. This causes symptoms of fatigue and shortness of breath on exertion.

Rheumatic heart disease causes one third of all Mitral Regurgitation. It may also occur as a congenital anomaly or as a degenerative disease. It may occur after marked dilation of the ventricle after myocarditis. In hypertrophic cardiomyopathy the enlarged muscular wall may pull the leaflet forward and cause mitral regurgitation. Degenerative changes following mitral valve prolapse or myocardial infarction may also cause regurgitation. It may also occur following an infection of the valve.

The echocardiogram shows a large amount of blood flowing backwards into the left atrium.

Regurgitant jet flowing back into the left atrium.

Physiologic Left Ventricular Hypertrophy

This is a common finding in athletes, specially those who train at high intensities for competitive sports. The walls of the heart are thickened and the cavities are enlarged in size, out of proportion to the body size. The heart is adapted to work at high intensities and to pump more blood than an untrained person. However contractility is normal. The diastolic property( the relaxation of the heart) is normal. This is in contrast to the diastolic properties in pathological hypertrophy, for example in hypertensive subjects. An estimate of the diastolic filling can be made by doppler blood flow across the mitral valve. This has always been shown to be normal in athletes.

It may be difficult to distinguish physiologic enlargement from Hypertrophic Cardiomyopathy.

Left ventricular hypertrophy (symmetrical).

Hypertrophic Cardiomyopathy

This is an abnormal enlargement of the heart as in left ventricular hypertrophy detailed above. It is however very important to distinguish from physiologic hypertrophy as it is associated with a high mortality. It is one of the most common causes of death in young athletes. Furthermore competitive sport is prohibited once this condition is diagnosed as it may lead to death. People with this abnormality have a propensity for going into an abnormal heart rhythm, specially during exercise, which may cause death. The abnormal muscle can obstruct blood flow out of the heart and pull on the mitral valve leaflet causing a leak across the valve, especially during forceful contractions that occur with exercise. This causes a characteristic ejection murmur at the left sternal border that increases with exercise and dehydration.

The obstruction to blood flow during contraction causes syncope or light headedness, dizziness, and a feeling of passing out on exertion. Occasionally patients may report palpitations.

This condition may be inherited and others in the family may have it. It may be a cause of unexplained death in the family at a young age. It is inherited as an autosomal dominant trait.

Distinguishing features from hypertrophy include--

The loud systolic murmur from the obstruction to blood flow.
A forth heart sound
A bizarre EKG showing severe hypertrophy and other abnormalities
On Echocardiogram the hypertrophy is not symmetric with contiguous segments not thickened to a similar degree.
The contour of the hypertrophic wall is irregular in contrast to smooth walls in physiologic hypertrophy.
The maximum thickening of the left ventricular wall usually does not exceed 16 mm in physiologic hypertrophy.
The left ventricular cavity is enlarged in physiologic hypertrophy. It is normal or reduced in size in hypertrophic cardiomyopathy.
The diastolic doppler flow pattern is abnormal in 80% of the patients with cardiomyopathy. It is always normal in physiologic hypertrophy.
Changes of physiologic hypertrophy show regression to normal with cessation of training, while the pathologic form shows no change.

Hypertrophic septum.

[IHSS Spectrum Image]
Dagger-shaped outflow velocities.

Marfans Syndrome

This is an inherited disorder, due to a gene mutation, causing a person to present with long thin extremities, reduced vision due to dislocation of the lens of the eye and aortic aneurysms- dilation of the root of the aorta. It is important in athletes as the root of the aorta may rupture causing sudden death. Marfans can usually be diagnosed from body habitus on physical exam in conjunction with the family history.

Echocardiogram shows dilated aortic root with aortic regurgitation. Mitral valve prolapse may be seen.

Myocarditis-Dilated Cardiomyopathy

Occasionally viruses may infect the heart and cause weakness of the heart muscle. The walls become thin and flabby and the cavity of the heart becomes enlarged. The heart does not contract very well.

Athletes can die, usually from an arrhythmia in this condition. They usually present with fatigue and exertional weakness.

The Nicholas Institute of Sports Medicine and Athletic Trauma

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