Valvular Heart Disease
Valvular heart disease is characterized by damage to or a defect in one of the four heart valves: the mitral, aortic, tricuspid or pulmonary.
The mitral and tricuspid valves control the flow of blood between the atria and the ventricles.
The pulmonary valve controls the flow of blood from the heart to the lungs, and the aortic valve governs blood flow between the heart and the aorta and the blood vessels to the rest of the body.
The mitral and aortic valves are the ones most frequently affected by valvular heart disease.
Normally functioning valves ensure that blood flows with proper force in the proper direction at the proper time.
In valvular heart disease, the valves become too narrow and hardened / stenotic to open fully, or are unable to close completely / incompetent.
A stenotic valve forces blood to back up in the adjacent heart chamber, while an incompetent valve allows blood to leak back into the chamber it previously exited. To compensate for poor pumping action, the heart muscle enlarges and thickens, thereby losing elasticity and efficiency. In addition, blood pooling in the chambers of the heart may create a greater tendency to clot, increasing the risk of stroke or pulmonary embolism.
The Valves of the Heart (Anterior View)
Types of Valvular Heart Disease
- Valve Affected Complication
- Mitral Valve disease Mitral Stenosis Mitral Regurgitation Mitral Valve Prolapse
- Aortic Valve Disease Aortic Stenosis Aortic Regurgitation
- Tricuspid Valve Disease Tricuspid Stenosis Tricuspid Regurgitation
- Pulmonic Valve Disease Pulmonic Stenosis Pulmonic Regurgitation
- Mitral Valve Disease Mitral Stenosis
The most common cause of Mitral Stenosis (MS) is Rheumatic Fever. Fifty percent of patients with Mitral Stenosis provide have a history of Acute Rheumatic fever that occurs about 20 yrs before the stenosis manifests. These patients present with rheumatic deformity of the valve. Other causes may include congenital stenosis of the mitral valve leaflets, as well as calcification from the mitral annulus onto the leaflets in elderly patients or endocarditis with large obstruction of the valve orifice.
In a normal heart, the mitral valve opens during left ventricular diastole, to allow blood to flow from the left atrium to the left ventricle. Blood flows in the proper direction because during this phase of the cardiac cycle the pressure in the left ventricle is lower than the pressure in the left atrium, and the blood flows down the pressure gradient. In the case of mitral stenosis, the valve does not open completely, and to transport the same amount of blood the left atrium needs a higher pressure than normal to overcome the increased gradient.
The normal area of the mitral valve orifice is about 4 to 6cm2. Under normal conditions, a normal mitral valve will not obstuct the flow of blood from the left atrium to the left ventricle during (ventricular) diastole, and the pressures in the left atrium and the left ventricle during ventricular diastole will be equal. The result is that the left ventricle gets filled with blood during early ventricular diastole, with only a small portion of extra blood contributed by contraction of the left atrium during late ventricular diastole.
When the mitral valve area goes below 2cm2, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may increase with increases in the heart rate or cardiac output. As the pressure gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood also increases. Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood decreases. When the heart rate exceeds a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion.
The constant pressure overload of the left atrium will cause the left atrium hypertrophy. As the left atrium increases in size, it becomes prone to develop atrial fibrillation. When atrial fibrillation develops, the atrial kick is lost.
In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick. The loss of the atrial kick due to atrial fibrillation can cause a steep decrease in cardiac output and sudden congestive heart failure.
Patients with mitral stenosis are prone to a series of hemodynamic changes that frequently cause deterioration of the patient's clinical status. A reduction in cardiac output, association with an accelerated heart rate and shortening of the diastolic time, frequently leads to congestive heart failure.
Therapy includes long term penicillin treatment to prevent recurrent acute rheumatic fever. Diuretics are prescribed to treat vascular congestion. Surgical options include Open mitral Commisurotomy as well as percutaneous balloon mitral valvuloplasty.
The pathophysiology of mitral regurgitation can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase
Acute mitral regurgitation causes a sudden volume overload of both the left atrium and the left ventricle. The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta , but also the blood that regurgitates into the left atrium (the regurgitant volume). The combination of the stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle.
With acute mitral regurgitation, the stroke volume of the left ventricle is increased, which is an increased ejection fraction, this happens due to complete emptying of heart. However, as it progresses the LV volume increases and the contractility deteriorates which leads to dysfunctional LV and a decrease in ejection fraction. The stroke volume increases by way of the Frank-Starling mechanism.
The regurgitant volume causes a volume overload and a pressure overload of the left atrium. The increased pressures in the left atrium inhibit drainage of blood from the lungs via the pulmonary veins. This causes pulmonary congestion.
If the mitral regurgitation develops slowly over months to years or if the acute phase can be managed with medical therapy, the individual will enter the chronic compensated phase this valve disease. In this phase, the left ventricle develops eccentric hypertrophy in order to better manage the larger than normal stroke volume. The eccentric hypertrophy and the increased diastolic volume combine to increase the stroke volume to abnormally high levels so that the forward stroke volume (forward cardiac output) approaches the normal levels.
In the left atrium, the volume overload causes enlargement of the chamber of the left atrium, allowing the filling pressure in the left atrium to decrease. This improves the drainage from the pulmonary veins, and signs and symptoms of pulmonary congestion will decrease.
These changes in the left ventricle and left atrium improve the low forward cardiac output state and the pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerances.
An individual may be in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction. The cause of entering the chronic decompensated phase is unknown. The decompensated phase is characterized by calcium overload within the cardiac myocytes.
In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation, and the stroke volume of the left ventricle will decrease. The decreased stroke volume causes a decreased forward cardiac output and an increase in the end-systolic volume. The increased end-systolic volume results in increased filling pressures of the ventricular and increased pulmonary venous congestion. The individual may again have symptoms of congestive heart failure.
The left ventricle begins to dilate during this phase. This causes a dilatation of the mitral valve annulus, which may worsen the extent of mitral regurgitation. The dilated left ventricle causes an increase in the wall stress of the cardiac chamber as well.
While the ejection fraction is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase of mitral regurgitation, it may still be of a normal range (i.e.: > 50 percent), and may not decrease until late in the course of the disease disease. A decreased ejection fraction in an individual with mitral regurgitation and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase.
Aortic Stenosis is often caused by age related degenerative calcific changes of the aortic valve. These calcific changes also develop in patients with congenitally deformed aortic valves. Younger patients experience calcification of the aortic valve that leads to stenosis.
When the aortic valve becomes stenotic, it causes a pressure gradient between the left ventricle and the aorta. The more constricted the valve, the higher the gradient between the Left Ventricle and the aorta.
In individuals with AS, the left ventricle has to produce an increased pressure in order to overcome the increased after load caused by the stenotic aortic valve and eject blood out of the Left Ventricle. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the myocardium of the Left Ventricle undergoes hypertrophy. Aortic stenosis results in all the walls of the left ventricle undergoing equal hypertrophy.
These individuals are not candidates for exercise programs. The danger of sudden death is present particularly during exercise. Patients with mild or moderate AS may have a normal exercise capacity. Angina, Dyspnea, and fatigue are common symptoms with exercise.
Aortic Regurgitation / Aortic Insufficiency
Aortic Regurgitation may result from diseases of the aortic leaflets or Dilatation of the Aortic root. Other causes may result from congenital abnormalities of the bicuspid valve, endocarditis, as well as rheumatic causes.
In aortic insufficiency, when the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve is not able to completely close. This causes a leaking of blood from the aorta into the left ventricle. This means that some of the blood that was already ejected from the heart is regurgitating back into the heart. The percentage of blood that regurgitates back through the aortic valve due to aortic insuffiency is known as the regurgitant fraction. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore an increase in the pulse pressure.
Since some of the blood that is ejected during systole regurgitates back into the left ventricle during diastole, there is decreased effective forward flow in Aortic Insufiency.
Aortic insufficiency causes both volume overload (elevated preload) and pressure overload (elevated after load) of the heart.
The pressure overload causes left ventricular hypertrophy . There is both concentric hypertrophy and eccentric hypertrophy in Aortic Insuffiency. The hypertrophy is due to the increased left ventricular systolic pressures associated with Aortic Insuffiency, as well as hypertrophy due to volume overload caused by the regurgitant fraction.
Patients are monitored with periodic examinations and assessment usually by ECG. Patients are also prescribed antibiotic prophylaxis to prevent endocarditis. Calcium Channel blockers may help by reducing vasodilation. Calcium channel blockers have been shown to reduce left ventricle enlargement, increase the left ventricle ejection fraction and thus delay the need for surgery.
Strenuous exercises should be avoided if weakening of the aortic wall is present. Patients with mild to moderate Aortic regurgitation can pursue normal activities.
Tricuspid Stenosis is rare and usually a result of rheumatic heart disease. It results from narrowing of the tricuspid valve. Other causes include infections and tumors. These individuals usually complain of fatigue and swelling in the lower extremity and abdominal regions. These patients have distended neck veins and significant edema.
This condition is usually functional more than structural. It develops because of right ventricular enlargement and not because of valve disease.
A sensitive sign of TR is a pulsatile liver because of regurgitation of right ventricular blood into the systemic veins.
This condition is rare and its cause is almost always congenital deformity of the valve. It is a narrowing or tightening of the pulmonary valve. Carcinoid syndrome is another rare cause of this condition in which encasement and immobilisation of the valve leaflets can occur. These individuals can present with heart failure, exert ional dyspnoea, syncope or chest pain caused by the inability to increase pulmonary blood flow during exercise.
This condition most commonly develops in the setting of severe pulmonary hypertension and results from dilatation of the valve ring by the enlarged pulmonary artery. This condition develops when the leaflets of the pulmonary valve do not close properly
Effects of Exercise Training
Mechanical function of the affected valve will not improve with exercise. The working capacity of skeletal muscles will however improve with training. This may assist the individual with performing activities of daily living that may have been previously unattainable at given cardiovascular workloads.
Significant mitral stenosis may limit exercise because demands of the exercising muscle may be greater than the cardiac output available.
Recommendations for Exercise Programming
Before commencement of an exercise programme the upper training rate and description of any symptoms should be documented from a diagnostic exercise test. The extent of the regurgitation and stenosis must also be established.
With Mitral Valve, - stenosis, - regurgitation and prolapse, physical activity is limited by individual symptoms.
Those individuals who are unable undergo surgery of the heart valves, the primary goal would be to improve their physical working capacity of the skeletal muscles.
Signs of heart failure must be documented and reported to the physician due to a progression of the left ventricle or valvular dysfunction.
Frequency should include 3 to 7 days per week with a goal of achieving duration of 20 to 60 minutes per session. Deconditioned people with valvular disease can use intermittent exercise of 5 to 15 minutes per session. Intensity of the exercise should be dictated by resting heart rate and adding 20 to 30 contractions per minute with a goal of reaching 40% to 70% of their aerobic capacity.