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Valvular heart disease involves damage or dysfunction of the heart valves. The mitral and aortic valves are most commonly affected. Stenosis and regurgitation are the main types of valve dysfunction, leading to enlargement of the heart and blood clot formation. Symptoms can vary from mild to severe, including congestive heart failure. Causes of valvular heart disease include aging, bacterial endocarditis, hypertension, and rheumatic fever. Diagnostic tests include auscultation, ECG, stress testing, echocardiogram, and cardiac catheterization. Mitral valve stenosis is caused by rheumatic fever and can lead to pulmonary hypertension and heart failure. Mitral valve regurgitation is caused by various factors including rheumatic fever and mitral valve prolapse. Symptoms worsen with enlargement of the left atrium. Treatment options include medication, valve replacement, and commissurotomy. Chapter 8, Valvular Heart Disease. This chapter's main topic is valvular heart disease. Valvular heart disease can involve any type of damage or dysfunction of the valves of the heart, including the mitral, aortic, pulmonic, or the tricuspid valve. The tricuspid and mitral valves control the amount of blood traveling from the atria to the ventricles. The pulmonic valve controls the blood flow to the lungs, and the aortic valve controls the blood flow from the left ventricle to the aorta. The valves most likely to be affected by valvular disease are the mitral and aortic valves, which are the left-sided valves. Each of the valves and their dysfunctions will be covered in this chapter. Valvular Disease Basics Valvular disease can involve stenotic or narrowed valves that inhibit blood flow through the valve itself, secondary to scar tissue or valve stiffening. The valve can also be regurgitant, in which it leaks blood back through the valve when the heart is actively pumping. Each of these deficits results in an enlargement of the heart or a thickening of the heart muscle. The heart muscle also loses its normal elasticity. Blood may also pool in the heart's chambers, causing blood clots to form that can break off and cause a pulmonary embolism or stroke. Mild cases may have no symptoms, while severe cases can lead to symptoms suggestive of congestive heart failure. Sudden valvular disease can happen after an MI has caused rupture of the tendons of a valve. This is most common with the mitral valve causing acute mitral regurgitation. Valvular heart disease that progresses more slowly may be asymptomatic even in severe cases, as the heart compensates for the abnormal valvular function. Typical symptoms of valvular disease are CHF symptoms, tiredness, palpitations, syncope, or dizziness as with aortic stenosis, weight gain, and fever with an infection of the valve. Common causes of valvular heart disease include degeneration of the valve secondary to the aging process, bacterial endocarditis, heart attack, hypertension, and rheumatic fever, which damages the heart valves. Certain tumors and connective tissue disease can damage the heart valves. Radiation for cancer can be linked to valvular heart disease, and methyl surguide used for migraines can also precipitate valvular damage. Diagnostic tests for valvular heart disease are numerous and start with a simple auscultation of the heart looking for heart murmurs from abnormal blood flow through the valves. An ECG can detect cardiac arrhythmia secondary to valvular disease. Stress testing with an exercise stress test can monitor the electrical activity of the heart. An echocardiogram can visualize the valves and show the amount of blood flowing through the valves. This is the best test for screening for valvular heart disease. A cardiac catheterization can look at pressure gradients across valves and detect regurgitation or stenosis. Mitral valve stenosis. Mitral valve stenosis, or MS, involves a narrowing of the opening of the mitral valve that blocks blood flow from the left atrium to the left ventricle. The cause of this in nearly all cases is rheumatic fever. The mitral valve leaflets become thicker and less mobile while there is fusion of the commissure, leading to thickened, matted cordae and a narrowed opening. Very rarely there can be mitral stenosis from annular calcification that has spread to involve the leaflets so they won't open properly. Mitral stenosis is sometimes a congenital problem associated with mitral regurgitation if the valves can't properly close. The heart responds to mitral stenosis by increasing the size and pressure of the left atrium and by increasing the pulmonary, capillary and venous pressures. This results in pulmonary hypertension and finally to right heart failure, triguspid regurgitation and pulmonic regurgitation. The dilatation of the left atrium results in atrial fibrillation, which is an independent risk factor for thromboembolism. The symptoms depend on the person and correlate poorly with the severity of the stenosis. These patients often present with exercise intolerance and eventually progress to atrial fibrillation and heart failure symptoms. The symptoms don't show up until 15 to 40 years after having rheumatic fever. Paroxysmal or chronic atrial fibrillation will reduce the degree of blood flow to the left ventricle, leading to shortness of breath and pulmonary edema. In patients who don't take anticoagulants, there is a 15% chance of experiencing an embolic event. Mitral stenosis can lead to core pulmonality and symptoms typical of right heart failure. On examination, there is a loud S1 from the sudden closure of the narrowed leaflets heard mainly at the apex of the heart. The S1 might be absent if the valve won't close. The S2 is split and there is a lowered decrescendo-crescendo diastolic murmur heard best over the apex. The murmur tends to increase with a valve salvo maneuver and with exercise. The murmur is extremely low-pitched. Severe disease may be linked to an aortic regurgitation murmur, a diastolic flow murmur from severe mitral regurgitation, or a gram-steel murmur, which is a soft decrescendo-diastolic murmur of pulmonic regurgitation heard on the left sternal border. The degree of mitral stenosis is graded using an echocardiogram. The normal orifice of the mitral valve is 4 to 5 square centimeters. Moderate disease involves an area of 1.5 to 2.5 centimeters. Severe disease is an area of less than 1.5 centimeters squared. Very severe disease is an area of less than 1 centimeter squared. An ECG will show an LA enlargement and a large P wave with a notched P wave in lead II. Chest X-ray will show a dilated LA appendage and widening of the heart with prominence of the pulmonary arteries and veins. Most patients progress from initial symptoms to severe cardiac disability within 7 to 9 years. The outcome is affected by the patient's age and degree of pulmonary hypertension when treated. There is a worse prognosis in the presence of atrial fibrillation or pulmonary hypertension. Frequent causes of death are pulmonary embolism, cerebral embolism, or heart failure. Treatment can include diuretic therapy, beta blockers, anticoagulation, valve replacement, or commissurotomy to open the valvular blockage. Intervention may be necessary when heart surgery is planned for other purposes or when the patient is symptomatic. Symptomatic patients with severe or very severe disease need a percutaneous balloon commissurotomy. If the patient has annular calcification, there is no point in doing a percutaneous procedure, instead the valve is replaced when all oral medications have failed to control the symptoms. Mitral valve regurgitation. Mitral regurgitation, or MR, is a weakness or incompetency of the mitral valve so that blood flows backward during a ventricular systole from the left ventricle to the left atrium. The two most common causes of MR are rheumatic fever and mitral valve prolapse. Less common causes of MR include a papillary muscle rupture from ischemia, infective endocarditis, acute LV dilatation from myocarditis or ischemia, congenital cleft mitral valve, connective tissue disorders, radiation heart disease, and mechanical failure of an artificial valve. When thickened valves and mitral stenosis do not close, there can be mitral regurgitation. Mitral valve regurgitation can be acute or chronic. Acute MR results in a cardiogenic shock and acute heart failure symptoms like shortness of breath, edema, weakness, and tiredness. Chronic mitral regurgitation may be asymptomatic at first and then will worsen as the left atrium enlarges with increases in the pulmonary artery pressure and venous pressure in the lungs. These symptoms will include orthopnea, tiredness, dyspnea, and palpitations, usually secondary to atrial fibrillation. These symptoms are present only when the disease is moderate to severe. On auscultation, the first S1 sound will be soft and the third sound, S3, will be heard when the LV is severely dilated. The presence of the S3 sound usually means heart failure is imminent. The classic murmur is an apical holosystolic murmur, worse in the left lateral decubitus position. The murmur will radiate to the axilla and will decrease withstanding or the Valsalva maneuver. A murmur or a thrill may also be palpable in severe cases. The difference between this murmur and tricuspid regurgitation is that the TR murmur is worse during inspiration. The echocardiogram can be done to evaluate the valve. It will determine the severity or grade of the murmur and look at the size and functionality of the left atrium and left ventricle. Moderate MR has a regurgitant volume of 30 to 60 mL and a regurgitant fraction of 40 to 50%. Severe primary MR has a regurgitant volume of more than 60 mL and a regurgitant volume of more than 50%. Severe secondary MR has a regurgitant volume of greater than 30 mL and a regurgitant fraction of greater than 50%. The ECG will show LA enlargement and hypertrophy of the left ventricle. There will be normal sinus rhythm with acute disease and atrial fibrillation with chronic disease. The chest X-ray will show pulmonary edema, left ventricular enlargement, and left atrial enlargement in chronic disease only. The chest X-ray may also depict increased pulmonary vascular congestion and frank pulmonary edema. The prognosis depends on the cause and severity of MR. As it becomes more severe, about 10% of patients per year will become symptomatic with about 10% of patients requiring surgery. Surgery involves doing a mitral valve replacement or repair while those in atrial fibrillation need anticoagulant therapy. If there is severe LV dysfunction, the treatments of choice include spironolactone, vasodilators, and vasodilating beta blockers. Pacing may be necessary if there is a bundle branch block. Digoxin and furosemide can help with heart failure symptoms. Prophylactic antibiotics are reserved for patients who have had their valves replaced. Patients with acute MR need their valve repaired or replaced urgently with an intra-aortic balloon pump, nitroprusside, or nitroglycerin before surgery. Chronic primary MR that is severe needs to be treated if the symptoms are severe or there is evidence of LV decompensation, such as an injection fraction less than 60% or high end diastolic pressure. For chronic secondary MR, the problem is with the muscle of the LV, so fixing the mitral valve is less helpful and riskier. These patients are generally treated medically. Replacement is only done when the MR is severe. Repair is always preferred over replacement, and if replaced, the mechanical valve tends to last longer. Lifelong anticoagulation is necessary if the patient has a mechanical valve. Warfarin is the only recommended anticoagulant after MR replacement surgery. Mitral valve prolapse. Mitral valve prolapse, or MVP, involves a billowing backward of the leaflets of the mitral valve into the left atrium and systole. The most common cause is idiopathic myxomatous degeneration of the valve. It is generally a benign condition but can lead to things like chordal rupture, mitral regurgitation, and endocarditis. It is generally asymptomatic but a few patients will have palpitations, dizziness, dyspnea, and chest pain. Mitral valve prolapse is the most common valvular disease affecting 1-3% of the population and usually arising in adolescence. It is generally caused by myxomatous degeneration of the mitral valve leaflets and the chordae tendineae. This means that there is a thinning of the collagen layer in the mitral valve with a buildup of mucoid material. The chordae become thinner and longer with enlargement of the leaflets that then become rubbery. This leads to a floppy valve. Most cases are idiopathic but there is an autosomal dominant and X-linked recessive disease that can cause this, including connective tissue disorders such as Ehlers-Danlos, Marfan, lupus, and polycystic kidney disease, and muscular dystrophies. It is seen more often in patients who have Graves' disease, sickle cell disease, von Willebrand's disease, and rheumatic heart disease. There can be mitral regurgitation without any myxomatous changes of the valve secondary to rupture of the cords or the papillary muscles. Transient mitral valve prolapse can happen when there is marked dehydration or when a gravid woman lies flat compressing the inferior vena cava. The most complication of MVP is mitral regurgitation. It can be an acute complication or a chronic complication. When MR occurs, there are secondary problems of atrial fibrillation, infective endocarditis, and acute heart failure. Most people with MVP have no symptoms or have nonspecific symptoms believed to be secondary to problems in adrenergic signaling instead of actual pathology of the valve. The symptoms are often precipitated by emotional stress, with palpitations being the most common symptoms of MVP. Auscultation of a person with MVP involves a sharp, mid-systolic click with tightening of the sub-valve apparatus. It is best heard in the apex with the patient lying on their left side. When MR develops, there can be a late systolic murmur. The valsalva maneuver will make the murmur longer and louder. The prognosis of MVP is usually quite good in those patients not developing mitral regurgitation. Those with MR will have left atrial and left ventricular enlargement with secondary arrhythmias like atrial fibrillation, secondary stroke, and infective endocarditis. The mortality rate at this time is about 2% to 4% per year. The major medical treatment is beta-blockers, which can block the excess of sympathetic tone seen in symptomatic patients. If atrial fibrillation develops, it needs to be treated. Aortic stenosis. Aortic stenosis, or AS, is a narrowed aortic valve that results in a blockage of blood flow from the left ventricle to the ascending aorta. The main cause is a congenital bicuspid aortic valve followed by idiopathic degenerative sclerosis and rheumatic fever. It will become symptomatic over the years, leading to shortness of breath with exertion, chest pain, and syncope. AS can develop in elderly patients, with the most common underlying cause being aortic sclerosis, which is degeneration of the valve with thickening and calcification of the valves. This will progress to aortic stenosis in about 15% of cases. Risk factors are similar to those seen in atherosclerosis. Psoriasis has been linked to an increased risk of atherosclerosis and aortic stenosis. In young people, the biggest risk factor for aortic stenosis is congenital bicuspid aortic valve, affecting 3 to 5 children out of 1,000. These people are also at greater risk for aortic dissection of a proximal aorta. In developing countries, rheumatic fever is the most common cause of AS. Rarely a child can be born with supravalvular AS, which is a congenital problem linked to other physical findings. Williams syndrome is one hereditary condition linked to AS. Aortic stenosis can be linked to aortic regurgitation and mitral regurgitation. The increased ventricular pressure secondary to aortic stenosis will lead to LV hypertrophy. Over time, there is a reduced ejection fraction and LV cavity enlargement. Patients can have pseudo-severe AS from mild valvular disease, but symptoms because they have other reasons to have left ventricular dysfunction and a low ejection fraction. These patients do not get better after a valve replacement because the problem is actually elsewhere in the heart. Congenital AS is not symptomatic in childhood, but becomes severe after age 20 with angina, exertional syncope, and dyspnea. These three symptoms are classic for AS. Other symptoms lead to arrhythmias and heart failure. Ventricular fibrillation can occur with sudden cardiac death. Dyspnea is worse on exertion because the cardiac output is too low. Exertional angina occurs in about 65% of patients, with about half of these actually having coronary artery atherosclerosis. Syncope tends to occur at risk from ventricular tachycardia or problems with aortic baroreceptors. Auscultation of the person's heart with AS shows a normal S1 and a single S2 because there is a delay of aortic valvular closure, so it matches with the pulmonic aspect of the S2. If the S2 is split, this finding rules out AS. There can be an ejection click after the S1. The murmur is a systolic crescendo-decrescendo ejection murmur heard over the left sternal border and radiating to the right clavicle. The louder the murmur, the more severe the AS, except when the LV begins to fail and then the murmur becomes shorter and softer. The murmur increases with valsalva maneuvers. The diagnosis is made through echocardiography with Doppler flow studies identifying the severity of the disease. Moderate AS is indicated with a peak aortic jet velocity of 3 to 4 meters per second. Severe AS has a peak aortic jet velocity of 4 to 5 meters per second. Very severe AS has a peak aortic jet velocity of greater than 5 meters per second. ECG will show left ventricular hypertrophy with a chest X-ray showing calcification of the aortic leaflets and evidence of heart failure. The heart size may or may not be enlarged. Exercise stress testing can bring out symptoms in people with no symptoms at rest. Exercise stress testing shouldn't be done on patients who are symptomatic at rest. The disease tends to progress over time, but some patients can have a rapid onset of symptoms. For this reason, patients with AS should be evaluated every 6 months to see what their ejection fraction and LV function is. Patients need a valve replacement when they become very symptomatic or when they are having heart surgery for other reasons. About half of patients will have sudden cardiac death. There are no medications that will slow the disease progression. Heart failure patients who are not surgical candidates can be managed with ACE inhibitors, diuretics, and digoxin. In general, the valve is replaced when the disease becomes severe and symptomatic or when the asymptomatic patient has an ejection fraction of less than 50%, are undergoing heart surgery for other reasons, or very severe disease. Young people with congenital AS can be treated with a balloon valvotomy, while other patients should have a surgical aortic valve replacement or percutaneous valve replacement. A bioprosthetic valve replacement doesn't require anticoagulation, but a mechanical valve requires lifetime anticoagulation therapy after surgery. Aortic regurgitation. Aortic regurgitation is also referred to as aortic insufficiency or AI. It involves a backflow or leakage of the aortic valve causing a reversing of flow during the ventricular diastole into the left ventricle. The typical symptoms are not unlike heart failure and include orthopnea, dyspnea on exertion, paroxysmal nocturnal dyspnea, cyanosis, angina, and palpitations. The main cause is dilatation of the aortic root, which is idiopathic 80% of the time. Less common causes of AI include osteogenesis imperfecta, syphilis, aging, reactive arthritis, hypertension, aortic dissection, and Bechet's disease. Any disease that involves connective tissue can cause AI by acting directly on these valves, such as Ehlers-Danlos syndrome, Marfan syndrome, lupus, and ankylosing spondylitis. Sudden onset AI can occur with dissection, trauma, or infective endocarditis. During AI, some of the blood initially ejected from the left ventricle reverses flow and goes back into the ventricle during diastole, causing an increase in pulse pressure and an effectively decreased ejection fraction. The systolic BP remains normal, but the diastolic BP drops. Catecholamines are released, which compensate for the decreased cardiac output by increasing the heart rate. When this fails, heart failure can develop, leading to reduced systolic blood pressure. There is volume overload in secondary left ventricular hypertrophy, which is concentric and eccentric. The exam will be significant for LV hypertrophy in a dilated aorta on chest X-ray. The ECG will show left ventricular hypertrophy. Cardiac chamber catheterization can be done to assess the degree of regurgitation. The exam will show the presence of an S3 gallop from LV dysfunction and an early decrescendo diastolic murmur, heard best at the third left intercostal space. There may also be an ejection systolic flow murmur. AI can be acute from endocarditis, trauma, or aortic dissection. This will suddenly increase the amount of blood in the left ventricle with an increase in pressure in the left ventricle and left atrium. Pulmonary edema soon follows. This is an emergency situation that results in death unless the valve is replaced urgently. AI can also be chronic with LV hypertrophy and dilatation of the left ventricle. The volume overload is compensated so the patient won't generally have heart failure. The patient may not have symptoms until the LV decompensates. Medical or surgical treatment is possible depending on the situation. Surgery is indicated if the EF falls to less than 50% or if there is severe dilatation of the left ventricle. Surgery must be done in acute AI. Medical treatment involves ACE inhibitors, angiotensin blockers, hydralazine, and nifedipine, all given to reduce LV wall stress and decrease the afterload. Patients should avoid strenuous activity and can be treated with digoxin, diuretic therapy, low-salt diet, and calcium channel blockers. Antibiotic prophylaxis is not recommended. Surgery is an open-heart surgery with valve replacement. Tricuspid stenosis. Tricuspid stenosis. Tricuspid stenosis, or TS, involves a narrowing of the tricuspid valve opening which blocks the flow of blood from the right atrium into the right ventricle. It is almost exclusively secondary to rheumatic fever. Patients will have liver congestion, fatigue, cold skin, and jugular venous distension. The jugular venous distension is a prominent finding of the disorder. Tricuspid regurgitation always accompanies TS. Less common causes of TS include lupus, congenital defects, metastatic cancer, and right atrial myxoma. There is hypertrophy of the right atrium which enlarges while the right ventricle is small and underfilled. Atrial fibrillation is a common sequela. The main physical finding is the jugular venous distension. Auscultation of the chest shows a soft opening snap and a mid-diastolic rumbling murmur similar to that of mitral stenosis. The two can be difficult to differentiate. The murmur is shorter in TS and stops before the next S1. It is worse on inspiration and best heard in the lower right and left parasternal borders. The echocardiogram will show a pressure gradient across the tricuspid valve with the thickened leaflets and reduced valvular motion. The RA is enlarged and can be seen on ECG as tall peaked waves in V1 and the inferior leads. Chest X-ray will show dilatation of the superior vena cava. Hepatic congestion will lead to elevated liver enzymes and cardiac catheterization will show increased RA pressure. Treatment almost never includes surgical replacement of the valve. Patients can have aldosterone antagonists and diuretics to improve heart function. This is uncommon disease so the best treatment approaches are not well known. Tricuspid regurgitation. Tricuspid insufficiency or TI is also called tricuspid regurgitation or TR. This involves a failure of the tricuspid valve to close during systole so blood flows backward from the right ventricle to the right atrium. This can be due to right ventricular dilatation or intrinsic abnormality in the valve. Patients with this will have symptoms of ascites and peripheral edema from right-sided heart failure. The patient will have a holosystolic heart murmur best heard over the lower left sternal border. The murmur increases with inspiration and decreases with expiration, which is carvalosine. A third heart sound may also be present. There will be a giant CV wave in the jugular vein with a palpable pulsatile liver. The murmur may be faint. The causes of TI can be from a congenital defect in the valve that more commonly is a problem of enlargement of the right ventricle causing it to leak. This can be secondary to pulmonary hypertension or other causes of right heart failure. When the right ventricle enlarges, it causes an internal derangement in the area that structurally affects the tricuspid valve. A right ventricular infarction, an inferior MI, and core pulmonality can all cause right ventricular dilatation. Primary TI is caused by rheumatic fever, myxomatous degeneration of the valve, Epstein anomaly, endocarditis, fibrosis, or trauma to the heart. Secondary TI is caused by LV valvular disease or LV dysfunction, lung disease, RV ischemia, pulmonary embolism, or carcinoid heart disease. There are geometric changes in the annulus of the valve with normal leaflets that aren't spatially in approximation with one another, leading to insufficiency. Tricuspid insufficiency is diagnosed by chest X-ray, which shows RA enlargement. The echocardiogram will show an abnormality of the valve. Cardiac catheterization will determine how severe the problem is. Pulmonary stenosis is not always surgical and can involve ACE inhibitors and diuretic therapy. Surgery, if necessary, can involve a bioprosthetic or mechanical valve. Pulmonic stenosis. Pulmonic stenosis or pulmonary stenosis is a fixed or dynamic obstruction of the outflow tract of the right ventricle into the pulmonary artery. It is a childhood disease that is usually congenital. It can affect the valve alone or parts above and below the valve. It can affect just the pulmonic valve or can be seen with other structural congenital heart problems. The pathophysiological result is right ventricular hypertrophy, and if the RV fails, there will be an increase in RA pressure and persistence of the foramen ovale at birth and cyanosis at birth. The presence of the patent ductus arteriosus will partially compensate for the shunting of blood from the right to left by reversing that shunt. The treatment of choice for PS is a percutaneous balloon valvuloplasty procedure. Pulmonic regurgitation. Pulmonic regurgitation is also referred to as pulmonic insufficiency or PI. In this case, the pulmonic valve is weak and allows backflow from the pulmonary artery into the right ventricle during ventricular diastole. If it is just found on echocardiogram, it is not serious and is more serious when detected during examination. The murmur is characteristic and is called the Graham-Steele murmur. In severe cases, it can lead to RV enlargement and right-sided heart failure. The murmur is a diastolic decrescendo murmur. The causes of PI include rheumatic heart disease, pulmonary hypertension, endocarditis, tetralogy of Fallot, and connective tissue diseases. It is diagnosed with an EKG and echocardiogram. The chest X-ray will show enlargement of the right ventricle and or right atrium. The treatment involves treating the underlying cause of the problem such as the reason behind pulmonary hypertension. In rare cases, the pulmonic valve is replaced. Treatment of valvular heart disease. The treatment of valvular heart disease involves lifestyle changes like smoking cessation, avoiding excessive use of alcohol, and reducing salt intake. Antibiotics might be recommended as a prophylaxis against vegetations, which can develop after surgery or dental work. Patients with rheumatic fever should have long-term antibiotic therapy. Antiplatelet drugs can prevent clots from forming along the valves. Stronger enteric regulation therapy is recommended with Warfarin if atrial fibrillation has developed from valvular regurgitation or if the valve is a replacement valve. Balloon dilatation procedures can be done to repair stenotic valves. A catheter with a balloon on the tip is inserted into the valve and blown up, dilating a stenotic valve. Surgery is another invasive technique, which is done to repair or replace a damaged valve. Replaced valves can be entirely prosthetic or harvested from pigs and other animals. The procedure increasingly being used for diseases like mitral stenosis is a percutaneous balloon commissurotomy, which can be done if the valves aren't heavily calcified. The procedure is guided by echocardiography and fluoroscopy. A balloon end of the catheter is passed through the narrowed valve and blown up, opening the valve. Severe disease is treated with a surgical commissurotomy. It is used for mitral stenosis. The valve is opened up using a dilator passed through the left ventricle in open-heart surgery. This type of procedure is performed only in cases of severe valvular dysfunction. In cases where the valve cannot be repaired, it is often replaced as an option. A valve can be artificial, mechanical, or biological. Some patients with an artificial valve will require heparin anticoagulation for the remainder of their lives. Key Takeaways Valvular heart disease involves either stenosis or regurgitation of one of the valves in the heart. Valvular diseases can be either congenital or acquired. Most valvular diseases have a characteristic murmur that can be identified on physical examination. Rheumatic heart disease is a major cause of acquired valvular disease. Quiz 1. What is the most common valvular condition occurring after a myocardial infarction? A. Aortic stenosis B. Mitral regurgitation C. Mitral stenosis D. Tricuspid regurgitation Answer B. The most common problem with an MI is necrosis of the tendon supporting the mitral valve leading to acute mitral regurgitation. Question 2. What is considered the best test for evaluating valvular heart disease? A. Exercise stress testing B. Electrocardiogram C. Halter monitor testing D. Angiogram E. Echocardiogram Answer E. An echocardiogram can directly visualize the valves and detect regurgitation, stenosis, and vegetations on the valve. It can monitor the flow through the valves. Question 3. The child is born with a persistent murmur and is found to have valvular disease from a congenital heart disease affecting the valves. Statistically, what is the most common valvular disease a child can be born with? A. Mitral stenosis B. Aortic stenosis C. Mitral valve regurgitation D. Pulmonary valve stenosis Answer D. The most common valvular disease in newborns is pulmonary valve stenosis, which doesn't have to be treated unless it is severe. Question 4. What valvular problem is identified by the Graham-Steele murmur? A. Mitral regurgitation B. Tricuspid regurgitation C. Pulmonic stenosis D. Pulmonic regurgitation Answer D. The murmur of pulmonic regurgitation is a soft decrescendo murmur heard on the left sternal border and is called the Graham-Steele murmur. Question 5. What is the most common cause of mitral regurgitation? A. Mitral valve prolapse B. LV enlargement C. MI with ruptured papillary muscles D. Malfunctioning prosthetic mitral valve Answer A. Mitral valve prolapse and rheumatic fever are the most common causes of mitral regurgitation. Question 6. What type of murmur is heard with mitral regurgitation? A. Crescendo-decrescendo diastolic murmur apex B. Holocystolic murmur apex C. Crescendo diastolic murmur left sternal border D. Harsh systolic murmur left sternal border Answer B. The main finding in mitral regurgitation is a holocystolic murmur heard at the apex. Question 7. When symptomatic, what is the most common symptom of mitral valve prolapse? A. Chest pain B. Vertigo C. Lightheadedness D. Palpitations Answer D. The most common symptom in patients with symptoms of MVP is palpitations. Question 8. What is the most common cause of aortic stenosis in a person aged 50 years in a developed country? A. Rheumatic fever B. Bicuspid aortic valve C. Williams syndrome D. Aortic sclerosis Answer B. The most common cause of aortic stenosis in a young person is having a bicuspid aortic valve from birth. Question 9. What is not part of the symptom triad present with aortic stenosis? A. Palpitations B. Syncope C. Chest pain D. Dyspnea Answer A. Each of these is a part of the aortic stenosis triad of symptoms except for the palpitations which is not one of these symptoms. Question 10. What murmur can be heard in tricuspid insufficiency? A. Decrescendo diastolic murmur B. Short systolic murmur C. Holosystolic murmur D. Split S2 without murmur Answer C. The main murmur heard in tricuspid insufficiency is a holosystolic murmur heard best over the lower left sternal border.
