Symptoms, Diagnosis, Treatment.docx

- Aortic Stenosis Signs & symptoms Aortic valve stenosis ranges from mild to severe. Aortic valve stenosis signs and symptoms generally develop when narrowing of the valve is severe. Some people with aortic valve stenosis may not experience symptoms for many years. Signs and symptoms of aortic valve stenosis may include: 

Abnormal heart sound (heart murmur) heard through a stethoscope

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Chest pain (angina) or tightness with activity

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Feeling faint or dizzy or fainting with activity

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Shortness of breath, especially when you have been active

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Fatigue, especially during times of increased activity

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Heart palpitations — sensations of a rapid, fluttering heartbeat

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Not eating enough (mainly in children with aortic valve stenosis)

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Not gaining enough weight (mainly in children with aortic valve stenosis)

The heart-weakening effects of aortic valve stenosis may lead to heart failure. Heart failure signs and symptoms include fatigue, shortness of breath, and swollen ankles and feet.

Diagnosis 

Echocardiography

Diagnosis of aortic stenosis is suspected clinically and confirmed by echocardiography. Two-dimensional transthoracic echocardiography is used to identify a stenotic aortic valve and possible causes, to quantify LV hypertrophy and degree of systolic dysfunction, and to detect coexisting valvular heart disorders (aortic regurgitation, mitral valve disorders) and complications (eg, endocarditis). Doppler echocardiography is used to quantify degree of stenosis by measuring jet velocity, transvalvular systolic pressure gradient, and aortic valve area.

Cardiac catheterization is necessary prior to intervention to determine whether coronary artery disease (CAD) is the cause of angina and, occasionally, to resolve inconsistency between clinical and echocardiographic findings. ECG typically shows changes of LV hypertrophy with or without an ischemic ST- and T-wave pattern. Chest x-ray findings may include calcification of the aortic cusps (seen on the lateral projection or on fluoroscopy) and evidence of HF. Heart size may be normal or only mildly enlarged. In asymptomatic patients with severe aortic stenosis, closely supervised exercise ECG testing is recommended in an attempt to elicit symptoms of angina, dyspnea, or hypotension—any of these symptoms, when due to the AS, is an indication for intervention. Failure to normally increase BP and development of ST segment depression are less predictive of adverse prognosis. Exercise testing is contraindicated in symptomatic patients. When there is LV dysfunction and the aortic valve gradient is low but the valve area is small, then low-dose dobutamine stress echocardiography distinguishes lowgradient AS from pseudostenosis.

Treatment 

Sometimes aortic valve replacement

Nothing has yet been proved to slow the progression of aortic stenosis. In randomized trials, statin therapy has been ineffective. Drugs that can cause hypotension (eg, nitrates) should be used cautiously, although nitroprussidehas been used as a temporizing measure to reduce afterload in patients with decompensated heart failure in the hours before valve replacement. Patients who develop heart failure but are too high risk for valve intervention benefit from cautious treatment with digoxin, diuretics, and ACE inhibitors. Timing of intervention The benefits of intervention do not outweigh the risks until patients develop symptoms and/or meet certain echocardiographic criteria. Thus, patients should have periodic clinical evaluations, including echocardiography and sometimes exercise testing, to determine the optimal time for valve replacement. Valve replacement is recommended for the following: Symptomatic patients (including those with symptoms or reduced effort tolerance on exercise testing) with 

Severe aortic stenosis

Asymptomatic patients with any one of the following: 

LV EF < 50%

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Moderate or severe AS when undergoing cardiac surgery for other reasons

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Abnormal exercise test showing a fall in blood pressure below baseline

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If surgical risk is low, then surgery may be considered if there is very severe AS, severe pulmonary hypertension without other explanation, or severe valve calcification with rapid progression

Choice of intervention Balloon valvotomy is used primarily in children and very young adults with congenital AS. In older patients who are not candidates for surgery, balloon valvuloplasty may be used as a bridge to valve replacement but this procedure has a high complication rate and provides only temporary relief. Surgical aortic valve replacement (SAVR) is the best choice for patients < 75 yr of age and for low-risk surgical patients. Transcatheter (percutaneous) valve replacement (TAVR)benefits patients with inoperable aortic stenosis (1) and patients > 75 yr of age at high surgical risk (2). The data are now extending this benefit to patients with intermediate risk (3, 4).( Surgery usually involves replacement with a mechanical or bioprosthetic valve, but in younger patients, the patient’s own pulmonic valve can be used, and a bioprosthesis is then used to replace the pulmonic valve (Ross procedure). Preoperative evaluation for CAD is indicated so that CABG and valve replacement, if indicated, can be done during the same procedure. An aortic bioprosthetic valve requires anticoagulation for 3 to 6 mo postoperatively, but a mechanical valve requires lifetime anticoagulation using warfarin. Newer directacting oral anticoagulants (DOAC) are ineffective and should not be used (see also Anticoagulation for patients with a prosthetic cardiac valve).

- Aortic Regurgitation Signs & Symptoms Most often, aortic valve regurgitation develops gradually, and your heart compensates for the problem. You may have no signs or symptoms for years, and you may even be unaware that you have the condition. However, as aortic valve regurgitation worsens, signs and symptoms may include: 

Fatigue and weakness, especially when you increase your activity level

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Shortness of breath with exercise or when you lie down

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Swollen ankles and feet

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Chest pain (angina), discomfort or tightness, often increasing during exercise

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Lightheadedness or fainting

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Irregular pulse (arrhythmia)

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Heart murmur

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Sensations of a rapid, fluttering heartbeat (palpitations)

Diagnosis 

Echocardiography

Diagnosis of aortic regurgitation is suspected based on history and physical examination findings and confirmed by echocardiography. Doppler echocardiography is the test of choice to detect and quantify the magnitude of regurgitant blood flow and grade overall severity of the AR. Two-dimensional echocardiography can quantify aortic root size and anatomy and LV function.

Echocardiography can also assess severity of pulmonary hypertension secondary to LV failure, detect vegetations or pericardial effusions (eg, in aortic dissection), and provide information about prognosis. Coarctation is associated with bicuspid valve and is detected by placing the ultrasound transducer at the suprasternal notch. Transesophageal echocardiography provides additional delineation of aortic dilatation and valve anatomy, which is especially useful when surgical repair is being considered. If the aorta is enlarged, gated CT or MRI is recommended to evaluate the entire thoracic aorta. MRI also can help assess LV function and degree of AR when echocardiographic images are suboptimal. ECG and chest x-ray should be done. ECG may show repolarization abnormalities with or without QRS voltage criteria of LV hypertrophy, left atrial enlargement, and T-wave inversion with ST-segment depression in precordial leads. Chest x-ray may show cardiomegaly and a prominent aortic root in patients with chronic progressive AR. If AR is severe, signs of pulmonary edema and HF may also be present. Exercise testing may help assess functional capacity and symptoms in patients with documented AR and equivocal symptoms.

Coronary angiography should be done before surgery, even if no angina is present because about 20% of patients with severe AR have significant CAD, which may need concomitant coronary artery bypass graft surgery. First-degree relatives of patients with a bicuspid valve should be screened using echocardiography because 20 to 30% will be similarly affected.

Treatment 

Aortic valve replacement or repair

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Sometimes vasodilators, diuretics, and nitrates

When aortic root dilatation is part of the mechanism of aortic regurgitation, angiotensin-receptor blockers may slow progression, making them favored drugs for patients with concomitant hypertension. Intervention is either surgical aortic valve replacement or (less commonly) valve repair. Percutaneous options are being developed. An aortic bioprosthetic valve requires anticoagulation for 3 to 6 mo postoperatively, but a mechanical valve requires lifetime anticoagulation using warfarin. Direct-acting oral anticoagulants (DOAC) are ineffective and should not be used Patients who are not candidates for surgery benefit from treatment of HF. Intra-aortic balloon pump insertion is contraindicated because the diastolic balloon inflation worsens AR. Beta-blockers should be used with caution because they block compensatory tachycardia and worsen AR by prolonging diastole. Patients with severe AR who do not meet the criteria for intervention should be reevaluated by physical examination and echocardiography every 6 to 12 mo. Antibiotic prophylaxis against endocarditis is no longer recommended for aortic regurgitation except for patients who have had valve replacement Intervention is indicated when 

AR is severe and is causing symptoms

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AR is severe and is causing LV dysfunction (EF < 50%, LV end-systolic dimension > 50 mm, or LV end-diastolic dimension > 65 to 75 mm)

Sometimes, intervention is done before AR becomes severe if the ascending aorta is dilated > 55 mm (> 50 mm in patients with Marfan syndrome and maybe for bicuspid aortic valve). When cardiac surgery is done for other indications, concomitant aortic valve intervention is indicated if AR is moderate or severe.

- Pulmonary Stenosis Signs & Symptoms Many children with pulmonic stenosis remain asymptomatic for years and do not present to a physician until adulthood. Even then many patients remain asymptomatic. When symptoms of pulmonic stenosis develop, they resemble those of aortic stenosis (syncope, angina, dyspnea). Visible and palpable signs reflect the effects of right ventricular (RV) hypertrophy and include a prominent jugular venous a wave (due to forceful atrial contraction against a hypertrophied RV), an RV precordial lift or heave, and a left parasternal systolic thrill at the 2nd intercostal space. Auscultation 

Widened S2 and delayed P2

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Harsh crescendo-decrescendo ejection murmur

On auscultation, the 1st heart sound (S1) is normal and the normal splitting of the 2nd heart sound (S2) is widened because of prolonged pulmonic ejection (P2, the pulmonic component of S2, is delayed). In RV failure and hypertrophy, the 3rd and 4th heart sounds (S3 and S4) are rarely audible at the left parasternal 4th intercostal space. A click in congenital PS is thought to result from abnormal ventricular wall tension. The click occurs early in systole (very near S1) and is not affected by hemodynamic changes. A harsh crescendo-decrescendo ejection murmur is audible and is heard best at the left parasternal 2nd (valvular stenosis) or 4th (infundibular stenosis) intercostal space with the diaphragm of the stethoscope when the patient leans forward. Unlike the aortic stenosis murmur, a pulmonic stenosis murmur does not radiate, and the crescendo component lengthens as stenosis progresses. The murmur grows louder immediately with Valsalva release and with inspiration; the patient may need to be standing for this effect to be heard.

Diagnosis 

Echocardiography

Diagnosis of pulmonic stenosis is confirmed by Doppler echocardiography, which can characterize the severity as 

Mild: Peak gradient < 36 mm Hg

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Moderate: Peak gradient 36 to 64 mm Hg

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Severe: Peak gradient > 64 mm Hg

ECG may be normal or show RV hypertrophy or right bundle branch block. Right heart catheterization is indicated only when 2 levels of obstruction are suspected (valvular and infundibular), when clinical and echocardiographic findings differ, or before intervention is done.

Treatment

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Sometimes balloon valvuloplasty

Prognosis of pulmonic stenosis without treatment is generally good and improves with appropriate intervention. Treatment of pulmonic stenosis is balloon valvuloplasty, indicated for symptomatic patients and asymptomatic patients with normal systolic function and a peak gradient > 40 to 50 mm Hg. Percutaneous valve replacement may be offered at highly selected congenital heart centers, especially for younger patients or those with multiple previous procedures, in order to reduce the number of open heart procedures. When surgical replacement is necessary, bioprosthetic valves are preferred due to the high rates of thrombosis of right-sided mechanical heart valves; anticoagulation is temporarily required (see Anticoagulation for patients with a prosthetic cardiac valve).

- Pulmonary Regurgitation Signs & Symptoms Pulmonic regurgitation is usually asymptomatic. A few patients develop symptoms and signs of RV dysfunction–induced HF. In RV failure, the most common symptoms are ankle swelling and fatigue. Sometimes patients feel a sensation of fullness in the abdomen or neck. Palpable signs are attributable to pulmonary hypertension and RV hypertrophy. They include a palpable pulmonic component (P2) of the 2nd heart sound (S2) at the left upper sternal border and a sustained RV impulse that is increased in amplitude at the left middle and lower sternal border. Auscultation 

High-pitched, early diastolic decrescendo murmur

On auscultation, the 1st heart sound (S1) is normal. The S2 may be split or single. When split, P2may be loud and audible shortly after the aortic component of S2 (A2) because of pulmonary hypertension, or P2 may be delayed because of increased RV stroke volume. S2 may be single because of prompt pulmonic valve closing with a merged A2-P2 or, rarely, because of congenital absence of the pulmonic valve. An RV 3rd heart sound (S3), 4th heart sound (S4), or both may be audible with RV dysfunction– induced HF or RV hypertrophy; these sounds can be distinguished from left ventricular heart sounds because they are located at the left parasternal 4th intercostal space and because they grow louder with inspiration. The murmur of PR due to pulmonary hypertension is a high-pitched, early diastolic decrescendo murmur that begins with P2 and ends before S1 and that radiates toward the mid-right sternal edge (Graham Steell murmur); it is heard best at the left upper sternal border with the diaphragm of the stethoscope while the patient holds the breath at end-expiration and sits upright. The murmur of PR without pulmonary hypertension is shorter, lower-pitched (rougher in quality), and begins after P2. Both murmurs may resemble the murmur of aortic regurgitation but can be

distinguished by inspiration (which makes the PR murmur louder) and by Valsalva release. After Valsalva release, the PR murmur immediately becomes loud (because of immediate venous return to the right side of the heart), but the aortic regurgitation murmur requires 4 or 5 beats to do so. Also, a soft PR murmur may sometimes become even softer during inspiration because this murmur is usually best heard at the 2nd left intercostal space, where inspiration pushes the stethoscope away from the heart. In some forms of congenital heart disease, the murmur of severe PR is quite short because the pressure gradient between the pulmonary artery and the right ventricle equalizes rapidly in diastole.

Diagnosis 

Echocardiography

Pulmonic regurgitation is usually incidentally detected during a physical examination or Doppler echocardiography done for other reasons. Mild PR is a normal echocardiographic finding that requires no action. An ECG and chest x-ray are usually obtained. ECG may show signs of RV hypertrophy; chest x-ray may show RV enlargement and evidence of conditions underlying pulmonary hypertension.

Treatment 

Treatment of cause

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Rarely valve replacement

Treatment is management of the condition causing pulmonic regurgitation. Pulmonic valve replacement is an option if symptoms and signs of RV dysfunction–induced heart failure develop, but outcomes and risks are unclear because the need for replacement is so infrequent.

- Tricuspid Stenosis Signs & Symptoms The only symptoms of severe tricuspid stenosis are fluttering discomfort in the neck (due to giant a waves in the jugular pulse), fatigue and cold skin (due to low cardiac output), and right upper quadrant abdominal discomfort (due to an enlarged liver). The primary visible sign is a giant flickering a wave with gradual y descent in the jugular veins. Jugular venous distention may occur, increasing with inspiration (Kussmaul sign). The face may become dusky and scalp veins may dilate when the patient is recumbent (suffusion sign). Hepatic congestion and peripheral edema may occur. Auscultation 

Soft opening snap

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Mid-diastolic rumble with presystolic accentuation

On auscultation, tricuspid stenosis is often inaudible but may produce a soft opening snap and a middiastolic rumble with presystolic accentuation. The murmur becomes louder and longer with maneuvers that increase venous return (exercise, inspiration, leg-raising, Müller maneuver) and softer and shorter with maneuvers that decrease venous return (standing, Valsalva maneuver). Findings of tricuspid stenosis often coexist with those of mitral stenosis and are less prominent. The murmurs can be distinguished clinically

Diagnosis 

Echocardiography

Diagnosis of tricuspid stenosis is suspected based on history and physical examination and confirmed by Doppler echocardiography showing a pressure gradient across the tricuspid valve. Severe tricuspid stenosis is signified by a mean forward gradient across the valve > 5 mm Hg. Two-dimensional echocardiography shows thickened leaflets with reduced movement and RA enlargement. ECG may show RA enlargement out of proportion to RV hypertrophy and tall, peaked P waves in inferior leads and V1. Chest x-ray may show a dilated superior vena cava and RA enlargement, indicated by an enlarged right heart border. Liver enzymes are elevated because of passive hepatic congestion. Cardiac catheterization is rarely indicated for evaluation of tricuspid stenosis. When catheterization is indicated (eg, to evaluate coronary anatomy), findings include elevated RA pressure with a slow fall in early diastole and a diastolic pressure gradient across the tricuspid valve.

Treatment 

Diuretics and aldosterone antagonists

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Rarely valve repair or replacement

Evidence to guide treatment of tricuspid stenosis is scarce. Symptomatic patients not undergoing intervention should receive a low-salt diet, diuretics, and aldosterone antagonists. Patients with severe tricuspid stenosis should undergo intervention if they are symptomatic or if cardiac surgery is being done for other reasons. Percutaneous balloon tricuspid commissurotomy might be considered for severe TS without accompanying tricuspid regurgitation.

- Tricuspid Regurgitation Signs & Symptoms Tricuspid valve regurgitation often doesn't cause signs or symptoms until the condition is severe. You may be diagnosed with this condition when having tests for other conditions. Noticeable signs and symptoms of tricuspid valve regurgitation may include: 

Fatigue

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Declining exercise capacity

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Swelling in your abdomen, legs or veins in your neck

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Abnormal heart rhythms

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Pulsing in your neck

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Shortness of breath with activity

You may also notice signs or symptoms of the underlying condition that's causing tricuspid valve regurgitation, such as pulmonary hypertension. Pulmonary hypertension symptoms may include fatigue, weakness, difficulty exercising and shortness of breath.

Diagnosis Echocardiography Mild tricuspid regurgitation is most often detected on echocardiography done for other reasons. More moderate or severe TR may be suggested by history and physical examination. Confirmation is by echocardiography.

Severe TR is characterized echocardiographically by ≥ 1 of the following:      

2-Dimensional failure of coaptation or flail Large regurgitant jet on color Doppler Large flow convergence zone proximal to the valve Vena contracta width > 7 mm Systolic flow reversal in the hepatic veins (specific for severe TR) Transtricuspid E wave dominant > 1 cm/sec

Dense, triangular, early peaking, continuous wave Doppler of TR jet When TR is moderate or severe, the peak regurgitant velocity will underestimate pulmonary pressure. Two-dimensional echocardiography detects the structural abnormalities present in primary TR. Cardiac MRI is now the preferred method for evaluating RV size and function, which typically should be done when echocardiographic image quality is inadequate. An ECG and chest x-ray are often done. ECG is usually normal but, in advanced cases, may show tall peaked P waves caused by right atrial enlargement, a tall R or QR wave in V1 characteristic of RV hypertrophy, or AF. Chest x-ray is usually normal but, in advanced cases with RV hypertrophy or RV dysfunction– induced HF, may show an enlarged superior vena cava, an enlarged right atrial or RV silhouette (behind the upper sternum in the lateral projection), or pleural effusion. Laboratory testing is not needed but if done may show hepatic dysfunction in patients with severe TR Cardiac catheterization is indicated for accurate measurement of pulmonary pressure when TR is severe and to evaluate coronary anatomy when surgery is planned. Catheterization findings include a prominent right atrial c-v pressure wave during ventricular systole.

Treatment 

Treatment of cause

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Sometimes annuloplasty or valve repair or replacement

Very mild tricuspid regurgitation is a normal finding and requires no action. Medical treatment of causes (eg, HF, endocarditis) is indicated. Patients with severe tricuspid regurgitation should undergo operation as soon as symptoms are present despite medical treatment or when there is moderate, progressive RV enlargement or dysfunction. During surgery for left-sided heart lesions, moderate or mild TR with dilated annulus > 40 mm should also undergo repair.

Surgical options include 

Annuloplasty

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Valve repair

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Valve replacement

Annuloplasty, in which the tricuspid valve annulus is sutured to a prosthetic ring or a tailored reduction in annulus circumferential size is done, is indicated when TR is due to annular dilation. Valve repair or replacement is indicated when TR is due to primary valve abnormalities or when annuloplasty is not technically feasible. Tricuspid valve replacement is indicated when TR is due to carcinoid syndrome or Ebstein anomaly. A bioprosthetic valve is used to reduce the risk of thromboembolism associated with the low pressures of the right heart; in the right heart, unlike the left heart, bioprosthetic valves last > 10 yr. A bioprosthetic valve requires temporary anticoagulation (see also Anticoagulation for patients with a prosthetic cardiac valve).

- Mitral Stenosis Signs & Symptoms You may feel fine with mitral valve stenosis, or you may have minimal symptoms for decades. Mitral valve stenosis usually progresses slowly over time. See your doctor if you develop: 

Shortness of breath, especially with exertion or when you lie down

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Fatigue, especially during increased physical activity

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Swollen feet or legs

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Heart palpitations — sensations of a rapid, fluttering heartbeat

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Dizziness or fainting

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Coughing up blood

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Chest discomfort or chest pain

Mitral valve stenosis symptoms may appear or worsen anytime your heart rate increases, such as during exercise. An episode of rapid heartbeats may accompany these symptoms. Or they may be triggered by pregnancy or other body stress, such as an infection. In mitral valve stenosis, pressure that builds up in the heart is then sent back to the lungs, resulting in fluid buildup (congestion) and shortness of breath. Symptoms of mitral valve stenosis most often appear in between the ages of 15 and 40 in developed nations, but they can occur at any age — even during childhood.

Mitral valve stenosis may also produce signs that your doctor will find during your examination. These may include: 

Heart murmur

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Fluid buildup in the lungs

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Irregular heart rhythms (arrhythmias)

Diagnosis 

Echocardiography

Diagnosis of mitral stenosis is suspected clinically and confirmed by echocardiography. Typically, 2dimensional echocardiography shows abnormal valve and subvalve structures. It also provides information about the degree of valvular calcification and stenosis and LA size. Doppler echocardiography provides information about the transvalvular gradient and pulmonary artery pressure. The normal area of the mitral valve orifice is 4 to 5 cm2. Severity is characterized echocardiographically as 

Moderate: Valve area 1.5 to 2.5 cm2

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Severe: Valve area < 1.5 cm2; symptoms are often present

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Very severe: Valve area < 1.0 cm2

However, the relationship between the area of the valve orifice and symptoms is not always consistent. Color Doppler echocardiography detects associated MR. Transesophageal echocardiography can be used to detect or exclude small LA thrombi, especially those in the LA appendage, which usually cannot be seen transthoracically. An ECG and chest x-ray are usually obtained. The ECG may show LA enlargement, manifest as a P wave lasting > 0.12 msec with prominent negative deflection of its terminal component (duration: > 0.04 msec; amplitude: > 0.10 mV) in V1; broad, notched P waves in lead II; or both. Right axis QRS deviation and tall R waves in V1 suggest RV hypertrophy. Chest x-ray usually shows straightening of the left cardiac border due to a dilated LA appendage, and widening of the carina. With barium in the esophagus, the lateral chest x-ray will show the dilated LA displacing the esophagus posteriorly. The main pulmonary artery (trunk) may be prominent; the descending right pulmonary artery diameter is ≥ 16 mm if pulmonary hypertension is significant. The upper lobe pulmonary veins may be dilated. A double shadow of an enlarged LA may be seen along the right cardiac border. Horizontal lines in the lower posterior lung fields (Kerley B lines) indicate interstitial edema associated with high LA pressure. Cardiac catheterization, indicated only for perioperative assessment of coronary artery disease (CAD) before surgical repair, can confirm elevated LA and pulmonary artery pressures, mitral gradient and valve area.

Treatment 

Diuretics and sometimes beta-blockers or calcium channel blockers

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Anticoagulation for AF



Commissurotomy or valve replacement

Asymptomatic patients with mitral stenosis require no treatment other than appropriate prophylaxis against rheumatic fever recurrence. Mildly symptomatic patients usually respond to diuretics and, if sinus tachycardia or AF is present, to beta-blockers or calcium channel blockers, which can control ventricular rate. Anticoagulation with a vitamin K antagonist (not a direct-acting oral anticoagulant [DOAC]) is indicated to prevent thromboembolism if patients have or have had AF, embolism, or a left atrial clot. Anticoagulation may also be considered in the presence of dense spontaneous contrast or an enlarged left atrium (M-mode diameter > 50 mm). All patients should be encouraged to continue at least low levels of physical exercise despite exertional dyspnea. Antibiotic prophylaxis against endocarditis is no longer recommended except for patients who have had valve replacement (see table: Recommended Endocarditis Prophylaxis During Oral-Dental or Respiratory Tract Procedures). Timing of intervention For moderate mitral stenosis, intervention may be indicated when there is ≥ 1 of the following: 

Cardiac surgery is required for other indications



Patients are symptomatic and have exercise-induced mean transmitral gradient > 15 mm Hg or pulmonary capillary occlusion pressure > 25 mm Hg

For severe mitral stenosis, intervention is indicated when there is ≥ 1 of the following: 

Any symptoms if the valve is suitable for percutaneous balloon commissurotomy (may be considered in asymptomatic patients)



Cardiac surgery is required for other indications

For very severe mitral stenosis, intervention is indicated for all patients (with or without symptoms) who are suitable candidates for percutaneous balloon commissurotomy. Choice of intervention Percutaneous balloon commissurotomy is the procedure of choice for younger patients and for patients without heavily calcified valve commissures, subvalvular distortion, LA thrombi, or severe MR. In this fluoroscopic- and echocardiographic-guided procedure, a transvenous catheter with an inflatable distal balloon is passed transseptally from the right atrium to the LA and inflated to separate fused mitral valve commissures. Outcomes are equivalent to those of more invasive procedures. Complications are uncommon but include MR, embolism, and tamponade.

Surgical commissurotomy may be used in patients with severe subvalvular disease, valvular calcification, or LA thrombi. In this procedure, fused mitral valve leaflets are separated using a dilator passed through the left ventricle (closed commissurotomy) via a thoracotomy, or by direct vision (open commissurotomy) via a sternotomy. Choice of procedure is based on surgeon’s experience and the morphology of the valve, although closed valvotomy is now done less frequently in Western countries. Because of its greater risks, surgery is usually deferred until symptoms reach New York Heart Association class III (see table: NYHA Classification of Heart Failure). During surgery, some clinicians ligate the left atrial appendage to reduce thromboembolism. Valve replacement is confined to patients with severe morphologic changes that make the valve unsuitable for balloon or surgical commissurotomy. Lifelong anticoagulation with warfarin is required in patients with a mechanical valve to prevent thromboembolism. A mitral bioprosthetic valve requires anticoagulation with warfarin for 3 to 6 mo postoperatively (see also Anticoagulation for patients with a prosthetic cardiac valve). Direct-acting oral anticoagulants (DOAC) are ineffective and should not be used. When the etiology is annular calcification, there is no benefit from percutaneous balloon commissurotomy because there is no commissural fusion. Furthermore, surgical valve replacement is technically demanding because of the annular calcification and often high risk because many patients are elderly and have comorbidities. Therefore, intervention is delayed until symptoms become severe despite use of diuretic and rate control drugs. Preliminary experience in inoperable patients suggests benefit from transcatheter implantation of a transcatheter aortic valve replacement (TAVR) bioprosthesis in the mitral position.

- Mitral Regurgitation Signs & Symptoms Acute mitral regurgitation causes the same symptoms and signs as acute heart failure (dyspnea, fatigue, weakness, edema) and cardiogenic shock (hypotension with resultant multisystem organ damage).Specific signs of mitral regurgitation may be absent. Chronic mitral regurgitation in most patients is initially asymptomatic, and symptoms develop insidiously as the LA enlarges, pulmonary artery pressure and venous pressure increase, and LV compensation fails. Symptoms include dyspnea, fatigue (due to heart failure), orthopnea, and palpitations (often due to atrial fibrillation). Rarely, patients present with endocarditis (eg, fever, weight loss, embolic phenomena). Signs develop only when mitral regurgitation becomes moderate to severe. Inspection and palpation may detect a brisk apical impulse and sustained left parasternal movement due to systolic expansion of an enlarged LA. An LV impulse that is sustained, enlarged, and displaced downward and to the left suggests LV hypertrophy and dilation. A diffuse precordial lift occurs with severe MR because the LA enlarges, causing anterior cardiac displacement, and pulmonary hypertension causes right ventricular hypertrophy. A regurgitant murmur (or thrill) may also be palpable in severe cases.

On auscultation, the 1st heart sound (S1) may be soft (or occasionally loud). A 3rd heart sound (S3) at the apex reflects a dilated LV and severe MR. The cardinal sign of mitral regurgitation is a holosystolic (pansystolic) murmur, heard best at the apex with the diaphragm of the stethoscope when the patient is in the left lateral decubitus position. In mild MR, the systolic murmur may be abbreviated or occur late in systole.

Diagnosis 

Echocardiography

Diagnosis of mitral regurgitation is suspected clinically and confirmed by echocardiography. Doppler echocardiography is used to detect regurgitant flow and pulmonary hypertension. Two-dimensional or 3-dimensional echocardiography is used to determine the cause and severity of MR (see table: Grading of Mitral Regurgitation), the presence and extent of annular calcification, and the size and function of the LV and LA and to detect pulmonary hypertension. When it is acute, severe MR may not be apparent on color Doppler echocardiography, but suspicion is raised when acute heart failure is accompanied by hyperdynamic LV systolic function. If endocarditis or valvular thrombi are suspected, transesophageal echocardiography (TEE) can provide a more detailed view of the mitral valve and LA. TEE is also indicated when mitral valve repair instead of replacement is being considered to evaluate the mechanism of MR in more detail. An ECG and chest x-ray are usually obtained initially. ECG may show LA enlargement and LV hypertrophy with or without ischemia. Sinus rhythm is usually present when MR is acute because the atria have not had time to stretch and remodel. Chest x-ray in acute MR may show pulmonary edema; abnormalities in cardiac silhouette are not evident unless an underlying chronic disorder is also present. Chest x-ray in chronic MR may show LA and LV enlargement. It may also show pulmonary vascular congestion and pulmonary edema with heart failure. Cardiac catheterization is done before surgery, mainly to determine whether coronary artery disease (CAD) is present. A prominent systolic c-v wave is seen on pulmonary artery occlusion pressure (pulmonary capillary wedge pressure) tracings during ventricular systole. Ventriculography can be used to quantify MR. Cardiac MRI can accurately measure regurgitant fraction and determine the cause of dilated myopathy with MR. Periodic exercise testing (stress ECG ) is often done to detect any decrease in effort tolerance, which would prompt consideration of surgical intervention. Periodic echocardiography is done to detect progression of MR.