Amer SULEMAN MD,
Kazi IMRAN MAJEED MD,
Wajahat MIRZA MD,
Mahvash AMER MBBS.
Mitral stenosis is a condition in which the mitral valve leaflets become thickened and the commissures fused along with thickening and shortening of the chordae tendineae. Mitral Stenosis is the leading cause of congestive heart failure in developing countries.
Mitral stenosis is almost always the result of rheumatic fever 1. Isolated involvement of mitral valve occurs in 25% of cases 2 while an additional 40% case have combined mitral stenosis and regurgitation 3. The history of rheumatic fever may or may not be elicited. In patients with rheumatic fever antibiotic prophylaxis with benzathine penicillin or penicillin VK has been shown to prevent recurrence. 4,5. Less common causes include congenital mitral stenosis 6, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), atrial myxoma, malignant carcinoid 7 and bacterial endocarditis. (Table 1)
CAUSES OF ACQUIRED MITRAL STENOSIS (Table 1)
- Rheumatic Fever
- Malignant Sarcoid
- Active Infective Endocarditis
- Whipple's Disease
- Massive Annular Calcification
Pure mitral stenosis (MS) develops in approximately 40% of all patients with rheumatic heart disease. After an episode of rheumatic fever, the latency period is 10-20 years or more before the onset of symptoms. The hall mark of mitral stenosis is comissural fusion 8. The normal area of the mitral valve orifice is 4-6 sq. cm. When this orifice is reduced to 2 sq.cm, increased left atrial pressure (LAP) is necessary for normal transmitral flow. Critical MS occurs when the opening is reduced to 1 sq. cm. At this stage, elevated left atrial pressure (LAP) is required to maintain a normal cardiac output 9 . This increase in LAP raises pulmonary venous and capillary pressures,12 resulting in exertional dyspnea. As the disease progresses, chronic elevation of LAP leads to pulmonary hypertension, tricuspid and pulmonary incompetence and eventual right heart failure.
Progressive dilation of the left atrium predisposes to two further complications 9. One is the development of mural thrombi. These thrombi embolize in 20% of patients. Patients at high risk for embolization are: over 35 years old, those with atrial fibrillation with a low cardiac output and those having a large left atrial appendage. The other significant complication is the development of atrial fibrillation (Afib) which occurs in up to 40% of patients. Loss of atrial contraction with the development of Afib decreases cardiac output by 20%. Since cardiac output is related to heart rate, Afib with a rapid ventricular response decreases diastolic filling time and further compromises cardiac output. The left ventricular function is often normal 11.
In the U.S.: The prevalence of MS has decreased due to the decline in rheumatic fever in the US and developed countries. The mitral valve is the valve most commonly affected with rheumatic heart disease.
Internationally: In underdeveloped areas, MS tends to progress more rapidly. Occasionally, patients can become symptomatic before the age of 20.
Mortality/Morbidity: Without surgical intervention, the progressive nature of the disease
results in an 85% mortality rate twenty years after the onset of symptoms.
Sex: Two-thirds of all patients with MS are female.
Age: The onset of symptoms is usually between the third and fourth decades.
Mitral Stenosis is a progressive disease in most patients. As depicted in figure below an average of 19 years elapses before the onset of dyspnea.
Recognised MS Dyspnea Valve Replacement/PMBV
0 ------------Time in years--------19
Before the surgical era the outlook for patients with this disease was unfavourable. From 1925 Rowe et al 17studied 250 patients with mitral stenosis. By 10 years 39% of patients had died, 22% had become more dyspneic, and 16% had developed at least one thromboembolic complication. By 20 years, 79% had died 8% had become more symptomatic, and 26% had developed at least one thromboembolic event. Progression of disease is the rule at least in the symptomatic group. The younger patients follow a more benign course then their old counter parts .
The diagnosis of mitral stenosis is suspected on history and confirmed by physical examination, electrocardiography and echocardiography. Cardiac catheterization may aid the diagnosis and treatment in selected individuals.
- History of acute rheumatic fever, although many patients do not recall this.
- History of murmur
- Effort induced dyspnea is the most common complaint and is often triggered by exertion, fever, anemia, onset of atrial fibrillation or pregnancy.
- Orthopnea progressing to paroxysmal nocturnal dyspnea.
- Effort induced fatigue
- Hemoptysis, due to rupture of thin dilated bronchial veins, is a late finding.
- Chest pain may be due to right ventricular ischemia, concomitant coronary atherosclerosis or secondary to a coronary embolism.
- Thromboembolism may be the first symptom of MS.
- Recumbent cough
The physical exam findings depend on how advanced the disease is and the degree of underlying cardiac decompensation.
- Peripheral and facial cyanosis, can be seen more if the patient is polycythemic
- Jugular venous distention, with positive hepatojugular reflex
- Respiratory distress, evidence of pulmonary edema (rales, etc.)
- Diastolic thrill palpable over apex.
- The murmur of mitral stenosis is best heard at the apex with little radiation. It is nearly holodiastolic with pre-systolic accentuation due to the atrial kick. It is usually described as low-pitched, decrescendo, and rumbling, and can be heard best with the patient in the left lateral decubitus position. The murmur appears about 0.08 seconds after S2, and is heralded by an "opening snap". This is a brief, loud sound which is caused as the stenotic valve suddenly halts its normal opening at the start of diastole.
- Loud S1 followed by S2 and opening snap best heard at left sternal border. This is succeeded by a low pitched rumbling diastolic murmur best heard over the apex, with the patient in the left lateral decubitus position. This may diminish in intensity with increasing stenosis. This S1 becomes more pronounced after exercise13,14.
- The duration of the diastolic murmur, not the intensity, correlates with the severity of mitral narrowing 13.The holosystolic murmur of mitral regurgitation may accompany the valvular deformity of mitral stenosis.
- Digital clubbing
- Systemic embolization
- Signs of right heart failure in severe MS include ascites, hepatomegaly and peripheral edema. If pulmonary hypertension is present there may be a right ventricular lift, an increased pulmonic second sound and a high-pitched decrescendo diastolic murmur of pulmonary insufficiency (Graham Steele's murmur).
- May give diastolic murmur and left sided failure but left ventricle is enlarged and murmur is usually parasternal and high pitched
Chronic Obstructive Pulmonary Disease and Emphysema
- May have cyanosis and edema, and can occur with MS, Patients with MS are frequently diagnosed as asthmatics.
Other Problems to be Considered
- Atrial Myxoma
Complete blood count (CBC), in cases of hemoptysis and to rule out anemia
Blood culture, in cases of suspected endocarditis
Chest X-Ray (CXR):
- Signs of pulmonary overload:
- Prominence of pulmonary arteries,
- Enlargement of right ventricle and
- Evidence of CHF (interstitial edema with kerley B lines).
- Left atrial enlargement with straightening of the left heart border, double density seen on CXR and also menifested by elevation of the left mainstem bronchus
- Pulmonary venous pattern changes with redistribution of flow toward the apices Prominent pulmonary arteries at the hilum with rapid tapering
- Kerley's B line Pulmonary edema pattern (late)
- In sinus rhythm, enlarged left atrium is signified by a broad notched P wave most prominent in lead II, with a negative terminal force in V1 15,16
- With severe pulmonary hypertension, right axis deviation and right ventricular hypertrophy can be seen.
- Atrial fibrillation is a common but nonspecific finding in MS.
Transthoracic two dimensional echocardiography is the most sensitive and specific non-invasive method for diagnosing mitral stenosis 25. With 2 dimensional echocardiography mitral valve area can be calculated using different techniques. With two dimensional ECHO, the size of the mitral orifice can be measured along with cardiac chamber sizes. The addition of color Doppler can evaluate the transvalvular gradient, pulmonary artery pressure and accompanying mitral regurgitation 22. Different methods used for mitral valve area assessment 20 are in Table 2
measurement in short axis view
most reliable, operator dependant
Pressure half time
(P ½ )
P ½ =0.29 x Deceleration time
*MVA= 220/ P ½ time
Unreliable in conditions with elevated left ventricle end diastolic pressure
assumption blood flow through different valves is equal
D2 LVOT x 0.785x TVI LVOT
In regurgitant lesions reliability decreases
PISA (Proximal Isovelocity Surface Area)
MVA= 2 x 3.14 r 2 x V1
Very reliable, operator dependant
*= mitral valve area
Two dimensional echocardiography is also useful in qualitative assessment of the valve. It can also be used to assess whether the valve is suitable for percutaneous mitral balloon valvuloplasty. An MGH (Massachusetts General Hospital) score of greater then 8-10 signify a poor outcome. Please see table 3 for MGH criteria
Transesophageal echocardiography (TEE) is useful for detecting vegetations smaller than 5 mm or thrombi in the left atrium not seen with transthoracic echocardiography.
INDICATIONS FOR CARDIAC CATHETERIZATION 23
Males with age greater than 35 years
Post menopausal females
Positive risk factors
History of illicit cocaine use
Prior PMBV (Percutaneous Mitral Balloon Valvuloplasty
Strong clinical suspicion of coronary artery disease
Hemodynamic findings at the time of catheterization may include 12:
- Increased left atrial or pulmonary capillary wedge pressure (PCWP)
- Increased left atrial or PCWP to left ventricular pressure gradient
- Calculated mitral valve orifice area
- Calcified mitral valve
- Concomitant mitral regurgitations
- Presence of coronary artery disease (CAD)
Emergency Department Care: 24,26,27,28
- Digitalis is of little if any benefit in patients with MS in sinus rhythm.
- In patients with atrial fibrillation, digitalis can be effective in slowing the ventricular rate.
- The addition of a beta-blocker to digitalis may be needed to achieve a ventricular rate of 60-70.
- In patients in whom a beta-blocker is contraindicated, a calcium channel blocker such as diltiazem may be used.
Diuresis for signs of pulmonary edema
- Anticoagulation is helpful in preventing thrombus formation and embolization in patients with atrial fibrillation.
- When possible, a period of three to four weeks of anticoagulation should precede chemical or electrical cardioversion to minimize the risk of systemic embolization.
For known or suspected mitral stenosis with hemodynamic instability, arrhythmia or embolization.
For new onset or progression of symptoms.
The goal of medical therapy is to control the rapid ventricular rate. In atrial fibrillation, the drug of choice is digitalis, however, a beta-blocker or calcium channel blocker may need to be added.
Drug Name Digoxin (Lanoxin) -
It is the drug of choice for rapid atrial fibrillation. It is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the Cardiovascular system. Its effects on the myocardium involve both a direct action on cardiac muscle that increases myocardial systolic contractions and indirect actions that result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.
Loading dose: 0.25 mg IV q6 up to 1 mg
Maintenance dose: 0.125 mg-0.25 mg qd
Between 2-5 y: Load 30-40 ug/kg PO
Between 5-10 y: Load 20-35 ug/kg PO
Older than 10 y: Load 10-15 ug/kg PO
IV doses are 80% of po doses Maintenance dosing is 25-35% of po loading doses
Avoid use in patients with documented hypersensitivity to this medication or related products and those diagnosed with beriberi heart disease, idiopathic hypertrophic subaortic stenosis, or constrictive pericarditis, or carotid sinus syndrome.
Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate,erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil.
Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid.
C - Safety for use during pregnancy has not been established.
Exercise caution in patients with renal insufficiencies, and electrolyte abnormalities
Hypokalemia may reduce the positive inotropic effect of digitalis.
Calcium, if administered IV, may produce arrhythmias in digitalized patients. Hypercalcemia predisposes the patient to digitalis toxicity and hypocalcemia can make digoxin ineffective until serum calcium levels are normal.
Magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity. Patients diagnosed with incomplete A-V Block may progress to complete block when treated with digoxin. Exercise caution in patients diagnosed with hypothyroidism, hypoxia, and acute myocarditis.
Beta-Blockers - Inhibit chronotropic, inotropic and vasodilatory responses to beta-adrenergic stimulation.
Metoprolol (Lopressor) - It is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions.
During IV administration, carefully monitor blood pressure, heart rate and ECG.
5 mg IV and repeat in 10 min up to 15 mg
Safety and efficacy in children have not been established.
Avoid use in patients with documented hypersensitivity to this drug or related products and those diagnosed with uncompensated congestive heart failure, bradycardia, asthma, cardiogenic shock, and A-V conduction abnormalities.
Aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease its bioavailability and plasma levels, possibly resulting in a decreased pharmacologic effect. Conversely, haloperidol, hydralazine, loop diuretics, and MAO inhibitors may increase metoprolol levels and thus its toxicity or pharmacologic effects.
C - Safety for use during pregnancy has not been established.
Beta-adrenergic blockade may reduce the signs and symptoms of acute hypoglycemia and may decrease the clinical signs of hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm. Monitor the patient closely and withdraw the drug slowly.
During the IV administration, carefully monitor blood pressure, heart rate, and ECG.
Calcium Channel Blocker - In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers inhibit movement of calcium ions across the cell membrane depressing both impulse formation (automaticity) and conduction velocity.
Diltiazem (Cardizem CD, Cardizem SR, Tiazac, and Dilacor) - During the depolarization, it inhibits the calcium ion from entering the slow channels or the voltage-sensitive areas of the vascular smooth muscle and myocardium.
0.25 mg/kg IV over 2 min.
Rebolus after 15 min if needed with 0.35 mg/kg.
Safety and efficacy in children have not been established.
Avoid use in patients with documented hypersensitivity to this drug or related products and in those diagnosed with severe CHF, sick sinus syndrome or second- or third-degree AV block, and hypotension (less than 90 mm Hg systolic).
Diltiazem may increase carbamazepine, digoxin, and cyclosporine levels when administered concurrently. Diltiazem, when administered concurrently with amiodarone, can cause bradycardia and a decrease in cardiac output. Similarly, diltiazem when administered concurrently with beta blockers may increase cardiac depression.
Cimetidine may increase diltiazem levels.
Diltiazem may increase theophylline levels.
C - Safety for use during pregnancy has not been
Exercise caution when administering to patients with impaired renal or hepatic function. Diltiazem may increase LFTs and hepatic injury may occur.
Further Inpatient Care:
- Cardiac catheterization is the ultimate method for detecting pressure gradient across the mitral valve, pulmonary artery pressure, associated mitral regurgitation, left ventricular function and coexistent atherosclerosis.
- It is often performed preoperatively in elderly patients with a history of angina or signs of severe MS clinically and by echocardiography.
- Balloon valvulotomy results in a decline in LAP and a prominent and sustained symptomatic improvement. Most commonly used in young patients without extensive valvular calcification, pregnant women or poor operative candidates.
- Mitral valve replacement is performed if leaflets are immobile, heavily calcified or if there is severe subvalvular scarring. Bioprosthetic or artificial mechanical valves can be used as replacements. The operative mortality is 1-2% for mitral commissurotomy and 2-5% for mitral valve replacement.
Bacterial endocarditis prophylaxis for dental and invasive procedures must be continued for life. Appropriate treatment of streptococcal pharyngitis to lessen the occurrence of rheumatic fever should be instituted promptly. Prophylaxis against recurrent streptococcal infection (and recurrent rheumatic fever) in patients with a history of rheumatic fever should be given for at least 25 years
- Thromboembolism 21
- Recurrent rheumatic fever
- Bacterial endocarditis
- Pulmonary hypertension
- Pulmonary edema
- Complications of balloon valvulotomy (e.g., stroke, cardiac perforation, development of mitral regurgitation).
- Complications of mitral valve replacement (e.g., paravalvular leakage, thromboemboli, infective endocarditis, mechanical dysfunction or bleeding due to anticoagulants).
Severity of disease is underestimated during periods of tachycardia because a decrease in cardiac output leads to a decrease in the intensity of the murmur. Failure to give patients with mitral valve disease antibiotic prophylaxis for beta-hemolytic streptococcal infections and prophylaxis for infective endocarditis. Failure to aggressively treat anemia or infections in patients with MS.
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TOP TEN SUGGESTED READINGS
1) Segal BL; Likoff W; Kingsley B. Echocardiography: Clinical application in mitral stenosis. JAMA, 193:161, 1966. Early description of the M-mode findings for mitral stenosis.
2) Nichol PM; Gilbert BW; Kisslo JA. Two-dimensional echocardiographic assessment of mitral stenosis. Circulation, 55:120, 1977. Initial article detailing the advantage of two-dimensional echocardiography in assessing the presence and severity of rheumatic mitral stenosis.
3) Holen J; Aaslid R; Landmark K; Simonsen S. Determination of pressure gradient in mitral stenosis with a non-invasive ultrasound Doppler technique. Acta Med Scand 199:455-460, 1976. Original description of Doppler measurement of transmitral pressure gradients.
4) David D; Lang RM; Marcus RH; et al. Doppler echocardiographic estimation of transmitral pressure gradients in mitral stenosis. Am J Cardiol 67:1161-1164, 1991. Detailed study of pressure-velocity relations across the stenotic mitral valve.
5) Libanoff AJ; Rodbard S. Evaluation of the severity of mitral stenosis and regurgitation. Circulation 33:218-226, 1966. Original description of pressure half-time with catheterization data.
6) Hatle L; Angelsen B; Tromsdal A. Non-invasive assessment of atrioventricular pressure half-time by Doppler ultrasound. Circulation 60:1096-1104, 1979. Application of pressure half-time concept to Doppler data.
7) Thomas JD; Wilkins GT; Choong CYP; et al. Inaccuracy of mitral pressure half- time immediately after percutaneous mitral valvotomy: Dependence on transmitral gradient and left atrial and ventricular compliance. Circulation 78:980-993, 1988. Evaluation of pressure half-time before and after mitral balloon commissurotomy illustrating reciprocal changes in left atrial and left ventricular compliance after valvuloplasty.
8) Rodriguez L. Validation of the proximal flow convergence method: Calculation of orifice area in patients with mitral stenosis. Circulation, in press. Application of the PISA method to determine mitral valve area.
9) Nakatani S; Masuyama T; Kokama K; Kitabatake A; Fujii K; Kamada T. Value and limitations of Doppler echocardiography in the quantification of stenotic mitral valve area: Comparison of the pressure half-time and the continuity equation methods. Circulation, 77-78, 1988. Important article describing the utility of the continuity equation to determine mitral valve area in rheumatic mitral stenosis.
10) Braverman AC; Thomas HD; Lee RT. Doppler echocardiographic estimation of mitral valve area during changing hemodynamic conditions. The article explains the effect of exercise on Doppler values of peak velocity, pressure half-time and mitral valve area as determined by the continuity equation and pressure half-time methods.
FOR THE EXPERTS:
Keren G; Pardes A; Miller HI; Scherez H; Laniado S. Pulmonary venous flow determined by Doppler echocardiography in mitral stenosis. Am J Cardiol 65:246, 1990.
First published 27.3.2000