MITRAL STENOSIS

Amer SULEMAN MD,
Kazi IMRAN MAJEED MD,
Wajahat MIRZA MD,
Mahvash AMER MBBS.

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INTRODUCTION

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
• SLE
• Malignant Sarcoid
• Mucopolysacchrhidosis
• Active Infective Endocarditis
• Gout
• Whipple's Disease
• Massive Annular Calcification

 Pathophysiology:

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.

Epidemiology:

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.

Natural History:

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

I--------------------I-------------------I------------------I------------------I Death

Rheumatic Fever

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 .

DIAGNOSIS :

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:

• 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.
• Palpitations
• Recumbent cough

Physical:

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 exercise^13,14.
• 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).

DIFFERENTIAL DIAGNOSIS

Aortic Regurgitation

• 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

Laboratory Studies:

Complete blood count (CBC), in cases of hemoptysis and to rule out anemia

Blood culture, in cases of suspected endocarditis

Electrolytes

Imaging Studies:

Chest X-Ray (CXR):

• Signs of pulmonary overload:

1. Prominence of pulmonary arteries,
2. Enlargement of right ventricle and
3. 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)

Electrocardiogram (EkG):

• 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.

 

Echocardiography:

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

 

TABLE 2

 

TECHNIQUE	METHOD	REMARKS
Direct measurement	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
Continuity Equation	assumption blood flow through different valves is equal MVA= D2 LVOT x 0.785x TVI LVOT TVI MV	In regurgitant lesions reliability decreases
PISA (Proximal Isovelocity Surface Area)	MVA= 2 x 3.14 r 2 x V1	Very reliable, operator dependant

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*= 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

TABLE 3¹⁸

FEATURE

Leaflet Mobility

Leaflet thickening

Calcification

Subvalvular Apparatus

Transesophageal echocardiography (TEE) is useful for detecting vegetations smaller than 5 mm or thrombi in the left atrium not seen with transthoracic echocardiography.

 

Cardiac Catheterization:

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)

TREATMENT:

Emergency Department Care: ^24,26,27,28

Upright posture

Rate Control:

• 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:

• 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.

Consultations:

Cardiology Consult:

For known or suspected mitral stenosis with hemodynamic instability, arrhythmia or embolization.

For new onset or progression of symptoms.

MEDICATION

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.

• Cardiac Glycosides 
• Beta-blockers
• Calcium Channel Blockers

Cardiac Glycosides - These agents alter the electrophysiologic mechanisms responsible for arrhythmia. 

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.

Adult Dose

Loading dose: 0.25 mg IV q6 up to 1 mg

Maintenance dose: 0.125 mg-0.25 mg qd

Pediatric Dose

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

Contraindications

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. 

Interactions 

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.

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

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.

Drug Name

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.

Adult Dose

5 mg IV and repeat in 10 min up to 15 mg

Pediatric Dose

Safety and efficacy in children have not been established.

Contraindications

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.

Interactions

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.

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

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. 

Drug Name

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.

Adult Dose

0.25 mg/kg IV over 2 min.

Rebolus after 15 min if needed with 0.35 mg/kg.

Pediatric Dose

Safety and efficacy in children have not been established.

Contraindications

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).

Interactions

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.

Pregnancy

C - Safety for use during pregnancy has not been

established.

Precautions

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.

Prevention:

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

Complications:

• 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).

MISCELLANEOUS

Medical/Legal Pitfalls:

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.

 

References

1. Kinkare, S.G. and Kulkarni, H.L. : Quantitative study of mitral valve in chronic rheumatic heart disease. Int. J. Cardiology. 16:271, 1987

2. Hortskotte, D. Niehues, R., and Strauer, B.E.: Pathomorphological aspects, aetiology and natural history of acquired mitral valve stenosis. Eur. Heart J. 12:55, 1991

3. Braunwald E., Valvular heart disease 4^th ed. E. Braunwald (ed). Philaedelphia, Saunders, 1992, p1007

4. Taranta A., Kleinberg E., Feinstein, AR, : A long term epidemiologic study of subsequent prophylaxis, streptococcal infections and clinical sequalae Ann. Intern. Med. (suppl 5):47-57, 1964.

5. Taranta A., Kleinberg E., Feinstein, AR,: Rheumatic fever in children and adolescents. Relationship of the rheumatic rate per streptococcal infections to pre-existing clinical features of patients. Ann. Int. Med. (suppl 5): 58-67, 1964

6. Ruckman, R. N., and Van Praagh, R.: Anatomic types of congenital mitral stenosis: Report of 49 autopsy cases with consideration of diagnostic and surgical implications. Am. J. Cardiol. 42:592, 1978

7. Roberts, W.C., Sjoerdsma, A.: The cardiac diseases associated with carcinoid syndrome (carcinoid heart disease). Am. J. Med. 36:5-34. 1964

8. Waller, B. F., : Rheumatic and non rheumatic conditions producing valvular heart disease. In Frankl, W.S., and Brest, A. N., (eds): Cardiovascular clinics. Valvular Heart Disease: Comprehensive evaluation and management. Philaedelphia, F.A. Davis, 1986, pp. 3-104.

9. Meisner, J.S., Keren G., Pajaro, O.E., Mani A. et al: Atrial contribution to ventricular filling in mitral stenosis. Circulation 84: 1469-1480, 1991

10. Beyer, R.W., Olmos A, Bermudez RF, Noll HE, Mitral valve resistance as a hemodynamic indicator in mitral stenosis. Am. J. Card. 69: 775-779, 1992

11. Gaasch WH, Folland ED: Left ventricular function in rheumatic mitral stenosis. Eur Heart J 12 (suppl B): 66-69, 1991

12. Abbo KM, Caroll JD, Hemodynamics of mitral stenosis: A review. Cathetrization and Cardiovascular Diagnosis, Suppl. 2:16-25, 1994

13. Barrington WW, Bashore T, Wooley CF: Mitral Stenosis Mitral dome excursion at M1 and mitral opening snap - The concept of reciprocal heart sounds. Am. Heart J. 115:1280-90, 1988

14. Ebringer R, Pitt A, Anderson ST, Hemodynamics factors inflencing opening snap interval in mitral stenosis. British Heart Journal, 32:350-354, 1970

15. Cooksey JD, Dunn M, Massie E, Clinical vectorcardiography and electrocardiography. 2^nd ed. Chicago, Year book publishers, 1977. P272

16. Cueto J, Toshima J, Et al: Vectorcardiographic studies in acquired valvular heart disease with reference to diagnosis of right ventricular hypertrophy. Circulation 33: 588, 1967

17. Row JC, Bland EF, Sprague HB, Ehite PD: The course of mitral stenosis without surgery: ten and twenty year perspectives. Ann Intern Med 52:741, 1960

18. Wilkins GT, Weyman AE, Abascal VM, Block PC, Palacios IF. Percutaneous balloon dilatation of the mitral valve-an analysis of echocardiographic variables related to outcome and the mechanism of dilatation. Br Heart J 1988; 60: 299-308.

19. Smith AD, Handshoe R, Handshoe S, et al: Comparative accuracy of two dimensional echocardiography and Doppler pressure half time methods in assessing severity of mitral stenosis in patients with and without prior commissurotomy. Circulation 73:100, 1986.

20. Feigenbaum H, Echocardiography in Heart Disease, 4^th ed, Philadelphia, Saunders, 1992, p81.

21. Abernathy W, Willis P: Thromboembolic Complications of Rheumatic Heart Disease. Cardiovasc Clin 1973; Vol 5: P.131-175.

22. Bortolotti U, Valente M, Agozzino L: Rheumatoid Mitral Stenosis Requiring Valve Replacement. Am Heart J 1984; Vol 107: P.1049

23. Braunwald E: Valvular Heart Disease. Heart Disease: A Text of Cardiovascular Medicine 1997; Vol 2: P.1007-1017.

24. Braunwald E: Valvular Heart Disease. Harrison's Principles of Internal Medicine 1991;P.938-942.

25. Duchak J, Chang S, Feigenbaum H: The Posterior Mitral Valve ECHO and the Echocardiographic diagnosis of Mitral Stenosis. Am J Cardio 1972; Vol 29: P.628-632.

26. Dunmire S, Ahrens B: Endocarditis and Acquired Valvular Heart Disease. Emergency Medicine Concepts and Clinical Practice 1992; Vol 2: P.1492-1493.

27. Gassach W, O'Rourke R, Cohn L: Mitral Valve Disease. The Heart Arteries and Veins 1994; 8th Ed: P.1483-1491.

28. Janz T: Valvular Heart Disease: Clinical approach to acute decompensation of left-sided lesions. Ann Emerg Med 1988; 17: P.201.

29. Kern M, Lewis L: Valvular Heart Disease. Principles and Practice of Emergency Medicine 1992; Vol 1: P.1313-1328.

30. Ornato J: Valvular Heart Disease. The Clinical Practice of Emergency Medicine 1996;p 612-616.

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.

 

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First published 27.3.2000

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