Valvular Heart Disease

Valvular Heart Disease Basic Science March 22, 2006

1. Information on valves may be accurately obtained by: • A. CXR • B. Transthoracic echocardiography (TTE) • C. Transesophageal echocardiography (TEE) • D. CT scan • E. Cardiac catheterization

TEE is more sensitive than TTE, especially for aortic and mitral valve lesions; even more so for mitral regurgitation. • Cardiac catheterization can give detail on mitral/aortic valve areas, calculated by the Gorlin formula.

2. What is true concerning the anatomy of the mitral valve? • A. The normal mitral valve has two leaflets; the lateral and medial leaflets. • B. The chordae tendineae attach the leaflets to two papillary muscles. • C. The two leaflets are identical mirror images of each other, forming a tight closure. • D. There is a fibrous continuity between the mitral and aortic valves.

The two leaflets are anterior and posterior. • The two leaflets have the same surface area but very different shapes. The base of the anterior leaflet accounts for 1/3 of the circumference of the mitral annulus and the posterior leaflet accounts for 2/3.

3. What is true concerning mitral stenosis? • A. Principal cause is rheumatic fever. • B. The normal cross-sectional area of the mitral valve is 4-6 cm2, and moderate stenosis occurs at 2 cm2 and severe stenosis occurs at 1 cm2. • C. There is normally a 5 mm Hg pressure gradient across a normal valve, with symptoms occurring once the gradient increases to greater than 10 mm Hg. • D. Symptoms usually occur with bradycardia and the heart’s inability to supply adequate cardiac output to overcome the pressure gradient across the valve.

There is normally no pressure gradient across the mitral valve. A pressure gradient of 20 mm Hg is needed to maintain adequate left ventricular filling across a 1 cm2 stenotic valve. • Contribution of an adequate left atrial “kick” is important in mitral stenosis, and loss of this contraction (with exertion or atrial fibrillation) often leads to symptoms.

4. Mechanical relief of mitral stenosis should be considered when: • A. The valve size is 2 cm2 or smaller. • B. The patient becomes symptomatic. • C. Pulmonary hypertension develops. • D. With worsening Left ventricular hypertrophy and dilatation. • E. Endocarditis develops in the valves.

Mechanical correction should be considered when the valve is 1 cm2 or less in area. • Left ventricular hypertrophy is not expected with isolated mitral stenosis. • Other causes for repair include systemic embolization (usually from a-fib).

5. What is true concerning balloon mitral valvuloplasty? • A. Treatment of choice in patients with pliable valves, without calcification or deformation of the chordae tendineae. • B. Contraindications include thickened, calcified mitral leaflets and absence of any mitral regurgitation. • C. Balloon inflation should increase the valve area to greater than 4 cm2. • D. Mortality rate is 0.5-2% with total complication rate of 3-6%. • E. Results compare favorably with surgical valvuloplasty in appropriately selected patients.

Moderate mitral regurgitation is a contraindication for valvuloplasty. • An area of 2 cm2 should be achieved, resulting in a significant decline in left atrial pressure with 20% increase in CO. • Complications include systemic embolism, cardiac perforation, and creation of mitral regurgitation (1-2% complication rate for each).

6. What is true concerning mitral valve replacement? • A. The mitral valve should be replaced if dense calcification precludes balloon valvuloplasty or open commissurotomy. • B. Should be openly replaced if there is concomitant mitral regurgitation. • C. The chordae tendineae should be divided, especially when excessively shortened or scarred. • D. Operative mortality is 1-2%. • E. The 5 year survival rate is 50-60%.

Efforts should be made to preserve the posterior, and in some cases the anterior leaflets and chordae tendineae; studies have shown an advantage to left ventricular function with preservation. • Operative mortality is 2-10%. • Five year survival rate is 70-90%.

7. Mitral regurgitation may be caused by: • A. Rheumatic fever. • B. Trauma. • C. Myocardial infarction. • D. Endocarditis. • E. Hypertension. • F. Diseases of collagen formation.

Rheumatic fever remains the #1 cause worldwide. • Chordal rupture can occur with trauma, MI, endocarditis and collagen disorders. • Hypertension is not a known etiology of mitral regurgitation.

8. Left ventricular ejection fraction typically: • A. Increases with mitral regurgitation. • B. Decreases. • C. Remains the same.

Because the left ventricle is ejecting into the aorta and left atrium, the EF is increased, but the left ventricle ultimately fails from chronic volume overload. Thus relatively normal parameters of systolic function (i.e. 40% EF) could indicate significant contractile dysfunction.

9. Management of mitral regurgitation includes: • A. Diuretics to decrease volume. • B. Inotropes to increase cardiac output. • C. ACE inhibitors to decrease afterload. • D. Nitroprusside in the setting of heart failure from acute regurgitation. • E. Tylenol for the fevers.

The mainstay of medical treatment is diuretics and ACE inhibitors. • Afterload reduction is key, since the blood will flow down the path of least resistance. • There is no role for inotropes or tylenol in mitral regurgitation (although tylenol is still ok for fevers).

10. Indications for surgery in mitral regurgitation include: • A. Ongoing symptoms despite medical management. • B. An identified structural abnormality, such as a ruptured chorda tendinea. • C. An EF of 20% or less. • D. An end-systolic diameter (ESD) of 60 mm or greater. • E. Development of pulmonary hypertension.

An EF of less than 60% suggests myocardial dysfunction and operative mortality increases. An ESD of 45 mm or more makes for a worse prognosis after surgery. • Thus even in the absence of symptoms patients should be referred for surgery if the EF is <60% or ESD is >45mm.

11. What is true regarding the anatomy of the aortic valve? • A. The valve consists of three cusps. • B. Coronary arteries arise from each of the three sinuses of Valsalva. • C. The coronary leaflets form commissures over the anterior leaflet of the mitral valve and the bundle of His. • D. The leaflets are divided into the left, right, and posterior coronary leaflets. • E. The normal area of the valve is 1-2 cm2.

There are two coronary arteries that arise from the sinuses: the left and right. • Thus the aortic leaflets are named after the coronary arteries: the left coronary leaflet, the right coronary leaflet, and the noncoronary leaflet. • The commissure between the left and noncoronary leaflets sits over the anterior leaflet of the mitral valve, while the commissure between the right and noncoronary leaflets sits on the left bundle of His. • Normal valve size is 3-4 cm2. Symptoms usually arise at 1 cm2 with critical stenosis at 0.7 cm2.

12. Aortic stenosis may be caused by: • A. Hypertension and the resultant left ventricular hypertrophy. • B. Rheumatic fever. • C. Idiopathic. • D. Congenital valvular deformities. • E. Chronic steroid use.

Left ventricular hypertrophy is a result of aortic stenosis, as the body compensates for the increased pressure gradient across the valve. There are unfortunately detrimental effects including increased myocardial mass, increasing oxygen demand, decreased ventricular compliance leading to increased wall tension, and thus decreased coronary artery flow. This all leads to chronic ischemia, cell death, and fibrosis. • Steroids have no known role in causing aortic stenosis (and if there is I apologize, as I just made this up).

13. The principle symptoms of aortic stenosis are: • A. Headache. • B. Angina. • C. Palpitations. • D. Syncope. • E. Nightmares. • F. Dyspnea.

The three principal symptoms are angina, syncope, and congestive heart failure, usually seen as dyspnea.

14. Viable treatment options for symptomatic aortic stenosis in a relatively healthy patient are: • A. Balloon angioplasty of the valve. • B. Open valvuloplasty (commissurotomy). • C. Minimally invasive laser valvulotomy. • D. Replacement of the valve. • E. Medical management.

Surgical replacement of the valve is the only solution with an acceptable long term outcome. • “The only potential role of aortic balloon valvuloplasty may be in aged, frail, and possibly senile patients whose long-term survival is poor.” • Answer C is complete nonsense.

15. Aortic insufficiency may be caused by: • A. Mixoid degeneration of the aortic root. • B. Trauma. • C. Rheumatic fever. • D. Endocarditis. • E. Annuloaortic ectasia.

Mixoid degeneration in Marfan’s, Ehlers-Danlos, and cystic medial necrosis. • Annuloaortic ectasia is an idiopathic dilatation of the aortic root and annulus, and is the most reason for aortic insufficiency despite normal leaflet morphology.

16. Treatment options for aortic insufficiency include: • A. Observation and close monitoring for patients with mild to moderate regurgitation who are asymptomatic. • B. Medical treatment with diuretics and afterload reduction agents in symptomatic patients. • C. Valve replacement before the left ventricle reaches 55 mm Hg in end-systolic volume. • D. Valve replacement once the end systolic volumes have reached 90 mL/m2 or greater. • E. Valve replacement in symptomatic patients.

Pts with mild to moderate regurgitation have a 10 yr survival rate of 85-95%. These pts can be followed with serial echocadiography or nuclear studies. • They should be maintained on diuretics and afterload reducers, but once symptoms develop, it means that the multiple compensatory mechanisms have failed and medical management is not enough. • To achieve optimal results valve replacement should take place before the left ventricle has undergone irreversible dilitation.

End

Valvular Heart Disease