Fication of Sports) or possible trauma.

MITRAL REGURGITATION

Mitral regurgitation, unlike MS, has a variety of etiologies,

the most common of which is mitral valve prolapse (myxomatous

mitral valve). Other common causes are rheumatic

heart disease, infective endocarditis, CAD, connective tissue

diseases (such as Marfan syndrome), and dilated cardiomyopathy.

The recommendations outlined in this section are

for patients with primary valvular MR rather than MR

secondary to CAD or other conditions causing LV dilation

(see Task Force 4: HCM and Other Cardiomyopathies,

Mitral Valve Prolapse, Myocarditis, and Marfan Syndrome,

and Task Force 6: Coronary Artery Disease).

Evaluation.Mitral regurgitation can be detected by the

characteristic physical findings and confirmed by Doppler

echocardiography. The severity of the MR is related to the

magnitude of the regurgitant volume, which results in LV

dilation and increased left atrial pressure. The increased LV

diastolic volume enhances total LV stroke volume enough to

accommodate the regurgitant volume and to maintain the

forward stroke volume within normal limits. The low

impedance presented by regurgitation into the left atrium

unloads the left ventricle during ventricular systole, such

that measures of LV pump function (e.g., ejection fraction)

tend to overestimate true myocardial performance (10).

The severity of chronic MR can be adequately judged by

noninvasive techniques, principally two-dimensional and

Doppler echocardiography. The larger the jet area, and the

wider the jet at its origin above the valve, the more severe

the regurgitation. The entry of the jet into the atrial

appendage or pulmonary vein or systolic reversal of the flow

in pulmonary veins are all indicators of severity. Various

measures of the severity of MR have been described (1,11).

In some patients with eccentric jets or those impinging on

the atrial wall, the assessment may be difficult (1). Generally,

the LV diastolic volume reflects the severity of chronic

MR. However, it should be noted that the upper limit of normal

LV size is increased in the healthy, highly trained athlete. In a

series of elite athletes, echocardiographic LV end-diastolic dimensions

as high as 66 mm were recorded in women (mean, 48

mm) and up to 70 mm in men (mean, 55 mm) (12). LV

end-diastolic dimensions greater than or equal to 55 mm were

observed in 45% of participants and greater than 60 mm in

14% of participants. Therefore, assessment of LV enlargement in

a highly trained athlete with known or suspected valvular heart

disease must take this issue into consideration. Hence, for

purposes of this discussion, an LV end-diastolic dimension

greater than 60 mm is considered likely to represent the

effects of LV volume overload due to valvular disease and

not per se to physiologically based exercise training.

Patients with chronic MR should be followed longitudinally

with serial echocardiograms (5). A decrease in ejection

fraction and/or increase in end-systolic volume with time is

a helpful marker of declining LV function and an indication

of having reached the limits of cardiac compensation.

1335 JACC Vol. 45, No. 8, 2005 Bonow et al.

April 19, 2005:1334–40 Task Force 3: Valvular Heart Disease

Effects of exercise.In general, exercise produces no signifi-

cant change or a mild decrease in the regurgitant fraction

because of reduced systemic vascular resistance. However,

patients with elevation of heart rate (increased systolic ejection

time per min) or blood pressure with exercise may manifest

marked increases in regurgitant volume and pulmonary capillary

pressures. Hence, static exercise that increases arterial

pressure is potentially deleterious. Ejection fraction usually

does not change or decreases slightly with exercise, although

the ejection fraction response may be completely normal in

young, asymptomatic subjects.

The etiology of MR may be important in making recommendations

concerning heavy physical activity. In patients with

MR secondary to previous infective endocarditis or ruptured

chordae, the valve tissues theoretically could be further damaged

or torn by marked sustained increases in LV systolic

pressure.

Recommendations:

Date: 2016-03-03; view: 734