During the process of wind-dampness Rebing, the mitral valve is most susceptible to involvement. It generally takes about two years from the initial infection to the formation of wind-dampness-related rheumatic mitral stenosis. Symptoms typically appear only when the degree of stenosis reaches 50% of normal. Therefore, clinically, it may take about 10 years for significant symptoms to manifest. As a result, severe mitral stenosis is relatively uncommon in childhood.

bubble_chart Diagnosis

(1) General Manifestations

1. Symptoms: Grade I may not present with symptoms. Children with grade II or higher stenosis may experience fatigue, palpitation, shortness of breath, and dyspnea after exertion, accompanied by grade I perioral cyanosis, flushed cheeks—the so-called "mitral facies." Severe cases may present with hemoptysis or bloody frothy sputum, orthopnea, and paroxysmal nocturnal dyspnea.
2. Signs: Precordial fullness may be observed. A low-pitched rumbling diastolic murmur, often localized, can be heard at the apex, usually accompanied by a diastolic tremor. The first heart sound at the apex is accentuated, and the pulmonary second sound is accentuated and split. A loud mitral opening snap (mitral opening sound) may be heard at the left sternal border of the 3rd–4th intercostal space or the upper inner apex. Active rheumatic carditis and left atrial enlargement with increased pressure often complicate atrial arrhythmias, such as atrial premature beats, atrial tachycardia, and atrial fibrillation, with the latter particularly suggesting active rheumatic activity. (2) X-ray Findings: May show left atrial and right ventricular enlargement, pulmonary artery prominence, and pulmonary congestion. (3) Electrocardiogram: Grade I cases may be normal. Severe cases show right axis deviation and right ventricular hypertrophy. Mitral P waves (PⅠ,Ⅱ) are widened, often notched, while PⅥ may be biphasic or even inverted, with P-wave amplitude exceeding 0.2 mV (indicating pulmonary hypertension). (4) Echocardiography: M-mode shows the disappearance of the double-peaked curve of the anterior mitral leaflet, replaced by a "plateau" pattern, with the posterior leaflet moving in the same direction as the anterior leaflet and reduced motion amplitude. Two-dimensional long-axis left ventricular view reveals enhanced mitral valve echoes, restricted opening, and left atrial and right ventricular enlargement. Short-axis view of the main pulmonary artery shows the mitral valve orifice in a "fish-mouth" shape, allowing measurement of its diameter. Doppler ultrasound detects a diastolic turbulent flow spectrum on the left ventricular side of the mitral orifice.

bubble_chart Treatment Measures

[Treatment]

For patients with mild mitral stenosis, no significant cardiac enlargement, and no obvious clinical symptoms, activity does not need to be overly restricted, but physical labor should be avoided to reduce cardiac load. Active prevention and treatment of wind-dampness activity and infective endocarditis. (1) For those with grade I cardiac insufficiency, a low-salt diet, β-blockers, or calcium channel blockers may be used to slow the heart rate. The use of digitalis preparations remains controversial. Some believe that the positive inotropic effect of digitalis enhances left ventricular contractility and increases cardiac output but also raises left atrial pressure, thereby worsening mitral stenosis symptoms. Conversely, others argue that digitalis drugs can increase left ventricular pressure and reduce left ventricular end-diastolic pressure, thereby lowering left atrial pressure. Therefore, they are generally not used in mild cases. (2) For patients with atrial fibrillation, small-dose rapid digitalis therapy may be considered; for persistent atrial fibrillation, electrical cardioversion can be applied. If the heart rate remains fast after cardioversion, β-blockers or calcium blockers may be added. (3) Surgical treatment: Patients with cardiac function at grade II or III and no concurrent active wind-dampness may be considered for surgical treatment, such as mitral commissurotomy or mitral valve plasty. However, in children, active wind-dampness is often present, so surgery should be postponed, and anti-wind-dampness treatment should be prioritized. For severe cases with mitral valve destruction, calcific stenosis, or concurrent mitral regurgitation, valve resection and artificial valve replacement are the only options. For younger patients, due to the unreliable durability of bioprosthetic valves, mechanical disc or ball-cage valves must be used, followed by long-term anticoagulation therapy. Postoperatively, about 20% of patients may develop "post-commissurotomy syndrome," which manifests 10 days to 2 months after surgery with left chest pain radiating to the left shoulder, accompanied by fever, sweating, cough, dyspnea, pleural or pericardial friction rubs, leukocytosis, and elevated erythrocyte sedimentation rate. The condition responds well to hormone therapy, improving within 1–2 weeks. The cause is unknown but may be related to an allergic reaction.