Tricuspid stenosis is more common in women and is mostly caused by wind-dampness heat. Similar to mitral stenosis, the pathological changes of wind-dampness-related tricuspid stenosis include fusion and shortening of the chordae tendineae, fusion of the valve leaflet tips, and the formation of a membrane-like orifice. Tricuspid stenosis may be accompanied by tricuspid regurgitation or coexist with damage to any other valve. The right atrium is significantly enlarged, with thickened atrial walls, and severe visceral static blood manifestations such as hepatosplenomegaly may also occur.

bubble_chart Etiology

Tricuspid stenosis is predominantly caused by wind-dampness heat, while other rare causes include congenital tricuspid atresia, right atrial tumors, and carcinoid syndrome. The clinical feature of right atrial tumors is rapid progression of symptoms; carcinoid syndrome is often accompanied by tricuspid regurgitation. Wind-dampness-related tricuspid stenosis rarely occurs alone and is almost always accompanied by mitral valve lesions, mostly mitral stenosis. Approximately 15% of patients with rheumatic heart disease have tricuspid stenosis, but only 5% are clinically diagnosed.

bubble_chart Pathological Changes

Tricuspid stenosis creates a diastolic pressure gradient between the right atrium and right ventricle. When exercise or inspiration increases tricuspid blood flow, the diastolic pressure gradient between the right atrium and right ventricle increases; when expiration reduces tricuspid blood flow, this pressure gradient decreases. If the mean diastolic pressure gradient exceeds 0.53 kPa (4 mmHg), it can elevate the mean right atrial pressure, leading to systemic venous congestion, manifested as jugular vein distension, hepatomegaly, ascites, and edema. In sinus rhythm, the right atrial a-wave becomes extremely elevated, potentially reaching the level of right ventricular systolic pressure. The resting cardiac output decreases and fails to increase during exercise; consequently, left atrial pressure, pulmonary capillary wedge pressure, and right ventricular pressure may not rise significantly.

(1) Symptoms Low cardiac output caused by tricuspid stenosis leads to fatigue, and systemic venous {|###|}static blood{|###|} can cause intractable {|###|}edema{|###|}, hepatomegaly, {|###|}ascites{|###|}, and other gastrointestinal symptoms, as well as general discomfort. The large "a" wave in jugular venous pulsation makes patients feel a throbbing sensation in the neck. Although patients often have concurrent mitral stenosis, clinical symptoms of mitral stenosis such as {|###|}hemoptysis{|###|}, paroxysmal nocturnal dyspnea, and acute pulmonary {|###|}edema{|###|} are rare. If a patient shows obvious signs of mitral stenosis but lacks clinical manifestations of pulmonary congestion, concurrent tricuspid stenosis should be considered.

(2) Signs

1. Cardiac auscultation A low-pitched rumbling mid-to-late diastolic murmur at the left lower sternal border, with presystolic accentuation. The murmur intensifies during upright inspiration and weakens during expiration or the straining phase of the Valsalva maneuver. A diastolic {|###|}tremor{|###|} may accompany the murmur, and an opening snap may be present. The pulmonary {|###|}stirred pulse{|###|} second heart sound is normal or diminished. In cases of {|###|}wind-dampness{|###|} etiology, mitral stenosis is often present, which may mask the signs of this condition.

2. Other signs Tricuspid stenosis often presents with obvious signs of right heart congestion, such as jugular venous distension with a prominent "a" wave that intensifies during expiration. Advanced cases may exhibit hepatomegaly, splenomegaly, {|###|}jaundice{|###|}, severe malnutrition, generalized {|###|}edema{|###|}, and {|###|}ascites{|###|}. The enlarged liver may show a pronounced presystolic pulsation.

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1. X-ray examination: The right atrium is significantly enlarged, with dilation of the inferior vena cava and azygos vein, but no pulmonary stirred pulse dilation.
2. Electrocardiogram examination: Right atrial hypertrophy, with tall and peaked P waves in leads II and V₁. Since most patients with tricuspid stenosis also have mitral stenosis, the electrocardiogram often shows biatrial hypertrophy. There are no signs of right ventricular hypertrophy.
3. Echocardiographic examination: The changes in the tricuspid valve are similar to those observed in mitral stenosis. M-mode echocardiography often shows thickened valve leaflets, slowed EF slope of the anterior leaflet, paradoxical movement during diastole with the septal leaflet, and calcification and thickening of the tricuspid valve. Two-dimensional echocardiography is more helpful in diagnosing tricuspid stenosis, characterized by doming of the leaflets during diastole, thickening, and restricted leaflet motion. Doppler ultrasound can estimate the transvalvular pressure gradient.

bubble_chart Diagnosis

The diagnosis can generally be made based on typical murmurs, right atrial enlargement, and symptoms and signs of systemic congestion. For cases with diagnostic difficulties, right heart catheterization can be performed. A mean diastolic pressure gradient across the tricuspid valve of more than 0.27 kPa (2 mmHg) confirms the diagnosis of tricuspid stenosis. Differential diagnosis should include conditions such as right atrial myxoma and constrictive pericarditis.

bubble_chart Treatment Measures

Strictly limit sodium intake and apply diuretics to improve the symptoms and signs of systemic congestion, especially to alleviate hepatic congestion and improve liver function. If symptoms are significant, with the mean right ventricular diastolic pressure reaching 0.53–0.67 kPa (4–5 mmHg) and the tricuspid valve orifice area less than 1.5–2.0 cm²

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