Early in the disease process of patients with Barlow syndrome, a characteristic midsystolic click can be appreciated, followed by a late systolic murmur; with disease progression the murmur becomes holosystolic, and the midsystolic click may become inaudible.[46] Acute mitral regurgitation Immediate intervention is often necessary in acute mitral regurgitation. Etiology can be organic or functional. Organic causes include rupture of a major chorda tendinea (in myxomatous mitral valve disease) or papillary muscle (due to myocardial infarction), leaflet perforation (of endocarditic origin), and dysfunction of a prosthetic valve due to endocarditis or paravalvular regurgitation. Regurgitation of functional etiology results from left ventricular abnormalities such as dyskinetic wall due to ischemia or dilated ventricle due to cardiomyopathy. https://www.textbookofcardiology.org/wiki/Valvular_Heart_Disease 26/39 7/4/23, 12:36 AM Valvular Heart Disease - Textbook of Cardiology Acute mitral regurgitation is associated with dyspnea and orthopnea, caused by sudden pulmonary congestion and edema. Acute papillary muscle rupture may mimic the presentation of a patient with a postinfarction ventricular septal defect.[49] On physical examination no signs of cardiac compensatory mechanisms are present. The increase in left atrial pressure diminishes the pressure gradient between the left ventricle and left atrium by midsystole. The murmur of mitral regurgitation is shortened and of decreased intensity, it may be soft, short of even inaudible. An S3 gallop usually is present. The volume overload is increasing the severity of MR over time, and leads to a greater percentage of the LV stroke volume being ejected in a retrograde fashion. Diagnostic Options Chest Radiography In chronic mitral regurgitation chest radiography demonstrates enlargement of the left ventricle and atrium. The mitral annulus may be calcified. In acute mitral regurgitation, no adaptive left atrium or ventricle enlargement has developed. Signs of interstitial or alveolar pulmonary edema may be present. Electrocardiography Signs of left ventricular hypertrophy and left atrial enlargement due to chronic volume overload may be seen on the electrocardiogram. Atrial fibrillation is a common finding late in the natural history of the disease. Q-waves may be seen in ischemic mitral regurgitation. In patients with acute mitral regurgitation, left atrial and ventricular enlargement may not be evident and the electrocardiogram may be normal or show only nonspecific findings. The resting electrocardiogram of patients with asymptomatic mitral valve prolaps is normal. A variety of ST-T-wave changes, including T-wave inversion and sometimes ST-segment depression, particularly in the inferior leads, can be found in patients with symptomatic mitral valve prolapse. Echocardiography Mitral valve pathology and pathophysiology is primary assessed by echocardiography. Left atrial and ventricular dimensions can be quantified. The etiology and mechanism of mitral regurgitation can be identified by echocardiography. Leaflet abnormalities and chordal morphology and function is assessed by echocardiography. Fused subvalvular apparatus due to rheumatic valvulitis and leaflet destruction due to endocarditis can be visualized by echocardiography. Myxoid degeneration of the mitral valve is characterized by an excess of tissue and by leaflets of more than 5mm thickness. Annular dilatation is characterized by a ratio of >1.3 anterior posterior diameter of the annulus to the length of the anterior leaflet in diastole. The regurgitation caused by annular dilatation and incomplete leaflet coaptation is directed straight back into the left atrium. In ischaemic MR, the apical displacement of the leaflets can be quantified by measuring the tenting area and the leaflet opening angles. https://www.textbookofcardiology.org/wiki/Valvular_Heart_Disease 27/39 7/4/23, 12:36 AM Valvular Heart Disease - Textbook of Cardiology Color doppler analysis can be used to grade the severity of the regurgitation and permits visualization of the origin, extent, direction, duration, and velocity of disturbed backward flow of the regurgitant leak or leaks into the left atrium.[46] MR is considered severe when the jet area is >10cm2 or >40% of the left atrial area. Cardiac Catheterization Coronary ischemic causes of mitral regurgitation can be identified by cardiac catheterization. Treatment Surgical The hemodynamic overload on the heart caused by mitral regurgitation can ultimately only be corrected by surgically restoring valve competence. For all valve surgery timing of surgery is essential. Irreversible left ventricular dysfunction will result in suboptimal results indelayed surgery. Due to the operative risk and risk of valve prosthesis surgery should however be delayed as long as possible Mitral valve regurgitation is surgically corrected by mitral valve replacement or repair. Mitral valve repair is generally found to be superior to replacement, with preservation of left ventricular function and part of the mitral valve apparatus [50] [51] [52] [53] and without the use of a prosthesis. In mitral valve regurgitation indication for valve surgery is influenced by symptomatic status, ventricular functional status, and the procedure to be performed. Repair might be considered in asymptomatic patients with normal left ventricular function or patients with severe impairment of left ventricular function who might not be candidates for mitral valve replacement. For most patients, mitral valve surgery is performed for the relief of symptoms or to prevent worsening of asymptomatic left ventricular dysfunction. Tricuspid stenosis Tricuspid stenosis (TS) is most commonly of rheumatic origin and combined with tricuspid regurgitation. The anatomical characteristics are similar to those of mitral stenosis, including fibrous leaflet thickening and fusion and shortening of the subvalvular apparatus. The preponderance of cases is in young women. Other aetiologies of right atrial obstruction are rare and include congenital tricuspid atresia, right atrial tumors and carcinoid syndrome The normal valve area of the tricuspid valve is 7 8cm2. Reduction of valve area to <2 cm2 causes a pressure gradient. A small diastolic pressure gradient (<5 mmHg), gradient between the right atrium and ventricle can be present due to tricuspid stenosis. The gradient is increasing on inspiration. A mean pressure gradient >5mmHg is considered indicative of significant TS and is usually associated with symptoms Clinical presentation https://www.textbookofcardiology.org/wiki/Valvular_Heart_Disease 28/39 7/4/23, 12:36 AM Valvular Heart Disease - Textbook of Cardiology A tricuspid opening snap and a characteristic mid-diastolic murmur may be audible along the left sternoid border on auscultation. Carvallo s sign, an increase of murmur intensity on inspiration, may be present. Distention of jugular veins, ascites, pleural effusion and peripheral edema may be present due to increased right atrial pressures. Reduced cardiac output causes symptoms of fatigue and malaise. The pulmonary congestion of mitral stenosis may be masked in severe tricuspid stenosis. Diagnostic Options Chest radiography Cardiomegaly with an increase in right atria and pulmonary artery size is demonstrated on chest radiography. Electrocardiography An increased P-wave amplitude is seen on the electrocardiogram if the patient is in normal sinus rhythm. Echocardiography The tricuspid valve structure and function is commonly assessed by echocardiography. The annular size can be measured and the right pressures can be evaluated. Tricuspid stenosis due to rheumatic disease is characterized by leaflet thickening with reduced motion and frequent commissural fusion. The chordae are shortened and thickened, and diastolic doming is present. Carcinoid syndrome is characterized by retraction of leaflets towards the apex during systole. A prolonged slope of antegrade flow across the tricuspid valve can be seen on Doppler. Tricuspid stenosis is considered severe when the mean transvalvular gradient is >5 mmHg. Treatment The therapeutic approach for tricuspid regurgitation is dictated by the aetiology of the regurgitation and overall condition of the patient. In a limited number of patients percutaneous balloon tricuspid dilatation has been performed. This is a treatment option in cases of isolated and pure tricuspid stenosis, but it frequently induces regurgitation.[54] Tricuspid balloon valvotomy, combining commissurotomy leaflet augmentation and annuloplasty, can be used to treat tricuspid stenosis; however, with this treatment the potential for inducing severe tricuspid regurgitation still exists. A biological prosthesis is preferred in case of tricuspid valve replacement,since it heas satisfactory long-term durability and mechanical prosthesis caries a higher risk of thrombosis. Tricuspid regurgitation https://www.textbookofcardiology.org/wiki/Valvular_Heart_Disease 29/39 7/4/23, 12:36 AM Valvular Heart Disease - Textbook of Cardiology Functional tricuspid regurgitation results from distortion of the architecture and coordinated actions of the tricuspid leaflets, annulus, chords, papillary muscles, and right ventricular (RV) wall. This distortion is most commonly caused by right ventricular dilation and dysfunction from left sided heart disease with pressure/volume overload conditions. Pressure volume overload conditions cause enlargement of the tricuspid annulus and the shaddle shape becomes more circular. The normal annular excursion can be reduced by 50% in severe tricuspid regurgitation.[55] Functional tricuspid regurgitation is a marker of poor prognosis in patients with left ventricular cardiomyopathy. Pure tricuspid regurgitation may result from rheumatic fever, infective endocarditis, carcinoid causes, rheumatoid arthritis, radiation therapy, anorectic drugs, trauma, Marfan s syndrome, tricuspid valve prolapse, papillary muscle dysfunction, or congenital disorders. Right ventricular infarction with severe regional wall motion abnormality or disruption of the papillary muscle may cause regurgitation. Right ventricular dilatation with annular enlargement and valvular incompetence can be seen in Eisenmenger syndrome and pulmonary hypertension. Clinical presentation A reduction in cardiac output related to tricuspid regurgitation, may cause symptoms of fatigue and weakness. Right-sided heart failure may cause ascites, congestive hepatosplenomegaly, pulsatile liver, pleural effusions, and peripheral edema. With progression of the disease, patients become cachexic, cyanotic and jaundice may be present. A parasternal pansytolic murmur increasing on inspiration may be appreciated on auscultation(Carvallo s sign). An S3, increasing with inspiration and decreasing with a Valsalva maneuve may be audible, as well as an increased P2 if pulmonary hypertension has developed. Diagnostic options Chest Radiography Cardiomegaly, increased right atrial and ventricular size and a prominent azygous vein can be demonstrated on chest x-ray. Chest Radiography may reveal pleural effusion, and ascites by upward diaphragmatic displacement. Echocardiography The tricuspid valve structure and function can be assessed echocardiographically and specific abnormalities can be identified. Distinction between primary and functional forms of tricuspid regurgitation can be made with echocardiography. The annular size can be measured. This imaging https://www.textbookofcardiology.org/wiki/Valvular_Heart_Disease 30/39 7/4/23, 12:36 AM Valvular Heart Disease - Textbook of Cardiology modality is used to evaluate the degree of regurgitation, pressures and ventricular function. Severe regurgitation is characterized by systolic flow reversal in the hepatic veins and a vena contracta diameter of more than 7 mm. Cardiac catheterization Cardiac catheterization is not necessary to diagnose tricuspid regurgitation. Increased right atrial and right ventricular end-diastolic pressures and the degree of pulmonary artery hypertension can be evaluated by catheterization. Pulmonary artery pressures of over 60 mmHg are usually due to left-sided lesions leading to secondary tricuspid regurgitation. Treatment Treatment strategy for tricuspid regurgitation is dictated by the aetiology and the underlying cause of the disease and the overall condition of the patient. Primary tricuspid regurgitation has a poor prognosis without treatment. Functional tricuspid regurgitation may improve following treatment of its cause. Correction of concomitant mitral regurgitation may worsen tricuspid regurgitation. Risk factors for persistence or worsening of tricuspid regurgitation are reduced right ventricular function and the diameter of tricuspid annulus. Medical When pulmonary hypertension is the underlying cause of tricuspid annular dilation, medical management alone may minimize the need for surgical intervention Surgical Surgical treatment can be recommended for primary tricuspid regurgitation, when there is pulmonary hypertension, important dilatation of the annulus (diameter >40mm or >21mm/m2). Surgical options for tricuspid regurgitation include annuloplasty or valve replacement with a mechanical valve or bioprosthesis. Functional tricuspid regurgitation may be repaired by suture annuloplasty (De Vega procedure) or by ring annuloplasty. Longterm outcomes of ring annuloplasty are superior to those of suture annuloplasty. Annuloplasty can be optimized by the use of intraoperative transesophageal echocardiography. Bioprostheses are generally preferred above mechanical prostheses for the tricuspid position, as mentioned in the section about tricuspid stenosis. Pulmonary valve stenosis Etiology and pathology Pulmonary valve stenosis can be caused congenital, carcinoid and rheumatic disorders or extrinsic compression. The typical domeshaped pulmonary valve stenosis is the most common form of right ventricular outflow tract obstruction. Stenosis is caused by fusion of the pulmonary valve lea ets and a https://www.textbookofcardiology.org/wiki/Valvular_Heart_Disease 31/39 7/4/23, 12:36 AM Valvular Heart Disease - Textbook of Cardiology narrowed central ori ce. The valve is usually mobile and associated with medial abnormalities the valve pulmonary stenosis may be associated with Noonan, Williams, Alagille, Keutel or rubella syndromes.[56] and dilation of trunk. Pulmonary The diagram shows a healthy heart and one suffering from Pulmonary valve stenosis Clinical presentation Most patients with mild to moderate pulmonary valve stenosis are asymptomatic. Severe pulmonary valve stenosis may cause exertional dyspnea and fatigue, chest pain, palpitations and syncope. On physical examination, thrill along the left sternal edge, and a long systolic ejection murmur with late peak may be appreciated. S2 may be widely split with reduced or absent P2. Diagnostic options Chest Radiography Chest radiography may show dilated pulmonary arteries, occasionally with calcification of the pulmonic valve. In case of severe pulmonary valve stenoisis, oligemic lung fields can be seen. Electrocardiography Right ventricular hypertrophy can be seen on electrocardiography as an axis deviation to the right. Right bundle branch block may also be present. Patients with Noonan syndrome invariably have a left bundle branch block. Echocardiography https://www.textbookofcardiology.org/wiki/Valvular_Heart_Disease 32/39 7/4/23, 12:36 AM Valvular Heart Disease - Textbook of Cardiology Transthoracic echocardiography confirms the diagnosis. The level of obstruction, valvular, supravalvular or right ventricular outflow tract, can be identified. Valvular stenosis is characterized by mildly thickened leaflets with restricted systolic excursion. The pressure gradient can be measured. Associated cardiac conditions can be demonstrated with echocardiography. Cardiac catheterization Cardiac catheterization is not necessary to diagnose pulmonic valve stenosis. Hemodynamic consequences and severity of pulmonary valve stenosis can be assessed with cardiac catheterization. Treatment Invasive intervention is recommended in case of symptomatic disease, or when the gradient across the valve is >40 mmHg. Medical Supportive and symptomatic treatment of right ventricular failure is recommended. Surgical The treatment of choice for stenosis at the valvular level is balloon valvuloplasty. Long-term results are satisfactory and the procedure relatively safe. Surgical valvotomy is very effective with minimal recurrence, however significant pulmonary regurgitation may occur. Pulmonary valve replacement is indicated if the patient is not suitable for balloon valvuloplasty or surgical valvotomy. Pulmonary valve regurgitation Etiology and pathology Physiologic pulmonic regurgitation, qualified as trace to mild, is present in nearly all individuals. Pulmonary valve regurgitation can be caused by valvular disease such as infective endocarditis (rarely involves pulmonic valve) or connective tissue disease, carcinoid, congenital heart disease, or it can be secondary to pulmonary hypertension, which causes dilation of the valve ring. Pulmonic regurgitation can result in impairment of right ventricular function and eventual clinical manifestations of right-sided volume overload and heart failure. Clinical presentation Patients are often asymptomatic. Symptoms of right-sided heart failure develop when the severity and duration of the regurgitation results in right ventricular enlargement and decompensation. Symptoms include dyspnea on exertion, light-headedness, lethargy, peripheral edema, chest pain, palpitations, and abdominal pain. Often these symptoms are accepted by the patient and attributed to poor physical https://www.textbookofcardiology.org/wiki/Valvular_Heart_Disease 33/39 7/4/23, 12:36 AM Valvular Heart Disease - Textbook of Cardiology fitness, causing a delay in presentation. The jugular venous pressure is usually increased in pulmonary valve regurgitation. A palpable impulse may be present at the left lower sternal border due to right ventricular enlargement. On auscultation P2 may be delayed due to increased right ventricular end- diastolic volume and increased ejection time with large stroke volume. P2 can be accentuated in case of pulmonary hypertension, The murmur of pulmonary regurgitation is heard best at the third to fourth intercostal space along the left sternal border and increases with inspiration. Diagnostic options Chest Radiography Chest radiography of patients with pulmonic regurgitation with tricuspid regurgitation may demonstrate cardiomegaly and enlargement of the right-sided heart contour. Pure pulmonic regurgitation may to have specific signs on chest radiography. Prominent central pulmonary arteries with enlarged hilar vessels and loss of vascularity in the peripheral lung fields suggest severe pulmonary hypertension. Electrocardiography Signs of right ventricular hypertrophy can be seen on the Electrocardiogram if pulmonary hypertension is present including a tall R wave in V1 or qR in V1, R wave greater than S wave in V1, R wave progression reversal in the precordial leads and Right axis deviation. A right bundle branch block can be present. Echocardiography Echodoppler is the main diagnostic tool for recognizing pulmonic regurgitation. Regurgitant jet and velocity is visualized by Doppler. The width of the regurgitating jet can be used to quantify the severity. Diastolic regurgitation as well as early peak flow velocity in systole suggests the presence of pulmonary hypertension. Echocardiography can reveal right ventricular hypertrophy and dilatation. Right ventricular volume overload is characterized by abnormal septal wall motion. Structural abnormalities of the pulmonic valve or congenital absence of the valve can be demonstrated by echocardiography. Treatment The right ventricle normally adapts to low-pressure volume, high-pressure volume overload in contrast, ultimately leads to heart failure. Determining the underlying cause of pulmonic regurgitation and possible coexisting pulmonary hypertension is essential for appropriate therapy. Treating the cause of pulmonary hypertension can relieve symptoms and decrease the severity of PR If medical management is insufficient, surgical treatment options should be evaluated. 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