Valvular Heart Disease

Valvular Heart Disease

Types Mitral Stenosis Mitral Regurgitation Mitral Valve Prolapse
Aortic Stenosis Aortic regurgitation Tricuspid valve is affected infrequently Tricuspid stenosis – causes Rt HF Tricuspid regurgitation –causes venous overload

Tricuspid Valve

Rheumatic Heart Disease
Inflammatory process that may affect the myocardium, pericardium and or endocardium Usually results in distortion and scarring of the valves

Rheumatic Heart Disease, cont.
Subjective symptoms Prior history of rheumatic fever General malaise Pain – may or may not be present Objective symptoms Temperature Murmurs Dyspnea polyarthritis

Diagnosis H/P WBC and ESR C-reactive protein Cardiac enzymes EKG Chest x-ray Echo Cardiac cath Cardiac output

Nursing Care Vital signs Rest and quiet environment Give antibiotics, digitalis, and diuretics Provide adequate nutrition Monitor I/O Explain treatment and home care

Mitral Stenosis Usually results from rheumatic carditis
Is a thickening by fibrosis or calcification Can be caused by tumors, calcium and thrombus Valve leaflets fuse and become stiff and the cordae tendineae contract These narrows the opening and prevents normal blood flow from the LA to the LV LA pressure increases, left atrium dilates, PAP increases, and the RV hypertrophies Pulmonary congestion and right sided heart failure occurs Followed by decreased preload and CO decreases

Mitral Stenosis, cont. Mild – asymptomatic
With progression – dyspnea, orthopneas, dry cough, hemoptysis, and pulmonary edema may appear as hypertension and congestion progresses Right sided heart failure symptoms occur later S/S Pulse may be normal to A-Fib Apical diastolic murmur is heard

Mitral Regurgitation Primarily caused by rheumatic heart disease, but may be caused by papillary muscle rupture form congenital, infective endocarditis or ischemic heart disease Abnormality prevents the valve from closing Blood flows back into the right atrium during systole During diastole the regurg output flows into the LV with the normal blood flow and increases the volume into the LV Progression is slowly – fatigue, chronic weakness, dyspnea, anxiety, palpitations May have A-fib and changes of LV failure May develop right sided failure as well

Mitral Valve Prolapse Cause is variable and may be associated with congenital defects More common in women Valvular leaflets enlarge and prolapse into the LA during systole Most are asymptomatic Some may report chest pain, palpitations or exercise intolerance May have dizziness, syncope and palpitations associated with dysrhythmias May have audible click and murmur

Aortic Stenosis Valve becomes stiff and fibrotic, impeding blood flow with LV contraction Results in LV hypertrophy, increased O2 demands, and pulmonary congestion Causes – rheumatic fever, congenital, arthrosclerosis Atherosclerosis and calcification is primary cause in the elderly Complications – right sided heart failure, pulmonary edema, and A-fib S/S – Early: dyspnea, angina, syncope Late: marked fatigue, debilitation, and peripheral cyanosis, crescendo- decrescendo murmur is heard

Aortic Regurgitation Aortic valve leaflets do not close properly during diastole The valve ring that attaches to the leaflets may be dilated, loose, or deformed The ventricle dilates to accommodate the ^ blood volume and hypertrophies Causes: infective endocarditis, congenital, hypertension, Marfan’s May remain asymptomatic for years Develop dyspnea, orthopnea, palpitations, ,and angina May have ^ systolic pressure with bounding pulse Have a high pitch, blowing, decrescendo diastolic murmur

Assessment for Valve Dysfunction
Subjective symptoms Fatigue Weakness General malaise Dyspnea on exertion Dizziness Chest pain or discomfort Weight gain Prior history of rheumatic heart disease

Assessment, cont. Objective symptoms Orthopnea Dyspnea, rales
Pink-tinged sputum Murmurs Palpitations Cyanosis, capillary refill Edema Dysrhythmias Restlessness

Diagnosis History and physical findings EKG Chest x-ray Cardiac cath
Echocardiogram

Medial Treatment Nonsurgical management focuses on drug therapy and rest Diuretic, beta blockers, digoxin, O2, vasodilators, prophylactic antibiotic therapy Manage A-fib, if develops, with conversion if possible, and use of anticoagulation

Interventions Assess vitals, heart sounds, adventitious breath sounds
^ HOB O2 as prescribed Emotional support Give medications I/O Weight Check for edema Explain disease process, provide for home care with O2, medications

Surgical Management of Valve Disease
Mitral Valve Commissurotomy Mitral Valve Replacement Balloon Valvuloplasty Aortic Valve Replacement Commissurotomy – excision of parts of the valve leaflets to enlarge the opening Replacement – tissue or mechanical Balloon – done in the cath lab to enlarge the opening

Mechanical Valve

Porcine Valve

Tissue Valve

Cardiac murmurs Cardiac murmurs are often the first sign of underlying valvular disease. May be systolic or diastolic, pathological or benign. Systolic murmurs may be due to physiological increases in blood velocity or might indicate as yet asymptomatic cardiac disease. Diastolic murmurs are almost always pathological and require further evaluation. An ECG and CXR, although readily available tests, provide limited diagnostic information. During the past 20 years, major advances have occurred in the understanding of natural history, diagnostic evaluation and the treatment of patients with valvular heart disease. The incidental finding of a cardiac murmur often raises the suspicion of underlying valvular disease and therefore requires careful evaluation. A heart murmur may be systolic or diastolic, pathological or benign. Most systolic murmurs do not signify cardiac disease, and many are related to physiological increases in blood flow velocity. On the other hand, a heart murmur may be an important finding in the diagnosis of undetected, as yet asymptomatic cardiac disease. Diastolic murmurs almost always represent pathological conditions and require further cardiac evaluation, as do most continuous murmurs. An ECG and chest X-ray are readily available investigations, but they provide limited information about the significance and aetiology of a heart murmur.

Echocardiography Echocardiography can evaluate valve function by the following imaging modalities: 2-D: Valve motion and morphology; LV size and function. Doppler: Blood flow velocity; valve gradients; haemodynamic data. Colour flow: Valvular regurgitation Echocardiography is the most useful investigation to assess the significance of a heart murmur and has the advantage of being a non-invasive test. 2-D echocardiography may indicate abnormal valvular motion and morphology and assesses left ventricular size and function. Doppler echocardiography identifies increased velocity of flow across stenotic valves from which the severity of stenosis may be determined. The presence of an abnormal regurgitant jet on Doppler colour flow imaging indicates valvular regurgitation and provides semiquantitative information about its severity.

Management of cardiac murmurs
Murmur + cardiac symptoms: refer to cardiologist. In asymptomatic patients with cardiac murmurs, an echo is indicated in the following instances: - Murmur + abnormal cardiac signs - Murmur + abnormal ECG or CXR - Diastolic or continuous murmurs - Pansystolic or late systolic murmurs

Aortic stenosis Aetiology
Aortic stenosis may be congenital or acquired. Congenital malformations may be tricuspid, bicuspid or unicuspid. Acquired causes include the following: - Degenerative disease - Rheumatic disease - Calcific e.g. end-stage renal failure, Paget’s disease - Miscellaneous e.g. rheumatoid involvement A normal aortic valve is formed of 3 cusps. Congenital malformations may be tricuspid, bicuspid or unicuspid. Unicuspid valves are often fatal in childhood. Bicuspid valves are not usually stenotic at birth and the changes causing stenosis resemble those occurring in acquired degenerative disease, but many decades earlier. The congenitally malformed tricuspid aortic valve has cusps of unequal size and some commissural fusion. Acquired degenerative aortic valve disease is the most common cause of aortic stenosis in the elderly. The cusps are immobilised by deposits of calcium resulting from years of normal mechanical stress on the valve. Hypertension, diabetes and hypercholesterolaemia are risk factors for this lesion. Rheumatic aortic stenosis is decreasing in frequency because of a decline in rheumatic fever. Stenosis results from fusion of the cusps producing an orifice that is reduced to a small round or triangular opening, often leading to both stenosis and regurgitation.

Aetiology of aortic stenosis
A: Normal aortic valve B: Congenital aortic stenosis C: Rheumatic aortic stenosis D: Calcific aortic stenosis E: Degenerative aortic stenosis

Aortic stenosis Grading and severity
Aortic valve area must be reduced to 25% of normal before significant circulatory changes occur. Grading of stenosis severity is as follows: - Normal valve area = 3-4cm2 - Mild stenosis = 1.5-3cm2 - Moderate stenosis = cm2 - Severe stenosis ≤ 1.0cm2 When stenosis is severe, the peak gradient across the aortic valve is usually > 60mmHg. The aortic valve area must be reduced to one quarter of its normal size before significant changes in the circulation occur. The normal valve area is 3-4cm2; mild stenosis = valve area of 1.5-3cm2; moderate stenosis = valve area of cm2; severe stenosis = valve area of <1.0cm2. When stenosis is severe and left ventricular function is normal, the peak aortic valve gradient derived by echocardiography is usually >60mmHg.

Pathophysiology of aortic stenosis
LV outflow obstruction LV systolic pressure Aortic pressure LV hypertrophy LV dysfunction Myocardial ischaemia LV failure

Aortic stenosis Natural history of aortic stenosis without operative treatment: Initially, there is a prolonged latent period during which the patient remains asymptomatic, despite gradually increasing aortic valve stenosis. In asymptomatic patients with an AV gradient >60mmHg, 50-60% will develop symptoms within 2-3 years. After the onset of symptoms, average survival is <2-3 years. The cardinal symptoms of aortic stenosis are angina, syncope and dyspnoea. Angina occurs in approximately two-thirds of patients with critical aortic stenosis, of whom about 50% have associated coronary artery disease. Syncope is usually due to reduced cerebral perfusion during exertion, in the face of vasodilatation and a fixed cardiac output. However, the possibility of arrhythmias should be borne in mind, particularly when syncope occurs at rest. Sudden death rarely occurs without preceding symptoms.

Aortic stenosis Physical findings Slow rising pulse
Reduced systolic and pulse pressure Systolic thrill over the aortic area Ejection systolic, crescendo-decrescendo murmur Soft or inaudible second heart sound ECG: LVH, AV node conduction defects The arterial pulse characteristically rises slowly, is low in amplitude and sustained. In the advanced stage, systolic and pulse pressure are both reduced. The apex beat is sustained and a systolic thrill is often palpable over the aortic area. Auscultatory findings include an ejection systolic, crescendo-decrescendo murmur, loudest over the aortic area and radiating to the neck and left sternal edge. The second heart sound is soft or inaudible. The ECG may demonstrate left ventricular hypertrophy or AV node conduction defects.

Aortic stenosis Medical therapy
Conservative treatment should be offered for mild to moderate aortic stenosis and to asymptomatic patients with severe aortic stenosis as follows: - Advise to report symptoms - Avoid vigorous exercise - Antibiotic prophylaxis for endocarditis - Regular follow-up ± echocardiography Conservative medical therapy should be offered to those with mild to moderate aortic stenosis and to asymptomatic patients with severe aortic stenosis as follows: - Advise to report symptoms - Avoid vigorous exercise - Antiobiotic prophylaxis for endocarditis - Regular follow-up ± echocardiography

Aortic stenosis Surgical therapy
Aortic valve replacement should be offered to the following: - Symptomatic pts with severe AS - Pts with severe AS undergoing CABG surgery - Pts with moderate AS undergoing CABG surgery - Asymptomatic pts with severe AS and LV dysfunction Balloon valvuloplasty can play a temporary role as a bridge to surgery in haemodynamically unstable patients, or as palliation for patients with serious comorbid conditions Aortic valve replacement should be offered to the following patients: Symptomatic patients with severe aortic stenosis Patients with severe aortic stenosis undergoing CABG surgery Patients with moderate aortic stenosis undergoing CABG surgery Asymptomatic patients with severe aortic stenosis and left ventricular dysfunction Balloon valvuloplasty can play a temporary role in the management of symptomatic patients who are not initially considered suitable for aortic valve replacement: Palliation for patients with serious comorbid conditions A bridge to surgery in haemodynamically unstable patients

Aortic stenosis Aortic valve replacement
In the absence of LV dysfunction, operative risk is 2-8%. Indicators of higher mortality are NYHA class, LV dysfunction, age, concomitant coronary artery disease, and aortic regurgitation. Valve replacement usually results in reduced LV volumes, improved LV performance and regression of LV hypertrophy. In the absence of LV dysfunction, operative risk is 2-8%. Risk factors for higher mortality are NYHA class, LV dysfunction, age, concomitant coronary artery disease, and aortic regurgitation. Successful valve replacement usually results in reduced LV volumes, improved LV performance and regression of LV hypertrophy.

Aortic regurgitation Aetiology
Either due to primary disease of the aortic valve or wall of the aortic root or both. Causes of primary aortic valve disease include: - Congenital eg. bicuspid aortic valve - Acquired: rheumatic valve disease, infective endocarditis, trauma, connective tissue disease. Causes of primary aortic root disease include: - Degenerative, cystic medial necrosis (eg. Marfan’s), aortic dissection, syphilis, connective tissue disease, hypertension. Aortic regurgitation is either due to primary disease of the aortic valve leaflets or wall of the aortic root or both. The causes of primary aortic valve disease include the following: - Congenital eg. bicuspid aortic valve - Acquired: rheumatic valve disease, infective endocarditis, trauma and connective tissue disease. The causes of primary aortic root disease causing dilatation of the ascending aorta and subsequent aortic regurgitation include the following: - Degenerative, cystic medial necrosis (eg. Marfan’s), aortic dissection, syphilis, connective tissue disease and hypertension.

Pathophysiology of aortic regurgitation
LV volume stroke volume diastolic BP LV mass systolic BP LV dysfunction myocardial ischaemia LV failure

Aortic regurgitation Clinical history
In chronic severe AR, the left ventricle gradually enlarges while the patient remains asymptomatic. Symptoms usually develop after cardiomegaly and LV dysfunction have occurred. Dyspnoea is the principal complaint. Syncope is rare and angina is less frequent than in aortic stenosis. In acute severe AR, LV decompensation occurs readily with fatigue , severe dyspnoea and hypotension. In chronic severe AR, the left ventricle gradually enlarges while the patient remains asymptomatic. Symptoms usually develop after cardiomegaly and LV dysfunction have occurred. Dyspnoea is the principal complaint. Syncope is rare and angina is less frequent than in aortic stenosis. In acute severe AR, LV decompensation occurs readily with clinical manifestations of cardiovascular collapse including fatigue , severe dyspnoea and hypotension.

Aortic regurgitation Physical findings Collapsing pulse.
Wide pulse pressure due to both raised systolic blood pressure and reduced diastolic blood pressure. Displaced, diffuse and hyperdynamic apex beat. Early blowing diastolic murmur. ECG: Left axis deviation, LV hypertrophy. CXR: Cardiomegaly, aortic calcification, aortic root dilatation. In addition to the physical findings listed above, a number of other clinical signs attributable to significant aortic regurgitation include: De Musset’s sign: Bobbing of the head with each heartbeat. Corrigan’s sign: Prominent carotid artery pulsations. Traube’s sign: Booming systolic and diastolic sounds heard over the femoral artery. Muller’s sign: Systolic pulsations of the uvula. Duroziez’s sign: Systolic murmur over the femoral artery when compressed proximally and diastolic murmur when compressed distally. Quincke’s sign: Capillary pulsations detected by transmitting light through the patient’s fingertips. Austin Flint murmur: Rumbling mid-diastolic murmur caused by mitral valve narrowing due to regurgitant blood flow directed at the anterior mitral leaflet and associated raised LV diastolic pressure.

Aortic regurgitation Management Medical treatment includes:
- Diuretics, digoxin, salt restriction - Vasodilators - Endocarditis prophylaxis Indications for surgical treatment depend on symptoms, and LV size and function. Without surgery, death usually occurs within 4 years of developing angina and within 2 years after onset of heart failure. Asymptomatic patients with mild or moderate AR do not require medical therapy, but should be followed up every months with repeat echocardiography. Digoxin may be given to patients with severe AR and LV dilatation. Although patients with severe AR and LV dysfunction require surgery, they respond at least temporarily to digoxin, salt restriction, diuretics and vasodilators.

Aortic regurgitation Surgical therapy
Severe acute AR requires prompt surgical intervention. Indications for valve replacement in pure, severe, chronic AR include: - Symptomatic patients with normal LV function - Symptomatic patients with LV dysfunction or dilatation - Asymptomatic patients with LV dysfunction or dilatation (EF<50% or end-systolic diameter > 55mm) Aortic valve and root replacement are indicated in patients with disease of the proximal aorta and AR of any severity when the aortic root diameter is ≥ 50mm. Since early demise due to left ventricular failure is frequent in patients with severe acute aortic regurgitation despite intensive medical management, prompt surgical intervention is indicated. Surgical intervention is usually deferred in patients with severe chronic AR who are asymptomatic with a good exercise tolerance and normal LV function. However, the onset of symptoms or left ventricular dysfunction and dilatation merits operative correction. Indications for aortic valve replacement in pure, severe, chronic aortic regurgitation include: - Symptomatic patients with normal left ventricular systolic function - Symptomatic patients with left ventricular dysfunction or dilatation - Asymptomatic patients with left ventricular dysfunction or dilatation (EF<50% or end-systolic diameter > 55mm) In general, aortic valve and root replacement are indicated in patients with disease of the proximal aorta and aortic regurgitation of any severity when the aortic root diameter is ≥ 50mm by echocardiography.

Aortic valve replacement and prognosis
Relation of preoperative LV function to postoperative survival The lower the preoperative ejection fraction and the higher the LV end-systolic diameter, the worse the postoperative outcome.

Mitral stenosis Aetiology Rheumatic fever is the predominant cause.
Rarely, mitral stenosis is congenital and observed almost exclusively in infants and young children. Miscellaneous rare causes include carcinoid, SLE, rheumatoid arthritis and mucopolysaccharidoses. Causes of left atrial outflow obstruction that may simulate mitral stenosis include left atrial myxoma, ball-valve thrombus, infective endocarditis with large vegetation and cor triatriatum. Rheumatic fever is the predominant cause of mitral stenosis. Rarely, mitral stenosis is congenital in aetiology and this is observed almost exclusively in infants and young children. Other possible causes include carcinoid, SLE, rheumatoid arthritis and mucopolysaccharidoses. Other causes of left atrial outflow obstruction may simulate mitral stenosis eg. left atrial myxoma, ball-valve thrombus, infective endocarditis with large vegetation and cor triatriatum (congenital membrane in the left atrium).

Rheumatic mitral stenosis
Rheumatic mitral stenosis is due to four forms of fusion: commissural (30%), cuspal (15%), chordal (10%) or combined (45%). The stenotic mitral valve is typically funnel-shaped; the orifice is frequently shaped like a fish mouth. Symptoms usuually occur in the 3rd or 4th decade, but mild MS in the aged is becoming more common. 25% of patients with rheumatic mitral valve disease have pure mitral stenosis and two-thirds are female. May be associated with an atrial septal defect – Lutembacher’s syndrome. Rheumatic mitral stenosis is due to four forms of fusion: commissural (30%), cuspal (15%), chordal (10%) or combined (45%). The stenotic mitral valve is typically funnel-shaped and the orifice is frequently shaped like a fish mouth. Symptoms commence most commonly in the third or fourth decade, although mild MS in the aged is becoming a more common finding. 25% of patients with rheumatic mitral valve disease have pure mitral stenosis and two-thirds are female. The combination of rheumatic mitral stenosis and an atrial septal defect is known as Lutembacher’s syndrome.

Mitral stenosis Pathophysiology Normal mitral valve area = 4-6cm2.
Usually, a mitral valve area ≤ 2.5cm2 must occur before the development of symptoms. A mitral valve area >1.5cm2 usually does not produce symptoms at rest. The first symptoms in mild mitral stenosis are usually precipitated by exercise, emotional stress, infection, pregnancy or fast atrial fibrillation. A mitral valve area ≤ 1cm2 equates to severe mitral stenosis. Pulmonary hypertension results from backward pressure, pulmonary arteriolar constriction and organic obliterative changes in the pulmonary vascular bed. The normal adult cross-sectional area of the mitral valve is 4-6 cm2. Narrowing of the valve area to 2.5cm2 must occur before the development of symptoms. A mitral valve area of >1.5cm2 usually does not produce symptoms at rest. However, an increase in transmitral flow or a decrease in the diastolic filling period may raise the left atrial pressure and thereby lead to the development of symptoms. Thus, the first symptoms of dyspnoea in patients with mild mitral stenosis are usually precipitated by exercise, emotional stress, infection, pregnancy or fast atrial fibrillation. In the presence of severe mitral stenosis (mitral valve area ≤ 1 cm2), left atrial pressure becomes chronically elevated leading to raised pulmonary venous and capillary pressures and the development of dyspnoea. Pulmonary hypertension in patients with mitral stenosis results from (i) passive backward transmission of the raised left atrial pressure; (ii) pulmonary arteriolar constriction triggered by left atrial and pulmonary venous hypertension; (iii) organic obliterative changes in the pulmonary vascular bed as a complication of longstanding and severe mitral stenosis.

Mitral stenosis Natural history
Long latent period of 20 to 40 years from the occurrence of rheumatic fever to onset of symptoms. Once symptoms develop, there is a further 10 years before symptoms become disabling. Once significant limiting symptoms occur, the 10-year survival rate is 5-15%. When there is severe pulmonary hypertension, mean survival falls to < 3 years. Mortality from untreated mitral stenosis is due to progressive heart failure (60-70%), systemic embolism (20-30%) and pulmonary embolism (10%). In developed countries, there is a long latent period of 20 to 40 years from the occurrence of rheumatic fever to the onset of symptoms. Once symptoms develop, there is another period of almost a decade before symptoms become disabling. Once significant limiting symptoms occur there is a 10-year survival rate of 5-15% and when there is severe pulmonary hypertension, mean survival drops to < 3 years. Mortality of untreated patients with mitral stenosis is caused by progressive heart failure in 60-70%, systemic embolism in 20-30% and pulmonary embolism in 10% of patients.

Mitral stenosis Clinical features
The main symptom is dyspnoea due to reduced lung compliance. Haemoptysis may also occur. Approximately 15% of patients experience angina due to either coincidental coronary artery disease, right ventricular hypertension or coronary embolisation. Embolic events may occur and 80% of such patients are in atrial fibrillation. The principal symptom is dyspnoea mainly due to reduced compliance of the lungs. Haemoptysis may also occur. Approximately 15% of patients experience angina which may be due to either coincidental coronary artery disease, right ventricular hypertension or coronary embolisation. The tendency for embolisation correlates inversely with cardiac output and directly with the patient’s age and size of the left atrial appendage. 80% of patients with systemic emboli are in atrial fibrillation.

Mitral stenosis Physical findings
Mitral facies – pinkish-purple patches on the cheeks. Tapping apex beat – palpable first heart sound. Right ventricular heave, loud P2 indicating pulmonary hypertension. Loud first heart sound. Opening snap. Rumbling, mid-diastolic murmur with presystolic accentuation in sinus rhythm. Characteristic physical findings include: - Mitral facies – pinkish-purple patches on the cheeks, present in patients with severe mitral stenosis, low cardiac output and systemic vasoconstriction. - Right ventricular heave and loud pulmonary component of the second heart sound - indicate the presence of pulmonary hypertension. - Tapping apex beat – palpable first heart sound indicating a pliable anterior mitral leaflet. - Opening snap - due to a sudden tensing of the valve leaflets at maximum opening of the mitral valve. - Low-pitched, rumbling mid-diastolic murmur with presystolic accentuation in sinus rhythm, best heard with the bell of the stethoscope at the apex with the patient’s breath held in expiration.

Mitral stenosis Echo evaluation
Assessment of valve morphology: degree of leaflet thickness, mobility and calcification and extent of subvalvular fusion. Estimation of left atrial size. Doppler echo: estimation of mitral valve area, transvalvular gradient and PA pressure. Echocardiography is the diagnostic tool of choice in the evaluation of a patient with mitral stenosis. 2-D imaging allows the assessment of mitral valve morphology including leaflet mobility, leaflet thickness, leaflet calcification, subvalvular fusion and appearance of the commisures. Left atrial size can also be measured. Doppler echocardiography allows the estimation of mitral valve area, mean transmitral pressure gradient and pulmonary artery pressure.

Mitral stenosis Medical treatment
The asymptomatic patient with mild mitral stenosis should be managed medically. Medical therapy includes: - Avoidance of unusual physical stress. - Salt restriction. - Diuretics if needed. - Control of heart rate – β-blocker or digoxin. - Anticoagulation for AF or prior embolic event. - Annual follow-up. - Echocardiography if deterioration in clinical condition. The asymptomatic patient with mild mitral stenosis (mitral valve area > 1.5cm2 and mean gradient <5mmHg) needs no further investigation as these patients usually remain stable for many years. Annual review is recommended and echocardiography should be repeated if there is a deterioration in symptoms or clinical signs. Medical therapy includes the following: - Avoid unusual physical stress - Salt restriction - Diuretics - Control of heart rate - Anticoagulation: patients with paroxysmal or chronic atrial fibrillation, or a prior embolic event. Antibiotic prophylaxis The asymptomatic patient with more severe mitral stensosis and pliable, noncalcified valves with little or no subvalvular fusion and no calcification in the commissures should be considered for balloon mitral valvuloplasty.

Mitral stenosis Management of symptomatic mitral stenosis
Patients with symptoms should undergo clinical re-evaluation with echocardiography. NYHA class II symptoms and mild mitral stenosis may be managed medically. NYHA class II symptoms and at least moderate stenosis (MVA≤1.5cm2 or mean gradient ≥5mmHg) may be considered for balloon valvuloplasty. NYHA class III or IV symptoms and severe mitral stenosis should be considered for balloon valvuloplasty or surgery. Patients who develop symptoms should undergo clinical re-evaluation with CXR, ECG and echocardiography. In general, patients with NYHA class II symptoms and mild mitral stenosis may be managed medically. Patients with NYHA class II symptoms and at least moderate stenosis (MVA≤1.5cm2 or mean gradient ≥5mmHg) may be considered for balloon mitral valvuloplasty. Patients with NYHA class III or IV symptoms and severe mitral stenosis have a poor prognosis if left untreated and intervention with balloon valvuloplasty or surgery should be considered.

Mitral stenosis Balloon mitral valvuloplasty
The technique involves passing a balloon flotation catheter across the interatrial septum after trans-septal puncture and dilating the balloon within the mitral valve orifice. Results of the procedure are highly dependent on the experience of the operator. 80-95% of patients have a successful procedure. Complications include severe MR, residual ASD, myocardial perforation, emboli, MI and death. Overall event-free survival is 50% to 65% over 3-7 years. The underlying mitral valve morphology is the most important factor in determining outcome. Relative contraindications include the presence of a left atrial thrombus and significant mitral regurgitation. Balloon mitral valvuloplasty emerged in the 1980s and has become an acceptable alternative to surgery in selected patients. The technique involves passing a balloon flotation catheter across the interatrial septum, after trans-septal puncture, and dilating the balloon within the mitral valve orifice. The results of the procedure are highly dependent on the experience of the operator. In experienced hands, the immediate results of balloon mitral valvuloplasty are similar to those of surgical mitral commisurotomy. The valve area usually doubles with a 50% to 60% reduction in the transmitral gradient; 80-95% of patients have a successful procedure defined as a mitral valve area >1.5cm2 and a decrease in left atrial pressure to ≤18mmHg in the absence of complications. However, there is a 4-5% complication rate including severe mitral regurgitation, residual atrial septal defect, myocardial perforation, emboli, myocardial infarction and death. The overall event-free survival rate is 50% to 65% over 3-7 years. The underlying mitral valve morphology is the most important factor in determining outcome. The procedure is usually more successful and with a better outcome in patients with noncalcified pliable valves and no commissural calcification. Relative contraindications include the presence of a left atrial thrombus and significant mitral regurgitation. In centres with skilled, experienced operators, balloon mitral valvuloplasty should be considered for symptomatic patients with moderate to severe mitral stenosis and favourable valve morphology in the absence of significant mitral regurgitation or a left atrial thrombus.

Mitral stenosis Mitral valve replacement
Mitral valve replacement is indicated in patients with severe mitral stenosis and contraindications to surgical commisurotomy or balloon valvuloplasty: - Restenosis following surgical commisurotomy or balloon valvuloplasty. - Significant mitral stenosis and regurgitation. - Extensive calcification of the subvalvular apparatus. Operative mortality ranges from 3-8% in most centres. Postponement of surgery until the patient reaches NYHA class IV symptoms should be avoided. Mitral valve replacement is an accepted surgical procedure for patients with severe mitral stenosis who are not candidates for open or closed surgical commisurotomy or balloon mitral valvuloplasty. Such patients include those with both significant mitral stenosis and regurgitation, or those with extensive calcification of the subvalvular apparatus. The operative mortality ranges from 3-8% in most centres. Postponement of surgery until the patient reaches NYHA class IV symptoms should be avoided because operative mortality is high and long term outcome suboptimal. However, surgery should not be denied because the outlook without surgical intervention is grave.

Mitral regurgitation Aetiology
Mitral regurgitation may be caused by abnormalities of the valve leaflets, chordae tendinae, papillary muscles or mitral annulus: Valve leaflets - myxomatous degeneration causing mitral valve prolapse - shortening, rigidity, deformity and retraction due to rheumatic heart disease - vegetations due to infective endocarditis Chordae tendinae - congenital, infective endocarditis, trauma, rheumatic fever, myxomatous Papillary muscles - myocardial ischaemia, congenital abnormalities, infiltrative disease Mitral annulus - dilatation eg. ischaemic or dilated cardiomyopathy - calcification due to degeneration, hypertension, aortic stenosis, diabetes, chronic renal failure The mitral valve apparatus involves the mitral leaflets, the chordae tendinae, the papillary muscles and the mitral annulus. Mitral regurgitation may therefore be caused by abnormalities of any of these structures: Abnormalities of the valve leaflets: - myxomatous degeneration causing mitral valve prolapse - shortening, rigidity, deformity and retraction by rheumatic heart disease - vegetations/infective endocarditis Abnormalities of the chordae tendinae: - congenital, infective endocarditis, trauma, rheumatic fever, mitral valve prolapse Abnormalities of the papillary muscles: - myocardial ischaemia, congenital abnormalities, infiltrative disease Abnormalities of the mitral annulus: - dilatation eg. ischaemic cardiomyopathy - calcification eg. degenerative, hypertension, aortic stenosis, diabetes, chronic renal failure

Mitral regurgitation Clinical features
Symptoms usually occur with LV decompensation: dyspnoea and fatigue. Physical findings include: - Pulse: sharp upstroke - Apex: displaced, hyperdynamic - Heart sounds: pansystolic murmur loudest at the apex, radiating to the axilla and accentuated by expiration. Symptoms Symptoms usually do not develop in patients with chronic mitral regurgitation until the left ventricle fails. The predominant symptoms are dyspnoea, fatigue and weakness. Examination - Pulse: sharp upstroke - Apex: displaced, hyperdynamic - Heart sounds: soft S1, pansystolic murmur loudest at the apex, radiating to the axilla and accentuated by expiration, wide splitting of S2, S3 present.

Mitral regurgitation Natural history
The natural history of chronic MR depends on the volume of regurgitation, the state of the myocardium and the underlying cause. Preoperative LV end-systolic diameter is a useful predictor of postoperative survival in chronic MR. The preoperative LV end-systolic diameter should be < 45mm to ensure normal postoperative LV function. Natural history The natural history of chronic mitral regurgitation depends on a combination of the volume of regurgitation, the state of the myocardium and the cause of the underlying disorder. Nevertheless, preoperative left ventricular end-systolic diameter is a useful predictor of postoperative survival in patients with chronic mitral regurgitation. The end-systolic diameter should be < 45mm before surgery to ensure normal postoperative left ventricular function.

Mitral regurgitation Medical treatment
Symptomatic patients may benefit from the following drug therapy whilst awaiting surgery: Vasodilator therapy Diuretics Digoxin / Beta-blockers in presence of atrial fibrillation. Endocarditis prophylaxis For the asymptomatic patient with chronic mitral regurgitation, there is no generally accepted medical therapy. Symptomatic patients may benefit from the following drug therapy whilst awaiting surgery: Vasodilator therapy Diuretics Digoxin / Beta-blockers in presence of atrial fibrillation. Endocarditis prophylaxis

Mitral regurgitation Surgical treatment
Surgery is indicated in the presence of symptoms or left ventricular end systolic diameter ≥45mm. The surgical procedure consists of either mitral valve repair or replacement. Mitral valve repair better preserves LV function and avoids the need for chronic anticoagulation. However, mitral valve repair is technically more demanding and often not possible to perform in severely deformed valves. The need for surgery in patients with chronic severe mitral regurgitation is dependent on symptomatic status and left ventricular function. Surgery is indicated in the presence of symptoms or left ventricular end systolic diameter ≥45mm. The surgical procedure consists of either mitral valve repair or replacement. Mitral valve repair has the advantage of better preserving left ventricular function and avoiding the need for chronic anticoagulation. However, the procedure is technically more demanding and often not possible to perform in severely deformed valves. Mortality rates for mitral valve surgery approximate to 1-4% in predominant mitral stenosis and 2-7% in predominant mitral regurgitation.

Mitral regurgitation Relationship of preoperative ejection fraction
to postoperative survival The lower the preoperative LV ejection fraction the worse the postoperative outcome.

Acute mitral regurgitation
Aetiology Important causes of acute mitral regurgitation include: Infective endocarditis causing disruption of valve leaflets or chordal rupture. Ischaemic dysfunction or rupture of papillary muscle. Malfunction of prosthetic valve. The causes of acute mitral regurgitation are diverse and represent acute manifestations of disease processes that may under other circumstances cause chronic mitral regurgitation. Important causes include: - Infective endocarditis causing disruption of valve leaflets or chordal rupture. - Ischaemic dysfunction or rupture of papillary muscle. - Malfunction of prosthetic valve.

Chronic versus Acute MR
Finding Chronic MR Acute MR Symptoms subtle onset obvious Appearance normal/mildly severely ill dyspnoeic Tachycardia not striking always present Apex beat displaced not displaced Systolic thrill common absent Murmur harsh pansystolic soft or absent early systolic component ECG-LVH usually present absent CXR severe cardiomegaly normal heart size As summarized in the table above, both the clinical features and haemodynamic findings between acute and chronic severe mitral regurgitation may differ widely. Many of the haemodynamic consequences derive from the difference in left atrial compliance in acute versus severe mitral regurgitation. Patients with acute mitral regurgitation usually have a normal-sized left atrium with normal or reduced atrial compliance leading to the rapid development of pulmonary oedema.

Acute mitral regurgitation
Medical therapy The following therapies may be beneficial in reducing the severity of MR - Vasodilator therapy - Inotropic therapy - Intra-aortic balloon counterpulsation Surgical therapy Indicated in patients with acute severe MR and heart failure. Higher mortality rates than for elective chronic MR, but unless treated aggressively, the outcome is usually fatal. Medical therapy Depending on haemodynamic status, the following therapeutic options may be beneficial in reducing the severity of mitral regurgitation: - Vasodilator therapy - Inotropic therapy - Intra-aortic balloon counterpulsation Surgical therapy Surgery is usually indicated in patients with acute severe mitral regurgitation and heart failure. Mortality rates are usually higher than for elective chronic mitral regurgitation, but unless such patients are treated aggressively, a fatal outcome is almost certain.

Mitral valve prolapse General features
Occurs in 2-6% of the general population Twice as common in women. Due to myxomatous proliferation of the mitral valve. Usually occurs as a primary condition, but may be a secondary finding in connective tissue diseases e.g. Marfan’s syndrome. Vast majority of patients are asymptomatic. Symptoms may include palpitations, dizziness, syncope, or chest discomfort. The principal physical finding is the mid-systolic click, followed by a late systolic murmur in the presence of regurgitation. This is the most common form of valvular heart disease, occurring in 2-6% of the population and is twice as common in women. It is due to myxomatous proliferation of the mitral valve causing an increased surface area of the valve, leading to impaired coaptation of the leaflet edges and resultant mitral regurgitation. The severity of mitral regurgitation depends on the extent of prolapse. It usually occurs as a primary condition unassociated with other disease, but can be a secondary finding in certain connective tissue diseases. It is found in approximately 90% of patients with Marfan’s syndrome. The vast majority of patients with MVP are asymptomatic. Patients may complain of palpitations, dizziness, syncope, chest discomfort, but whether these symptoms are truly attributable to the MVP is often unclear. The principal cardiac auscultatory finding is the midsystolic click resulting from sudden tensing of the mitral valve apparatus as the leaflets prolapse into the left atrium during systole. In the presence of regurgitation, the midsystolic click is followed by a late systolic murmur.

Mitral valve prolapse Echocardiographic criteria
M-mode criterion:  2mm posterior displacement of one or both leaflets. 2-D echo findings: Systolic displacement of one or both leaflets within the left atrium in the parasternal long-axis view; leaflet thickening, redundancy, chordal elongation and annular dilatation. The diagnosis of mitral valve prolapse is even more certain when leaflet thickness is >5mm. Echocardiography is useful in the risk stratification of patients with mitral valve prolapse. Echocardiography is the most useful investigation for defining mitral valve prolapse: - M-mode criterion:  2mm posterior displacement of one or both leaflets - 2-D echo findings may include: Systolic displacement of one or both mitral leaflets within the left atrium in the parasternal long-axis view; leaflet thickening, redundancy, chordal elongation and annular dilatation. The diagnosis of mitral valve prolapse is even more certain when leaflet thickness is >5mm. Echocardiography is useful in the risk stratification of patients with mitral valve prolapse

Mitral valve prolapse Natural history
In most patients, mitral valve prolapse is associated with a benign prognosis. Complications may occur in patients with a systolic murmur, thickened leaflets an increased LV or LA size, especially in men > 45 years old: Complications include progressive mitral regurgitation, infective endocarditis, cerebral emboli, arrhythmias and rarely sudden death. Natural history In most patients, mitral valve prolapse is associated with a benign prognosis. Complications may occur in patients with a systolic murmur, thickened leaflets an increased LV or LA size, especially in men > 45 years old: Complications include progressive mitral regurgitation, infective endocarditis, cerebral emboli, arrhythmias and rarely sudden death.

Mitral valve prolapse Management
Asymptomatic patients without MR or arrhythmias have an excellent prognosis – follow-up every 3-5 years. Patients with a typical systolic murmur should receive endocarditis prophylaxis. Patients with a long systolic murmur may show progression of MR and should be reviewed annually. Patients with previous embolic events should be given antiplatelet / anticoagulant therapy. Severe MR requires surgery, often mitral valve repair. Asymptomatic patients without mitral regurgitation or arrhythmias have an excellent prognosis and may be followed-up every 3-5 years. In patients with a typical systolic murmur indicating mitral regurgitation, endocarditis prophylaxis should be given. Patients with a long systolic murmur may show progression of mitral regurgitation and should be reviewed annually. Severe mitral regurgitation requires surgery, often mitral valve repair. Antiplatelet / anticoagulant therapy should be recommended to patients with previous embolic events.

Prosthetic valves Prosthetic valves may be divided into 2 broad categories: Mechanical valves Very good durability. Require long-term anticoagulation. May cause mild haemolysis. Bioprosthetic (tissue) valves Porcine variety most commonly used. Limited durability. Anticoagulation for first 3 months only.

Mechanical valves Designs and flow patterns of different types of mechanical valves

Prosthetic valves Mechanical versus tissue valves
No difference in survival, haemodynamics or in probability of developing endocarditis, valve thrombosis or systemic embolism. Valve-related failure is much more common with tissue valves. Anticoagulant-related bleeding occurs with mechanical valves. Elderly patients tend to receive tissue valves.

Tricuspid stenosis Always rheumatic in origin and when present accompanies mitral valve involvement. The anatomical changes and physiological principles are similar to those of mitral stenosis. The low cardiac output state causes fatigue; abdominal discomfort may occur due to hepatomegaly and ascites. The diastolic murmur of tricuspid stenosis is augmented by inspiration. Medical management includes salt restriction and diuretics. Surgical treatment should be carried out in patients with a valve area <2.0cm2 and a mean pressure gradient >5mmHg. Tricuspid stenosis, although very uncommon, is always rheumatic in origin and when present accompanies mitral valve involvement. The majority of cases of rheumatic tricuspid valve disease present with tricuspid regurgitation or a combination of stenosis and regurgitation. The anatomical changes resemble those of mitral stenosis. The physiological principles are also similar to those of mitral stenosis but reflect changes to the systemic venous circulation rather than the pulmonary venous system. The low cardiac output characteristic of tricuspid stenosis, causes fatigue and abdominal discomfort may occur due to hepatomegaly and ascites. The diastolic murmur of tricuspid stenosis, unlike mitral stenosis is augmented by inspiration. Medical management includes salt restriction and diuretic therapy. Surgical treatment should be carried out in patients with a valve area <2.0cm2 and a mean pressure gradient >5mmHg. A porcine bioprosthesis is the preferred choice of valve because of the high risk of thrombosis with mechanical valves in this position. Other causes of obstruction to right atrial emptying are rare and include congenital tricuspid atresia, right atrial tumours and the carcinoid syndrome.

Tricuspid reurgitation
Most common cause is annular dilatation due to RV failure of any cause; may also be caused by intrinsic valve involvement Well tolerated in the absence of pulmonary hypertension; in the presence of pulmonary hypertension, cardiac output declines and RV failure may worsen. Symptoms and signs result from a reduced cardiac output, ascites, painful congestive hepatomegaly and oedema. The pansystolic murmur of TR is usually loudest at the left sternal edge and augmented by deep inspiration. Severe functional TR may be treated by annuloplasty or valve replacement. Severe TR due to intrinsic tricuspid valve disease requires valve replacement. Aetiology The most common cause of tricuspid regurgitation is annular dilatation due to right ventricular failure of any cause eg. mitral valve disease, right ventricular infarction, congenital heart disease, primary pulmonary hypertension and rarely cor pulmonale. Causes of TR due to intrinsic valve involvement include Ebstein’s anomaly, atrioventricular canal defects, rheumatic heart disease, carcinoid syndrome, myxomatous degeneration and infective endocarditis. Clinical features TR is generally well tolerated in the absence of pulmonary hypertension. However, in the presence of pulmonary hypertension, cardiac output declines and right-sided heart failure may worsen. Therefore, the symptoms and signs of TR result from a reduced cardiac output, ascites, painful congestive hepatomegaly and oedema. The pansystolic murmur of tricuspid regurgitation is usually loudest at the left sternal edge and augmented by deep inspiration. Management TR in the absence of pulmonary hypertension usually does not require surgical treatment. Patients with severe TR and rheumatic heart disease require ring annuloplasty. The management of severe functional TR is controversial and may be treated by annuloplasty or valve replacement. Severe TR due to intrinsic tricuspid valve disease eg. Ebstein’s anomaly or carcinoid usually requires valve replacement.

Pulmonary stenosis Most commonly due to congenital malformation and usually an isolated anomaly. Survival into adulthood is the rule, infective endocarditis is a risk and right ventricular failure is the most common cause of death. Rheumatic involvement of the pulmonary valve is very uncommon and rarely leads to serious deformity. Carcinoid plaques may lead to constriction of the pulmonary valve ring. Pulmonary stenosis is most commonly due to congenital malformation and usually an isolated anomaly. Survival into adulthood is the rule, infective endocarditis is a risk and right ventricular failure is the most common cause of death. Rheumatic involvement of the pulmonary valve is very uncommon and rarely leads to serious deformity. Carcinoid plaques may lead to constriction of the pulmonary valve ring.

Pulmonary regurgitation
Most common cause is ring dilatation due to pulmonary hypertension, or dilatation of the pulmonary artery secondary to a connective tissue disorder. May be tolerated for many years unless complicated by pulmonary hypertension. The clinical manifestations of the primary disease tend to overshadow the pulmonary regurgitation. Physical examination reveals a right ventricular heave and a high-pitched, blowing, early diastolic decrescendo murmur over the left sternal edge, augmented by deep inspiration. Pulmonary regurgitation is seldom severe enough to require specific treatment. Surgery may be required because of intractable RV failure. Aetiology Most common cause is dilatation of the valve ring secondary to pulmonary hypertension, or to dilatation of the pulmonary artery secondary to a connective tissue disorder. The second most common cause is infective endocarditis. Pulmonary regurgitation may also result from congenital malformations, trauma, carcinoid syndrome or iatrogenic causes. Clinical features Isolated pulmonary regurgitation may be tolerated for many years unless it is complicated by pulmonary hypertension. In most patients, the clinical manifestations of the primary disease overshadow the pulmonary regurgitation. Physical examination reveals a hyperdynamic right ventricle producing a right ventricular heave in the left parasternal area. The murmur of pulmonary regurgitation is a high-pitched, blowing, early diastolic decrescendo murmur heard best over the left sternal edge and augmented by deep inspiration. Management Pulmonary regurgitation is seldom severe enough to require specific treatment. Surgery is required only occasionally because of intractable right ventricular failure, preferably with a porcine bioprothesis.

Valvular Heart Disease

Similar presentations

Presentation on theme: "Valvular Heart Disease"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Valvular Heart Disease

Similar presentations

Presentation on theme: "Valvular Heart Disease"— Presentation transcript:

Similar presentations

About project

Feedback