valvular heart disease
DESCRIPTION
TRANSCRIPT
VALVULAR HEART DISEASE
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CARDIAC MURMURSAuscultatory sound, particularly a periodic sound of short
duration of cardiac or vascular origin 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 and most continuous murmurs are almost always pathological and require further evaluation.
An ECG and CXR, although readily available tests, provide limited diagnostic information. 2
CHARACTERISTICS OF MURMURS
Benign
Early to midsystolic
Soft (I-III/VI)
Vary with respiration
Present during normal exam and work-up
Pathologic
All diastolic murmurs
All pansystolic murmurs
Late systolic murmurs
Very loud murmurs
Continuous murmurs 3
EXAMPLES OF MURMURS
Benign
Flow
Pathologic
Diastolic: MS, TS, AI, PI
Pansystolic (holosystolic): MR, TR, VSD
Loud murmurs: >III/VI
Continuous: Patent ductus arteriosus
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MURMURS BY POSITION
Systolic
Right Upper Sternal Border (RUSB)
Aortic Stenosis (AS)
Left Upper Sternal Border (LUSB)
Pulmonary Insufficiency (PI)
Left Lower Sternal Border (LLSB)
Tricuspid Regurgitation (TR)
Ventricular Septal Defect (VSD)
Hypertrophic Cardiomyopathy (HCM)
Apex
Mitral Regurgitation (MR) 5
MURMURS BY POSITION
Diastolic
Left Upper Sternal Border (LUSB)
Pulmonary Insufficiency (PI)
Left Lower Sternal Border (LLSB)
Tricuspid Stenosis (TS)
Apex
Mitral Stenosis (MS)
3rd Intercostal Space (ICS), Lower Sternal Border (LSB)
Aortic Insufficiency (AI)
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CONTINUOUS MURMURS
Require continuous pressure gradient for continuous blood flow
Occurs at artery-vein connections
Patent Ductus Arteriosus (PDA)
Arteriovenous Malformation (AVM)
Venous Hum
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MANAGEMENT OF CARDIAC MURMURS
Murmur + cardiac symptomsRefer 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
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ECHOCARDIOGRAPHYMost useful investigation to assess significance of heart murmurAdvantage of being non-invasive test
Echocardiography can evaluate valve function by the following imaging modalities:
2-D: Valve motion and morphologyLV size and function
Doppler: Blood flow velocityValve gradientsHemodynamic data
Color flow: Valvular regurgitationSemi-quantitation about severity
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HEART VALVES
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AORTIC STENOSISAortic stenosis may be congenital or acquiredCongenital malformations:
Tricuspid – cusps of unequal size and some commissural fusion Bicuspid – not usually stenotic at birth; changes resemble those occurring in acquired degenerative disease, but many decades earlierUnicuspid – often fatal in childhood
Acquired causes:Degenerative disease – most common cause of aortic stenosis in the elderly; deposits of calcium resulting from years of normal mechanical stress on the valve; hypertension, diabetes and hypercholesterolemia are risk factorsRheumatic disease – decreasing in frequency because of a decline in rheumatic fever; fusion of the cusps producing an orifice that is reduced to a small round or triangular opening, often leading to both stenosis and regurgitation Calcific – e.g. end-stage renal failure, Paget’s diseaseMiscellaneous – e.g. rheumatoid involvement
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PATHOPHYSIOLOGY OF AORTIC STENOSIS
Aortic stenosis
LV outflow obstruction
LV systolic pressure Aortic pressure
LV hypertrophy
LV dysfunction Myocardial ischemia
LV failure
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AORTIC STENOSIS
Symptoms
Fatigue
Dyspnea on exertion (DOE)
Angina
Exertional Syncope
Heart Failure (HF)
Sudden Cardiac Death (SCD)
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AORTIC STENOSIS
Physical findings
Slow rising pulse – low in amplitude and sustained
Reduced systolic and pulse pressure in advanced stages
Systolic thrill palpable over aortic area
Ejection systolic, crescendo-decrescendo murmur loudest over the aortic area and radiating to the neck and left sternal edge
Soft or inaudible second heart sound
ECG: LVH, AV node conduction defects15
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
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AORTIC STENOSISSurgical therapy
Aortic valve replacement should be offered to the following:
Symptomatic pts with severe ASPts with severe AS undergoing CABG
surgeryPts with moderate AS undergoing CABG
surgeryAsymptomatic pts with severe AS and LV
dysfunctionBalloon valvuloplasty can play a temporary role as a bridge to surgery in hemodynamically unstable patients, or as palliation for patients with serious comorbid conditions
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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. 18
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AORTIC REGURGITATION
Either due to primary disease of the aortic valve, wall of the aortic root, or both
Causes of primary aortic valve disease include:Congenital – bicuspid aortic valve Acquired – rheumatic valve disease, infective
endocarditis, trauma, connective tissue disease
Causes of primary aortic root disease include:Degenerative – cystic medial necrosis,
Marfan’s syndrome, Reiter’s syndrome, aortic dissection, syphilis, connective tissue disease, hypertension
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PATHOPHYSIOLOGY OF AORTIC REGURGITATION
Aortic regurgitation
LV volume stroke volume diastolic BP
LV mass systolic BP
LV dysfunction myocardial ischemia
LV failure
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AORTIC REGURGITATIONClinical 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. Dyspnea 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 dyspnea and hypotension.
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AORTIC REGURGITATION
Physical findingsCollapsing 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.
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AORTIC REGURGITATION
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AORTIC REGURGITATION
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.32
AORTIC REGURGITATION
ManagementMedical treatment includes:
Diuretics, digoxin, salt restrictionVasodilators 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.
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AORTIC REGURGITATION
Surgical therapySurgical intervention is usually deferred in patients with severe chronic AR
who are asymptomatic with a good exercise tolerance and normal LV functionSevere acute AR requires prompt surgical intervention due to early demise
from left ventricular failure despite intensive medical managementIndications for valve replacement in pure, severe, chronic AR include:
Symptomatic patients with normal LV functionSymptomatic patients with LV dysfunction or dilatationAsymptomatic 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 by echocardiography
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• Subaortic membrane demonstrated with an aortogram. The aortic regurgitation outlines the membrane (arrow) as well as fills the left ventricle.
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Aortic regurgitation image acquired in end diastole showing lack of apposition of the aortic valve leaflets(arrowed). Note also the dilated aortic root.
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MITRAL STENOSIS
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
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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
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MITRAL STENOSIS
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 – increase in transmitral flow or a decrease in the diastolic filling period
A mitral valve area ≤ 1cm2 equates to severe mitral stenosis – left atrial pressure becomes chronically elevated leading to raised pulmonary venous and capillary pressures and the development of dyspnea
Pulmonary hypertension results from backward pressure, pulmonary arteriolar constriction and organic obliterative changes in the pulmonary vascular bed
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MITRAL STENOSISLong 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%) 42
MITRAL STENOSISClinical features
The main symptom is dyspnea due to reduced lung compliance Hemoptysis may also occur – increased pulmonary pressuresApproximately 15% of patients experience angina due to either coincidental coronary artery disease, right ventricular hypertension or coronary embolizationHeart failure (HF) symptoms – both left sided with paroxysmal nocturnal
dyspnea (PND) or orthropnea and right sided with jugular venous pressure (JVP), lower extremity edema, hepatomegaly, and ascites
Hoarseness – secondary to left atrial compression of recurrent laryngeal nerve, enlarged tracheobronchial lymph nodes and dilated
pulmonary arteryTendency for embolization correlates inversely with cardiac output and
directly with the patient’s age and size of the left atrial appendageEmbolic events may occur and 80% of such patients are in atrial fibrillation
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MITRAL STENOSISPhysical findings
Mitral facies – pinkish-purple patches on the cheeks 2° to low cardiac output and systemic vasoconstrictionTapping apex beat – palpable S₁ indicating a pliable anterior mitral leafletRight ventricular heave, loud P2 indicating pulmonary hypertensionLoud first heart sound – elevated pressure in the left atria (LA) slamming the valve shutOpening snap – due to a sudden tensing of the valve leaflets at maximum opening of the mitral valveRumbling, mid-diastolic murmur with presystolic accentuation in sinus rhythm
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MITRAL STENOSIS
Echo evaluation
Diagnostic tool of choice
2-D imaging:
Assessment of valve morphology – degree of leaflet thickness, mobility, calcification, extent of subvalvular fusion, and appearance of the commisures
Estimation of left atrial size
Doppler echo:
Estimation of mitral valve area, transvalvular gradient and PA pressure
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MITRAL STENOSISAsymptomatic patients with mild mitral stenosis (valve
area >1.5cm² and mean gradient <5mmHg) should be managed medically
No further investigation as these patients usually remain stable for many years
Annual review recommended and echocardiography repeated if there is deterioration in symptoms or clinical signsAsymptomatic patients 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
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MITRAL STENOSIS
Medical treatmentAvoidance of unusual physical stressSalt restrictionDiuretics if neededControl of heart rate – β-blocker or digoxinAnticoagulation for AF or prior embolic eventSBE prophylaxisAnnual follow-upEchocardiography if deterioration in clinical condition
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MITRAL STENOSIS
Management of symptomatic mitral stenosisPatients with symptoms should undergo clinical re-evaluation with CXR, EKG, and echocardiographyNYHA class II symptoms and mild mitral stenosis may
be managed medicallyNYHA class II symptoms and at least moderate stenosis
(MVA ≤1.5cm2 or mean gradient ≥5mmHg) may be considered for balloon valvuloplastyNYHA class III or IV symptoms and severe mitral stenosis have a poor prognosis if left untreated and should be considered for balloon valvuloplasty or surgery
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MITRAL STENOSISBalloon mitral valvuloplasty
Involves passing a balloon flotation catheter across the interatrial septum after trans-septal puncture and dilating the balloon within the
mitral valve orificeResults highly dependent on experience of operator – valve area usually
doubles with a 50% to 60% reduction in the transmitral gradient80-95% of patients have successful procedureComplications include severe MR, residual ASD, myocardial perforation,
emboli, MI and deathOverall event-free survival is 50% to 65% over 3-7 yearsUnderlying mitral valve morphology most important factor in determining
outcomeProcedure usually more successful and better outcome if noncalcified pliable valves and no commissural calcificationRelative contraindications include presence of left atrial thrombus and significant mitral regurgitation
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MITRAL STENOSIS
Mitral valve replacementMitral valve replacement indicated in patients with severe mitral stenosis and contraindications to surgical commisurotomy (repair) or balloon valvuloplasty:
Restenosis following surgical commisurotomy or balloon valvuloplasty
Significant mitral stenosis and regurgitationExtensive 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.
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Dilated left atrium with mitral stenosis and calcified plaques on the atrial wall (circle), possibly caused by chronic hypertension
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Calcified Mitral Valve Requiring Replacement Due To Mitral Valve Stenosis
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Mitral valve stenosis is the narrowing of the opening of the heart's mitral valve. Here, thickened valve halves (cusps or
leaflets) do not open and close properly and causes interference with blood flow.
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Viewed via the open left atrium is a “fishmouth” mitral valve as a long term sequel of rheumatic fever.
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Rheumatic aspect of mitral valve with anterolateral commissural fusion prior to commissurotomy and Gregori-Braile ring
implantation
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MITRAL REGURGITATION
Abnormality prevents the valve from closing
Blood flows back into the right atrium during systole
During diastole the regurgitant output flows into the LV with the normal blood flow and increases the volume into the LV
Progression is slow – fatigue, chronic weakness, dyspnea, anxiety, palpitations
May have A-fib and changes of LV failure
May develop right sided failure as well
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MITRAL REGURGITATIONMitral 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 endocarditisChordae tendinae
congenital, infective endocarditis, trauma, rheumatic fever, mitral valve prolapse
Papillary musclesmyocardial ischemia, congenital abnormalities,
infiltrative disease Mitral annulus
dilatation, eg. ischemic or dilated cardiomyopathycalcification due to degeneration, hypertension,
aortic stenosis, diabetes, chronic renal failure
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MITRAL REGURGITATION
Clinical featuresSymptoms usually occur with LV decompensation dyspnea, fatigue, and weaknessPhysical findings include:
Pulse: sharp upstrokeApex: displaced, hyperdynamicHeart sounds: pansystolic murmur loudest at the apex, radiating to the
axilla and accentuated by expiration; soft S₁, wide splitting of S₂, and S₃ present
EKG
LAE
Atrial fibrillation
LVH
CXR
Cardiomegaly
LVH/LAE
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MITRAL REGURGITATION
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MITRAL REGURGITATION
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
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MITRAL REGURGITATIONMedical treatment
In asymptomatic patients with chronic mitral regurgitation, no generally accepted medical therapy – monitor with echo
Symptomatic patients may benefit from the following drug therapy while awaiting surgery:
Low sodium diet
Afterload reduction
Vasodilator therapy – Nitroprusside, ACE inhibitors, hydralazine
Preload reduction
Diuretics
Digoxin / Beta-blockers in presence of atrial fibrillation
Endocarditis prophylaxis
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MITRAL REGURGITATIONSurgical treatment
Symptomatic – Class II, III, IVNeed for surgery dependent on symptomatic status and left ventricular functionSurgery is indicated in the presence of symptoms or left ventricular end systolic diameter ≥45mm Surgical procedure consists of either mitral valve repair or replacement Mitral valve repair better preserves LV function and avoids the
need for chronic anticoagulation but technically more demanding and often not possible to perform in
severely deformed valvesMortality rates for mitral valve surgery approximate to 1-4%
in predominant mitral stenosis and 2-7% in predominant mitral regurgitation
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ACUTE MITRAL REGURGITATION
Causes are diverse and represent acute manifestations of disease processes that may under other circumstances cause chronic mitral regurgitation:
Infective endocarditis causing disruption of valve leaflets or chordal rupture
Ischemic dysfunction or rupture of papillary muscle
Malfunction of prosthetic valve79
ACUTE MITRAL REGURGITATION
Medical therapyThe following therapies may be beneficial in reducing the
severity of MR depending on hemodynamic statusVasodilator therapyInotropic therapyIntra-aortic balloon counterpulsation
Surgical therapyIndicated in patients with acute severe MR and heart
failureHigher mortality rates than for elective chronic MR, but
unless treated aggressively, the outcome is usually fatal
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Chronic versus Acute MR
Finding Chronic MR Acute MR
Symptoms subtle onset obviousAppearance normal/mildly severely ill
dyspneicTachycardia not striking always presentApex beat displaced not displacedSystolic thrill common absentMurmur harsh pansystolic soft or absent early
systolic componentECG-LVH usually present absentCXR severe cardiomegaly normal heart size
Intra-aortic Balloon Counterpulsation
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MITRAL REGURGITATION
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MITRAL VALVE PROLAPSEMost common form of valvular heart disease
Other terms: Floppy valve, Barlow’s syndrome
Occurs in 2-6% of the general population
Twice as common in women
Due to myxomatous proliferation of the mitral valve causing an increased surface area of the valve
Severity of mitral regurgitation depends on the extent of prolapse
Usually occurs as a primary condition (congenital) but may be a secondary
finding in RHD, cardiomyopathy, MI, or connective tissue diseases, e.g. Marfan’s syndrome (90%)
Vast majority of patients are asymptomatic
Symptoms may include palpitations, dizziness, syncope, or chest discomfort
The principal physical finding is the mid-systolic click resulting from sudden tensing of the mitral valve apparatus as the leaflets prolapse into the left atrium during systole, followed by a late systolic murmur in the presence of regurgitation
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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
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MITRAL VALVE PROLAPSEManagement
Asymptomatic patients without MR or arrhythmias have an excellent prognosis – follow-up every 3 – 5 years
Patients with a typical systolic murmur indicating MR 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
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MITRAL VALVE PROLAPSEMost MVP patients are at negligible or moderate risk of developing
endocarditis. The AHA/ACC guidelines define negligible risk as “not higher than in the general population,” therefore not requiring prophylaxis. According to the guidelines, patients whose valves prolapse without leaking are at negligible risk.
Mitral valve prolapse patients at moderate risk are patients with MVP associated with any leaking, thickening or degeneration of the mitral valve, and should receive prophylaxis prior to undergoing procedures that put them at risk of bacteremia (bacteria in the blood). More specifically, patients with prolapsing and leaking mitral valves, as identified on physical and Doppler- echocardiographic examination, should receive endocarditis prophylaxis. Thickened valve leaflets are an indication for prophylaxis, as is the presence of myxomatous degeneration of the mitral valve.
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Mitral Valve Before Surgery After Surgery
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PROSTHETIC VALVES
Prosthetic valves may be divided into 2 broad categories:
Mechanical valves
Very good durability
Require long-term anticoagulation
May cause mild hemolysis
Bioprosthetic (tissue) valves
Porcine variety most commonly used
Limited durability
Anticoagulation for first 3 months only
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PROSTHETIC VALVES
Mechanical versus tissue valves
No difference in survival, hemodynamics 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
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Designs and flow patterns of different types of mechanical valves
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TRICUSPID STENOSIS
Very uncommon – always rheumatic in origin and when present accompanies mitral valve involvement
Majority of cases of rheumatic tricuspid valve disease present with tricuspid regurgitation or a combination of stenosis and regurgitation
Anatomical changes and physiological principles similar to those of mitral stenosis but reflect changes to the systemic venous circulation rather than the pulmonary venous system
Low cardiac output state causes fatigue and abdominal discomfort may occur due to hepatomegaly and ascites
Diastolic murmur of tricuspid stenosis augmented by inspiration, unlike mitral stenosis
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TRICUSPID STENOSIS
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
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 tumors and the carcinoid syndrome
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TRICUSPID REGURGITATION
Most common cause is annular dilatation due to RV failure of any cause – mitral valve disease, right ventricular infarction, congenital heart disease, primary pulmonary hypertension and rarely cor pulmonale
May also be caused by intrinsic valve involvement – Ebstein’s anomaly, atrioventricular canal defects, rheumatic heart disease, carcinoid syndrome, myxomatous degeneration and infective endocarditis
Well tolerated in the absence of pulmonary hypertensionIn the presence of pulmonary hypertension, cardiac output
declines and RV failure may worsen
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TRICUSPID REGURGITATION
Symptoms and signs result from a reduced cardiac output, ascites, painful congestive hepatomegaly and edema
The pansystolic murmur of TR is usually loudest at the left sternal edge and augmented by deep inspiration
TR in the absence of pulmonary hypertension usually does not require surgical treatment
Patients with severe TR and rheumatic heart disease require ring annuloplasty
Management of severe functional TR is controversial and may be treated by annuloplasty or valve replacement
Severe TR due to intrinsic tricuspid valve disease requires valve replacement
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Tricuspid regurgitation is a disorder involving backflow of blood from the right ventricle to the right atrium during contraction of the right ventricle. It is
caused by damage to the tricuspid heart valve or enlargement of the right ventricle.
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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
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PULMONARY REGURGITATION
Most common cause is ring dilatation due to pulmonary hypertension or dilatation of pulmonary artery secondary to connective tissue disorder
Second most common cause is infective endocarditis
May also result from congenital malformations, trauma, carcinoid syndrome, or iatrogenic causes
If isolated, may be tolerated for many years unless complicated by pulmonary hypertension
Clinical manifestations of primary disease tend to overshadow the pulmonary regurgitation
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PULMONARY REGURGITATION
Physical examination reveals a hyperdynamic right ventricle producing a right ventricular heave in the left parasternal area 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 only occasionally because of intractable RV failure preferably with a porcine bioprothesis
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SURGICAL LINKS
http://www.orlive.com/wfubmc/videos/mitral-valve-repair-surgery
http://www.orlive.com/medtronic/videos/minimally-invasive-heart-valve-surgery
http://www.orlive.com/nyp/videos/innovations-in-transcatheter-valve-therapies
http://www.orlive.com/davinci/videos/early-intervention-in-the-treatment-of-mitral-valve-disease1
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