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

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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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