VALVULER VALVULER HEART DISEASEHEART DISEASE

Yrd.Doç.Dr.Olcay ÖZVERENYrd.Doç.Dr.Olcay ÖZVEREN

Aortic StenosisAortic Stenosis

Pathology :Pathology :

Obstruction to left ventricular (LV) Obstruction to left ventricular (LV) outflow outflow

Causes :Causes : a congenital bicuspid valve with a congenital bicuspid valve with

superimposed calcification superimposed calcification calcification of a normal trileaflet valve calcification of a normal trileaflet valve

((senilesenile or or degenerativedegenerative ) ) rheumatic disease rheumatic disease

The risk factors of calcific ASThe risk factors of calcific AS

Similar to those for vascular Similar to those for vascular atherosclerosisatherosclerosis : :

..elevated serum levels of LDL elevated serum levels of LDL cholesterol and lipoprotein(a) cholesterol and lipoprotein(a)

.Diabetes.Diabetes

.Smoking.Smoking

.hypertension. .hypertension.

Rheumatic Aortic Stenosis Rheumatic Aortic Stenosis Rheumatic AS results from Rheumatic AS results from adhesions and adhesions and

fusions fusions of the of the commissures and cusps commissures and cusps and and vascularization of the leaflets vascularization of the leaflets of the valve of the valve ring, leading to ring, leading to retraction and stiffening of retraction and stiffening of the free borders of the cuspsthe free borders of the cusps..

Calcific nodules develop on both surfaces, Calcific nodules develop on both surfaces, and the orifice is reduced to a small round and the orifice is reduced to a small round or triangular opening or triangular opening

The rheumatic valve is The rheumatic valve is often regurgitant,often regurgitant, as well as stenotic. as well as stenotic.

Patients with rheumatic AS invariability Patients with rheumatic AS invariability have rheumatic involvement of the mitral have rheumatic involvement of the mitral valvevalve . .

PathophysiologyPathophysiology

Classification of the Classification of the Severity of ASSeverity of AS

SymptomsSymptoms exertional dyspnea (exertional dyspnea (LV diastolic dysfunction, LV diastolic dysfunction,

with an excessive rise in end-diastolic pressure with an excessive rise in end-diastolic pressure leading to pulmonary congestion and the limited leading to pulmonary congestion and the limited

ability to increase cardiac output with exerciseability to increase cardiac output with exercise ) ) Angina (Angina (precipitated by exertion and relieved by precipitated by exertion and relieved by

rest. Angina results from the combination of the rest. Angina results from the combination of the increased oxygen needs of hypertrophied myocardium increased oxygen needs of hypertrophied myocardium and reduction of oxygen delivery secondary to the and reduction of oxygen delivery secondary to the

excessive compression of coronary vesselsexcessive compression of coronary vessels ) ) Syncope (Syncope (reduced cerebral perfusion that occurs reduced cerebral perfusion that occurs

during exertion when arterial pressure declines during exertion when arterial pressure declines consequent to systemic vasodilation in the presence of consequent to systemic vasodilation in the presence of

a fixed cardiac outputa fixed cardiac output ) ) heart failure heart failure

Physical Examination Physical Examination parvus and tardus carotid impulseparvus and tardus carotid impulse ( (slow-slow-

rising, late-peaking, low-amplitude carotid pulse .rising, late-peaking, low-amplitude carotid pulse . However, in patients with associated AR or in older However, in patients with associated AR or in older patients with an inelastic arterial bed, systolic and pulse patients with an inelastic arterial bed, systolic and pulse pressures may be normal or even increasedpressures may be normal or even increased. ). )

The cardiac impulse is sustained and The cardiac impulse is sustained and becomes displaced inferiorly and laterally becomes displaced inferiorly and laterally ..

systolic thrillsystolic thrill ( (It is palpated most readily in the It is palpated most readily in the second right intercostal space or suprasternal notch and second right intercostal space or suprasternal notch and is frequently transmitted along the carotid arteries.is frequently transmitted along the carotid arteries. ) )

AuscultationAuscultation The ejection systolic murmurThe ejection systolic murmur Typically is late peaking and heard best Typically is late peaking and heard best at the base of the heart, with at the base of the heart, with

radiation to the carotidsradiation to the carotids . . Cessation of the murmur before A2 is helpful in differentiation from a Cessation of the murmur before A2 is helpful in differentiation from a

pansystolic mitral MR murmur.pansystolic mitral MR murmur.In patients with calcified aortic valves, the systolic murmur is loudest at the In patients with calcified aortic valves, the systolic murmur is loudest at the

base of the heart, but high-frequency components may radiate to the apex base of the heart, but high-frequency components may radiate to the apex ((Gallavardin phenomenonGallavardin phenomenon), ), in which the murmur may be so prominent in which the murmur may be so prominent that it is mistaken for the murmur of MR. that it is mistaken for the murmur of MR.

A A louderlouder and and later peaking later peaking murmur indicates more severe stenosismurmur indicates more severe stenosis..When the When the left ventricle fails left ventricle fails and stroke volume falls, the systolic and stroke volume falls, the systolic

murmur of AS becomes murmur of AS becomes softersofter; rarely, it disappears altogether. ; rarely, it disappears altogether. The slow rise in the arterial pulse is more difficult to recognizeThe slow rise in the arterial pulse is more difficult to recognize

The intensity of the systolic murmur varies from The intensity of the systolic murmur varies from beat to beatbeat to beat when the duration of diastolic filling varies, as in AF or when the duration of diastolic filling varies, as in AF or following a premature contraction. This characteristic is following a premature contraction. This characteristic is helpful in helpful in differentiating AS from MRdifferentiating AS from MR, in which the , in which the murmur is usually unaffected. murmur is usually unaffected.

Splitting of the second heart soundSplitting of the second heart sound helpful in excluding the diagnosis of severe AS because helpful in excluding the diagnosis of severe AS because

normal splitting implies the aortic valve leaflets are flexiblenormal splitting implies the aortic valve leaflets are flexible enough to create an audible closing sound (A2). enough to create an audible closing sound (A2).

Diagnostic Evaluation Diagnostic Evaluation ModalitiesModalities

Echocardiography (Echocardiography (definition of valve anatomy, including the cause of AS and the severity of valve calcification, evaluation of LV hypertrophy and systolic function, mean transaortic pressure gradient with calculation of the ejection fraction, and for measurement of aortic root dimensions and detection of associated

mitral valve disease.).) Cardiac Catheterization Cardiac Catheterization

and Angiography and Angiography Computed Tomography Computed Tomography Cardiac MR Cardiac MR

Clinical OutcomeClinical Outcome

2 years in patients 2 years in patients with heart failure with heart failure

3 years in those 3 years in those with syncopewith syncope

5 years in those 5 years in those with angina with angina

Asymptomatic Symptomatic

The average rate of hemodynamic progression :The average rate of hemodynamic progression :

annual decrease in aortic valve area of annual decrease in aortic valve area of 0.12 cm2/year0.12 cm2/year

an increase in aortic jet velocity of an increase in aortic jet velocity of 0.32 m/sec/year0.32 m/sec/year

an increase in mean gradient of an increase in mean gradient of 7 mm Hg/year7 mm Hg/year. .

Exercise test is helpful :Exercise test is helpful : Symptoms on treadmill exercise Symptoms on treadmill exercise a a decrease in blood pressure with exertion decrease in blood pressure with exertion An An elevated BNP elevated BNP level may be helpful when level may be helpful when

symptoms are equivocal or when stenosis symptoms are equivocal or when stenosis severity is only moderate. severity is only moderate.

Management Management Symptomatic patients with severe Symptomatic patients with severe

AS are usually operative candidates AS are usually operative candidates because medical therapy has little to because medical therapy has little to offer .offer .

Medical therapy may be necessary Medical therapy may be necessary for patients considered to be for patients considered to be inoperable , HF , HT, CAD.inoperable , HF , HT, CAD.

Diüretics ,ACE inh. ,Statins,Diüretics ,ACE inh. ,Statins, DC Cardiversion in AF DC Cardiversion in AF

Surgical TreatmentSurgical Treatment

Aortic RegurgitationAortic Regurgitation

Causes and PathologyCauses and Pathology

Valvular DiseaseValvular Disease calcific AR calcific AR infective endocarditis infective endocarditis trauma trauma congenitally bicuspid congenitally bicuspid

valve valve Rheumatic fever Rheumatic fever SLESLE rheumatoid arthritisrheumatoid arthritis ankylosing spondylitisankylosing spondylitis Takayasu disease, Takayasu disease, Whipple disease,Whipple disease,

Aortic Root DiseaseAortic Root Disease Marfan syndrome; Marfan syndrome; aortic dilation related to aortic dilation related to

bicuspid valvesbicuspid valves aortic dissection, aortic dissection, osteogenesis imperfecta,osteogenesis imperfecta, syphilitic aortitis,syphilitic aortitis, ankylosing spondylitis,ankylosing spondylitis, the Beh?et syndrome,the Beh?et syndrome, giant cell arteritis, giant cell arteritis, systemic hypertensionsystemic hypertension

Pathophysiology Pathophysiology

Clinical PresentationClinical Presentation exertional dyspneaexertional dyspnea AnginaAngina SyncopeSyncope heart failureheart failure

Physical FindingsPhysical Findings Quincke's PulseQuincke's Pulse: Capillary pulsation visible on the : Capillary pulsation visible on the

fingernail beds fingernail beds or tipsor tips Musset's SignMusset's Sign: Head bobbing with each heartbeat: Head bobbing with each heartbeat Müller’s SignMüller’s Sign: Systolic pulsation of the: Systolic pulsation of the uvulauvula Corrigan’s PulseCorrigan’s Pulse: Water-hammer pulse. Rapid distention : Water-hammer pulse. Rapid distention

and collapse of arteriel pulseand collapse of arteriel pulse Hill’s SignHill’s Sign: Popliteal cuff pressure : Popliteal cuff pressure more than 60 mmHg more than 60 mmHg

above brachial cuff pressureabove brachial cuff pressure Duroziez’s SignDuroziez’s Sign:: To-and-fro To-and-fro murmur over the femoral murmur over the femoral

artery with the artery compressedartery with the artery compressed Traube’s signTraube’s sign: : Pistol-shot sounds. Pistol-shot sounds. Prominent systolic and Prominent systolic and

diastolic sounds over the femoral arteriesdiastolic sounds over the femoral arteries Increased pulse pressure (SBP increases and DBP Increased pulse pressure (SBP increases and DBP

decreases.)decreases.)

Diastolic Murmur In ARDiastolic Murmur In AR

•In moderate AR, a relatively loud early desending diastolic murmur is heard.•With more severe AR, the murmur becomes longer, and will usually decrease in intensity.•The classic murmur caused by the regurgitant flow is best heard along the lower left sternal border. In some cases (Marfan’s Syndrome, VSD w/AR , aortic dissection or aneurysm) it is best heard at the right sternal border.• A lower-pitched mid-diastolic murmur is heard over apex this indicates what is called an Austin Flint murmur which indicates severe AR. (The murmur is not the regurgitant flow over the aortic valve, but rather vibrations in a restricted Mitral Valve when the left atrium empties and is met with the opposite flow from the aortic valve.)•In addition to the diastolic murmur(s), a systolic flow murmur like in aortic stenosis may be heard. This is not necessarily indicating a calcified valve, as the increased velocity resulting from ventricular overload will also cause flow vibrations)

Diagnostic Evaluation Diagnostic Evaluation ModalitiesModalities EchocardiographyEchocardiography ( (bicuspid valve, thickening bicuspid valve, thickening

of the valve cusps, other congenital abnormalities, of the valve cusps, other congenital abnormalities, prolapse of the valve, a flail leaflet, or vegetation )prolapse of the valve, a flail leaflet, or vegetation )

Electrocardiography Electrocardiography (left axis deviation and a (left axis deviation and a pattern of LV diastolic volume overload, pattern of LV diastolic volume overload, characterized by an increase in initial forces characterized by an increase in initial forces (prominent Q waves in leads I, aVL, and V3 through (prominent Q waves in leads I, aVL, and V3 through V6) and a relatively small wave in lead V1 )V6) and a relatively small wave in lead V1 )

Radiography Radiography Cardiac Magnetic Resonance Imaging Cardiac Magnetic Resonance Imaging Angiography Angiography

electrocardiographyelectrocardiography

Chest x rayChest x ray

echocardiographyechocardiography

Disease CourseDisease Course

asymptomatic symptomatic

Management Management Medical TreatmentMedical Treatment : :There is no specific therapy to There is no specific therapy to

prevent disease progression in chronic AR. prevent disease progression in chronic AR. Systemic arterial hypertension, should be treated

because it increases the regurgitant flow; vasodilating agents such as ACE inhibitors or ARB are preferred, and beta-blocking agents should be used with great caution.

Chronic medical therapy may be necessary for Chronic medical therapy may be necessary for some patients who refuse surgery or are some patients who refuse surgery or are considered to be inoperable because of comorbid considered to be inoperable because of comorbid conditions. These patients should receive an conditions. These patients should receive an aggressive heart failure regimen with ACE aggressive heart failure regimen with ACE inhibitors (and perhaps other vasodilators), inhibitors (and perhaps other vasodilators), digoxin, diuretics, and salt restriction; beta digoxin, diuretics, and salt restriction; beta blockers may also be beneficial. blockers may also be beneficial.

Surgical TreatmentSurgical Treatment

Acute Aortic RegurgitationAcute Aortic Regurgitation Causes: Causes: infective endocarditis, aortic dissection, traumainfective endocarditis, aortic dissection, trauma The characteristic features of acute AR are The characteristic features of acute AR are tachycardia tachycardia

and an increase in LV diastolic pressures.and an increase in LV diastolic pressures. The sudden The sudden increase in LV fillingincrease in LV filling causes the LV diastolic causes the LV diastolic

pressure to pressure to rise rapidly rise rapidly above left atrial pressure during above left atrial pressure during early diastole .early diastole .

Premature closure of the mitral valvePremature closure of the mitral valve, together with , together with tachycardia that also shortens diastole, reduces the time tachycardia that also shortens diastole, reduces the time interval during which the mitral valve is open.interval during which the mitral valve is open.

The tachycardia may compensate for the The tachycardia may compensate for the reduced reduced forward stroke volumeforward stroke volume, and the LV and aortic systolic , and the LV and aortic systolic pressures may exhibit little change. pressures may exhibit little change.

Acute severe AR may cause Acute severe AR may cause profound hypotension and profound hypotension and cardiogenic shock .cardiogenic shock .

Weakness, severe dyspneaWeakness, severe dyspnea, and , and profound hypotension profound hypotension secondary to the reduced stroke volume and elevated left secondary to the reduced stroke volume and elevated left atrial pressure .atrial pressure .

Physical Examination Physical Examination tachycardia, severe peripheral tachycardia, severe peripheral

vasoconstriction, and cyanosis, and vasoconstriction, and cyanosis, and sometimes pulmonary congestion and edema. sometimes pulmonary congestion and edema.

S1S1 may be may be soft or absent soft or absent because of because of premature closure of the mitral valve, and premature closure of the mitral valve, and the sound of mitral valve closure in mid or the sound of mitral valve closure in mid or late diastole is occasionally audible. Closure late diastole is occasionally audible. Closure of the mitral valve may be incomplete, and of the mitral valve may be incomplete, and diastolic MRdiastolic MR may occur may occur

The early diastolic murmur of acute AR is The early diastolic murmur of acute AR is lower pitched and shorter than that of lower pitched and shorter than that of chronic AR because as LV diastolic pressure chronic AR because as LV diastolic pressure rises, the (reverse) pressure gradient rises, the (reverse) pressure gradient between the aorta and left ventricle is rapidly between the aorta and left ventricle is rapidly reduced. reduced.

Echocardiography:Echocardiography:In acute AR the In acute AR the echocardiogram reveals a dense, diastolic Doppler echocardiogram reveals a dense, diastolic Doppler signal with an end-diastolic velocity approaching signal with an end-diastolic velocity approaching zero and premature closure and delayed opening zero and premature closure and delayed opening of the mitral valve. LV size and ejection fraction of the mitral valve. LV size and ejection fraction

are normal.are normal. Electrocardiography:Electrocardiography: In acute AR, the ECG may In acute AR, the ECG may

or may not show LV hypertrophy, depending on or may not show LV hypertrophy, depending on the severity and duration of the regurgitation. the severity and duration of the regurgitation. However, nonspecific ST-segment and T wave However, nonspecific ST-segment and T wave changes are common.changes are common.

Radiography :Radiography :In acute AR, there is often evidence In acute AR, there is often evidence of marked pulmonary venous hypertension and of marked pulmonary venous hypertension and pulmonary edema.pulmonary edema.

Management Management Early death caused by LV failure is frequent in Early death caused by LV failure is frequent in

patients with acute severe AR despite intensive patients with acute severe AR despite intensive medical management, prompt surgical intervention is medical management, prompt surgical intervention is indicated.indicated.

Even a normal ventricle cannot sustain the burden of Even a normal ventricle cannot sustain the burden of acute, severe volume overload. acute, severe volume overload.

While the patient is being prepared for surgery, While the patient is being prepared for surgery, treatment with an intravenous positive inotropic treatment with an intravenous positive inotropic agent (dopamine or dobutamine) and/or a vasodilator agent (dopamine or dobutamine) and/or a vasodilator (nitroprusside) is often necessary. (nitroprusside) is often necessary.

In hemodynamically stable patients with acute AR In hemodynamically stable patients with acute AR secondary to active infective endocarditis, operation secondary to active infective endocarditis, operation may be deferred to allow 5 to 7 days of intensive may be deferred to allow 5 to 7 days of intensive antibiotic therapy . However, AVR should be antibiotic therapy . However, AVR should be undertaken at the earliest sign of hemodynamic undertaken at the earliest sign of hemodynamic instability or if echocardiographic evidence of instability or if echocardiographic evidence of diastolic closure of the mitral valve develops. diastolic closure of the mitral valve develops.

MITRAL STENOSIS

MITRAL VALVE ANATOMYMITRAL VALVE ANATOMY

1. Rheumatic Fever2. Congenital Mitral

Stenosis

Etiology

1.Increased left atrial pressure2.Pulmonary vasoconstriction3.Pulmonary Hypertension4.Right Ventricular Failure5.Decreased cardiac output

Pathophysiology

Right Heart Failure:

Hepatic Congestion

JVD

Tricuspid Regurgitation

RA Enlargement

Pulmonary HTN

Pulmonary Congestion

LA Enlargement

Atrial Fib

LA Thrombi

LA Pressure

RV Pressure Overload

RVH

RV Failure LV Filling

PathophysiologyPathophysiology

SymptomsSymptoms Fatigue Fatigue PalpitationsPalpitations CoughCough Chest painChest pain SOBSOB Left sided failureLeft sided failure

OrthopneaOrthopnea PNDPND Exercise Exercise

PalpitationPalpitation Hoarseness (Ortner’s Hoarseness (Ortner’s

syndromesyndrome

AfibAfib Systemic embolismSystemic embolism Pulmonary infectionPulmonary infection HemoptysisHemoptysis Right sided failureRight sided failure

Hepatic CongestionHepatic Congestion EdemaEdema

Exertion Fever Anemia Pregnancy Atrial Fibrillationhypertiroid

Precipitating Factors

Recognizing MitralRecognizing Mitral Stenosis Stenosis

Palpation:Palpation: Small volume pulseSmall volume pulse Tapping apex-Tapping apex-

palpable S1palpable S1 +/- palpable opening +/- palpable opening

snap (OS)snap (OS) RV liftRV lift Palpable S2Palpable S2

ECG:ECG: LAE, AFIB, RVH, RADLAE, AFIB, RVH, RAD

Auscultation:Auscultation: Loud S1- as loud as S2 in Loud S1- as loud as S2 in

aortic areaaortic area A2 to OS interval inversely A2 to OS interval inversely

proportional to severityproportional to severity Diastolic rumble: length Diastolic rumble: length

proportional to severityproportional to severity In severe MS with low In severe MS with low

flow- S1, OS & rumble may flow- S1, OS & rumble may be inaudiblebe inaudible

© Continuing Medical Implementation

…...bridging the care gap

Mitral Stenosis: Physical Mitral Stenosis: Physical ExamExam

First heart sound (S1) is accentuated and snappingFirst heart sound (S1) is accentuated and snapping Opening snap (OS) after aortic valve closureOpening snap (OS) after aortic valve closure Low pitch diastolic rumble at the apexLow pitch diastolic rumble at the apex Pre-systolic accentuation (esp. if in sinus rhythm)Pre-systolic accentuation (esp. if in sinus rhythm)

S1 S2 OS S1

Common Murmurs and Common Murmurs and TimingTiming

Systolic MurmursSystolic Murmurs Aortic stenosisAortic stenosis Mitral insufficiencyMitral insufficiency Mitral valve prolapseMitral valve prolapse Tricuspid insufficiency Tricuspid insufficiency

Diastolic MurmursDiastolic Murmurs Aortic insufficiencyAortic insufficiency Mitral stenosisMitral stenosis

S1 S2 os S1

•Accentuated precordial thrust of right ventricle •Elevated neck veins •Ascites•Edema

Signs: Later findings of right ventricular failure

Hemoptysis Embolism Pulmonary infection EndocarditisAtrial fibrillation

Complications

Chest XRay Double density of left atrial enlargement Right ventricular enlargement Posterior displacement of esophagus Mitral valve calcification Kerley B Lines

Echocardiogram Mitral valve leaflet changes

Inadequate separation of valve leaflets Valve leaflet calcification and thickening

Doppler estimates transvalvular gradient

Radiology

Mitral Stenosis - upper lobe Mitral Stenosis - upper lobe blood diversionblood diversion

Trivial enlargement of the transverse diameter of the heart. Left atrium causes double outline (opposite right arrow) and is somewhat dilated. Left atrial appendage is dilated, causing a prominence of the left border (opposit left arrow). Upper lobe vessels larger than lower lobe vessels, that is, upper lobe blood diversion. An arrow points to a dilated upper lobe vein.

Mitral Stenosis - septal line Mitral Stenosis - septal line shadows. Kerley "B" shadows. Kerley "B"

Horizontal short line shadows, septal (Kerley "B") lines above the costo-phrenic recesses, indicating interstitial oedema of the septa, often with haemosiderin in the adjacent alveoli.

Mitral Stenosis - hilar Mitral Stenosis - hilar oedema oedema

Hilar vessels indistinct, peri-hilar haze. Also upper lobe blood diversion and septal line shadows. Arrow points to a Kerley "A" line, due either to septal oedema or oedema around an intercommunicating lymphatic during its course from a perivenous to a pericardial position or vice versa.

echocardiographyechocardiography

Slow, progressive, life-long course Latent period of 20 to 40 years after Rheumatic Fever Rapid acceleration of symptoms in later life

Prognosis

Rheumatic Fever prophylaxis until age 35 years Benzathine Penicillin G 1.2 MU IM monthly

OR Penicillin VK 125-250 mg PO bid

Treat complications and associated conditions Atrial Fibrillation Congestive Heart Failure Anticoagulation for history of emboli

Beta blocker. Digitalis.diüretics

Management

Open Mitral valvotomyPercutaneous balloon valvuloplastyMitral Valve Replacement

Surgery

MITRAL REGURGITATION

MITRAL VALVE MITRAL VALVE ANATOMYANATOMY

Rheumatic Heart Disease Mitral Valve Prolapse Ischemic Heart Disease and papillary muscle dysfunction Left Ventricular dilatation Mitral annular calcification Hypertrophic Cardiomyopathy Infective endocarditis Congenital mitral regurgitation

Etiology

Early or compensated mitral regurgitation Volume overload Left Ventricular Hypertrophy Left atrial enlargement

Late or decompensated mitral regurgitation Left Ventricular Failure Decreased ejection fraction Pulmonary congestion

Pathophysiology

Pathophysiology of mitral Pathophysiology of mitral regurgitationregurgitation

In the normal heart, left ventricular (LV) contraction during systole forces blood exclusively through the aortic valve into the aorta; the closed mitral valve prevents regurgitation into the left atrium (LA). In mitral regurgitation (MR), a portion of the LV output is forced retrograde into the LA, so that forward cardiac output into the aorta is reduced. In acute MR, the LA is of normal size and is noncompliant, such that the LA pressure rises markedly and pulmonary edema may result. In chronic MR, the LA has enlarged and is more compliant, such that LA pressure is less elevated and pulmonary congestive symptoms are less common if LV contractile function is intact. There is LV enlargement and eccentric hypertrophy due to the chronic increased volume load.

PathophysiologyPathophysiology

The severity of MR and the ratio of The severity of MR and the ratio of forward cardiac flow (cardiac output) to forward cardiac flow (cardiac output) to backward flow are determined by several, backward flow are determined by several, interacting factors: interacting factors: 1)  the size of 1)  the size of the the mitral orifice mitral orifice during regurgitation during regurgitation

2)  the 2)  the systemic vascular resistance systemic vascular resistance opposing forward flow from the ventricle opposing forward flow from the ventricle

3)  the 3)  the compliance of the left atrium compliance of the left atrium 4)  the 4)  the systolic pressure gradient systolic pressure gradient

between the LV and the LA between the LV and the LA 5)  5)  the duration of regurgitation the duration of regurgitation

during systole during systole (not all regurgitation is (not all regurgitation is holo-systolic)holo-systolic)

Dyspnea Fatigue Weakness Cough

Symptoms

Holosystolic Murmur at Apex Harsh, medium pitched pansystolic murmur Murmur obliterates M1

Radiation Axilla Upper sternal borders Subscapular region

Soft or diminished First Heart Sound (S1) P2 heart sound augmented S2 Heart Sound with wide split S3 Gallop rhythm (indicative of severe disease) Accentuated and displaced precordial Apical Thrust Systolic thrill

Physical findings

MURMURMURMUR

Electrocardiogram Left Ventricular Hypertrophy Left Axis Deviation

Chest XRay Enlarged left atrium Dilated left ventricle

Echocardiogram Enlarged left atrium Hyperdynamic left ventricle Doppler assess severity

Laboratuary findings

CHEST X-RAY CHEST X-RAY

echocardiographyechocardiography

Annual or semi-annual echocardiogram Assess ejection fraction Assess end-systolic dimension

Management

Anticoagulation in Atrial Fibrillation Treat Congestive Heart Failure

Diuretics Digoxin

Afterload reduction ACE Inhibitor Hydralazine Nitroprusside (especially acute

MR)

Monitoring

Mitral Valve repair or replacement Repair before Heart Failure develops

Keep ejection fraction >60% Keep end-systolic dimension <45 mmIndications

Cardiopulmonary Symptoms (NYHA Class II-IV)Left Ventricular function impaired

Surgery

Tricuspid Valve Tricuspid Valve DiseasesDiseases

The forgotten The forgotten valvevalve

Tricuspid Valve AnatomyTricuspid Valve Anatomy

TV annulussTV annuluss• The tricuspid valve is the most apically The tricuspid valve is the most apically

(or caudally) placed valve with the (or caudally) placed valve with the largest orifice among the four valves.largest orifice among the four valves.

• The tricuspid annulus is oval-shaped The tricuspid annulus is oval-shaped and when dilated becomes more and when dilated becomes more circular.circular.

• 20% larger than MV annulus .20% larger than MV annulus .

• Normal TV annulus= 3.0Normal TV annulus= 3.0 - - 3.5 cm 3.5 cm

LeafletsLeaflets

the tricuspid valve has three distinct leaflets the tricuspid valve has three distinct leaflets described as septal, anterior, and posterior.described as septal, anterior, and posterior.

The septal and the anterior leaflets are The septal and the anterior leaflets are larger.larger.

The posterior leaflet is smaller and appears The posterior leaflet is smaller and appears to be of lesser functional significance since to be of lesser functional significance since it may be imbricated without impairment of it may be imbricated without impairment of valve function.valve function.

LeafletsLeaflets

The septal leaflet is in immediate The septal leaflet is in immediate proximity of the membranous ventricular proximity of the membranous ventricular septum, and its extension provides a basis septum, and its extension provides a basis for spontaneous closure of the for spontaneous closure of the perimembranous ventricular septal defect.perimembranous ventricular septal defect.

The anterior leaflet is attached to the The anterior leaflet is attached to the anterolateral margin of the annulus and is anterolateral margin of the annulus and is often voluminous and sail-like in Ebstein’s often voluminous and sail-like in Ebstein’s anomaly.anomaly.

Papillary Muscles & Papillary Muscles & ChordaeChordae

There are three sets of small papillary There are three sets of small papillary muscles, each set being composed of up to muscles, each set being composed of up to three muscles.three muscles.

The chordae tendinae arising from each The chordae tendinae arising from each set are inserted into two adjacent leaflets.set are inserted into two adjacent leaflets.

the anterior set chordae insert into half of the anterior set chordae insert into half of the septal and half of the anterior leaflets.the septal and half of the anterior leaflets.

The medial and posterior sets are similarly The medial and posterior sets are similarly related to adjacent valve leaflets.related to adjacent valve leaflets.

Etiology of Primary Etiology of Primary Tricuspid Valve DiseaseTricuspid Valve Disease

• CongenitalCongenital——Cleft valve generally in association with atrioventricular Cleft valve generally in association with atrioventricular

canal defectcanal defect——Ebstein’s anomalyEbstein’s anomaly——Congenital tricuspid stenosisCongenital tricuspid stenosis——Tricuspid atresiaTricuspid atresia• Rheumatic valve disease, generally in association with Rheumatic valve disease, generally in association with

rheumatic mitral valve diseaserheumatic mitral valve disease• Infective endocarditisInfective endocarditis• Carcinoid heart diseaseCarcinoid heart disease• Toxic (eg, Phen-Fen valvulopathy or methysergide Toxic (eg, Phen-Fen valvulopathy or methysergide

valvulopathy)valvulopathy)• Tumors (eg, myxoma)Tumors (eg, myxoma)• Iatrogenic—pacemaker lead traumaIatrogenic—pacemaker lead trauma• Trauma—blunt or penetrating injuriesTrauma—blunt or penetrating injuries• Degenerative—tricuspid valve prolapseDegenerative—tricuspid valve prolapse

Etiology of Secondary or Etiology of Secondary or Functional Tricuspid Valve Functional Tricuspid Valve

DiseaseDisease

• Right ventricular dilatationRight ventricular dilatation• Right ventricular hypertensionRight ventricular hypertension• Global right ventricular dysfunction Global right ventricular dysfunction

resulting from cardiomyopathy, myocarditis, resulting from cardiomyopathy, myocarditis, or longstanding right ventricular or longstanding right ventricular hypertension with fibrosishypertension with fibrosis

• Segmental dysfunction secondary to Segmental dysfunction secondary to ischemia or infarction of the right ventricle, ischemia or infarction of the right ventricle, endomyocardial fibrosis, arrhythmogenic endomyocardial fibrosis, arrhythmogenic right ventricular dysplasiaright ventricular dysplasia

Clinical PresentationsClinical Presentations

Pure or predominant tricuspid Pure or predominant tricuspid stenosisstenosis

Pure or predominant tricuspid Pure or predominant tricuspid regurgitationregurgitation

MixedMixed

Tricuspid valve disease—Tricuspid valve disease—SymptomsSymptoms

• Fatigue Fatigue • Liver/gut congestion Liver/gut congestion • Right upper quadrant discomfort Right upper quadrant discomfort • Dyspepsia Dyspepsia • Indigestion Indigestion • Fluid retention with leg edema Fluid retention with leg edema • Ascites Ascites

Tricuspid valve disease Tricuspid valve disease ausculatory findingsausculatory findings

Stenosis Stenosis : Low-to medium-pitch : Low-to medium-pitch diastolic rumble with inspiratory diastolic rumble with inspiratory accentuationaccentuation

Regurgitation :Regurgitation : Soft, early, or holosystolic Soft, early, or holosystolic

murmur Augmented with inspiratory effort murmur Augmented with inspiratory effort (Caravallo’s sign) (Caravallo’s sign)

Prolapse Prolapse : Systolic click : Systolic click

• Substantial tricuspid regurgitation may existSubstantial tricuspid regurgitation may exist

without the classic ausculatory findings. without the classic ausculatory findings. Thus, clinical evaluation including cardiac Thus, clinical evaluation including cardiac auscultation cannot be used to exclude auscultation cannot be used to exclude tricuspid valve disease.tricuspid valve disease.

Transthoracic Transthoracic Echo Echo ViewsViews

Transesophageal ViewsTransesophageal Views

Transesophageal ViewsTransesophageal Views

Key Diagnostic FeaturesKey Diagnostic Features

Mild TR is seen in up to 60% and Moderate Mild TR is seen in up to 60% and Moderate TR in up to 15% of healthy individuals.TR in up to 15% of healthy individuals.

Mild or worse TR in a valve with thin Mild or worse TR in a valve with thin leaflets,leaflets,

normal coaptation, and normal-appearingnormal coaptation, and normal-appearing

supporting structures, suggests supporting structures, suggests regurgitationregurgitation

is physiologic or functional .is physiologic or functional .

Key Diagnostic FeaturesKey Diagnostic Features

In carcinoid disease, the leaflets are In carcinoid disease, the leaflets are thickenedthickened

and retracted with a fixed orifice usually and retracted with a fixed orifice usually leadingleading

to predominant regurgitation and less to predominant regurgitation and less severe stenosis.severe stenosis.

Approximately 30% of patients with MVP Approximately 30% of patients with MVP have redundancy and prolapse of the have redundancy and prolapse of the tricuspid valve, leading to TR.tricuspid valve, leading to TR.

TR & TS SeverityTR & TS Severity

PAP based on TR VelocityPAP based on TR Velocity

Mild increased PAP = 2.6 - 2.9 m/s Mild increased PAP = 2.6 - 2.9 m/s (27-33 mmhg)(27-33 mmhg)

Moderate increased PAP = 3.0 - 3.9 Moderate increased PAP = 3.0 - 3.9 m/s (36-60 mmhg)m/s (36-60 mmhg)

Severe increased PAP = 4.0Severe increased PAP = 4.0≤ ≤ (64 (64 mmhgmmhg ≤ ≤ ))

European Guideline for TV European Guideline for TV managmentmanagment

AHA/ACC Guideline for TV AHA/ACC Guideline for TV managmentmanagment