Valvular heart disease assessment of lesion severity

Valvular Heart DiseaseValvular Heart DiseaseAssessment of Lesion severityAssessment of Lesion severity

Dr Awadhesh kumar sharma

DM Cardiology

PGIMER &Dr RML Hospital,New Delhi

In managing the patient with valvular heart disease (VHD) three major issues must be addressed:-

Assessment of the severity of disease, The effect the disease is having or is likely to have on the

patient and his/her cardiovascular system The timing and type of intervention to be used to correct

the lesion.

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: WB Saunders; 2007:1625-1712.

The distinction between mild, moderate and severe disease is thought crucial since it is believed that, in most cases, mild and moderate disease are tolerated indefinitely (unless severity worsens) and only severe disease (as defined) causes symptoms and cardiac dysfunction.


Classification of the severity of valve lesions should be based on multiple criteria, including the initial findings on the physical examination, which should then be correlated with data from a comprehensive TTE.

Intervention should primarily be performed on patients with severe VHD


Classification of progression of VHD

J Am Coll Cardiol. March 2014.Online first.

OBJECTIVE ASSESSMENT OF DISEASE SEVERITY

The physical examination In this age of high-tech diagnostic modalities, the physical

examination, and the skill applied when performing it, seem to be diminishing.

However, the importance of the physical exam cannot be overemphasized because it lays the Bayesian foundation for all tests that follow.

Mitral stenosis (MS)

Etiology Most commonly rheumatic fever ——rheumatic heart disease （ RHD ） Symptoms commence mostly in 2nd~4th decade 2/3 of all patients are female 25% of all patients with RHD have pure MS

40% have combined MS and mitral regurgitation (MR)

J Am Coll Cardiol. 1994;24:152-8.

Clinical features s/o severe MS

PND Pulmonary edema Orthopnea Atrial fibrillation Ortner syndrome Short A2-OS interval Long duration of diastolic murmur


Laboratory examination

Electrocardiography (ECG)Left atrial enlargement Mitral valve P wave P-wave duration in lead II ＞ 0.12 s Large terminal negative P force in lead V1

Right ventricular hypertrophy

Arrhythmia Premature atrial contraction → atrial fibrillation

Radiological findings

“Mitral valve heart”

Marked enlargement of LAEnlargement of RVDilatation of PA

Pulmonary congestionInterstitial edema (manifested as Kerley B lines)

EchocardiographyThe most valuable technique for diagnosing MS, and determining its severity

M-mode echoM-mode echo ：： Thickened, calcified leaflets open poorly, close slowly (EF slope↓) The double peaks disappear Both leaflets move anteriorly during early diastole

Two-dimensional echo:Two-dimensional echo: Fusion, thickening, doming of the valve leaflets, and poor leaflet separation in diastole; mitral orifice area↓

Eur J Echocardiogr. 2009;10:1-25.

Mitral stenosis

Moderate MS

Severe MS

Hemodynamic changes

MS involves mainly LA and RV

1. Effect of MS on left atrioventricular pressure gradient and left atrial pressure (LAP)

MVA transvalvular gradient LAP

Normal 4 ～ 6cm2

Mild MS ＞ 1.5cm2 <5 mmHg ↑

Moderate 1.0 ～ 1.5cm2 5-10mmHg ↑↑

Severe ＜ 1.0cm2 ≥10mmHg 25mmHg


Mitral stenosis

Doppler echoDoppler echo ：：Most accurate noninvasive technique for quantifying the severity of MS

Spectrum Doppler: measure transvalvular gradient, MVAColor Doppler: display high velocity color jet

Provide other important informationCardiac chamber size (LA, RV)Left ventricular contractilityPulmonary arterial pressureOther coexisted valvular or congenital abnormalities Mural thrombi


Cardiac catheterization Its value in assessment of patients with MS or suspected MS has been largely superseded by echocardiography

If surgery is planned, coronary angiography is performed to ascertain whether or not bypass grafting is indicated in patients at risk of having coexisting coronary artery disease


2014 AHA/ACC Valvular Heart Disease Guidelines


Mitral regurgitation (MR)EtiologyMitral valve apparatus and/or LV structural and

functional abnormality

RHD: common(1/3); + MS and/ or aortic valve disease

Mitral valve prolapse (MVP) myxomatous degeneration, floppy and redundancy

Ischemic heart disease (or CAD) papillary muscle dysfunction

Mitral annular calcification

Severe dilatation of LV result in dilatation of the mitral annulus and lateral movement of papillary muscle

Infective endocarditis valve leaflets destruction, perforation, retraction; valve closure interfered by vegetation

Other causes: Rupture of the chordae congenital abnormalities obstructive hypertrophic cardiomyopathy

Hemodynamic changesMR involves mainly LA and LVChronic MRCompensation: MR→ LV volume↑→LV, LA↑→ LVEDV↑→ SV↑→ CO↑, EF↑

Decompensation: Left HF, LAP and LVEDP↑ → pulmonary congestion, pulmonary hypertension, right HF (hepatomegaly, edema, and ascites) CO↓

Acute MR MR →LA, LV volume↑→LVEDP↑→LAP↑→ ↓ pulmonary congestion, pulmonary edemaSV and CO↓

Clinical manifestationsSymptomsChronic MR Mild— no symptom Severe— left-sided heart failure Weakness, fatigue (CO↓) Dyspnea (pulmonary congestion)

RHD: symptoms occur late, once present, LV dysfunction is usually irreversible

MVP: asymptomatic, or atypical chest pain, palpitation, fatigue; in severe MR, left HF occur at late stage

Acute Mild— mild exertional dyspnea

Severe— acute left HF, pulmonary edema, or cardiac shock

Circulation. 2003;108:2432-2438.

Physical examination

Cardiac impulse at apex Hyperdynamic Displaced laterally, inferiorly (Chronic)

Changes of heart sounds S1↓(RHD) or normal (MVP, CAD) S3 (severe MR): prominent

Mid or late systolic click （ MVP ）（ Acute: P2↑ ， S4 ）

Circulation. 2003;108:2432-2438.

Systolic murmurRHD ： Pansystolic, blowing, high-pitched murmurPansystolic, blowing, high-pitched murmur maximal at the apex Anterior valve lesion, radiate to the axilla and back Posterior leaflet abnormality, radiate to the base

MVP ： mid- to late-systolic murmurDysfunction of papillary muscles: Variable (early, mid, late or holosystolic)

Rupture of the chordae: musical

(Acute MR: not pansystolic murmur, but lower-pitched,

decrescendo, and softer than the murmur of chronic MR)

Circulation. 2003;108:2432-2438.

Severe MR

Hyperdynamic LV type apex Systolic thrill over apex S3 Functional flow mid diastolic murmur

Circulation. 2003;108:2432-2438.


ECGChronic (severe) MR: LA dilation, Atrial fibrillation LV enlargement and non-specific ST-T changes

Acute MR: sinus tachycardia

Radiological findingsChronic (severe) MR: Cardiomegaly with LA, LV↑; pulmonary congestion, interstitial edema with Kerley B lines (left HF) C-shaped calcification of mitral annulus

Acute MR: Normal cardiac silhouette or mild LA dilation overt pulmonary congestion, edema


Echocardiography1 、 Display anatomy of the mitral valve apparatus Useful in determining the etiology of MR (2D)2 、 Confirm the existence of MR Doppler (color, spectrum): reveal high-velocity jet into LA

during systole Sensitivity~100%

Estimate the severity of MR ＜ 4

cm2 Mild （ Color flow jet area ） 4~8 cm2 Moderate ＞ 8

cm2 Severe

3 、 Measure cardiac chamber sizes, evaluate LV function, pulmonary artery pressure, provide data concerning other valvular lesions


Calculating (PISA)

Apical 4Ch view Narrow sector width Minimise depth Zoom Adjust Colour Doppler

alaising velocity (20-40 cm/s)

PISA

Measure the radius of the hemisphere. (red/blue interface)

– PISA radius =2πr2 (cm2)

• Mild MR: <0.4

• Severe MR:>1.0

Colour Doppler Indicators of Mitral Regurgitation Severity

Mild Moderate Severe

Colour Doppler

Jet area (cm2) Nyquist 50-60cm/s

<4 >10

Ratio of jet area to left atrial area (%)

<20 >40

Vena contracta width (cm)

<0.3 >0.7

PISA radius (cm) at Nyquist 40cm/s

<0.4 >1.0

Continuous wave and Pulse wave Doppler

Continuous wave spectral Strength

– Apical 4Ch view CW of regurgitant jet

• Faint in mild mitral regurgitation

• Denser in moderate and severe regurgitation.

Peak Mitral Valve E velocity

Increased mitral valve E velocity (>1.2m/s) may indicate significant regurgitation.

– Assumes ejection fraction is>40%)

Decreased mitral valve DT (<150msec) may indicate significant regurgitation.

– Assumes normal diastolic LV function.

Pulmonary Vein Systolic Flow Reversal

PW doppler 1cm into the pulmonary veins

– Systolic S (systolic) wave is normally larger than the D (diastolic) wave.

– If D wave is larger there is blunting of forward flow.

– S wave inversion demonstrates systolic flow reversal (indicative of severe MR).

Limitation

Eccentric jets may affect pulmonary vein flow

Determination of Pulmonary Artery Pressures at Rest and Exercise

Multimodality Indicators of Mitral Regurgitation Severity

Mild Moderate Severe

Multimodality

Regurgitant volume (mL/beat)

<30 30-59 >60

Regurgitant fraction (%)

<30 30-49 >50

Effective regurgitant orifice area (cm2)

<0.20 0.20-0.39 >0.40

Regurgitant Volume, Regurgitant Fraction and ERO

Regurgitant volume Step 1

– A4ch view measure diameter of the mitral annulus.

• CSAMV =0.785 X (mitral annulus diameter)2

Regurgitant volume

Step 2– Apical 4Ch view measure

the VTI of the mitral inflow (using PWD)

– Commonly at valve tip level.

• VTIMV in cm Step 3. Stroke Volume

– SVMV (mL/beat) =CSAMV X VTIMV

Regurgitant volume

Step 4– In PLAx measure the

diameter of the LVOT (cm).

– Calculate CSA of the LVOT (cm2)

• CSALVOT = 0.785 x (LVOT diameter)2

Regurgitant volume

Step 5

– In the Ap5 Ch view measure the VTI of the LVOT outflow (using PWD)

• VTILVOT (cm)

Step 6. Stroke volume

– SVLVOT = CSALVOT x VTILVOT

Regurgitant Volume/Fraction

Step 6– Mitral regurgitant volume (RV)(mL)

• RV =SVMV – SVLVOT

– Mild MR:<30 Mod MR:31-59– Severe MR:>60

Step 7– Mitral regurgitant Fraction (MF)(cm2)

• RF = RV / SVMV (x100)– Mild MR:<30 Mod MR:31-49– Severe MR:>50

Regurgitant orifice area

Step 8– Measure the VTI of the

mitral regurgitation VTIMR (cm) (using CWD)

– Calculate Regurgitant Orifice Area (ROA) in cm2

• ROA = RV / VTIMR

– Mild MR:<0.20– Mod MR:0.21-0.39– Severe MR:>0.40

Regurgitant Orifice Area PISA method

Step 1. Measure the radius of the hemisphere. (red/blue interface)

– PISA =2πr2 (cm2)

– Calculate regurgitant flow rate

– RFR mL/s =PISA X aliasing velocity

Regurgitant orifice area

Step 2. CWD of the mitral regurgitation. Measure peak velocity (VMR) in cm/s.

Calculate Regurgitant Orifice Area in cm2.

– ROA =Regurgitant flow rate / VMR

Common pitfalls

Measuring regurgitant jet area or VC width on colour doppler with inappropriate colour gain settings

Underestimating severity of eccentric jets on CFD. Failure to align the doppler beam with regurgitant flow

during CW doppler interrogation. Inaccurate measurement of mitral valve orifice area or

LVOT diameter when calculating RV. Trying to calculate RV when there is coexistant aortic

regurgitation. Failure to average several readings when the patient is in

AF.

Radionuclide angiography and MRIEvaluate LV function

Estimate the severity of regurgitation The regurgitant fraction can be estimated from the ratio of LV to RV (LV/RV) stroke volume

Cardiac catheterizationConfirm the diagnosis of MR and estimate its severity, evaluate cardiac function andpulmonary artery pressureCoronary angiography is performed todetermine presence of CAD prior to surgery






Aortic stenosis (AS)

EtiologyRHD Common, + AR and mitral valve disease

Degenerative calcific AS Common in the elderly, accompanied by calcification of the mitral annulus Congenital abnormalities Calcific stenosis of congenitally bicuspid aortic valve Congenital aortic stenosis

Hemodynamic changesNormal aortic orifice area (AOA): 3.0~4.0 cm2AOA ≤1.0cm2, LVSP↑, with significant transvalvular gradient

Compensation AS→LV pressure load↑

Concentric LVH→compliance↓→LVEDP↑→LAH

Maintain systolic wall stress and CO ↑LVEDV

Decompensation LVEDV↑→wall stress↑, myocardial ischemia, fibrosis → left HF

Classic symptom triad

Dyspnea Angina Syncope

Classic symptom triad

Once any of these classic symptoms develop, prognosis dramatically worsens.

Thus, within 5 years of the development of angina, approximately 50% of patients will die unless aortic valve replacement is performed.

For syncope, 50% survival is 3 years For congestive heart failure, 50% survival is only 2

years unless the valve is replaced. Angina 5yrs, Syncope 3yrs, and CHF 2yrs.

Severe AS

Triad of angina,dyspnoea and syncope Heaving apex Slow rising small volume pulse Reverse splitting of S2 Long duration of systolic murmur Late peaking of murmur Presence of S4


ECGSevere: LVH and secondary ST-T changes,

LA↑ ， arrhythmias

Radiological findingsNormal size or slightly enlarged heart

Calcification of the aortic valve

Poststenotic dilatation of the ascending aorta

Pulmonary congestion

EchocardiographyEstablish a diagnosis, and determine the severity of AS

M-mode and 2D echo Observe aortic valve opening, thickening and calcificationHelpful in determining the etiology of AS

Also invaluable in detecting associated mitral valve disease and in assessing LV performance, hypertrophy, and dilatation


Doppler echo

Allows calculation of the aortic valve gradient

Estimate the severity of the stenosis ＜ 20 mmHg Mild AS MPG 20~40 mmHg Moderate AS ＞ 40 mmHg Severe AS

Color Doppler flow imaging is helpful in the detection and determination of the severity of any accompanying aortic regurgitation


Enriquez-Sarano, M. et al. N Engl J Med 2004;351:1539-1546

Jet of Aortic Regurgitation, as Shown by Color-Flow Imaging


Classification of the Severity of Aortic Regurgitation


Quantitation of Aortic Regurgitation by the Convergence of the Proximal Flow

Cardiac catheterization

Determine the severity of AS by measuring systolic LV and aortic pressure simultaneously, and calculating the valve area

An average pressure gradient of ＞ 40mmHg or peak pressure gradient of ≥ 70mmHg represent severe AS

Coronary angiography is performed in most adults to assess for concomitant coronary disease

Cath data

“Pull back” tracing can be used in pt with NSR but not accurate in irregular rhythms or low-out put states.

In low cardiac output, the stenosis may be severe, with a mean gradient <50mm Hg per echo.

Gorlin equation can be used to calculate AVA from pressure gradients, independent of CO.

AVA= (1000)(CO) (44)(SEP)(HR)(√P)





Aortic regurgitation (AR)

Etiology

Primary disease of the aortic valves

and/ or aortic root

Aortic valve disease① RHD ： most common, about 2/3 + AS and/or mitral valve disease

② Infective endocarditis③ Congenital deformity: bicuspid valves

④ Myxomatous degeneration of the aortic valve

Aortic root dilatation① Marfan syndrome② Aortic dissection (involve annulus or leaflets) ③ Syphilitic aortitis

Clinical practice: aortic regurgitation. NEngl J Med. 2004;351:1539-1546.

Valvular Abnormalities leading to AR

Nodular Rheumatic Disease Aortic Root Dilation

Endocarditis

Hemodynamic changes

Chronic ARCompensation ： AR→LV volume↑→ LV↑, LVEDV↑→ SV↑(CO)

Decompensation: LV systolic dysfunction→ LV failure (EF↓, LVESV↑)

Acute ARAR →LV volume↑→ LVDP↑→ LAP↑ ↓ ↓CO↓ pulmonary congestion pulmonary edema


Clinical manifestationsSymptomsChronic ARAsymptomatic for many yearsPalpitation, precordial discomfort, head pounding

(related to SV↑)LV failure (dyspnea, fatigue): occur at late stage

Angina pectoris or chest pain: less common

Acute ARmild—no symptomsevere—Acute LV failure and hypotension (pulmonary edema)


Physical examinationChronic, severe AR

① Peripheral arterial signs: Owing to wide pulse pressure: SBP↑, DBP↓

Water-hammer pulse Water-hammer pulse (rapid rise and fall)

“Pistol shot soundsPistol shot sounds” (booming systolic & diastolic sounds heard over femoral artery) Duroziez’s signDuroziez’s sign (systolic, diastolic murmur over partially compressed femoral artery) Quincke’s sign Quincke’s sign (subungual capillary pulsations)

de Musset’s sign de Musset’s sign (head bobs with each heartbeat )

② Apical impulse: diffuse and forceful, displaced laterally and inferiorly (hyperactive, enlarged LV)

③ Heart sound: An S3 gallop is common with LV failure


④ Heart murmurs

Aortic diastolic murmur:Aortic diastolic murmur:

High-pitched, blowing, decrescendo pattern

When AR is due to primary valvular disease, the diastolic murmur is best heard along the left sternal border in the 3rd and 4th intercostal spaces

However, when it is due mainly to dilatation of the ascending aorta, the murmur is often more readily audible along the right upper sternal border

Austin-Flint murmur: apical mid or late diastolic low-pitched murmur: common in severe AR, owing to partial closure of MV by the regurgitant jet

Circulation. 2005;112(1):125-134.

Ejection systolic murmur: common harsh at the base of the heart accompanied by a systolic thrill

Acute ARS1 soft or absent ， P2↑ ， S3 and S4AR murmur: lower pitched and shorter than that of chronic ARAustin-Flint murmur: brief

Circulation. 2005;112(1):125-134.

Laboratory examinationECG Acute: sinus tachycardia; nonspecific ST-T changes

Chronic: LV enlargement and hypertrophy, arrhythmias

Circulation. 2005;112(1):125-134.

Radiological findings

Acute AR: cardiac size normal or slightly enlarge,signs of pulmonary congestion, pulmonary edema

Chronic: LV enlargement, associated with dilatation of the ascending aorta Severe, aneurysmal dilatation of the aorta suggests aortic root disease Marfan syndrome)

Pulmonary congestion （ LV heart failure ）

Chronic Acute

LVE with normal pulmonaryvasculature

Normal size LV with pulmonaryvascular congestion

Echocardiography Confirm diagnosis, estimate severity, identify the cause

2-D echo: Structural changes of the valve leaflets and/or aortic root

M mode echo: Diastolic fluttering of the anterior leaflet of the mitral valve is an important echocardiographic finding in AR Serial assessments of LV size and function

Doppler echo: Sensitive, accurate noninvasive technique for detecting AR

LVOT diastolic regurgitant jet, estimate the severity of AR

Cardiac catheterization Quantify the severity of AR Evaluate the coronary and aortic root anatomy

J Am Soc Echocardiogr.2003;16:777-802.

AMVL fluttering

Color Flow – top mild, bottom moderate

Regurgitant jet width/LVOT diameter ratio greater than or equal to 60 percent

Vena contracta greater than 6 mm

Regurgitant jet area/LVOT area ratio greater than or equal to 60 percent

Holodiastolic flow reversal in the descending thoracic or abdominal aorta

vitrag24-www.medicalgeek.com

Assessing Severity of AR

Assess severity by impact on peripheral signs and LV- Duration of murmur >2/3 of diastole Bisferiens pulse Hills sign>60 mmHg Apical impulse down & out Austin flint murmur Marked peripheral sign

Circulation. 2005;112(1):125-134.

Features AS > AR AR > AS

Symptoms:Anginal pain, blackoutPalpitation

++++

++++

Pulse Low volumeBisferians pulse

High volumeCorrigan’s pulse

Pulse pressure Normal to low Wide

Peripheral signs +/- +

Apex Heaving Hyperdynamic

Thril Always systolic Rarely

S3 Absent May be present

S4 May be present Absent

Ejection click Present Rare

Diastolic murmur Very short Classic murmur of AR

Systolic murmur Classic murmur of AS Function systolic murmur +/-

Chest X-Ray Calcification + Cardiomegaly

ECG Pressure overload Volume overload

vitrag24-www.medicalgeek.com





Tricuspid stenosis

Uncommom valvular lesion Rheumatic heart disease Congenital TS Carcinoid syndrome

Severe TS

Giant a wave in JVP Duration of diastolic murmur over tricuspid

valve Signs of right heart failure

N Engl J Med. 1997;337:32-41.

ECG- Absence of evidence of RVH Right atrial abnormality Chest X ray Prominence of right atrium and SVC

N Engl J Med. 1997;337:32-41.



Tricuspid regurgitation Primary disorders of the tricuspid apparatus Rheumatic disease Prolapse Congenital disease (Ebstein’s) IE Radiation Carcinoid Blunt chest wall trauma RV endomyocardial biopsy related trauma Intra-annular RV pacemaker or implantable cardioverter-

defibrillator leads.

N Engl J Med. 1997;337:32-41.

Approximately 80% of cases of significant TR are

functional in nature and related to tricuspid

annular dilation and leaflet tethering in the setting

of RV remodeling due to pressure and/or volume

overload.


Tricuspid stenosis





Pulmonary stenosis

Pulmonic stenosis is essentially a congenital disorder.

Less common etiologies include carcinoid and obstructing vegetations or tumors.

Assessment with TTE alone is usually sufficient for diagnosis and clinical decision making.

N Engl J Med. 1997;337:32-41.

Pulmonary stenosis



Pulmonary regurgitation

Mild-to-moderate PR seen on echocardiography is common and does not require further follow-up or intervention if asymptomatic with normal RV size and function.

Significant PR in patients is uncommon. Primary PR that follows in the wake of childhood surgery

for tetralogy of Fallot or other congenital lesions may progress insidiously




We urgently need research on almost every aspect of VHD to ensure that patients who already have VHD receive optimal therapy and to prevent VHD in those at risk.

Approaches to improving outcomes in patients with VHD include –

1) National and international registries and RCTs

2) Continuous evaluation of outcomes data at each Heart Valve Center of Excellence

3) Focus on patient-centric care with involvement of the patient in the decision-making process.

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Valvular heart disease assessment of lesion severity