valvular heart disease. goals and objectives discuss the common etiologies of valvular stenosis and...

VALVULAR HEART DISEASE

Goals and Objectives

• Discuss the common etiologies of valvular stenosis and regurgitation.

• Recognize the signs and symptoms of severe valvular stenosis and regurgitation

• Be able to quickly identify and treat acute mitral and aortic regurgitation

• Identify patients who should be referred for surgical replacement of their valves

Mitral Stenosis

Etiology of Mitral Stenosis

• Rheumatic heart disease: 77-99% of all cases

• Infective endocarditis: 3.3%

• Mitral annular calcification: 2.7%

• Congenital: rare

Mitral Stenosis Overview

• Definition: Obstruction of LV inflow that prevents proper filling during diastole

• Normal MV Area: 4-6 cm2

• Transmitral gradients and symptoms begin at areas less than 2 cm2

• Rheumatic carditis is the predominant cause• Prevalence and incidence: decreasing due

to a reduction of rheumatic heart disease.

MS Pathophysiology• Progressive fibrosis ,thicking ,calcifications of of valve

leaflets and fusion of commisures leads to gradual narrowing of mitral valve orifice,symptoms begin at areas less than 2 cm2

restricted blood flow from LA to LV and LA pressure rises -Leads to left atrial enlargement and atrial fibrillation(very common)….. pulmonary congestion(reduced lung compliance) pulmonary venous hypertension –Progressive and gradual rise in pulm.venous HTN leads to increase pulm.vascular resistance and pulm.arterial HTN leading to RVH-later RV dilatation and RT heart Failure .

•

SYMPTOMS• Breathlessness (pulmonary congestion) dominant •

•Fatigue (low cardiac output) • •Palpitation (atrial fibrillation) • •Haemoptysis (pulmonary congestion, pulmonary embolism) ••Cough (pulmonary congestion) • •Chest pain (pulmonary hypertension) • •Oedema, ascites (right heart failure)•Thromboembolic complications (e.g. stroke, ischaemic limb)

SIGNS• Dyspneaic,Mitral facies -malar flush(pinkish-

purple patches on the cheeks)• JVP normal or raised• Pluse usually irregular due to Atrial fibrillation

LOCAL:• Palpation : Apex tapping(loud S1), • RV heave, loud P2

(pulmonary hypertension)-diastolic thrill.

• • Auscultation Loud first heart sound, opening snap ,Mid-diastolic murmur •

• Crepitations, pulmonary oedema, effusions• Signs of right-sided heart failure: in advanced disease

• Diastolic murmur: – Low-pitched diastolic rumble most prominent at

the apex. – Heard best with the patient lying on the left side

in held expiration – Intensity of the diastolic murmur does not

correlate with the severity of the stenosis

Heart Sounds in MS

• Loud S1-Opening snap: heard at the apex when leaflets are still mobile – Due to the abrupt halt in leaflet motion in early

diastole, after rapid initial rapid opening, due to fusion at the leaflet tips.

– A shorter S2 to opening snap interval indicates more severe disease.-

Heart Sounds in MS

Investigations

• ECG: may show atrial fibrillation and LA enlargement

• CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV

• ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area,other lesions

• Cardiac catheterization

Management of MSSerial echocardiography:

– Mild: 3-5 years– Moderate:1-2 years– Severe: yearly

• Medications: MS is a mechanical problem and medical therapy does not prevent progression -blockers, CCBs, Digoxin which control heart rate

in atrial fibrillation– Anticoagulant to prevent thromboembolization in

atrial fib.– Duiretics for fluid overload and pulm .congestion

Management of MS

• Rheumatic fever prophylaxis• IE prophylaxis: Patients with prosthetic valves or

a Hx of IE for dental procedures.

Nonmedical managment• Mitral balloon valvuloplasty and valve

replacement(MVR)

• Symptomatic mod/sever MS +favorable anatomy• Asymptomatic mod/sever MS +pulm.HTN

+favorable anatomy(Isolated mitral stenosis • No mitral regurgitation, Mobile, non calcifiedvalve/subvalve apparatus on echo • LA free of thrombus )

• Valve replacement(MVR)

Mitral Regurgitation

• Definition: Backflow of blood from the LV to the LA during systole

• Mild (physiological) MR is seen in 80% of normal individuals.

Chronic Mitral Regurgitation Overview

Acute MR

• Endocarditis

• Acute MI:

• Malfunction or disruption of prosthetic valve

-Mitral valve prolapse

-Dilatation of the LV and mitral valve ring (e.g. coronary artery disease, cardiomyopathy)

-Rheumatic fever

-Ischaemia or infarction of the papillary muscle

-Myocardial infarction

Etiologies of Chronic Mitral Regurgitation

Mitral valve prolapse

• Occurs in 5% of adults

• Floppy MV, caused by congenital anomalies or degenerative myxomatous changes, Marfans syndrome.

• Asymptomatic,atypical chest pain ,benign arrythmia ,small risk of embolic stroke

• Mid systolic click and late systolic murmur

• Prognosis is good

Pathophysiology of MR• Pure Volume Overload

• Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility,LV dilatation.– Progressive left atrial dilation and right ventricular

dysfunction due to pulmonary hypertension.– Progressive left ventricular volume overload leads to

dilation and progressive heart failure.

SYMPTOMS

Asymptomatic

•Dyspnoea (pulmonary venous congestion)

Fatigue (low cardiac output)

• Palpitation (atrial fibrillation, increased stroke volume)

• Oedema, ascites (right heart failure)

Systemic embolization { stroke , ischaemic limb etc.. }

Signs

• Pulse :Atrial fibrillation/flutter

• Cardiomegaly: displaced hyperdynamic apex beat

• Apical pan.systolic murmur ± thrill • Soft S1, apical S3.

• Signs of pulmonary venous congestion (crepitations, pulmonary oedema, effusions) • Signs of pulmonary hypertension and right heart failure.

Investigations in MR

• ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR

• CXR: LA enlargement, central pulmonary artery enlargement.

• ECHO: Estimation of LA, LV size and function. Valve structure assessment– TEE if transthoracic echo is inconclusive– Cardiac catheterization.

Management of MR

• Medications

• Mild –moderate MR can be treated medically

a) Vasodilator such as hydralazine,ACE inhibitors

b) Rate control for atrial fibrillation with -blockers, CCB, digoxin in AF

c) Anticoagulation in atrial fibrillation and flutter

d) Diuretics for fluid overload

• Serial Echocardiography: – Mild: 2-3 years– Moderate: 1-2 years– Severe: 6-12 months

• IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

Surgical

• Repair or MVR

• Sever even asymptomatic

• Progressive cardiomegaly or progressive deterioration of LV function by ECHO

Treatment of Acute MR

• Balloon Pump

• Nitroprusside even if hypotensive

• Emergent Surgery

Aortic Stenosis

Aortic Stenosis Overview:

• Normal Aortic Valve Area: 3-4 cm2

• Symptoms: Occur when valve area is 1/4th of normal area.

• Types:

– Supravalvular

– Subvalvular

– Valvular

Etiology of Aortic Stenosis

• Congenital(Bi-cusped).Bi-cusped).• Rheumatic.

• Degenerative/Calcific.

Patients under 70: >50% have a congenital cause

Patients over 70: 50% due to degenerative

Evaluation of AS

Cardiac catheterization: Should only be done for a direct measurement if symptom severity and echo severity don’t match OR prior to replacement when replacement is planned.

Pathophysiology of Aortic Stenosis• A pressure gradient develops between the

left ventricle and the aorta. (increased afterload)

• LV function initially maintained by compensatory pressure hypertrophy

to maintain the cardioac output

• When compensatory mechanisms exhausted, LV function declines and pulm.edema supervenes.

Presentation of Aortic Stenosis

- Asymptomatic mild/moderate

- Syncope: (exertional)

- Angina: (increased myocardial oxygen demand; demand/supply mismatch)

- Dyspnea: on exertion due to heart failure (systolic and diastolic)

- Sudden death

Physical Findings in Aortic Stenosis

• Slow rising carotid pulse (pulsus tardus)• Thrusting apex beat (LV pressure overload) • Narrow

pulse pressure

• Heart sounds- soft and split second heart sound, S4 gallop due to LVH.

• Systolic ejection murmur- cresendo-decrescendo character. This peaks later as the severity of the stenosis increases.– Loudness does NOT tell you anything about

severity

Investigations• ECG Left ventricular hypertrophy ,LBBB• Chest X-ray May be normal; sometimes enlarged

LV and dilated ascending aorta on PA view, calcified valve on lateral view.

• Echo Calcified valve with restricted opening, hypertrophied LV) Doppler • Measurement of severity of stenosis • Detection of associated aortic regurgitation.

• Cardiac catheterisation • Mainly to identify associated coronary artery disease • May be used to measure gradient between LV and aorta.

Management of AS

• General- IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis.

• Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS

• Aortic Balloon Valvotomy- shows little benefit.

• Surgical Replacement: Definitive treatment

Simplified Indications for Surgery in Aortic Stenosis

• Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)

• Any patient with decreasing EF

• Any patient undergoing CABG with moderate or severe AS

Aortic Regurgitation

Aortic Regurgitation Overview

• Definition: Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps.

Etiology of Acute AR

• Endocarditis

• Aortic Dissection

• Physical Findings:– Wide pulse pressure– Diastolic murmur– Florid pulmonary edema

Treatment of Acute AR

• True Surgical Emergency:

• Positive inotrope: (eg, dopamine, dobutamine)

• Vasodilators: (eg, nitroprusside)

• Avoid beta-blockers

• Do not even consider a balloon pump

Etiology of Chronic AR

Cusps defects

•Congenital -Bicuspid aortic valve

•Rheumatic •Infective endocarditis

Aortic root dilatation Marfan.

Pathophysiology of AR

• Combined pressure AND volume overload

• Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure.

Symptoms

• Asymptomatic until 4th or 5th decade

• Progressive Symptoms include:- Dyspnea: exertional, orthopnea, and

paroxsymal nocturnal dyspnea- Nocturnal angina: due to slowing of heart rate

and reduction of diastolic blood pressure.- Palpitations: due to increased force of

contraction.

Peripheral signsPeripheral signs• Pulses Large volume or ‘collapsing’ pulse.

• Corrigan pulseCorrigan pulse• Increased pulse pressure• Bounding peripheral pulses • Capillary pulsation in nail beds: Quincke’s sign •

Femoral bruit (‘pistol shot’) • Duroziez’s sign • • Head nodding with pulse: de Musset’s sign.

• Hill’s signHill’s sign JVP may be normal or elevatedJVP may be normal or elevated•

Signs

Central Signs•Apex : Hyperdynamic and displaced apical impulse.•Diastolic thrill.

•AuscultationAuscultation High pitched, blowing, decrescendo diastolic High pitched, blowing, decrescendo diastolic murmur at LSB, best heard at end-expiration & murmur at LSB, best heard at end-expiration & leaning forward.leaning forward.Austin-Flint murmur indicates severity (mid to Austin-Flint murmur indicates severity (mid to late diastolic murmur)late diastolic murmur)Systolic murmur related to high flow stateSystolic murmur related to high flow state

Investigations• ECG Initially normal, later left ventricular

hypertrophy and T-wave inversion • Chest X-ray Cardiac dilatation, maybe aortic

dilatation Features of left heart failure • Echo Dilated LV •Hyperdynamic LV • Doppler

detects reflux • Fluttering anterior mitral leaflet • Cardiac catheterisation (may not be required) •

Dilated LV • Aortic regurgitation • Dilated aortic root.

Management of AR

• General: IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis.

• Medical: Vasodilators (ACEI’s), Nifedipine improve stroke volume and reduce regurgitation only if pt symptomatic or HTN.

• Serial Echocardiograms: to monitor progression.

• Surgical Treatment: Definitive Tx

Simplified Indications for Surgical Treatment of AR

• ANY Symptoms at rest or exercise

• Asymptomatic treatment if:

– EF drops below 50% or LV becomes dilated.

Tricuspid stenosis

Almost always rheumatic

The low cardiac output state causes fatigue; abdominal discomfort may occur due to hepatomegaly and ascites

The diastolic murmur of tricuspid stenosis is augmented by inspiration. •Medical management includes salt restriction and diuretics.• Surgical treatment in patients with a valve area <2.0cm and a mean pressure gradient >5mmHg.

Tricuspid regurgitation

Most common cause is annular dilatation due to RV failure of any cause

Symptoms and signs result from a reduced cardiac output, ascites, painful congestive hepatomegaly and oedema.

The pansystolic murmur of TR is usually loudest at the left sternal edge and augmented by deep inspiration.

Severe functional TR may be treated by annuloplasty or valve replacement. Severe TR due to intrinsic tricuspid valve

disease requires valve replacement.

Pulmonary stenosis

Most commonly due to congenital malformation

Survival into adulthood is the rule, infective endocarditis is a risk and right ventricular failure is the most common cause of death.

Carcinoid plaques may lead to constriction of the pulmonary valve ring.

Pulmonary regurgitation

•Most common cause is ring dilatation due to pulmonary hypertension, or dilatation of the pulmonary artery secondary to a connective tissue disorder.May be present and well-tolerated for many years

•The clinical manifestations of the primary disease tend to overshadow the pulmonary regurgitation.

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