Valvular Heart Disease

dr. Kiki Rizky

Pembibing : dr. Ilham Udin SpJP

Overview

Valvular heart disease 10% to 20% cardiac surgical procedures in US The primary causes

age-associated calcific valve changes and

inherited or congenital conditions

Rheumatic valve disease United States and Europe

Primary prevention of rheumatic fever

Increase in life expectancy in the last half of the 20th century Degenerative valve increasing problem

Indonesia???

Anatomy of the heart

Aortic Stenosis
There are three primary causes of valvular AS:

A congenitally abnormal valve with superimposed calcification (unicuspid or bicuspid) Calcific disease of a trileaflet valve Rheumatic valve disease

Rare causes: metabolic diseases (eg, Fabry's disease), SLE, Paget disease, and alkaptonuria.
Calcific AS has also been associated with chronic kidney disease.

Aortic Stenosis
Congenital malformations of the aortic

Unicuspid valve

severe obstruction in infancy the most frequent malformations found in fatal valvular AS in children often they are not responsible for serious narrowing of the aortic orifice during childhood have normal valve function until late in life, when superimposed calcific changes result in valve obstruction

Bicuspid valve

Aortic Stenosis
Calcific aortic valve disease is characterized by aortic valve leaflet thickening and calcification in patients with a congenital bicuspid valve or an anatomically normal trileaflet valve The pathobiology of calcific aortic valve disease is characterized by three primary processes:

lipid accumulation

inflammation
calcification

Disease progression in calcific aortic stenosis

Aortic Stenosis
Rheumatic valve disease

fusion of the commissures between the leaflets, with a small central orifice. Histologic studies show typical changes due to rheumatic disease. The rheumatic process typically involves the mitral valve as well

10

Major types of aortic valve stenosis

Pathophysiology of AS

11

Signs and symtoms

There are three classic symptoms associated with AS: Heart failure (HF)

12

diastolic dysfunction inability of the LV to increase the cardiac output during exercise

Syncope or dizziness

Exercise-induced vasodilation A transient bradyarrhythmia on exertion Abnormalities in the baroreceptor response

Angina

Increased LV oxygen demand Compression of intramyocardial coronary arteries Reduced diastolic coronary perfusion time during tachycardia Reduced coronary flow reserve

Signs and symtoms

13

Sudden cardiac death Arrhythmias

Atrial fibrillation Ventricular arrhythmias

Endocarditis Bleeding tendency

Embolic events
Coronary disease

Physical examination

14

Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus) Heart sounds- soft and split second heart sound, S4 gallop due to LVH. Systolic ejection murmur- cresendodecrescendo character. This peaks later as the severity of the stenosis increases.

Loudness does NOT tell you anything about severity

CXR

15

Other tests
ECG Left Ventricle Hipertrophy Echocardiography is the most valuable test for diagnosis, quantification and follow-up of patients with AS.

16

Two measurements obtained are:

Left ventricular size and function: LVH, Dilation, and EF Doppler derived gradient and valve area (AVA)

Cardiac catheterization

in symptomatic patients in whom noninvasive tests are inconclusive or provide discrepant results from clinical findings regarding the severity of AS (ACC/AHA 2006)

Cardiovascular magnetic resonance Computed tomography

Management of AS

17

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

18

Management strategy for patients with severe aortic stenosis

Aortic Regurgitation

19

Inadequate closure of the aortic valve leaflets. Induced by:

Damage to and dysfunction of the aortic valve leaflets Distortion or dilatation of the aortic root and ascending aorta.

Major causes of aortic regurgitation

Leaflet abnormalities
Rheumatic fever Endocarditis (bacterial or marantic) Trauma Bicuspid aortic valve Rheumatoid arthritis Myxomatous degeneration

20

Aortic root or ascending aorta

Systemic hypertension Aortitis (eg, syphilis) Reactive arthritis Ankylosing spondylitis Trauma Dissecting aneurysm Marfan syndrome Ehlers-Danlos syndrome Pseudoxanthoma elasticum

Ankylosing spondylitis
Acromegaly Fenfluramine-phentermine

Inflammatory bowel disease

Osteogenesis imperfecta Annuloaortic ectasia

21

Pathophysiology of aortic regurgitation

22

Signs and symtoms

23

Asymptomatic until 4th or 5th decade Rate of Progression: 4-6% per year 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

A sense of pounding and an uncomfortable awareness of the heartbeat. Atypical chest pain mechanical interaction between the heart and the chest wall.

Physical findings

24

Wide pulse pressure ("water hammer" or Corrigan pulse) Hyperdynamic and displaced apical impulse

Auscultation

Diastolic blowing murmur at the left sternal border Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate Systolic ejection murmur: due to increased flow across the aortic valve

Hyperdynamic pulse
deMusset's sign A head bob occurring with each heart beat.

25

Traube's sign A pistol shot pulse (systolic and diastolic sounds) heard over the femoral arteries. Duroziez's sign A systolic and diastolic bruit heard when the femoral artery is partially compressed.

Quincke's pulses Capillary pulsations in the fingertips or lips.

Mueller's sign Systolic pulsations of the uvula. Becker's sign Visible pulsations of the retinal arteries and pupils. Hill's sign Popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg. Mayne's sign More than a 15 mmHg decrease in diastolic blood pressure with arm elevation from the value obtained with the arm in the standard position. Rosenbach's sign Systolic pulsations of the liver. Gerhard's sign Systolic pulsations of the spleen.

Initial evaluation of AR

26

ECG: Left axis deviation, Left ventricular hypertrophy.

CXR: enlarged cardiac silhouette (LV) and aortic root enlargement

ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation) Aortography: Used to confirm the severity of disease

Medical therapy

29

Vasodilators Vasodilators such as CCB and ACE inhibitors may influence LV size and function and slow the rate of progression of AR.

Other forms of medical therapy has a limited role in AR.

Symptomatic valve replacement.

Management strategy

30

Acute AR

Etiology

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

Mitral Stenosis

33

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.

34

Pathophysiology of mitral stenosis

35

Progressive Dyspnea (70%): LA dilation pulmonary congestion (reduced emptying)

worse with exercise, fever, tachycardia, and pregnancy

Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation. Right heart failure symptoms: due to Pulmonary venous HTN Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure

Signs and symtoms

36

The symptoms induced by MS are primarily related to the severity of the valvular stenosis as reflected by the left atrial pressure, pulmonary pressures, pulmonary vascular resistance, and cardiac output. Not noticed by patient slow progression of disease is "matched" by a gradual reduction in activity.

Signs and symtoms

37

Dyspnea low cardiac output Hemoptysis The increased pulmonary pressures and vascular congestion Thromboembolism Chest pain Infective endocarditis

Right-sided heart failure

Hoarseness compression of the recurrent laryngeal nerve

Physical findings

38

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 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.

Loud Opening S1 snap:

Representation of MS

39

CXR

40
CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV ECG: may show atrial fibrillation and LA enlargement ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

Management of MS
Serial echocardiography:

41

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

Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression

-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling Duiretics for fluid overload

Identify patient early who might benefit from percutaneous mitral balloon valvotomy. IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

Management of MS

42

Mitral balloon valvotomy

43

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

44

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

Etiology
Acute MR

45

Endocarditis Acute MI: Malfunction or disruption of prosthetic valve

Chronic MR

Myxomatous degeneration (MVP) Ischemic MR Rheumatic heart disease Infective Endocarditis

Pathophysiology of MR

46

Pure Volume Overload Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility

Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension. Progressive left ventricular volume overload leads to dilation and progressive heart failure.

The Natural History of MR

Compensatory phase: 10-15 years Patients with asymptomatic severe MR have a 5%/year mortality rate

Once the patients EF becomes <60% and/or becomes symptomatic, mortality rises sharply
Mortality: From progressive dyspnea and heart failure

Signs and symptoms

48

Auscultation: soft S1 and a holosystolic murmur at the apex radiating to the axilla

S3 (CHF/LA overload)

In chronic MR, the intensity of the murmur does correlate with the severity.

Exertion Dyspnea: ( exercise intolerance) Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

Imaging studies 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

Management of MR
Medications
a) b) c)

Vasodilator such as hydralazine Rate control for atrial fibrillation with -blockers, CCB, digoxin Anticoagulation in atrial fibrillation and flutter

d)

Diuretics for fluid overload

Management of MR

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.

Management MR

52

Acute MR

Etiology

Endocarditis Acute MI: Malfunction or disruption of prosthetic valve

Acute MR
Management:

Myocardial infarction: Cardiac cath or thrombolytics Most other cases of mitral regurgitation is afterload reduction:

Diuretics and nitrates nitroprusside, even in the setting of a normal blood pressure.

Do not attempt to alleviate tachycardia with betablockers. Mild-to-moderate tachycardia is beneficial in these patients because it allows less time for the heart to have backfill, which lowers regurgitant volume.

Treatment of Acute MR

Balloon Pump Nitroprusside even if hypotensive Emergent Surgery

56