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Cardiology > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

Valvular Heart Disease (VHD)

A

Can be defined by the Location (Valve) and Physiology (Stenosis vs. rEgurgitation) and can occasionally be both Stenotic and Regurgitant, and involve Multiple Valves

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2
Q

VHD Epidemiology

A
  • The age adjusted prevalence is 2.5%, however the prevalence is highly dependent on Age, reaching 13% in those >75 years
  • The most common etiologies, requiring intervention are: AS, Primary MR, Secondary MR, and AR
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3
Q

RF for VHD

A
  1. Advancing age
  2. Genetic Conditions -→ Congenital BV, Marfan’s, Turners’, and Downs Syndrome
  3. Infectious → Rheumatic Fever, IE
  4. Cardiovascular → Previous MI, Hypertension
  5. Renal → CKD
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4
Q

Ddx for VHD

A
  1. The DDX for any murmur is any other valve that could be causing the same noise during that phase of the Cardiac Cycle i.e. Diastolic or Systolic
  2. Ddx for Systolic Murmurs include → AS/PS, MR/TR.
    1. Systolic murmurs can also be caused by left ventricular outflow tract obstruction (LVOTO) either by a congential sub aortic membrane or seen in hypertrophic cardiomyopathy (HCM)
  3. Ddx for Diastolic Murmurs include → AR/PR, MS, TS (Very rare)
  4. VSD → Holo or Pansystolic murmur
  5. Continuous murmurs can also be heard if the patient has a Fistula for dialysis or in the case of a PDA
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5
Q

Mitral Valve

Anatomy

A
  • The mitral valve consists of the Fibrous Annulus
  • Anterior and Posterior leaflets
  • Chordae Tendineae
  • and the papillary muscles (Fig. 30.73).
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6
Q

Mitral Stenosis

Epidemiology

A
  • Prevelance is estimated at <0.1%
  • MS is largely a remnant of prior Rheumatic Infection, and secondary to the decline of Rheumatic Fever in the Industrialized world, this too has subsequently declined
  • However, it is still prevelaent in developing nations so In low- to medium-income countries this affects nearly 20million people.
  • The condition is more common in women than men.
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7
Q

Mitral Stenosis

Most common cause

A
  • Mitral stenosis is commonly due to rheumatic heart disease following previous rheumatic fever due to infection with a group A β- haemolytic streptococcus
  • Inflammation leads to Commissural Fusion and a reduction in Mitral Valve Orifice Area, causing the characteristic DOMING pattern seen on ECHO.
  • Over many years the condition progresses to Valve Thickening, Cusp Fusion, Calcium Deposition, a Severely Narrowed (stenotic) valve orifice and Progressive immobility of the valve cusps.
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8
Q

Mitral Stenosis

Other causes

A
  1. Congenital Mitral Stenosis
  2. Lutembacher’s syndrome (the combination of Acquired Mitral Stenosis and an ASD)
  3. Mitral Annular Calcification, rarely; this may lead to mitral sten-
    osis if extensive, particularly in Elderly Patients and those with
    End-Stage Renal disease
  4. Carcinoid tumours metastasizing to the lung, or primary bron-
    chial carcinoid.
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9
Q

Mitral Stenosis

Pathophysiology

A
  1. When the normal valve orifice area of 4–6cm2 is reduced to less than 1cm2, severe mitral stenosis is present.
  2. In order for sufficient CO to be maintained, the Left Atrial Pressure increases and Left Atrial Hypertrophy and Dilation occur.
  3. Consequently, Pulmonary Venous, Pulmonary Arterial and Right Heart Pressures also increase.
  4. The increase in Pulmonary Capillary Pressure is followed by the development of Pulmonary Oedema, particularly when the rhythm deteriorates to atrial fibrillation with Tachycardia and loss of coordinated Atrial Contraction.
  5. This is partially prevented by Alveolar and Capillary Thickening and Pulmonary Arterial Vasoconstriction (Reactive Pulmonary Hypertension). Pulmonary Hypertension leads to RVH, Dilation and Failure, with subsequent TR.
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10
Q

Mitral Stenosis

Symptoms

A
  1. Usually, there are no symptoms until the valve orifice is moderately stenosed (area <2 cm2).
    1. In Europe, this does not usually occur until several decades after the first attack of rheumatic fever, but in low- to medium-income countries severe stenosis may occur at 10–20years of age
  2. Dyspnea: Progressively severe dyspnoea develops from the elevation in Left Atrial Pressure, Vascular Congestion and Interstitial Pulmonary Oedema.
  3. Cough: A cough productive of Blood-tinged, Frothy Sputum or Frank Haemoptysis may occur.
  4. RHF Sx: The development of Pulmonary Hypertension eventually leads to right heart failure and its symp- toms of Weakness, Fatigue and Abdominal or Lower limb swelling.
  5. Palpitations: The large left atrium predisposes to atrial fibrillation, giving rise to symptoms such as palpitations.
    1. Atrial fibrillation may result in Systemic Emboli, most commonly to the Cerebral Vessels, producing neurological sequelae, but Mesenteric, Renal and Peripheral Emboli are also seen.
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11
Q

Mitral Stenosis

Signs

A
  1. Face
    1. Severe mitral stenosis with pulmonary hypertension is associated with the so-called mitral facies or malar flush.
    2. This is a bilateral, cyanotic or dusky pink discoloration over the upper cheeks, which is due to arteriovenous anastomoses and vascular stasis.
  2. Pulse
    1. A Small-Volume Pulse is typical in mitral stenosis.
    2. This may be regular early on in the disease process (patient in sinus rhythm)
    3. but as the disease progresses, an ‘irregularly irregular’ pulse (atrial fibrilla- tion) may occur and may cause symptomatic clinical deterioration.
  3. Jugular veins
    1. Right heart failure may develop, leading to jugular venous disten- sion.
    2. When pulmonary hypertension or tricuspid stenosis is present, the ‘a’-wave will be prominent, provided that atrial fibrillation has not supervened.
  4. Palpation
    1. There is a Tapping Impulse felt Parasternally on the left side.
    2. This is the result of a Palpable FIRST heart sound combined with left Ventricular backward displacement produced by an Enlarging Right Ventricle.
    3. A Sustained Parasternal impulse due to Right Ventricular hypertrophy may also be felt.
  5. Auscultation
    1. S1: Auscultation (see Fig. 30.74) reveals a loud first heart sound if the mitral valve is pliable but this will not occur in calcific mitral stenosis.
    2. Opening Snap: As the valve suddenly opens with the force of the increased left atrial pressure, an ‘OPENING SNAP will be heard.
    3. Mid-Diastolic Murmur: This is followed by a Low-Pitched, ‘Rumbling’, Mid-Diastolic Murmur, best heard with the bell of the stethoscope held lightly at the apex and the patient lying on the Left side in Expiration.
    4. If the patient is in Sinus rhythm, the murmur becomes Louder at the end of Diastole as a result of Atrial Contraction (pre-systolic accentuation).
    5. Graham Steell Murmur: Pulmonary Hypertension may result in Pulmonary Valvular Regurgitation, which causes an Early Diastolic Murmur in the pulmonary area, known as a Graham Steell murmur.
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12
Q

Mitral Stenosis: Ix

CXR

A
  1. The chest X-ray may show Left Atrial Enlargement with Straightening of the left heart border and a ‘Double Shadow’ on the border of the right and left atria (see Fig. 30.14).
  2. Late in the course of the disease a Calcified mitral valve may be seen on a penetrated or lateral view.
  3. Pulmonary Vascular Congestion and enlargement of the main pul- monary arteries may also be apparent in severe disease.
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13
Q

Mitral Stenosis: IX

ECG

A
  1. In sinus rhythm the ECG may show a bifid P wave owing to delayed left atrial activation (Fig. 30.75).
  2. However, Atrial fibrillation is frequently present.
  3. As the disease progresses the ECG features of Right Ventricular Hypertrophy (right axis deviation and, perhaps, tall R waves in lead V1) may develop (Fig. 30.76).
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14
Q

Mitral Stenosis IX:

ECHO

A
  1. TTE is able to determine Left Atrial Size and the degree of Thickening, Calcification and Mobility of the mitral leaflets, as well as the degree of commissural fusion (Fig. 30.77).
    1. The severity of the mitral stenosis (Box 30.42) can be defined by Mitral Valve Area on two- dimensional echocardiography, with Continuous Wave (CW) Doppler to measure the pressure half-time (the time taken for the pressure to halve from the peak value) and mean pressure drop across the valve
    2. CW Doppler may also be used to estimate pulmonary artery pressure through measurement of the degree of Tricuspid Regurgitation.
  2. TOE is performed to detect the presence of left atrial thrombus (see p. 1040) or to carry out a detailed assessment prior to consideration of surgical or percutaneous intervention.
  3. The Wilkins score is an echocardiographic assessment of the mitral valve (degree of Valve Thickening, Calcification and Mobility of the mitral leaflets, and Subvalvular Apparatus and is also used to determine suitability for Percutaneous Mitral Valvuloplasty.
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15
Q

Mitral Stenosis IX:

ECHO

A
  1. TTE is able to determine Left Atrial Size and the degree of Thickening, Calcification and Mobility of the mitral leaflets, as well as the degree of commissural fusion (Fig. 30.77).
    1. The severity of the mitral stenosis (Box 30.42) can be defined by Mitral Valve Area on 2D ECHO, with Continuous Wave (CW) Doppler to measure the Pressure Half-Time (the time taken for the pressure to halve from the peak value) and Mean Pressure Drop across the valve
    2. CW Doppler may also be used to estimate Pulmonary Artery Pressure through measurement of the degree of Tricuspid Regurgitation.
  2. TOE is performed to detect the presence of LA Thrombus (see p. 1040) or to carry out a Detailed assessment prior to consideration of surgical or percutaneous intervention.
  3. The Wilkins score is an echocardiographic assessment of the mitral valve (degree of Valve Thickening, Calcification and Mobility of the mitral leaflets, and Subvalvular Apparatus and is also used to determine suitability for Percutaneous Mitral Valvuloplasty.
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16
Q

Mitral Stenosis: IX

Cardiac Catheterization

A

Left and right heart catheterization may be required in patients with severe mitral stenosis referred for intervention

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17
Q

Mitral Stensosi: Pharmacotherapy

A
  1. Early symptoms of mitral stenosis, such as mild dyspnoea, can usually be treated with low doses of diuretics.
  2. BB+CB improve Exercise Tolerance.
  3. The onset of Atrial Fibrillation requires treatment with BB or DC cardioversion and anticoagulation to prevent Atrial Thrombus and systemic embolization. (WARFARIN, NOACs are not licensed)
  4. Patients with moderate-severe mitral stenosis who develop persistent symptoms or pulmonary hypertension are appropriate for interven- tion.
  5. There are four operative measures.
  6. Intervention either with Surgery or Percutenaous Mitral Commissurotomy is chosen depending on Multiple Clinical Factors and Echocardiographic Anatomical Variables
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18
Q

Mitral Stenosis: Management

Trans-Septal Balloon Valvolotomy

A
  1. A catheter is introduced into the right atrium via the femoral vein under local anaesthesia in the cardiac catheter laboratory.
  2. The inter- atrial septum is then punctured and the catheter advanced into the left atrium and across the mitral valve.
  3. A balloon is passed over the catheter to lie across the valve and then inflated briefly to split the valve commissures.
  4. As with other valvotomy techniques, significant regurgitation may result, necessitating valve replacement (see later).
  5. This procedure is ideal for patients with Pliable Valves in whom there is little involvement of the Subvalvular Apparatus and Minimal Mitral Regurgitation.
  6. Contraindications include Heavy Calcification** or more than **Mild Mitral Regurgitation** and **Thrombus in the left atrium.
  7. TOE must be performed prior to this technique in order to exclude Left Atrial Thrombus.
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19
Q

Mitral Stenosis: Management

Closed Valvotomy

A
  1. This operation is advised for patients with Mobile, Non-calcified and Non-regurgitant mitral valves.
  2. The fused cusps are forced apart by a Dilator introduced through the Apex of the LV and guided into position by the surgeon’s finger inserted via the Left Atrial Appendage.
  3. Cardiopulmonary Bypass is NOT needed for this operation.
  4. Closed valvotomy may produce a good result for 10years or more.
  5. The valve cusps often re-fuse and another operation may eventually be necessary.
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20
Q

Mitral Stenosis: Management

Open Valvotomy

A
  1. This operation is often preferred to closed valvotomy.
  2. The cusps are carefully dissected apart under direct vision.
  3. Cardiopulmonary bypass is required.
  4. Open dissection reduces the likelihood of causing Traumatic Mitral Regurgitation.
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21
Q

Mitral Stenosis: Management

Valve Replacement

A
  1. Replacement of the mitral valve is necessary if:
  2. Mitral regurgitation is also present
  3. There is a badly Diseased or Calcified stenotic valve that cannot
    be re-opened without producing significant Regurgitation
  4. There is severe MS and Thrombus in the Left Atrium despite Anticoagulation.
  5. Artificial valves (see p. 1102) may work successfully for more
    than 20 years.
  6. Anticoagulants are generally necessary to prevent the formation of thrombus, which might obstruct the valve or embolize.
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22
Q

Mitral Regurgitation

Epidemiology

A

MR is the 2nd most common VHD (after AS) in hospitalized patients, and is the most common in the General Population

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23
Q

Mitral Regurgitation

Subdivision

A
  1. Mitral regurgitation can occur due to abnormalities of the valve leaflets, the annulus, the chordae tendineae or papillary muscles, OR the left ventricle.
  2. SO MR is subdivided into Primary or secondary MR
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24
Q

Mitral Regurgitation

Primary

A
  • Primary (AKA Organic) MR is due to abnormalities in the Mitral Valve Apparatus, examples include
  • Degenerative (Myxomatous) disease
  • Mitral Valve Prolapse (more commonly seen in CT Disorders)
  • Collagen diseases (e.g. Marfan’s and Ehlers–Danlos syndromes)
  • Rheumatic Autoimmune Diseases (e.g. Systemic Lupus Erythematosus)
  • Rheumatic Heart Disease
  • Perforation (seen in IE)
  • Papillary Muscle Rupture (Post-Myocardial Infarction)
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25
Q

Mitral Regurgitation

Secondary

A
  • Secondary (AKA Functional/ISchemic) MR is due to LV Dilation, which results in Annular Dilation often leading to Poor Co-Aptation between the Leaflets.
  • The Mitral Leaflets themselves are structurally normal–but the abnormally Dilated Ventricle causes Abnormal Function
  • The underlying Aetiology of the Ventricular Dilation is often Secondary to a Prior MI (Ischemic) or Dilated Cardiomyopathy
  • Myocardium (dilated and hypertrophic cardiomyopathy)
  • and disorders caused by drugs, including Centrally Acting Appetite Suppressants (Fenfluramine) and Dopamine Agonists (Cabergoline).
  • The most frequent causes of mitral regurgita- tion are
    • Degenerative (Myxomatous) disease
    • Ischaemic Heart Disease
    • Rheumatic Heart Disease
    • Infectious Endocarditis.
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26
Q

Mitral Regurgitation

Pathophysiology

A
  1. Regurgitation into the LA produces Left Atrial DILATION but little increase in Left Atrial Pressure if the Regurgitation is long- standing, as the Regurgitant Flow is accommodated by the large LA.
  2. With Acute Mitral Regurgitation the normal compliance of the Left Atrium does not allow much dilation and the left atrial pressure rises.
  3. Thus, in Acute Mitral Regurgitation the left atrial v- wave is greatly increased and Pulmonary Venous Pressure rises, leading to Pulmonary Oedema.
  4. Since a proportion of the Stroke Volume is regurgitated, the Stroke Volume increases to maintain the forward CO and the Left Ventricle therefore enlarges.
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27
Q

Mitral Regurgitation

Classification

A
  1. The Carpentier classification (Fig. 30.78) uses Mitral Leaflet motion to divide patients into different classes according to the mechanism of regurgitation,
  2. which can be useful when considering surgical intervention.
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28
Q

Mitral Regurgitation

Sx

A
  1. MRcan be present for many years and the cardiac dimensions greatly increased before any symptoms occur.
  2. Dyspnoea and Orthopnoea develop because of Pulmonary Venous Hypertension that arises as a direct result of the MR and secondarily as a consequence of LVF.
  3. Fatigue and Lethargy develop because of the Reduced Cardiac Output.
  4. In the late stages of the disease the symptoms of RHF also occur and eventually lead to congestive cardiac failure.
    1. Cardiac cachexia may develop.
    2. Thromboembolism is less common than in mitral stenosis but Subacute Infective Endocarditis is much more common
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29
Q

Mitral Regurgitation

Signs: The physical signs of Uncomplicated Mitral Regurgitation are:

A
  1. Apex Beat: Laterally displaced (forceful) diffuse apex beat and a systolic thrill (if severe).
  2. S1: Soft first heart sound, owing to the incomplete apposition of the valve cusps and their partial closure by the time ventricular systole begins.
  3. Pansystolic Murmur: Pansystolic murmur, due to the occurrence of regurgitation throughout the whole of systole, being loudest at the apex but radiating widely over the precordium and into the axilla.
  4. Mid-systolic click, which may be present with a floppy mitral valve (see later); it is produced by the Sudden Prolapse of the valve and the tensing of the Chordae Tendineae that occurs during systole. This may be followed by a Late Systolic murmur ow- ing to some regurgitation.
  5. S3: Prominent third heart sound (S3), owing to the sudden rush of blood back into the Dilated LV in Early Diastole (some- times a Short Mid-diastolic flow murmur may follow the third heart sound).
  6. The signs related to AFib, Pulmonary Hypertension and Left and Right HF develop later in the disease. The onset of atrial fibrillation has a much less dramatic effect on symptoms than in mitral stenosis.
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30
Q

Mitral Regurgitation: IX

CXR

A
  • The chest X-ray may show LA and LV enlargement.
  • There is an increase in the cardiothoracic ratio
  • and Valve Calcification may be present.
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31
Q

Mitral Regurgitation: IX

ECG

A
  1. The ECG shows the features of left atrial delay (bifid P waves)
  2. and left ventricular hypertrophy (Fig. 30.79), as manifested by tall R waves in the left lateral leads (e.g. leads I and V6) and deep S waves in the right-sided precordial leads (e.g. leads V1 and V2).
    1. (Note that S in V1 plus R in V5 or R in V6 >35mm indicates left ventricular hypertrophy.)
    2. Left ventricular hypertrophy occurs in about 50% of patients with MR
  3. Atrial fibrillation may be present.
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32
Q

Mitral Regurgitation: IX

ECHO

A
  1. The echocardiogram (Fig. 30.80) shows a dilated LA and LV
  2. There may be specific features of Chordal or Papillary Muscle Rupture.
  3. The severity of regurgitation can be assessed with the use of colour Doppler, looking at the Narrowest Jet Width (Vena Contracta) and Area, and Calculating the Regurgitant Fraction, Vol- ume or Orifice Area.
  4. Useful information regarding the severity of the condition can be obtained indirectly by observing the dynamics of ventricular function.
  5. TOE can be helpful to identify Structural Valve Abnormalities before surgery (see Fig. 30.80) and intraoperative TOE can aid assessment of the Efficacy of valve repair.
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33
Q

Mitral Regurgitation: IX

Cardiac Catheterization

A

Left and right heart catheterization is appropriate for patients referred for surgical repair or replacement.

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34
Q

Mitral Regurgitation: Management

Conservative

A
  1. Pharmacotherapy → No evidence to support the use of pharmacotherapy in Chronic MR without HF. However, if there is presence of HF–use standard Pharmacotherapy for HF
  2. Mild to Moderate Mitral regurgitation can be managed conservatively by following the patient with Serial Echocardiograms
  3. Prophylaxis against Endocarditis is discussed….
  4. When patients are not suited to Surgical Intervention or when surgery will be performed at a later date, management involves tx with Diuretics, ACEi and possibly Anticoagulants
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35
Q

Mitral Regurgitation:

Surgical Intervention

A
  1. The purpose of Surgical Intervention is to try and reduce the progression of LV Dilation, subsequent decreasing EF, LA Dilation and AFib due to the Regurgitation
  2. Current ESC guidelines recommend surgical intervention in patients with
  3. Symptomatic Severe MR, LVEF of >30% and End Diastolic Dimension of less than 55mm
  4. and in Asymptomatic patients with primary Severe MR with LV dysfunction (End Diastolic Dimension >45mm and/or EF of <60%)
  5. Surgery should also be considered in Asymptomatic patients with Primary Severe MR with Preserved LV function and Atrial Fibrillation and/or Pulmonary Hypertension (elevated Systolic Pulmonary Artery Pressure)
  6. Secondary MR is rarely operated on unless there is another reason for Surgery such as CABG or AVR, due to the singifcant Operative Mortality and High rates of recurrent MR, and no evidence of Survival Benefit.
  7. The advantages of Surgical Intervention are diminished in more advanced disease
  8. Sudden Torrential MR, as seen with Chordal or Papillary Muscle Rupture or IE, necessitates emergency Mitral Valve Replacement
  9. A Percutaenous Mitral Valve Repair (MitraClip) may be appropriate in selected patients unsuitable for Cardiac Surgery
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36
Q

Prolapsing (Billowing) Mitral Valve

i.e. Barlow’s Syndrome or Floppy Mitral Valve

A
  1. It is due to excessively large Mitral Valve Leaflets, an Enlarged Mitral Annulus, Abnormally long Chordae, or Disordered Papillary Muscle Contraction
  2. Histology ay demonstrate Myxomatous Degeneration of the MV Leaflefts
  3. Prolapsing Mitral Valve is more commonly seen in Young Women than in Men or Older Women, and has a Familiar Incidence
  4. It’s cause is unknown but it is associated with Connective Tissue Disorders (Marfan’s Syndrome, Ehlers Danlos Syndrome and Pseudoxanthoma Elasticum)
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37
Q

Aortic Stenosis

Definition

A

AS is a chronic progressive disease that limits LV outflow, leading to symptoms of Chest Pain, Breathlessness, Syncope and Presyncope and Fatigue

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38
Q

AS Epidemiology

A
  • AS is the most common Valve Disease requiring intervention in the US and EU
  • There frequency increases with age–25% at 65 years and rising to 48% over aged 75
  • The number of Elderly with aS is expected to increase by 2-3 times in the next 50 years
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39
Q

Aortic Stenosis

Causes

A
  1. Aortic Valve Stenosis includes Calcific Stenosis of a Trileaflet AV, Stenosis of a Congenitally Bicuspid Valve, and Rheumatic AS
  2. Calcific Aortic Valvular Disease (CAVD) is the most common cause of AS and occurs mainly in the elderly.
    1. Calcific AS has traditionally through to be due to “wear and teat” and part of the Degenerative Process, however, recent studies have shown a complex Multifactorial Pathobiological process involving Inflammation, a/w Traditional CV RF
    2. This is an Inflammatory Process involving Macrophages and T Lymphocytes, initially with Thickening of the Subendothelium and Adjacent Fibrosis.
    3. The lesions contain Lipoproteins, which Calcify, increasing Leaflet Stiffness and Reducing Systolic Opening
    4. This can occur in a Tri or Bileaflet AV
    5. Risk Factors for CAVD include Old Age, Male Sex, Elevated Lipoprotein and LDL Cholesterol, Hypertension, Diabetes and Smoking
  3. Bicuspid Aortic Valve (BAV)
    1. Is the most common form of Congenital Heart Disease, occurring in 1-2% of live births, in about 9% of cases, it is familial
    2. Patients with Familial Bicuspid Valve tend to present at an earlier age (So in young patients, BAV is the most predominant pathology)
    3. BAV is associated with Aortic Coarcation, Root Dilation and, potentially, Aortic Dissection, and patient should have regular follow up Echocardiography → NB ALWAYS LOOK FOR COARCTATION OF AORTA IN A PATIENT WITH BAV
  4. Rheumatic Fever can produce Progressive Fusion, Thickening and Calcification of the AV
    1. In Rheumatic Heart Disease, the Aortic Valve is affected in about 30-40% of cases and there is usually associated Mitral Valve Disease
  5. Other causes of Valvular Stenosis include Chronic Kidney Disease, Paget’s disease of Bone, Previous Radiation Exposure and SLE
  6. Valvular AS should be distinguished from other causes of obstruction to LV emptying, which include
    1. Supravalvular Obstruction → A Congenital Fibrous Diaphragm above the aV, often associated with Learning Difficulties and Hypercalcemia (William’s Syndrome)
    2. Subvlavular AS → A Congenital condition in which a Fibrous Ridge or Diaphragm is situated immediately below the AV
    3. Hypertrophic Cardiomyopathy → Septal Muscle Hypertrophy obstructing LV outflow
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40
Q

Aortic Stenosis

Pathophysiology

A
  1. Obstructed LV Emptying leads to increased Left Ventricular Pressure and Compensatory LV Hypertrophy
  2. In turn, this results in relative Ischemia of the LV Myocardium and consequent Angina, Arrhythmias, and LV Failure
  3. The obstruction to LV Emptying is relatively more severe on Exercise
    1. Normally, exercise causes a many-fold increase in Cardiac Output, but when there is Severe Narrowing of the AV Orifice, the CO can hardly increase
    2. Thus, the BP Falls, Coronary Ischemia Worsens, the Myocardium fails and Cardiac Arrhythmias develop
    3. LV Systolic Function is typically preserved in patients with AS
41
Q

Aortic Stenosis

Symptoms

A
  1. There are usually no symptoms until AS is moderately severe (when the Aortic Orifice is reduced to ⅓ of it’s normal size)
  2. At this stage, Exercise-induced Syncope, Angina, and Dyspnoea develop
  3. When symptoms occurs, the prognosis is poor: on average, death occurs within 2-3 years if there has been no surgical intervention
42
Q

Aortic Stenosis: Signs

Pulse

A

The Carotid pulse is Small-Volume and Slow-Rise or Plateaue in nature

43
Q

Aortic Stenosis Signs

Precordial Palpation

A
  1. The Apex Beat is not usually displaced because Hypertrophy (as opposed to Dilation) does not produce noticeable Caridomegaly.
  2. However, the Pulsation is Sustained and Obvious
  3. A Double Impulse is sometimes felt because the 4th heart sound or Atrial Contraction (kick) may be palpable
  4. A systolic thrill may be felt in the Aortic Area.
44
Q

Aortic Stenosis

Auscultation

A
  1. The most obvious Auscultatory finding in AS is an Ejection Systolic Murmur that is usually “Diamond Shaped” (Crescendo-Decrescendo)
  2. The murmurs is usually longer when the disease is more severe, as a longer Ejection Time is needed.
  3. The murmur is usually roughly in quality
  4. Best heard at Base of HeartRight 2nd Intercostal Space (i.e. in the Aortic Area)
  5. Loudest/Accentuated on expiration and with leaning forward  As is the case with all Left sides Murmers
  6. Radiating to Carotids and Apex/Praecordium but not Axilla
  7. The Intensity of the murmur is not a good guide to the severity of the condition because it is lessened by a reduced CO. In severe cases, the murmur may be inaudible
  8. Other Findings include
    1. Systolic Ejection click, unless the valve has become immobile and calcified: When the LV is pushing against that Stenotic area it will eventually blow that Valve open and when it does you will hear a systolic ejection click and then as the valve opens all the blood will be moved out in a rush giving a Crescendo and then it will decrease giving Decrescendo Murmur (followed by a Crescendo-Decrescendo Murmur is heard)
    2. S2 soft, Split S2, S4 (of a Left Atrial kick into a stiff ventricle)
      1. Soft or Inaudible Aortic 2nd Heart Sound when the AV becomes immobile
      2. Reversed Splitting of the Second Heart Sound (Splitting on Expiration)
      3. Prominent 4th Heart sound, caused by Atrial Contraction and heard unless coexisting MS prevents this
45
Q

Aortic Stenosis: IX

CXR

A
  1. This reveals a relatively Small Heart with Prominent, Dilated, aScending Aorta
  2. This occurs because Turbulent blood flow above the Stenosed AV produces so-called ‘Post-Stenotic Dilation’
  3. The AV may be calcificed
  4. the CTR increases when HF occurs
46
Q

Aortic Stenosis: IX

ECG

A
  1. The ECG shows LV Hypertrophy and Left Atrial Delay
  2. A LV “Strain” pattern due to “Pressure Overload” (Depressed ST Segments and T Wave inversion in leads oriented towards the LV i.e leads I, AVL, V5, and V6 is common when disease is severe
  3. Usually, Sinus Rhythm is present but Ventricular Arrhythmias may be recorded
47
Q

Aortic Stenosis: IX

ECHO

A
  1. Echocardiography readily demonstrates the Thickened, Calcified and Immobile Aortic Valve Cusps and the presence of LV hypertrophy
  2. It can be used to determine the severity of AS
  3. TOE is rarely indicated
48
Q

Aortic Stenosis: IX

Cardiac Catheterization

A

CC is rarely necessary since all fo this information can be gained non-invasively with ECHO and CMR

Coronary Angiography is required before surgery/is recommended

49
Q

Aortic Stenosis: IX

CMR and Cardiac CT

A

The techniques are indicated for assessing the Thoracic Aorta for the presence of Aneurysm, Dissection or Coarctation but are rarely needed

50
Q

Aortic Stenosis: Pharamcological Management

A
  1. Pharmacological Approach → THERE IS NO pharmacological tx that is shown to slow progression fo AS. Comorbidites should be treated
51
Q

AS: Surgical Indications

A
  1. Severe AS is determined on TTE by a Vmax >4m/s, Mean gradient >40mmHg, and Aortic Area >/1cm2
  2. In patients with Aortic Stenosis, Symptoms are a good index of Severity and all Symptomatic, appropriate patients should have AV Replacement
  3. Early intervention in all patients (without Severe comorbidites and a life expectancy >1 year) with Severe Symptomatic AS is recommended
  4. Patients with a BAV and Ascending Aorta of over 50mm OR Expanding at more than 5mm per year, should be considered for Surgical Intervention
  5. Asymptomatic Patients should be under regular review for assessment of sx and ECHO
  6. Surgical Intervention for Asymptomatic People with Severe AS is recommended in those with:
    1. Symptoms or Hypotension during an exercise Test
    2. an LVEF of less than 50% (not due to any other cause)
    3. Moderate to Severe Stenosis undergoing CABG, Surgery of the Ascending Aorta or other Cardiac Valve
      1. Peak Velocity through the AV >5.5m/s
      2. Systolic Pulmonary Artery Pressure >60mmhg
      3. Rapid increase in Velocity through the Valve at >0.3m/s/year
  7. Antibiotic Prophylaxis against IE is discussed on page 1106.
  8. Percutaneous Valve Replacement
    1. A novel treatment for patients unsuitable for Surgical AV replacement is Trancatheter AV Implantation (TAVI), with a Balloon Expandable Stent Valve
    2. Valve implantation has been shown to be successful (86%) with a procedural mortality of 2% and 30-day mortality of 12%
    3. Good results have been reported in follow up studies, and this technique may replace the need for surgery
  9. Decision on whether the patient should get a TAVI versus Surgically implanted AV is made by the MDT
  10. AS in Childhood or Adolescence
    1. Provided that the valve is not severely deformed or heavily calcified, Critical AS in Childhood or Adolescence can be treated by Valvotomy (Performed under Direct Vision by the Surgeon or by Balloon Dilation using Xray Visualization)
    2. This produces temporary relief from obstruction
    3. AVR will usually be needed a few years later
  11. Patients who are Older (generally >75 years old), with multiple co-morbidites, Prior CABG/Valve Surgery, etc may benefit more from TAVI than Surgical Repair, and conversely, Younger, Healthier patients should be treated with Surgical Repair.
  12. Surgical AVR is the traditional intervention, and the long-term Durability of Implanted Valves are known, whereas the outcomes of >10 years are not known in TAVI cohort. However, there is significant research in this field
  13. If patients re not fit for either Surgery or TAVI, a Balloon Valvuloplasty may be considered. This carrie s a much higher risk of stroke
    1. Balloon Dilation (Valvuloplasty) has been tried in adults, especially in the Elderly, as an alternative to surgery. Generally, results are poor and such treatment is reserved for patients unfit for surgery or as a bridge to surgery (as Systolic Function will often improve)
52
Q

AS: Surgical Options

A
  1. AS in Childhood or Adolescence
    1. Provided that the valve is not severely deformed or heavily calcified, Critical AS in Childhood or Adolescence can be treated by Valvotomy (Performed under Direct Vision by the Surgeon or by Balloon Dilation using Xray Visualization)
    2. This produces temporary relief from obstruction
    3. AVR will usually be needed a few years later
    4. Balloon Dilation (Valvuloplasty) has been tried in adults, especially in the Elderly, as an alternative to surgery. Generally, results are poor and such treatment is reserved for patients unfit for surgery or as a bridge to surgery (as Systolic Function will often improve)
  2. Percutaneous Valve Replacement
    1. A novel treatment for patients unsuitable for Surgical AV replacement is Trancatheter AV Implantation (TAVI), with a Balloon Expandable Stent Valve
    2. Valve implantation has been shown to be successful (86%) with a procedural mortality of 2% and 30-day mortality of 12%
    3. Good results have been reported in follow up studies, and this technique may replace the need for surgery
  3. Decision on whether the patient should get a TAVI versus Surgically implanted AV is made by the MDT
53
Q

AS prognosis

A
  • In Aortic stenosis, mortality is associated with presenting symptoms.
  • Angina :50% 5 year mortality
  • Syncope : 50% 3 year mortality
  • Dyspnoea (Heart failure): 50% 2 year mortality
54
Q

AR

Causes

A
  1. Prevalence of Moderate or Severe AR is estimated at less than 1%
  2. More commonly seen in patients with BAV, IE, or with Aprtopoathies such as Marfan;s Syndrome, AD, and Syphilis.
  3. Can occur in diseases affecting the AV, such as Endocarditis,
  4. and Diseases affect the Aortic Root, such as Marfan’s Syndrome
  5. Acute AR
    1. Acute Rheumatic Fever
    2. IE
    3. Dissection of the Aorta
    4. Ruptured Sinus of Valsalva Aneurysm
    5. Failure of Prosthetic Valve
  6. Chronic AR
    1. Rheumatic Heart Disease
    2. Syphilis
    3. Arthritides → Reactive Arthritis, Ankylosing Spondylitis, Rheumatoid Arthritis
    4. Hypertension (Severe)
    5. Bicuspid Aortic Valve
    6. Aortic Endocarditis
    7. Marfan’s Syndrome
    8. Osteogenesis Imperfecta
55
Q

AR

Pathophysiology

A
  1. AR is reflux of blood from the Aorta through the AV into the LV during Diastole
  2. If Net CO is to be maintained, the Total Volume of blood pumped into the Aorta must increase and, consequently, LV size must enlarge.
  3. Because of the Aortic runoff during Diastole, Diastolic Blood Pressure falls and Coronary Perfusion is decreased.
  4. In addition, the Larger LV size is mechanically less efficient, so that the demand for Oxygen is greater and Cardiac Ischemia develops
56
Q

AR

Symptoms

A
  1. In AR, significant symptoms occur late and do not develop until LV Failure develops
  2. Angina Pectoris may arise
  3. Varying grades of Dyspnoea occur, depending on the extent of LV Dilation and Dysfunction
  4. Arrhythmias are relatively uncommon
57
Q

AR

Signs: Pulse

A
  1. The signs of AR are many and are due to the Hyperdynamic Circulation, Reflux of blood into the LV and Increased LV size.
  2. The pulse is Bounding or Collapsing
  3. The following signs, which are rare, also indicate a Hyperdynamic Circulation
    1. Quincke’s Sign → Capillary Pulsation in the Nail beds
    2. de Musset’s Signs → Head nodding with each Heart Beat
    3. Duroziez’s Signs → A To-and-Fro Murmur heard when the Femoral Artery is auscultated with Pressure applied distally (if found, it is a sign of severe AR)
    4. Pistol Shot Femoral → A Sharp bang heard on Auscultation over the Femoral Arteries in the time with each Heart Beat
58
Q

AR: Signs

Palpation + Auscultation

A
  1. The Apex Beat is displaced Laterally and Downwards and is forceful in quality
  2. On Auscultation, there is a high-pitched Early Diastolic Murmur best heard at the Left Sternal Edge in the 4th intercostal space with the patient leaning forwards and the breath held in Expiration
  3. Because of the Volume Overload, there is commonly and Ejection Systolic Flow Murmur
  4. The Regurgitant Jet can impinge on the Anterior Mitral Valve Cusp, causing a Mid-Diastolic Murmur (Austin Flint Rumble)
59
Q

AR: IX

CXR

A
  1. LV enlargement, and possibly, Dilation of the Ascending Aorta.
  2. The Ascending Aortic wall may be calcified in Syphilis, and the AV Calcified if Valvular Disease is responsible for the Regurgitation.
60
Q

AR: IX

ECG

A
  1. The ECG appearances are those of LV Hypertrophy due to “Volume Overload”
    1. Tal R Waves and Deeply Inverted T waves in the Left-Sided Chest Leads. and Deep S waves in the Right sided leads
  2. Normally, Sinus Rhythm is present
61
Q

AR: IX

ECHO

A
  1. The ECHO demonstrates Vigorous cardiac contraction and a Dilated LV
  2. The Aortic Root may also be Enlarged
  3. Diastolic Fluttering of the Mitral Leaflets or Septum occurs in Severe AR (Producing the Austin Flint Rumble)
  4. The Severity of AR is assessed with a combination of Color Doppler (Extent of the Regurgitant jet, Width of the Vena Contracta) and CW Doppler (Diastolic Flow Reversal in the Descending Thoracic Aorta, Pressure half-time)
  5. TOE may provide additional information about the Valves and Aortic Root
62
Q

AR: IX

Cardiac Catheterization

A
  1. CC is appropriate for patients requiring Valvular Intervention, although CTCA or CT Angiography may be an alternative in younger patients
63
Q

AR: IX

CMR and Cardiac CT

A
  1. These techniques may be indicated for assessing the Thoracic Aorta in cases of Aortic Dilation or Dissection
  2. CMR can be used to quantify Regurgitant Volume
64
Q

AR: Management

Medical

A
  1. The underlying cause of AR (e.g. Syphilitic Aortitis or IE) may require specific treatment
  2. Patient with Acute AR may need treatment with Vasodilators and Inotropes
  3. Treatment of AR is mostly symptomatic; relief with Diruretics and ACE/ARBs
  4. There is not evidence that tx with these medications in Normotensive indivudals slows or reverses the natural disease progression, however, in Marfan’s Disease there is evidence that tx with BB and ACEi/ARBs may reduce the Aortic Root Dilation (slow it down)
  5. ACEi are useful in patients with LV Dysfunction
65
Q

AR: Management

Surgical

A
  1. Because sx do not develop until the Myocardium Fails, and because the Myocardium does not recover fully after Surgery, Operative replacement may be performed before significant sx occur
  2. Aortic Surgery is indicated in
    1. Acute Severe AR (e.g. Endocarditis)
    2. Severe Symptomatic Patients (Dyspnoea, NYHA Class II-IV, Angina) → with Chronic Severe AR
    3. Asymptomatic patients with an LVEF of 50%
    4. Surgery should be considered in Severe AR Asymptomatic patients whose LV is starting to Dilate→ Asymptomatic patients with an LVEF of >50% but with a Dilated LV (End-Diastolic Dimension >70mm or Systolic Dimension >50mm)
    5. In patients with Marfan’s; Dilated Aortic Root or Those undergoing CABG or surgery of the Ascending Aorta or Other Cardiac Valve, the threshold is lower for intervention
  3. Both Mechanical Protheses and Tissue Valves are used.
    1. Tissue valves are preferred in the Elderly and in cases where Anticoagulants must be avoided, but are Contraindicated in Children and Young Adults because of the rapid Calcification and Degeneration of the Valves
  4. Antibiotic Prophylaxis against IE is NOT recommended
66
Q

TS: Causes

A
  1. Rarely seen
  2. This uncommon valve lesion, which is seen much more often in women than in men, is usually due to Rheumatic Heart Disease and is frequently associated with Mitral and/or Aortic Valve disease
  3. Tricuspid Stenosis is also seen in the Carcinoid Syndrome
67
Q

TS: Pathophysiology

A
  1. Tricuspid valve Stenosis results in a Reduced CO, which is restored towards normal when the RA Pressure increases
  2. The resulting Systemic Venous congestion produces Hepatomegaly, Ascites, and Dependent Oedema
68
Q

Review of Tricuspid Valve

A
69
Q

TS: Symptoms

A
  1. Patients with TS are likely to have Left Sided Rheumatic Valve Disease that may be the main driver of symptoms
  2. Symptoms of Prominent TS include Abdominal Pain (Hepatomegaly), Abdominal Distention (Ascites) and Peripheral Oedema.
70
Q

TS: Signs

A
  1. The patient remains in Sinus Rhythm, which is unusual, and there is a prominent Jugular Venous a-Wave → This Presystolic Pulsation may also be felt over the Liver
  2. There is usually a Rumbling Mid-Diastolic Murmur, which is heart best at the Lower Left Sternal Edge and is louder on Inspiration → It may be missed because of the murmur of coexisting MS
  3. A Tricuspid Opening Snap may occasionally be heard
  4. Hepatomegaly, Abdominal Ascites, and Dependent Oedema may be present.
71
Q

TS: IX

A
  1. On the CXR, there may a prominent Right Atrial Bulge
  2. On the ECG, the Enlarged RA is shown by Peaked, Tall P Waves (>3mm) in Lead II
  3. The ECHO may show a Thickened and Immobile TV but this is not so clearly seen as an Abnormal Mitral Valve
72
Q

TS: Management

A
  1. Medical Management consists of Diuretic Therapy and Salt Restriction
  2. TS is NOT treated surgically (RCSI book)
  3. Tricuspid Valvotomy is occasionally possible but Tricuspid Valve Replacement is often necessary
  4. Usually, other valves also need replacement becuase TV is rarely an isolated lesion
73
Q

TR

A
  1. Functional TR → Due to Increased RV Pressure or volume causing RV Annular Dilation
    1. Identifying the Underlying Aetiology is key
    2. Cor Pulmonale, MI or Pulmonary Hypertension
    3. Pulmonary Hypertension is often secondary Left Sided HF, but can include Acute/Chronic PE, Idiopathic Hypertension, or Severe Lung Disease
  2. Primary/Organic TR → Due to an Inherent Abnormality in the Valve Leaflets, causes
    1. May occur with Rheumatic Heart Disease, IE (IVDU),
    2. Carcinoid Syndrome,
    3. Traumatic Injury,
    4. Ebtein’s Anomaly (A Congenitally malpositioned TV) and other Congenital Abnormalities of the AV Valve
74
Q

TR: Symptoms

A

The Valvular Regurgitation gives rise to High Right Atrial and Systemic Venous Pressures

Patients may experience the Sx of Right Heart Failure.

75
Q

TR: Signs

A
  1. Include a Large Jugular Venous “cv-wave” and a Palpable Liver that Pulsates in Systole
  2. Usually, a RV impulse may be felt at the Left Sternal Edge,
  3. and there is a Blowing Pansystolic Murmur, best heard on Inspiration at the Lower Left Sternal Edge
  4. Atrial Fibrillation is common
76
Q

TR: IX

A

An ECHO shows dilation of the RV with Thickening of the Valve

77
Q

TR: Management

A
  1. Functional TR usually disappears with medical management
  2. Surgery is indicated in Symptomatic px with Severe TR who are undergoing Left-Sided Intervention
  3. Severe Organic TR may require operative repair of the TV (Annuloplast or Annuloplication)
  4. Very occasionally, TV replacement may be necessary
  5. In IV Drug users, with IE of the TV, Surgical removal of the Valve is recommended to Eradicate the infection. This is usually well tolerated in the short-term.
  6. The Insertion of a Prosthetic Valve for this condition is sometimes necessary.
78
Q

Pulmonary Valve Epidemiology

A

PS and PR are rarely seen in the adult populations, they are more often seen in Pediatric Cardiology a/w ToF

79
Q

PS: Causes

A
  1. This is usually a Congenital Lesion but may rarely result from Rheumatic Fever or from the Carcinoid Syndrome
  2. Congenital PS may be associated with ToF, Noonan’s Syndrome or Congenital Rubella Syndrome
  3. PS may be Valvular, Subvalvular, or Supravalvular.
80
Q

PS: Clinical Fx

A
  1. The Obstruction too RV emptying results in RV Hypertrophy, which in turn, leads to RA Hypertrophy
  2. Severe Pulmonary Obstruction may be incompatible with life, but lesser degree of obstruction give rise to Fatigue, Syncope and the Sx of RHF.
  3. Mild Pulmonary stenosis may be Asymptomatic
  4. Physical Signs are characterized by a Harsh, Mid-Systolic Ejection Murmur, best heard on Inspiration, to the Left of the Sternum in the Second Intercostal Space
    1. This murmur is often associated with a thrill
  5. The Pulmonary closure sound is usually Delayed and Soft
  6. There may be a Pulmonary Ejection sound if the Obstruction is Valvular
  7. A RV Fourth Sound and a Prominent Jugular Venous a-wave are present when the Stenosis is moderately severe
  8. A right ventricular Heave (Sustained Impulse) may be felt.
81
Q

PS: IX

A
  1. The CxR usually shows a prominent Pulmonary Artery owing to Post-Stenotic Dilation
  2. The ECG demonstrates both RA and RV Hypertrophy, although it may sometimes be normal, even in Severe PS
  3. A Doppler ECHO is the investigation of choice
82
Q

PS: Management

A
  1. PR and PS can be treated Surgically but is often left to specialized centers who have experience in Adult Congenital Heart Disease
  2. Management of Severe PS requires Pulmonary Valvotomy (Balloon Valvotomy or Direct Surgery)
83
Q

PR

A
  1. This is the most common Acquired Lesion of the PV
  2. It results from Dilation of the PV Ring, which occurs with Pulmonary Hypertension (Graham Steell Murmur)
  3. IT may also occur follow ToF Repair
  4. IT is characterized by a Decresendo Diastolic Murmur, beginning with the Pulmonary Component of the 2nd Heart sound that is difficult to Disntguish from the Murmur of AR
  5. PR usually causes no sx and tx is rarely necessary
84
Q

Prosthetic Valves: Intro

A
  • There is no ideal replacement for our own normally functioning, native heart valves
  • There are two options for valve prostheses: Mechanical or Tissue (Bioprosthetic)
  • Tissue Prostheses are derived from Human (Homograft) or Porcine or Bovine (Xenograft) sources
  • A valve replacement from within the same patient (i.e. Pulmonary to Aortic Valve Position) is termed an Autograft
  • The valves consist of Two basic components
    • An opening to allow blood to flow through
    • and an Occluding mechanism to regular the flow
      • Mechanical Prostheses rely on Artificial Occluders: A ball and Cage (Starr-Edwards), Tilting Disc (Bjork Shiler), or Double Tilting Disc (St. Jude)
85
Q

Mechanical versus Tissue Valves

A
  • Mechanical Valves, being Artificial Structures, are more durable than their Tissue counterparts, which tend to degenerate after 10 years.
  • However, Artificial Structures are more Thrombogenic. → Mechanical Valves require Formal Anticoagulation for the lifetime of the Prosthesis
86
Q

Mechanical Valve Anticoagulation

A
  • The Target INR is determined by what Type** of valve is inserted, **Where** it is positioned, and where the patient has **additional RF for Thromboelbolism (Mitral, Tricuspid, Pulmonary Valve Disease; Previous Thromboembolism; AFib, LA diameter >50mm; Mitral Stenosis; LVEF <35%; Hypercoagulable State)
87
Q

Mechanical Valve Anticoagulation

Low Thrombogenecity Valve INR

A
  • (Carbomedics** (Aortic Position), **Medtronic Hall, St. Jude Medical. (without Silzone):
  • INR 2.5 without and 3 with additional RF
88
Q

Mechanical Vale Anticoagulation

Medium Thrombogenecity Valve INR

A
  • (Bjork-Shiley, other Bileaflet Valves):
  • INR 3.0 without and 3.5 with additional RF
89
Q

Mechanical Valve Anticoagulation

High Thrombogenecity Valve INR

A
  • (Killehei-Kaster, Omniscience, Starr-Edwards):
  • INR 3.5 without and 4 with additional RF
90
Q

Tissue Valve Anticoagulation

A
  1. Tissue Valves require anticoagulation for a limited Post-Op period only, while the Suture lines Endothelialize
  2. The ESC recommends 3 months with a target INR of 2.5, although some centers use Low-Dose Aspirin 75-100mg daily)
  3. It can then be discontinued unless another RF for Thromboembolism (e.g. AFib) persists
  4. There is currently no role for DOACs
91
Q

Prosthetic Valves Auscultation

A
  1. On auscultation, Tissue Valve Heart Sounds are comparable to those of a native valve
  2. Mechanical Valve HS are generally louder and both opening and closing sounds can be heard
92
Q

Prosthetic Valves Complications

A
  • VIP BEAST
  • V: Valve Obstruction, Valve Dehiscence.
  • I: INR monitoring, Infective Endocarditis
  • P: Paravalvular regurgitation, Prosthetic mismatch
    • The Prosthesis can become detached from the Valve Ring, resulting in a Para-prosthetic Leak
  • B: Bleeding
  • E: Embolization
  • A: Anemia (the smaller the ring leaks, the severer the hemolysis)
  • S: Structural failure
    • Evidence of Structural Failure can b detected by Simple Auscultation, with eCHO as the initial investigation of choice.
    • TTE is non0invasive but scattering of Echoes by Mechanical Valves makes assessment difficult
    • TOE provides Alternative Views and Higher Image Resolution, making it the investigation of choice when Prosthetic Valve Edncoarditis is suspected.
  • T: Thrombosis
    • The prosthetic Valve occluding mechanism can be interrupted by Vegetations but also by Thrombosis and Calcification, resulting in either Stenosis or Regurgitation
    • Lifelong anticoagulation is required
    • Warfarin should be used with Metallic Valves whereas a DOAC may be used with Bioprosthetic
  • reStenosis may occur usually >10 yrs after replacement
    *
93
Q

Prosthetic Valves IE Prophylaxis

A
  • All Prostheses carry a risk of infection
  • Prosthetic Valve Endocarditis is a/w significant Morbidity and Mortality → Prevention is the Cornerstone of Management
  • Patient education about Abx prophylaxis is vital and should be reinforced at Clinic Visits
  • Details of Abx prophylaxis indicated in patients undergoing different types of interventional procedures are given on p.161 and in box 8.7
  • Additional Prophylaxis indicated in patients at higher risk of Endocarditis are discussed on p1106
  • This must be borne in mind when managing a patient with a Prosthetic Heart Valve and steps should be taken to minimize the risk involved.
    *
94
Q

Prosthetic Valves Intterruption of Anticoagulatn Therapy

A
  1. For Minor** Surgical Procedures, including Dental Extraction and Diagnostic Endoscopy, Anticoagulation **should not be interrupted**, although the **Target INR should be reduced to 2.0
  2. Percutaneous Arterial Puncture** is safe with an INR **below 2.0, although Radial Catheterization may be possible at higher INR levels
  3. For Major** surgical procedures, Anticoagulation should be **discontinued 5 days before the procedure and IV Unfractionated Heparin or Subcutaneous LMWH commenced when the INR is below 2.0
95
Q

Pregnancy and Prosthetic Heart Valves

A
  1. Pregnancy is a Hypercoagulable state due to increased levels of Fibrinogen and Factors VII, VIII, and X, Decreased Levels of Protein S activity, Venous Hypertension and Stasis.
  2. The types of Valve prosthesis for use in women of childbearing age are as follows:
  3. Bioprosthetic Valves are preferable during pregnancy, as they are less Thrombogenic and do not require Anticoagulation
  4. However, Valve dEgradation in women of childbearing age has been shown to be as high as 50% at 10 years and 90% at 15 years; Women with a BV may require Redo Valve Surgery
  5. Mechanical HEart Valves are excellent Durability but are Thrombogenic and require Life-Long Anticoagulation with Warfarin.
    1. Pregnancy in women with a Mechanical HV is associated with increased Maternal Mortality (1-4%) due to Valve Thrombosis because Safe Anticoagulation in these patients is complex.
    2. Warfarin crosses the Placenta and is a/w a 5-12% risk of Embryopathy during the First tRimester
    3. Warfarin also has an Anticoagulant effect on the Fetus, which may lead to Spontaneous Fetal Intracranial Hemorrhage.
    4. Many women will choose Unfractionated Heparin or LMWH, as these drugs do not cross the Placenta or cause Fetal Embryopathy
    5. However, Unfractionated Heparin may not provide consistent Therapeutic Anticoagulation during Pregnancy and there is a High incidence (25%) of Valve Thrombosis
    6. LMWH provides a more consistent Anticoagulant effect when given twice daily, with Dose Adjustment to maintain Anti-Xa- levels of 0.8-1.2 U/mL 4 hours after administration
96
Q

VHD Ix: Bloods

A
  1. Fasting Lipids/HbA1C → Screen for Hypercholestrolemia and Diabetes as they are RF for CVD
  2. Liver Function Test → Elevated Liver Enzymes from Hepatic Congestion Secondary to RHF
97
Q

VHD Ix: Imaging

A
  1. CT Coronary Angiogram → CTCA is useful in calculating the Calcium Score which can be helpful to identify Severe AS when ECHO is equivocal
    1. The calcium score is a calculation of calcium volume within the heart.
    2. A normal calcium score is zero to 100 between 100-300 indicates a moderate risk of heart disease.
    3. A score of 1000 puts you at significant risk
  2. Cardiac MRI → This may be considered but depends on Findings on ECHO. Gold Standard Imaging modality to assess Ventricular Dysfunction and can help to determine Ischemic or Non-Ischemic Cardiomyopathies
  3. CT-TransCatheter AV Implantation (TAVI) → A CT from the Femoral Arteries to the Coronary Sinus of the Aorta is completed to assess if a Percutaneous Approach to Repair is possible
98
Q

VHD IX: Procedure

A
  1. Exercise ECHO → Useful in determining MR sEverity as it can become more severe with Tachycardia
  2. Coronary Angiogram → Necessary to determine if there is any underlying Coronary Artery Disease which be present in up to 30% of patients with AS
  3. Echocardiogram (PRIMARY IX for diagnosis)
    1. TTE is the key diagnostic tool for diagnosis of CHD
    2. TOE is invasive, but facilitates better image quality
    3. The use of Doppler ECHO allows calculation of Gradients across Valves which is useful in grading the Severity of Valvular Disease
99
Q

VHD management

A
  1. The management of the Majority VHD is Conservative, as it is often due to a Slow Degenerative Process and the Dlerly population has multiple co-morbidities.
  2. This risk-Benefit Ratio to an intervention needs to be carefully Calculated and Discussed with the patient
  3. Acute: In rare cases, where there is acute change (AR or MR)–usually causing Acute Decompensated HR, treat as ADHF and request URGENT SURGICAL OPINION

Cardiology (4 decks)

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