Aortic Stenosis (and Valve Replacement) Flashcards

1
Q

What is the diagnosis?

A 78-year-old man presents to his primary care physician with 2 months of progressive shortness of breath on exertion. He first recognised having to catch his breath while gardening and is now unable to walk up the stairs in his house without stopping. Previously he was healthy and active. On physical examination there is a loud systolic murmur at the right upper sternal border radiating to the carotid vessels.

A

Aortic stenosis

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2
Q

Describe the aortic stenosis murmur.

A

Crescendo decrescendo systolic murmur - flow during systole is slowest at the very start and end and fastest in the middle

Ejection systolic murmur

Heaving apex beat

Slow rising pulse and narrow pulse pressure

Also:

  • soft/absent S2
  • S4
  • thrill
  • duration of murmur
  • left ventricular hypertrophy or failure

Typically grade _>_3/6

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3
Q

How common is AS?

A

MOST COMMON valvular disease in the US/EU

Second most common cause of cardiac surgery

10% of those >80yrs affected

Preceded by aortic sclerosis - 25% of _>_65yrs have aortic sclerosis

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4
Q

Define aortic sclerosis.

A

Aortic valve thickening without flow limitation

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5
Q

What are the risk factors for AS?

A

Age >60

Congenital bicuspid valve

Rheumatic heart disease

CKD

Other:

  • High LDL
  • Hyperlipoproteinaemia
  • HTN
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6
Q

What causes aortic stenosis?

A
  1. Senile calcification - most common (80% - older patients >65yo)
  2. Congenital bicuspid valve (~20% - younger patients <65yo)

Other:

  • William’s syndrome (supravalvular aortic stenosis)
  • Rheumatic fever
  • Subvalvular: HOCM
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7
Q

What is the pathophysiology of aortic stenosis?

A
  1. Calcification is no longer thought to be due to age “wear and tear”
  2. But thought to be an active process whereby valvular endocardium is damaged due to abnormal flow or other trigger
  3. Damage causes atherosclerosis → fibrosis and calcium deposition
  4. This causes limit to aortic leaflet mobility and eventually stenosis

In rheumatic disease the process is autoimmune inflammatory

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8
Q

What investigations would you do for aortic stenosis?

A

Main investigations:

*Echo + Doppler* - diagnostic. Will show elevated pressure gradient across the aortic valve

ECG - abnormal in 90% with AS. LVH and absent Q waves. Often also conduction problems e.g. LBBB or complete AV block (due to septal calcification),

CXR - to assess for pulmonary congestion or other lung pathology

Other:

CT angiography for concomitant coronary heart disease. Normal CT also for measuring aortic valve calcium score.

Cardiac catheterisation - more direct measure of the elevated aortic pressure gradient

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9
Q

What are the symptoms of aortic stenosis?

A

Symptoms:

  • Exertional syncope/presyncope, angina, dyspnoea = SAD
  • Fatigue
  • HF symptoms: paroxysmal nocturnal dyspnea (PND), orthopnoea, oedema.

Signs:

  • Slow rising pulse (carotid parvus et tardus)
  • ESM*, S4, S2 diminished and single (due to decreased mobility of aortic valve leaflets)
  • Signs of heart failure
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10
Q

Is aortic stenosis a systolic or diastolic murmur?

A

Systolic

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11
Q

How can you distinguish aortic stenosis murmur from other systolic murmurs? Where is it best heard?

A
  • Best heard in aortic area
  • Radiates to carotids
  • Louder during squatting
  • Quieter in Valsalva and handgrip
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12
Q

How do you manage aortic stenosis?

A

Asymptomatic:

  • observe
  • OR consider surgery if valvular gradient >40mmHg or LV systolic dysfunction

Symptomatic:

Valve replacement

Medical:

  • HTN (ACEi/ARB)
  • statins
  • aspirin/clopidogrel post-TAVI
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13
Q

What are the valve replacement options in AS?

A

Access types: surgical or percutaneous

  • Surgical AVR (SAVR) = young, low/medium operative risk patients.
  • Transcatheter AVR (TAVR) = for patients with a high operative risk. Older patients
  • Balloon valvuloplasty = inserting balloon to open up the valve
    • may be used in children with no aortic valve calcification
    • in adults limited to patients with critical aortic stenosis who are not fit for valve replacement - does not improve mortality but improves symptoms

Valve types: mechanical or tissue

  • Mechanical - best for younger patients, last whole life but need lifelong warfarin
  • Tissue/Bioprosthetic - bovine/porcine. Last 15-20yrs , lifelong anticoagulation not necessary.
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14
Q

What are the complications of untreated AS?

A

Symptom onset indicates poor prognosis - average survival of only 2-5yrs without valve replacement

Acute heart failure -due to afterload burden

Sudden cardiac death due to ventricular arrhythmia

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15
Q

What are the complications of AS treatment?

A

After any open heart surgery there will be poor LV function

Infection of prosthetic valve

Thrombosis secondary to mechanical valve

Re-stenosis

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16
Q

What is the prognosis with AVR?

A

SAVR - <70yrs old have 1.3% risk of death from surgery, 99% life expectancy at 5yrs and 85% at 10yrs

TAVR- 20% absolute reduction in mortality at 1yr, 30% alive at 3yrs compared to 5% on standard therapy

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17
Q

Rarely, what bleeding disorder may patients with AS acquire?

A

von Willebrand deficiency - due to turbulent flow across a stenotic valve. Will present with epistaxis and bruising.

18
Q

What common HTN medications should not be used in AS?

A
  • NITRATES - can reduce afterload quickly so cause hypotension. Do not use in AS.
19
Q

Which of these are signs of aortic stenosis?(4)

  • Angina
  • Sinus tachycardia
  • Dizziness
  • Ejection systolic murmur radiating to the carotids
  • Narrow pulse pressure
A

Angina, dizziness, ESM radiating to carotids, narrow pulse pressure

Aortic stenosis – can present with angina, dyspnoea, dizziness and faints. Signs – slow rising pulse, narrow pulse pressure, heaving undisplaced apex, aortic thrill, ejection systolic murmur heard at the left sternal edge and radiating to the carotids. Aortic sclerosis is senile degeneration of the valve. There is an ejection systolic murmur, no carotid radiation and a normal pulse.

20
Q

What happens during S1?

A

S1 - closing of the mitral and tricuspid valves (AV valves)

21
Q

What happens during S2? When might you get a physiological splitting of S2?

A

S2 - closing of the aortic and pulmonary valves (semilunar valves)

Normal, physiologic splitting of S2: inspiration lowers intrathoracic pressure, increasing the compliance of the pulmonary vascular bed,–> increased right heart filling –> RV systole is lengthened, causing the pulmonic valve to close after the aortic valve, resulting in splitting of the second sound at 3LICS or 4LICS.

.

22
Q

What are S3 and S4?

A

gallop rhythm heart sounds

23
Q

When might you get paradoxical, peristent or wide splitting of S2?

A

Paradoxical splitting: results from delayed onset or prolongation of left ventricular systole e.g. in prolonged LV emptying, aortic stenosis, LBBB– eliminated on inspiration

Persistent splitting: results from delayed onset or prolongation of right ventricular systole, or shortened duration of left

  • Widened split S2 – prolong PV emptying – pulmonay stenosis, RBBB
  • Fixed Split S2 – ASD

S1: Normal wide splitting S1 – RBBB, LV pacing, ectopic beats

24
Q

What causes S3?

A
  • Caused by early diastole
  • Associated with rapid ventricular filling e.g. HF (the ventricles and chordae are stiff and weak so they reach their limit much faster than normal)
  • Can be normal in children, young adults and pregnant women because the heart functions so well that the ventricles easily allow rapid filling.

“Kentucky”

  • heard 0.1sec after second heart sound
  • like rapid ventricular filling causing chordae tendinae to pull their full length and twang like guitair strings
25
Q

What is shown on this ECG?

A

LVH

Absence of Q waves

Seen in AS

26
Q

What causes S4?

A
  • Happens during late diastole
  • Caused by atrial contraction against a stiff ventricle (hypertrophy)
  • Pathological - HTN, aortic stenosis, hypertrophic cardiomyopathy

“Tennessee”

  • occurs before S1
  • rare to hear
27
Q

What is Erb’s point?

A

Listen to “Erb’s point”. This is in the third intercostal space on the left sternal boarder and is the best area for listening to heart sounds (S1 and S2).

28
Q

What are the grades of murmurs?

A

Grade 1: murmur is faint and heard only with effort

Grade 2: murmur is faint but easily detected

Grade 3: murmur is loud

Grade 4: murmur is very loud and associated with a palpable thrill

Grade 5: murmur is so loud that it can be heard with only the edge of the stethoscope

Grade 6: murmur is extremely loud and heard even when the stethoscope is no longer in contact with the patient.

29
Q

Why might a holosystolic murmur be present at the apex in AS?

A

Uncommon but this is called Gallavardin’s phenomenon, whereby AS mimicks the murmur of MR.

30
Q

What does TAVI stand for?

A

Transcatheter aortic valve implantation

31
Q

What is the origin of bioprosthetic valves?

A

Bovine Porcine

32
Q

What is the mechanism of mechanical valves?

A

The most common type now implanted is the bileaflet valve. *Ball-and-cage valves are rarely used nowadays*

33
Q

What are the advantages and disadvantages of bioprosthetic valves?

A

D - Structural deterioration and calcification over time. A - long term anticoagulation not necessary

34
Q

How long is anticoagulation given post-bioprosthetic valve insertion?

A

NICE does not recommend it at all unless there are other reasons why they might need anticoagulation e.g. AF Aspirin (or clopidogrel if C/I) given long-term

35
Q

What are the advantages and disadvanatges of mechanical valves?

A

A - low failure rate D - increased risk of thrombosis so long-term anticoagulation necessary

36
Q

What anticoagulation is used for mechanical valves?

A

Warfarin *DOACs not advised Aspirin only given in addition if there are additional indications e.g. ischaemic heart disease *

37
Q

What is the desired INR range for mechanical valves?

A

INR 3 = aortic valves INR 3.5 = mitral valves

38
Q

What are some medications that interact with warfarin?

A

Thyroxine - increases warfarin levels → high INR

Trimethoprim, NSAIDS - enhance warfarin effect → high INR

Cranberry juice → high INR

Amiodarone, ciprofloxacin → high INR

Carbamazepine - increased breakdown of warfarin → low INR (NB: carbamazepine also increases thyroxine metabolism)

39
Q

What are the stages of AS?

A
40
Q

What is the doppler aortic jet velocity in severe aortic stenosis?

A

>4m/sec - a high velocity means worse survival.

41
Q

What factors are used in classification of the severity of AS?

A

NB: pressure gradient = e.g. if the pressure in aorta is 120 and the one in the LV is 220 then the pressure gradient is 100.

42
Q

What is the management algorithm for severe AS? If the AS is asymptomatic what test can be done?

A

If the patient is asymptomatic you would do an exercise test and decide whether they need the SAVI based on that . You can also look at BNP or cardiac biomarkers.