VALVE DISEASE

VALVE DISEASE

CARDIAC ANATOMY 101

 

CARDIAC PHYSIOLOGY 101

Systole                        AV/PV – opens

 S1-S2              MV/TV – closes

Diastole           AV/PV – closes

 S2-S1              MV/TV – opens

NORMAL VALVE FUNCTION NORMAL VALVE FUNCTION

•         Maintain forward flow and prevent reversal of flow.

•         Valves open and close in response to pressure differences (gradients) between cardiac chambers.

ABNORMAL VALVE FUNCTION

• Valve Stenosis
• Obstruction to valve flow during that phase of the cardiac cycle when the valve is normally open.
• Hemodynamic hallmark -“pressure gradient”  ~ flow// VA
• Valve Regurgitation, Insufficiency, Incompetence
• Inadequate valve closure --→ back leakage
• A single valve can be both stenotic and regurgitant; but both lesions cannot be severe!!
• Combinations of valve lesions can coexist
• Single disease process
• Different disease processes
• One valve lesion may cause another
• Certain combinations are particularly burdensome (AS & MR)

MITRAL VALVE COMPETENCE:

• Integrated function of several anatomic elements

1. Posterior LA wall
2. Anterior & Posterior valve leaflets
3. Chordae tendineae
4. Papillary muscles
5. Left ventricular wall where the papillary muscles attach

 MITRAL VALVE DISEASE:  ETIOLOGY

• Mitral Stenosis

v     Rheumatic  - 99.9%!!!

v     Congenital

v     Prosthetic valve stenosis

v     Mitral Annular Calcification

v     Left Atrial Myxoma

•  Acute Mitral Regurgitation

v     Infective endocarditis

v     Ischemic Heart disease

-     Papillary ms rupture

v     Mitral valve prolapse

-     Chordal rupture

v     Chest trauma

•  Chronic Mitral Regurgitation

v     Ischemic Heart disease

-     Papillary ms dysfunction

-     Inferior & posterior MI

v     Mitral Valve prolapse

v     Infective endocarditis

v     Rheumatic

v     Prosthetic

v     Mitral annular calcification

v     Cardiomyopathy

-     LV dilatation

-     IHSS

MITRAL REGURGITATION-PATHOPHYSIOLOGY

MITRAL REGURGITATION-PATHOPHYSIOLOGY

MITRAL REGURGITATION-PATHOPHYSIOLOGY

MITRAL REGURGITATION-PATHOPHYSIOLOGY

• MR: Leakage of blood into LA during systole
• 10 Abnormality -Loss of forward SV into LA
• Compensatory Mechanisms

1        Increase in SV (& EF)

2        Forward SV + regurgitant volume

3        LV (LA) dilatation

4        Left Ventricular Volume Overload (LVVO)

MITRAL REGURGITATION : SYMTOMS & PE

Symptoms

•         Fatigue and weakness

•         Dyspnea and orthopnea

•         Right sided HF

•         MVP Syndrome (if present)

Physical Exam

•          Holosystolic Apical Blowing Murmur

•          Laterally displaced apical impulse

•          Split S2 (but is obscured by the murmur)

•          S3 Gallop (increased volume during diastole)

•          Radiation depends on the etiology

MITRAL REGURGITATION : SURGICAL INTERVENTION

MITRAL STENOSIS

MITRAL STENOSIS

MITRAL STENOSIS-PATHOPHYSIOLOGY

• MV gradientè Incr LA pr
• Pulmonary HTN
• Passive
• Reactive- 2nd stenosis
• RV Pressure Overload
• RVH
• RV failure
• Tricuspid regurgitation
• Systemic Congestion
• Paradoxes of MS
• Disease of Pulm Arts & RV
• LV unaffected (protected)
• As RV fails, pulmonary symptoms diminish

MITRAL STENOSIS : CLINICAL SYMPTOMS

• Symptoms related to severity of MVA reduction-
• Symptoms unrelated to severity of MS-
• Atrial fibrillation
• Systemic thromboembolism
• Symptoms due to Pulmonary HTN and RV failure-
• Fatigue, low output state
• Peripheral edema and hepato-splenomegaly
• Hoarseness –recurrent laryngeal nerve palsy

MITRAL STENOSIS :  PHYSICAL FINDINGS

• Auscultatory findings
• S1 – variable intensity; increased early, progressively decreases
• OS –opening snap, variable intensity
• A2-OS interval – varies inversely with severity of MS; shortens as MVA diminishes
• Low-pitched diastolic rumble @ apex
• Duration of murmur correlates with severity of MS
• Pre-systolic accentuation
• Increased P2
• Body habitus – thin, asthenic, female
• Low BP
• LA lift & RV tap

MITRAL VALVE DISEASE : TREATMENT

• Medical Rx for Class I & II
• HR control – Dig & BB
• Anticoagulation
• Afib, >40yrs, LAE, MR, prior  embolic event
• Surgical Rx -Class III &IV
• Balloon Mitral Valvuloplasty
• Commissural fusion
• pliable, noncalcified leaflets
• No MR of LA thrombus
• Mitral Valve Surgery
• Open commissurotomy
• MV replacement

MEDICAL MANAGEMENT - MS

• CHF
• Salt restriction and intermittent diuretics
• See MD immediately if sudden onset SOB
• May have A-fib with flash pulmonary edema 

• Exertional symtpoms
• Consider –ve chonotropic agents (BB,CCB) 

• Atrial fibrillation
• Rate control and anticoagulation
• May consider anticoagulation if stroke w/o Afib

BALLOON MITRAL COMMISSUROTOMY

AORTIC VALVE DISEASE:  ETIOLOGY

• Aortic Stenosis
• Degenerative calcific (senile)
• Congenital – Uni or bicuspid
• Rheumatic
• Prosthetic

• Acute Aortic Insufficiency
• Infective endocarditis
• Acute Aortic Dissection
• Marfan’s Syndrome
• Chest trauma
• Chronic Aortic Insufficiency
• Aortic leaflet disease
• Infective endocarditis
• Rheumatic
• Bicuspid Aortic valve
• Prolapse & congenital VSD
• Prosthetic
• Aortic root disease
• Aortic aneurysm/dissection
• Marfan’s syndrome
• Connective tissue disorders
• Syphilis
• HTN
• Annulo-aortic ectasia

 AORTIC STENOSIS - PATHOPHYSIOLOGY

• Normal AVA 2.5-3.0cm2
• Severe AS <1.0cm2
• Critical AS <0.7cm2; <0.5cm2/m2
• Hemodynamic Hallmark
• Systolic pressure gradient
• AV grad ~ AV flow//AVA
• AV flow = CO/SEP (systolic ejection period)
• 50-100mmHg gradients are common in severe AS

RELATIONSHIP BETWEEN AV GRADIENT AND FLOW FOR DIFFERENT AORTIC VALVE AREAS

• Like Mitral Stenosis – as flow increases so does the gradient.
• Unlike Mitral Stenosis –
• Resting flows are higher
• smaller AV area
• shorter SEP
• Larger gradients
• Significant (>50mmHg) gradient can be present at rest in asymptomatic individuals.

 

Aortic Stenosis: Natural History & Clinical Symptoms

• Asymptomatic for many years
• Symptoms develop when valve is critically narrowed and LV function deteriorates
• Bicuspid AV  5th - 6th decade
• Senile AS  7th-8th decades
• Classic Symptom Triad
• Angina pectoris – 5 years
• CHF   1-2 years
• Syncope 2-3 years
• Sudden Death
• Natural History Studies-
• Pts grad 25mmHg –20% chance of intervention in 15 years
• Pts with asymptomatic severe AS require close f/u
• Gradient progression
• 6-10mmHg/yr
• Risk Factors
• Age > 70
• CAD, hyperlipidemia
• Chronic renal failure

 AORTIC STENOSIS: NATURAL HISTORY

AORTIC STENOSIS

AORTIC STENOSIS:  PHYSICAL FINDINGS

Severity of AS	Mild	Moderate	Severe
Carotid pulse	normal	Slow rising	Parvus et Tardus
LV apical impulse	normal	heaving	Heaving & sustained
Auscultation
S4 gallop	-	+/-	++
Systolic ejection Click	+	+/-	-
SEM, peaking	Early systole	midsystole	mid-to-late systole
S2	normal	Normal or single	Single or paradoxical

AORTIC STENOSIS: MEDICAL THERAPY   

• No medical therapy prolongs life
• Theoretical benefit of statins, but trials –ve so far 

• Treatment of CHF can reduce symptoms
• Diuretics, ACEi, Digoxin have all been used 

• Atrial fibrillation worsens symptoms
• Needs aggressive rate control or cardioversion 

• All patients should be considered for OR
• Age is NOT a contraindication to surgery, but increases risk of complications

AORTIC STENOSIS: WHEN TO OPERATE?

Indication for Aortic Valve Repair	Class
Severe AS (AVA <1.0cm2) with symptoms	I
Severe AS undergoing CABG or CVS surgery	I
Severe AS and impaired LV function (LVEF < 50%)	I
Moderate AS undergoing CABG or CVS surgery	IIa
Asymptomatic patients:  - critical AS if operative mortality very low (<1%)  - severe AS with exercise induced hemodynamic changes  - severe AS and risk of rapid progression (age, calcified, CAD)	IIb IIb IIb

REMINDER

• Class I: There is evidence and/or general agreement that a given procedure or treatment is useful and effective
• Class II: There is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment

-     IIa:  Weight of evidence/opinion is in favor of usefulness/efficacy

-      IIb:  Usefulness/efficacy is less well established by evidence/opinion.

•  Class III: There is evidence and/or general agreement that the procedure/treatment is not useful and in some cases may be harmful.

AORTIC INSUFFICIENCY- PATHOPHYSIOLOGY

• 10 abnormality – LVVO
• Severity of LVVO
• Size of regurgitant orifice
• Diastolic pressure gradient between Ao & LV
• HR or duration of diastole
• Compensatory Mechanisms
• LV dilatation & eccentric LVH
• Increased LV  diastolic compliance
• Peripheral vasodilation
  
  

LV VOLUME VS PRESSURE OVERLOAD

Feature		LVPO (AS)	LVVO (MR,AI)
LV Volume		normal	Dilated**
Wall thickness		Conc. LVH	Normal to slightly increased
LV compliance		“stiff” noncompliant	Increased compliance
LV diastolic Pr		increased	Normal to slightly increased
LV systolic Pr		Increased**	Normal to slightly increased
LVEF		normal	increased

CHRONIC AORTIC REGURGITATION: 

PHYSICAL FINDINGS

•         Widened Pulse Pressure  > 70mmHg   (170/60)

•         Low diastolic pressure  <60mmHg

•         Hyperdynamic LV –

•         DeMusset’s signs

•         Corrigan’s pulse

•         Quincke’s pulsations,

•         Durozier’s murmur

•         Auscultation:

•         Diminished A2

•         Descrescendo diastolic blowing murmur @ LSB

•         Austin-Flint murmur – diastolic flow rumble @ apex

•         Due to interference with trans-mitral filling by impignement from aortic regurgitant jet.

•         DDx - mitral stenosis(increases intensity with amyl nitrite)

AORTIC REGURG – AUSTIN FLINT MURMUR

Due to the vibration of the anterior leaflet of the mitral valve as it is buffetted simultaneously by the blood jets from the left atrium and the aorta.

AORTIC REGURGITATION

Treatment of Asymptomatic Aortic Regurg

Medical Therapy – treats the symptoms not the cause

1. Serial Check ups with Echos (eval EF, Severity AR)
2. SBE Prophylaxis
3. Vasodialators (Nifedipine, ACE-I)
4. Diuretics

Treatment of Symptomatic Aortic Regurg

            Aortic Valve Replacement

                        Bioprosthetic vs Mechanical AVR

CONCLUSION

• Normal valves : maintain forward flow and prevent reversal of flow.
• Aortic, mitral, tricuspid and pulmonal valves.
• Treatment : medical and intervention (non surgical and surgical.