1. Regurgitant Valvular
Heart Diseases
Presenter:
Dr. Rebil Heiru (Internal Medicine Resident, R3)
Moderator:
Dr. Senbeta Guteta (Consultant Internist, Cardiologist)

2. Outlines:
Aortic Regurgitation
Mitral Regurgitation
Tricuspid Regurgitation
Pulmonic Regurgitation
References

3. Aortic Regurgitation

4. Anatomy

6. AR: is Leakage/back flow of blood into LV during diastole
due to ineffective coaptation of the aortic cusps.

9. Epidemiology

11. • 42/44 (95.5%) had mitral
valve involvement
• 88.7% MR
• Aortic valve involvement in
13.6% of definite RHD...All
were AR

12. Pathophysiology of AR
Pathophysiology of AR is depends on whether the AR is acute or chronic.
Is due to combined pressure and volume overload
Acute AR: sudden LV volume overload…> increase LVEDP…increase
pulmonary venous pressure…> dyspnea and pulmonary edema
Chronic AR: gradual LV volume overload ….>LV dilation and LVH.
Early phase… increase preload…> increase or normal EF…> remains
asymptomatic
As AR progress…EF falls, LVEDV increase, LVEDP increase….>
symptoms(dyspnea), lower coronary perfusion gradient…….> subendocardial
and myocardial ischemia

13. Pathophysiology of Chronic AR

15. Clinical Presentation
• Asymptomatic until 4th or 5th decade
• Progressive Symptoms include:
- Dyspnea, orthopnea, PND
- Chest pain.
• Nocturnal angina >> exertional angina
• ( HR  diastolic aortic pressure and increased LVEDP thus 
coronary artery diastolic flow)
• Angina pectoris is prominent late in the course with extreme
reductions in diastolic pressures
- Palpitations: due to increased force of contraction.
- PVCs symptoms

16. Peripheral Signs of Severe AR
• Quincke’s sign: capillary pulsation
• Corrigan’s sign: water hammer
pulse
• Bisferiens pulse
• De Musset’s sign: systolic head
bobbing
• Mueller’s sign: systolic pulsation of
uvula
• Durosier’s sign: femoral retrograde
bruits
• Traube’s sign: pistol shot femorals
• Hill’s sign:BP Lower extremity >BP
Upper extremity by
• > 20 mm Hg - mild AR
• > 40 mm Hg – mod AR
• > 60 mm Hg – severe AR

17. AR: Physical Exam
• Widened pulse pressure
• Systolic – diastolic = pulse pressure
• Muffled Korotkoff sound
• Apex:
Enlarged
displaced
hyper-dynamic
Palpable S3

18. Auscultation
• Diastolic murmur beginning immediately after A2 + wide PP
• Decresendo murmur
• Pt sitting and leaning fwd, breath held in deep expiration
• Lt 3rd and 4th ICS (Valvular)
• Rt parasternal area (aortic root)
S1 S2 S1

19. Central Signs of Severe AR
• Aortic diastolic murmur
• duration correlates with severity
(chronic AR)
• in acute AR murmur shortens
as Aortic DP=LVEDP
• in acute AR - mitral pre-closure
• Assess severity by impact on
peripheral signs and LV
•  peripheral signs = 
severity
•  LV =  severity
• S3
• Austin -Flint
• LVH
• radiological cardiomegaly

20. Investigation
ECHO:
oidentifying the cause of AR
o demonstrate a bicuspid valve, thickening of the valve cusps,
other congenital abnormalities, prolapse of the valve, a flail
leaflet, or vegetation
o leaflet anatomy and motion, the size and shape of the aortic
root
omeasurement of LVED and LVES dimensions and volumes,
EF, and mass
TEE when TTE is inconclusive… Aortic root
Doppler echo and color flow Doppler imaging
for the diagnosis and quantitative evaluation of AR

21. Investigations
ECG: Initially normal, later LVH
and T-wave inversion
Chest X-ray: Cardiac dilatation,
may be aortic dilatation, features of
left heart failure
Cardiac catheterization:(may not
be required), Dilated LV, Aortic
regurgitation, Dilated aortic root.
Cardiac Magnetic Resonance
Imaging
recommended when
echocardiographic evaluation of
regurgitation is suboptimal
Accurately quantifies the
severity of AR on the basis of
the antegrade and retrograde
flow volumes in the ascending
aorta

23. Disease Course
Asymptomatic Patients with Chronic Aortic
Regurgitation:
Patients with mild to moderate AR and those with severe AR
with a normal LVEF and only mild ventricular dilation may
engage in aerobic forms of exercise.
However, patients with AR who have limitations of cardiac
reserve and evidence of declining LV function should not
engage in competitive sports or strenuous activities.

25. Disease Course
Asymptomatic Patients with Chronic Aortic Regurgitation:
Depressed LVEF is among the most important determinants of
mortality after AVR…LV dysfunction may become irreversible and may
not improve after AVR.
Measures of LV systolic volume and systolic function are the most
important predictors of clinical course in asymptomatic
Moderately severe or even severe chronic AR often is associated with
a generally favorable prognosis for many years.

26. Disease Course
Asymptomatic Patients with Chronic Aortic Regurgitation:
Quantitative measures of AR severity and LV size and systolic function predict clinical
outcome
10 yr survival in mild AR 94% ±4%, compared with 69% ±9% in those with
severe AR
Normal LV function (~good prognosis)
• Progression to symptoms or LV dysfunction is < 6%/year
• Progression to asymptomatic LV dysfunction is < 3.5%/year
• Sudden death =0.2%
• Abnormal LV function
• Progression to cardiac symptoms is 25%/year
Symptomatic (Poor prognosis)
• Mortality is > 10%/year

30. Symptomatic Patients with Chronic
Aortic Regurgitation
• Once the patient with AR becomes symptomatic, the downhill course
becomes rapidly progressive
• Data compiled in the presurgical era…death usually occurred within
4 years after the development of angina pectoris and within 2 years
after the onset of HF.
• Even in the current era, 4-year survival without surgery in patients
with NYHA Class III or IV symptoms is only approximately 30%

31. Treatment of Chronic Aortic
Regurgitation
No specific therapy to prevent disease progression in chronic AR is
currently available
There is no evidence that vasodilating drugs reduce severity of AR or alter
the disease course in patients with significant AR in the absence of
systemic hypertension.
Recommendations for GDMT for hypertension and HF apply to patients
with chronic asymptomatic AR, as for the general population.
ACEI and BB for asymptomatic chronic AR… no definitive studies.
BB… paradoxical rise in BP

32. Treatment of Chronic Aortic
Regurgitation
• Medical Treatment:

33. Surgical Aortic Valve Replacement
Any Symptoms at rest or exercise
Asymptomatic patients:
either with EF of 55% or less or with severe LV dilation (LVESD >50
mm or 25 mm/m2 when indexed to body size).

35. Prognosis after Surgery
Substantial reductions in heart size and in LV diastolic volume and mass occur in
most patients.
The operative risk of AVR for patients with AR depends on
• the general condition of the patient
• the state of LV function
• the skill and experience of the surgical team.

36. cont….
Mortality ranges from 3% to 8% in most medical centers.
 advanced cases late mortality reaches 5% to 10%/year
after surgical relief of AR there will be early rapid and then slower, long-
term reductions in
o LV mass, EF, myocyte hypertrophy and ventricular fibrosis content.

38. Treatment of Acute AR
intravenous positive inotropic agent (dopamine or dobutamine) and/or a
vasodilator (nitroprusside).
prompt surgical intervention
If an acute aortic dissection is the cause for the AR, the aorta will also
need to be fixed during surgery

39. Mitral
Regurgitation
Mitral Valve Apparatus:
 Valve leaflets
 Chordae tendinea
 Papillary muscle
 Mitral valve annulus

40. Overview
Backflow of blood from the LV to the LA during systole
Mild (physiological) MR can be seen in normal individuals.
For clinical purposes, MR is classified as
primary and secondary (or functional) MR
o Ischemic MR is subset of secondary MR
o Primary and secondary MR are two distinctly d/t disease conditions, with
d/t pathophysiology, outcomes, and management considerations.
Acute vs Chronic MR
Based on leaflet motion

43. Pathophysiology of chronic
primary MR
Ventricular compensatory
 Volume Overload
o Frank-Starling: Increased preload --> LV Dilatation --> increased
stroke volume
o Initially -- Increased LV Ejection Fraction --> increased stroke volume
o (Eventually -- LV systolic function deteriorates and CHF ensues)
Myocardial contractility
Left Atrial Compliance
o Acute: rapidly increasing LA/PV pressure….>pulmonary edema
o Chronic: slow enlargement of the LA with low pressures

47. The severity of MR and the ratio of forward cardiac flow and
backward flow are determined by:
1) the size of the mitral orifice during regurgitation
2) the SVR opposing forward flow from the ventricle
3) the compliance of the left atrium
4) the systolic pressure gradient between the LV and the LA
5) the duration of regurgitation during systole (not all regurgitation is holo-
systolic)

48. Effect of MR on LA pressure depends on LA Compliance
ACUTE MR (non-compliant LA) CHRONIC MR (compliant LA)
Normal LA size Dilated LA
Increased LA pressure LA pressure normal or slow increase
"V" waves on PCW tracing Absence of V waves
Pulmonary Edema Low output state

49. Clinical features
 Until late asymptomatic
Acute MR: Dyspnea (pulmonary venous congestion)
Chronic MR: weakness, fatigue and low output state
Palpitation (atrial fibrillation, increased stroke volume)
 RV failure (less common than with MS)
Systemic embolization { stroke , ischemic limb etc.. }

50. Physical examination
Pulse :Atrial fibrillation/flutter
 Cardiomegaly: lateral displaced hyperdynamic apex beat
 Apical pan/holosystolic murmur ± thrill
 Soft S1, apical S3.
 Signs of pulmonary venous congestion (crepitations, pulmonary edema,
effusions)
 Signs of pulmonary hypertension and right heart failure.

51. Diagnosis and Evaluation
• ECHO:
• Cause, underlying disease, Chamber size, severity of regurgitation
• Jet morphology… mechanism of MR (opposite from the most significant anatomic
lesion) except in functional MR
• Quantitative measurements
• TEE
• when TTE images are inadequate
• Whether MVR or clipping is feasible or MVR is necessary
• Detailed anatomy of MV
• 3D Echo
• directly demonstrates pathology (surface rendering)
• Multiple images--- localization of the pathology
• Stress echo
• Can be used to establish the presence of symptoms in patients with chronic primary
MR and exercise tolerance

58. Other Diagnostic Evaluation
Modalities :
ECG: LAE & Afib , LVH (1/3) with severe
MR, RVH (15%)
CXR: Cardiomegaly LV enlargement +
LA enlargement, Calcification (dense C
shaped opacity)
 Combined MS + MR…
Cardiac Magnetic Resonance
Imaging.
 Accurate measurement of regurgitant
flow
 The most accurate non invasive
testing (LVSEDV,ESV and mass)
⁻ indicated in chronic primary MR to
assess LV and RV volumes,
function or MR severity
Cardiac Computed
Tomography:
 Sizing mitral annulus and quantifying
degree of annular calcification
 particularly useful for planning MVR
Left Ventricular Angiography.
• when discrepancy b/n
noninvasive testing and clinical
symptoms
• Assess Severity of MR, LV
function, need for surgery
• Qualitative but clinically useful
estimate of severity of MR

59. Disease course
Natural history of Chronic primary MR is highly variable and depends on:
oThe volume of regurgitation
o State of the myocardium
o Cause of underlying disorder.
o Asymptomatic mild MR - stable for many years
o Asymptomatic severe MR- progression to symptoms, LV dysfunction,
pulmonary HTN, or AF is 30-40% at 5 years.

60. cont….
5 year survival is 30% in patients who are candidates for operation,
presumably b/c of symptoms, but who declined surgery
In Severe MR due to flail leaflets
₋ annual mortality without surgery is 3%
₋ at 20 years 60%
₋ it is high in those with LV Dysfunction (LVEF of 60% or less)

66. Management of MR
Medical management
In patients with primary MR, there is no convincing evidence
that vasodilator therapy reduces MR severity.
However, GDMT for LV systolic dysfunction or systemic HTN
should be implemented as in any patient with these
conditions.

69. Mitral valve Surgery
Only effective treatment is valve repair/replacement
Optimal timing is determined by:
• Presence/absence of symptoms
• Functional state of ventricle
• Feasibility of valve repair
• Presence of Afib/PHTN
• Presence/expectation of patient

70. cont….
Surgical mortality depends on the patient's clinical and hemodynamic
status particularly:
₋ LV function
₋ age
₋ presence of comorbid conditions such as renal, hepatic, or pulmonary
disease
₋ the skill and experience of the surgical team

71. MV Repair vs. Replacement
Valve replacement:
oMortality 2-7%
oAnti-coagulation
oDecreased LVEF
Prosthesis related complications
Mechanical prosthetic valve
dysfunction/ thrombosis
Valve repair
oMortality 2-3%
oNo anticoagulation (unless Afib)
oPreservation of LVEF
Valve repair always preferable
Feasible in 70-90% of patients
High volume surgeon (20
procedures/yr)

72. Indication for surgery
Asymptomatic patients :
LV dysfunction (EF <60% and /or LV end-diastolic diameter of 40 mm)
AF or pulmonary hypertension
Symptomatic patients :
 Patients with severe primary MR and moderate or severe symptoms
(NYHA Class II, III, and IV) should generally be considered for surgery.

74. MV Repair vs. Replacement
Repair of primary degenerative MR most often is successful in:
1) children and adolescent with pliable valves
2) adults with MR secondary to MVP
3) cases with annular dilatation
4) cases with chordal rupture
5) cases with perforation of a mitral leaflet caused by infective
endocarditis

75. Percutaneous mitral valve repair
Mitra Clip is safe (Everest I) but less effective than surgical repair (Everest II)
 Residual MR by creating 2 regurgitant orifice – similar to Alfieri procedure
Reduce symptoms by reducing MR, reverse LV remodeling
For patients:
o with chronic severe MR with symptoms NYHA 3-4 despite medical therapy for
HF and are not candidate for surgery
o Favorable anatomy for repair procedure
o Reasonable life expectancy

76. Surgical results
Operative mortality is 1-9% in many centers
Mortality was significantly lower in the repair than replacement
patients (1.4% vs 5.4% in 2007-10)
The mortality rate in mitral valve surgery with CABG is
6.2%... 25% in pts with LV dysfunction

77. Indicators for Poor Prognosis in MR
1. Symptoms of heart failure
2. Left ventricular ejection fraction (LVEF) < 50% with symptoms
3. Acute-onset MR
4. Acute flail of mitral valve leaflets
5. Significant MR accompanying acute myocardial infarction

78. Surgical result
A large proportion of operative
survivors after MVR or repair exhibit:
• improved clinical status
• quality of life
• Exercise tolerance
If operation done before development
of serious symptoms or marked LV
dysfunction:
• Severe PHTN is reduced
• LVEDV and LV mass decrease
• coronary flow reserve increases.
• Depressed contractile function
improves

79. Treatment of Chronic Secondary
MR
Medical Management
GDMT for HF with reduced LVEF in patients with severe secondary MR
(I-A)
Treatment should be provided, in conjunction with a cardiology expert,
in the management of HF (I-C)

80. Surgical Treatment in chronic secondary MR
If patient has persistent symptoms despite optimal medical therapy
Reasonable if severe secondary MR undergoing surgery for CABG
but Several randomized trials have provided conflicting data on concomitant
MV repair in pts undergoing CABG.
 POINT Trial
 RIME Trial
 CTSN Trial
Transcatheter Treatment of secondary MR
COAPT trial Vs MITRA-FR

81. CABG alone VS CABG + MV repair

82. COAPT trial

83. Eur Heart J Cardiovasc Imaging, Volume 20, Issue 6, June 2019, Pages 620–624, https://doi.org/10.1093/ehjci/jez073
The content of this slide may be subject to copyright: please see the slide notes for details.
Utility vs. futility of MitraClip procedure according to severity of MR
and LV systolic dysfunction. EROA, ...

84. MV repair vs replacement in secondary
chronic MR

87. Treatment of Acute MR
Medical Treatment
Afterload reduction -IV nitroprusside and add inotropic agent (I. e
dobutamine) if hypotension
intra-aortic balloon pump
Emergent Surgery - mitral valve repair or replacement
Surgical mortality rates are higher in patients with:
acute MR and refractory HF (NYHA Class IV)
those with prosthetic valve dysfunction
those with active infective endocarditis

88. Tricuspid Regurgitation

90. Pathophysiology TR
The RA and RV end-diastolic pressures often are elevated in TR whether
the condition is caused by:
oorganic disease of the tricuspid valve
o is secondary to RV systolic overload.
Determination of the pulmonary artery (or RV) systolic pressure may be
helpful in deciding whether the TR is primary or secondary to RV dilation

94. Clinical presentation of TR
In absence of PHTN or RV failure, TR generally is well tolerated.
Manifested with of right-sided HF: reduced CO, ascites, painful congestive
hepatomegaly, and massive edema

95. Physical Examination
The RV impulse is hyperdynamic and thrusting in quality.
High pitch blowing holosystolic murmur varying with respiration(carvallo
sign) in xiphoid area
Large pulsations in neck, pulsatile enlarged liver, widespread edema, RV
S3(increase with respiration)
In TR 2ndary to PHTN
P2 is accentuated
 systolic murmur usually is high pitched, pansystolic
loudest in the 4th intercostal space in the parasternal region

96. Investigation
ECHO:
 to estimate the severity of TR and assess pulmonary artery pressure (PAP) and RV
function, RV and RA chamber size , mass, valve anatomy and motion
ECG:
nonspecific or Incomplete right bundle branch block, Q waves in lead V1, and AF are
often found.
CXR:
marked cardiomegaly, and the right atrium is prominent, distention of the azygos vein
and the presence of a pleural
effusion.
Cardiac Magnetic Resonance Imaging:
for determining the 3 D geometric relationships between the right ventricle and the
tricuspid annulus and leaflets in patients with functional TR

97. Echo…

98. Management
Medical
 Diuretic therapy treats the systemic congestion in patients with severe symptomatic TR (2a)
 In patients with secondary TR, treatment of the underlying primary cause may decrease the
severity of the TR (2a)
Surgery:
• Severe functional TR may be treated by annuloplasty or valve replacement.
• Severe TR due to intrinsic tricuspid valve disease requires valve replacement.
• Tricuspid valve repair accounts for 73% of tricuspid valve operations.
• For TVR, bio prostheses are increasingly being used and now account for 46% of
TVRs.

99. Treatment…
• Treatment of secondary TR is targeted at pulmonary
hypertension or myocardial disease.
• Outcomes of patients with severe primary TR are poor with
medical management.
• Surgical treatment is performed for selected patients with
• TR at the time of surgery for left-sided valve lesions to treat severe TR (Stages C and
D) and
• to prevent later development of severe TR in patients with progressive TR (Stage B).
• Severe isolated TR
• Mild TR with annular dilatation

100. Treatment…
• There is renewed interest in earlier surgery for patients with
severe isolated TR before the onset of severe RV dysfunction or
end-organ damage.
• This interest is attributable to
• 1) an increasing no. of patients presenting with RHF from isolated TR
• 2) more advanced surgical techniques, and
• 3) better selection processes, resulting in a lower operative risk with
documented improvement in symptoms
• There is growing interest in the development of catheter-based
therapies for these patients with severe isolated TR.

102. Pulmonary regurgitation

103. Pulmonary regurgitation
Most common cause is ring dilatation due to pulmonary hypertension, or
dilatation of the pulmonary artery secondary to a connective tissue disorder.

104. Clinical Presentation
Asymptomatic or well-tolerated for many years.
The clinical manifestations of the primary disease tend to overshadow the
pulmonary regurgitation
The right ventricle is hyperdynamic
 palpable systolic pulsations in the left parasternal area
enlarged pulmonary artery often produces systolic pulsations in the 2nd left
intercostal space.
the diastolic murmur of PR is low-pitched and usually is heard best at the 3rd and
4th left intercostal spaces adjacent to the sternum.

105. Cont….
Electrocardiography.
o an rSr (or rsR) configuration in the right precordial leads.
o RV hypertrophy.
Radiography.
o Both the pulmonary artery and right ventricle are usually enlarged, but these
signs are nonspecific.
Cardiac Magnetic Resonance Imaging.
o assess pulmonic valve anatomy
o recognize any obstruction above or below the valve
o measure pulmonary artery dilation
o quantify PR severity.
o evaluation of RV dilation and systolic function

106. Echocardiography
Right chamber Size , RV hypertrophy, RV function , abnormal motion of
septum and motion of pulmonic valve.
Doppler echo - is extremely accurate in detecting PR and in helping
estimate its severity

108. Management
None to treat underlying lesions responsible for PHTN
PVR with a pulmonary allograft.

109. References
Braunwald’s Heart Diseases 11th edition
Uptodate 2018
AHA VHD guideline 2020
Harrison’s principles of internal medicine 20 ed

110. THANK YOU