The document provides an overview of various valvular heart diseases including their etiology, pathophysiology, clinical manifestations, diagnostic evaluation, and treatment. It discusses conditions such as aortic stenosis, aortic insufficiency, mitral regurgitation, mitral stenosis, and tricuspid regurgitation. The document is intended as an educational reference for medical professionals on approaches to evaluating and managing patients with valvular heart disease.

1. Johnstone Kayandabila, MD
Feb, 2017.
Department of Internal Medicine
Kilimanjaro Christian Medical Center
KCMC

2. Contents
1. Aortic Stenosis (AS)
2. Aortic Insufficiency (AI)
3. Mitral Regurgitation (MR)
4. Mitral Stenosis (MS)
5. Mitral Valve Prolapse (MVP)
6. Tricuspid Regurgitation
7. Prosthetic Heart Valves

3. Introduction

4. Distribution of VHD in the Euro Heart Survey
ESC, 2007

5. Approach to the cardiac patient
 Inspection
Body habitus - marfans
Face + neck - mitral
facies, cyanosis, JVP,
carotid pulse
Chest wall – scars, apex
beat.
Hands – cyanosis,
stigmata of endocarditis
Etiology
Physical Exam
Assessing Severity
Natural History
Prognosis
Timing of Surgery

6.  Palpation
Pulse - rate, rhythm ,character, volume, equality
Thrills - Aortic + pulmonary areas, apex, LSE
Heaves - with right ventricular hypertrophy (left
sternal edge)
Apex - hypertrophied, dilated.
Palpable sounds
1st
(mitral stenosis, tapping apex),
2nd
– pulmonary or systemic hypertension

7.  Auscultation
Split up the cardiac cycle
○ first and second sounds
○ Added sounds
○ Systole
○ Diastole
List with breath held in expiration (most murmurs
are left sided)
Track murmurs across the chest wall
Always listen for an early diastolic murmur in
expiration at the left sternal edge

8. Investigations for murmurs
 FBC, TFT’s – flow murmurs.
 CXR
 ECG
 Echocardiogram
 Angiography (prior to surgery)
 If endocarditis suspected:
Blood cultures, CRP, urine dipstick and
microscopy, trans oesophageal echocardiogram

9. SYSTOLIC AND DIASTOLIC MURMURS
 SYSTOLIC
 Flow murmurs
 Aortic stenosis
 Hypertrophic obstructive
cardiomyopathy
 Mitral regurgitation
 Ventricular septal defect
 Pulmonary stenosis
 Coarctation
 Tricuspid regurgitation
 DIASTOLIC
 Aortic regurgitation
 Mitral stenosis
 Pulmonary regurgitation

11. MURMURS AND THE
CARDIAC CYCLE
Aortic stenosis
Mitral Regurgitation
1 2
1 2
Mitral valve prolapse with
late regurgitation
1 2

12. Evaluation of cardiac patient

13. Epidemiology
 Primary VHD ranks below Coronary HD, HTN,
obesity, & DM as major threat to the public health
 Has significant morbidity & mortality rates.
 Rheumatic fever – dominant cause of VHD in LIC.
 Prevalence of RF 1/100,000 school-age children in
Costa Rica, 150/100,000 in China. RHD; 12-65% of
hosp admissions due to CV-d’se. (Harrison, 2015)
 RHD incidence at Muhimbili by Echo 5.4% btn 10-
19 yo; Females>Males (Luggajo, 2009)

14. Cont’
 Globally, about 15-20 million people live
with RHD; new cases 300,000, & CFR
233,000/yr
 Highest mortality reported in Southeast
Asia, 7.6/100,000.

15. A 71 yo M is evaluated for symptoms of HF. On physical
exam, the apical impulse is enlarged and displaced laterally
and a grade 2/6 midsystolic murmur is heard at the right
upper sternal border that radiates to the carotid arteries.
Echo shows hypokinesis & LVEF of 30%, calcified aortic valve
cusp with diminished mobility, and transvalvular mean
gradient is 26 mmHg.
The correct answer is;
a) Severe AS with cardiomyopathy
b) Low transvalvular gradient is due to LV dysfunction
c) Treatment is by cardiac catheterization or valve
replacement
d) All the above
e) None of the above

16. A 71 yo M is evaluated for symptoms of HF. On physical
exam, the apical impulse is enlarged and displaced laterally
and a grade 2/6 midsystolic murmur is heard at the right
upper sternal border that radiates to the carotid arteries.
Echo shows hypokinesis & LVEF of 30%, calcified aortic valve
cusp with diminished mobility, and transvalvular mean
gradient is 26 mmHg.
The correct answer is;
a) Severe AS with cardiomyopathy
b) Low transvalvular gradient is due to LV dysfunction
c) Treatment is by cardiac catheterization or valve
replacement
d) All the above
e) None of the above

17. Aortic Stenosis (AS)
Etiology;
 Calcific: predominant cause in patients > 70y
 Risk factors;
 HTN,
 ↑chosterolaemia,
 ESRD
 Congenital
 Bicuspid AoV →premature calcification (40-60yrs)
 cause in 50% of pts <70 y
 William syndrome
 RHD: AS usually a/c by AI & MV disease
 DDx: subvalvular- HCMP, membranous subAo
stenosis , supravalvular AS

18. Pathogeneis of calcific aortic
stenosis
Harrison 19th
Edition, 2015. pp. 1530.

19. Major causes of Aortic valve
disease
 Table 283-1, pp.1529
Valve lesion Etiologies
Aortic stenosis Congenital (bicuspid, unicuspid)
Degenerative calcific
Rheumatic fever, Radiation
Aortic
regurgitation
Valvular
Congenital (bucuspid)
Endocarditis, Rheumatic fever
Myxomatous (prolapse), Traumatic
Syphilis, Ankylosing spondylitis
Root disease
Aortic dissection, Cystic medial
degeneration
Marfan’s syndrome, Bicuspid aortic valve
Nonsyndromic familial aneurysm
Aortitis
HTN
Harrison, pp. 1529

20. Aortic valves
DEGENERATIVE AORTIC VALVE DISEASE
BICUSPID AORTIC VALVE

21. Clinical manifestations
 Usually indicates AVA 1 cm2
or concomitant CAD
 Cardinal features
 Angina: ↑O2 demand (hypertrophy) + ↓O2 supply (↓ cor
perfusion pressure) +/- CAD
 Syncope (exertional): peripheral vasodil. w/ fixed CO → ↓MAP
→ ↓cerebral perfusion.
 Heart failure: outflow obstruct + diastolic dysfxn → pulm.
edema; precip. by AF & AV dissociation (↓ LV filling)
 Acquired von Willebrand disease
of vWF (NEJM 2003;349:343)
 2
per y, but
varies; Circ 1997;95:2262), until sx develop
 Mean survival based on sx: angina = 5 y; syncope = 3 y; CHF = 2 y

22. Physical exam
 Midsystolic crescendo-decrescendo murmur at RUSB,
 harsh, high-pitched, radiates to carotids, apex (holosystolic =
Gallavardin effect)
 ↑ w/ passive leg raise,
 ↓ w/ standing & Valsalva
 In contrast, dynamic outflow obstruction (eg, HCMP) ↓ w/
passive leg raise & ↑ w/ standing & Valsalva
 Ejection click after S1 sometimes heard with bicuspid AoV
 Signs of severity:
 late-peaking murmur, paradoxically split S2 or
 inaudible A2, small and delayed carotid pulse (“pulsus parvus
et tardus”),
 LV heave,
 S4 (occasionally palpable)

23. Diagnostic studies
 ECG: LVH, LAE, LBBB, AF (in late disease)
 CXR:
 cardiomegaly,
 AoV calcification,
 post-stenotic dilation of ascending aorta,
 pulmonary congestion
 Echo:
 valve morphology,
 estimate pressure gradient &
 calculate aortic valve area, EF
 Cardiac cath:
 pressure gradient ( ) across AoV,∇
 AVA,
 r/o CAD (in 50% of calcific AS)

24. ECG in Aortic Valve disease
LVH
LAE
LBBB
AF (in
late
disease)

25. CXR in Aortic Valve disease

26. Fig. 283-2: management strategy for patients with
aortic stenosis (pp.2101)

27. Classification of Aortic Stenosis
Stage Mean
Gradient
(mmHg)
Jet vel.
(m/s)
AVA
(cm2)
LVEF
Normal 0 1 3-4 Normal
Mild < 25 <3 >1.5 Normal
Moderate 25-40 3-4 1.0 – 1.5 Normal
Severe,
compensated
>40 >4 < 1.0* Normal
Severe,
decompensate
d
Variable Variable <1.0* ↓
AVA index (AVA relative to BSA) < 0.6 cm2/m2 also qualifies for severe
AS.

28. Treatment
 Management decisions are based on
symptoms: once sx develop surgery is needed.
If asx wt preserved EF; HTN can be Rx’d; BB, ACE-I
Nitroglycerin: relieves angina sx
HMG-CoA reductase inhibitors (statins); lower
progression of leaflet calcification & AVA reduction.
The need for endocarditis prophylaxis is restriced to
AS patients with a prior h/o endocarditis
Harrison, 19th
Edition, pp. 1532. 2015

29.  Medical therapy:
used in sx Pts who are not operative candidates
○ diuresis,
○ control HTN, maintain SR;
○ digoxin if low EF or AF
○ avoid venodilators (nitrates) & negative
inotropes (CCB & B-blockers) in severe AS
○ avoid vigorous physical exertion once AS
moderate-severe
○ ? nitroprusside if p/w CHF w/ sev.AS, EF
35%, CI 2.2, & normal BP
(NEJM 2003;348:1756)

30.  Balloon Ao valvotomy: 50% ↑ AVA & ↓
peak ,∇ but 50% restenosis by 6–12 mo & ↑
risk of peri-PAV stroke/AI (NEJM
1988;319:125)
 ∴ bridge to AVR or palliation
 Transcatheter AoV implantation (TAVI);
bioprosthetic valve mounted on balloon
expandable stent (JACC 2009;53:1829);

31. Indications for Aortic Valve
Replacement AVR is indicated in those with;
 Severe AS (AVA < 1 cm2)
 Or 0.6 cm2/m2 body surface
area with sx
 LV systolic dysfunction (EF<
50%) with sx
 BAV disease and an aneurysmal
root or ascending aorta
(maximal dimension > 5.5 cm)
 Aneurysmal disease wt aortic
diameters 4.5 – 5.0 cm in positive
FHx of an aortic catastrophe
 Rapid aneurysm growth > 0.5
cm/year
 Asx moderate or severe AS who
are referred for coronary artery
bypass grafting surgery.
 NOTE: Perioperative risk; 15 – 20%
 Relative Indications;
 Abnormal response to treadmill
exercise
 Rapid progression of AS (in
conditions wt compromised access
to health care)
 Very severe AS
 Aortic jet velocity > 5 m/s
 Mean gradient > 60 mmHg
 Low operative risk
 Excessive LVH in the absence of
systemic HTN
 NOTE: Perioperative risk; 15 – 20%

33. Aortic Insufficiency (AI)
 Introduction
 Confer to Table 283-1
AR may be caused by primary valve disease
or by primary aortic root disease.

34. Introduction:
 Isolated AR is rare without association
with mitral valve disease.
 Patients wt congenital BAV disease may
develop predominant AR & about 20%
will require aortic valve surgery btn 10 &
40 yrs of age

35. Etiology
 Valve disease (43%)
 RHD (usually mixed AS/AI and concomitant MV disease)
 Bicuspid AoV: natural hx: 1/3 → normal, 1/3 → AS, 1/6
→AI, 1/6 → endocarditis →AI
 Infective endocarditis
○ valvulitis: RA, SLE; anorectics (fen/phen) & other
serotoninergics (NEJM 2007;356:29,39)
 Root disease (57%)
 HTN
 aortic aneurysm or dissection, annuloaortic ectasia,
Marfan syndrome
 aortic inflammation: giant cell, Takayasu’s, ankylosing
spond., reactive arthritis, syphilis (Circ 2006;114:422)

36. Pathophysiology
 Total SV ejected by the LV (effective forward
SV + Volume of Regurgitant flow) ↑ in AR.
 In severe AR, the volume of regurgitant flow
may equal the effective forward SV.
 In AR, the entire LV-SV is ejected into a
high-pressure LA, the aorta
 An ↑ in the LV end-diastolic volume (↑pre-
load) → major hemodynamic compensation
of AR→ LVH → ↑ LV systolic tension
 All changes reflect the Laplace’s law.

37.  In chronic AR, LV preload & afterload both↑ ↑ failure of
adaptive mechanism → ↓LV function → ↑↑ End-diastolic
volume & pressure (> 40 mmHg) → ↓forward SV & EF =>
sx development
 The reverse pressure gradient from Aorta to LV,
↓progressively during diastole → decrescendo nature of the
diastole murmur.
 Early sign of LV dysfunction is ↓EF
 In advanced stages; LA, PA wedge, PA, & RV pressures
all elevate with lowering of forward CO at rest.
 Myocardial ischemia is resulted by;
 Increased myocardial oxygen requirements by LV dilatation,
LVH, ↑ LV systolic tension, & compromised coronary blood flow
 Subendocardium is more susceptible even in absence of
epicardial CAD.
 In acute AR; the valve is unprepared;

38. Clinical manifestations
 Acute: sudden ↓ forward SV and ↑LVEDP
(noncompliant ventricle) → pulmonary
edema +/- hypotension & cardiogenic shock
 Chronic: clinically silent while LV dilates (to
↑ compliance to keep LVEDP low) more than
it hypertrophies → chronic volume overload
→ LV decompensation → CHF
 Natural hx: variable progression (unlike AS,
can be fast or slow); once decompensation
begins, prognosis poor w/o AVR (mortality

39. Physical examination
 Early diastolic decrescendo murmur at LUSB
 (RUSB if dilated Ao root); ↑/ sitting forward, expir, handgrip;
severity of AI α duration of murmur (except in acute and
severe late); Austin Flint murmur: mid-to-late diastolic rumble
at apex (AI jet interfering w/ mitral inflow): SOFT MURMUR
 Wide pulse pressure due to ↑ stroke volume,
hyperdynamic pulse → many of classic signs; pulse
pressure narrows in late AI with T LV fxn; bisferiens
(twice-beating) arterial pulse
 diffuse and laterally displaced point of maximal impulse;
soft S1 (early closure of MV); +/- S3 (≠ ↓ EF but rather
just volume overload in AI): AT THE 4th
interspace

40. Austin Flint - Murmur
LV
AV
MV
AR
Diastolic
Filling
1 2
Anterior leaflet of mitral valve vibrates between AR and filling jets
1

41. Classic Eponymous Signs in Chronic AI (South Med J. 1981; 74: 459)
Sign Description
Corrigan’s pulse “water hammer” pulse (ie, rapid rise/fall or
distention/collapse)
Hill’s sign (popliteal SBP – brachial SBP) > 60 mmHg
Duroziez’s sign to-and-fro murmur heard over femoral artery w/ light
compression
Pistol shots
sounds
Pistol shot sound heard over femoral artery
Trabe’s sound Double sound heard over femoral artery when compressed
distally
de Musset’s sign Head-bobbing with each heartbeat (low Se)
Muller’s sign Systolic pulsations of the uvula
Quincke’s pulses Subungual capillary pulsations (low Sp)
Arterial pulse

42. CXR:
 In chronic severe AR;
Downward displaced apex to the left
cardiomegaly
ascending Ao dilatation in presence of aortic
root aneurysm
Lateral view; aorta filling the entire
retrosternal space

43. Diagnostic studies
• ECG:
LVH, ST-segment depression, TWI in
leads I, aVL, V5, & V6 (‘LV-strain) in pts
with chronic severe AR;
LAD +/- QRS prolongation denote
diffuse myocardial disease/patchy
fibrosis, signify poor prognosis

44. Echo: (TTE/TEE)
 severity of AI
o severe = width of regurgitant jet > 65% LV outflow tract,
o vena contracta > 0.6 cm,
o regurg fraction ≥50%,
o regurg orifice ≥ 0.3 cm2
,
o flow reversal in descending Ao
 LV size & function
o LV size ↑in chronic AR, systolic function is normal until
myocardial contractility declines
o TEE – provides detailed anatomic assessment of the
valve, root, & portions of aorta.

45. Cardiac MRI
 Is indicated in patients whom;
 TTE is limited by poor acoustical windows or
 inadequate semiquantitative assessment of LV
function or severity of the regurgitation.
 It allows accurate assessment of aortic size &
contour
 NOTE: Echo, cardiac MRI, chest CT-
angiography are more sensitive than CXR for
detecting root & ascending aortic enlargement
 Cardiac catheterization & angiography

46. Treatment
 Acute decompensation (consider ischemia
and endocarditis as possible precipitants)
surgery usually urgently needed for acute severe
AI which is poorly tolerated by LV
IV afterload reduction (nitroprusside) and inotropic
support (dobutamine) +/- chronotropic support (↑
HR →↓ diastole →↓ time for regurgitation)
pure vasoconstrictors and IABP contraindicated
 In chronic AI, management decisions based
on LV size and fxn (and before sx occur)
Circ 2008;118:e523

47.  Medical therapy:
vasodilators (nifedipine, ACEI, hydralazine) if
severe AI w/ sx or LV dysfxn & Pt not operative can
didate or to improve hemodynamics before AVR;
 no clear benefit on clinical outcomes or LV fxn
when used to try to prolong compensation in
asx severe AI w/ mild LV dilation & normal LV
fxn
NEJM 2005;353:1342

48. Indication for Valve Replacement in
Aortic Regurgitation
 ACC/AHA Class I
Symptomatic patients with preserved LVF
(LVEF >50%)
Asymptomatic patients with mild to moderate LV
dysfunction (EF 25-49%)
Patients undergoing CABG, aortic or other
valvular surgery
 ACC/AHA Class II a
Asymptomatic patients with preserved LVEF but
severe LV dilatation (EDD>75 mm or ESD >
55mm)

49. Indication for Valve Replacement in
Aortic Regurgitation
 ACC/AHA Class II b
Patients with severe LV dysfunction (EF < 25%)
Asymptomatic patients with normal systolic
function at rest (EF >0.50) and progressive LV
dilatation when the degree of dilatation is
moderately severe (EDD 70 to 75 mm, ESD 50
to 55 mm).
 ACC/AHA Class III
Asymptomatic patients with normal systolic function
at rest (EF >0.50) and LV dilatation when the degree
of dilatation is not severe (EDD <70 mm, ESD <50
mm).

51. Mitral Regurgitation (MR)

52. MITRAL VALVE STRUCTURE
ETIOLOGIES OF MR

53. Harrison pp., 3984

54. Etiology
 Leaflet abnormalities:
 myxomatous degeneration
(MVP),
 endocarditis,
 calcific RHD,
 valvulitis (collagen-vascular
disease),
 congenital,
 anorectic drugs
 Functional:
 infero-apical papillary muscle
displacement due to ischemic
LV remodeling or other causes
of DCMP;
 LV annular dilation due to LV
dilation
 Ruptured chordae
tendinae:
myxomatous
endocarditis
spontaneous
trauma
 Acute papillary muscle
dysfxn b/c of ischemia or
rupture during MI [usu.
Posteromedial papillary m.
vs. anterolateral]
 HCMP
Lancet 2009;373:1382

55. Clinical manifestations
 Acute: pulmonary edema,
hypotension, cardiogenic shock
 Chronic: typically asx for yrs, then as
LV fails → progressive dyspnoea on
exertion, fatigue, AF, PHT
 Prognosis: 5-y survival w/ medical
therapy is 80% if asx, but only 45% if sx
NEJM 2004;351:1627

56. Physical examination
 High-pitched, blowing, holosystolic murmur
at apex;
 radiates to axilla; +/- thrill; ↑ w/ handgrip (Se 68%, Sp
92%),
 ↓w/ Valsalva (Se 93%) (NEJM 1988;318:1572)
 ant. leaflet abnormal → post. jet heard at spine
 post. leaflet abnormal → ant. jet heard at sternum
 Lateral displaced hyperdynamic point of
maximal impulse, obscured S1, widely split S2 (A2
early b/c T LV afterload, P2 late if PHT); S3
 Carotid upstroke brisk (vs. diminished and
delayed in AS)

57. Diagnostic studies
 ECG: LAE, LVH, +/- AF
 CXR: dilated LA, dilated LV, +/- pulmonary
congestion
 Echo:
 MV anatomy
 MR severity: jet area, jet width at origin, or effective
regurgitant orifice (predicts survival, NEJM
2005;352:875);
 LV fxn (EF should be supranormal if compensated, ∴
EF 60% w/ sev. MR LV dysfxn);TEE if TTE
inconclusive or pre/intraop to guide repair vs. replace
 Cardiac cath: prominent PCWP cv waves,
LVgram for MR severity & EF

58. Classification of Mitral Regurgitation
Severity Regurgitation
fraction
Jet area
(% of LA)
Jet width
(cm)
ERO
(cm2)
Angio
(see footnote)
Mild <30% <20 <0.3 <0.2 1+
Moderate 30-49% 20-40 0.3-0.69 0.2-0.39 2+
Severe ≥50% >40 ≥0.70 ≥0.40 3/4+
1+ = LA clears w/ each beat; 2+ = LA does not clear, faintly opac. After several
beats; 3+ = LA & LV opac. equal

59. RADIOLOGICAL FEATURES OF MITRAL REGURGITATION

60. WHEN TO
INTERVENE IN
MITRAL
REGURGITATION

61. Treatment
 Acute decompensation -consider ischemia and
endocarditis as precipitants
 IV afterload reduction (nitroprusside), +/- inotropes
(dobuta),
 IABP,
 avoid vasoconstrictors
 Medical: benefit (incl ACEI) in asx pts; indicated if∅
sx but not an operative candidate
 ↓preload (↓CHF and MR by ↓ MV orifice):
 diuretics,
 nitrates (espec if ischemic/fxnal MR)
 if LV dysfxn: ACEI, βB (carvedilol), +/-biV pacing; maintain
SR
Circ 2008;118:e523; NEJM 2009;361:2261

62. • Surgery
○ Surgery usually needed for acute severe MR as
prognosis is poor w/o MVR
 repair [preferred if feasible] vs. replacement w/
preservation of mitral apparatus)
 sx severe MR,
 asx severe MR and EF 30–60% or
 LV sys. diam. 40 mm
 consider MV repair for asx severe MR w/ preserved
EF, esp. if new AF or PHT

64. Mitral Stenosis (MS)

65. Mitral Stenosis – Aetiology
 Rheumatic Fever
Commissural fusion and thickening 30%
Cuspal thickening 15%
Chordal 10%
Remainder combined
Pure MS 25%
Combined MS/MR 40%

66. Etiology
 Rheumatic heart
disease: fusion of
commissures →“fish
mouth” valve
-from autoimmune
rxn to strep infxn;
 Mitral annular
calcification :
encroachment upon
leaflets → functional
MS
 Congenital,
infectious
endocarditis w/ large
lesion, myxoma,
thrombus
 Valvulitis (SLE,
amyloid, carcinoid)
or infiltration
(mucopolysaccharid
oses)

67. Mitral Stenosis - Presentation
 Dyspnoea
 Haemoptysis
Sudden Haemorrhage (bronchial venous bleed)
Blood stained sputum associated with PND
Pink frothy sputum with acute pulmonary oedema
Pulmonary infarction ( late)
Blood stained sputum associated with COPD
 Chest pain
 Thrombo embolism (20% of patients during life)
Directly related to age, cardiac output and size of left
atrium
 Ortners syndrome – LA compression of RLN
Lancet 2009;374:1271

68. Physical exam
 Low-pitched mid-diastolic rumble at apex
 w/ presystolic accentuation
 Best heard in left lateral decubitus position during
expiration
 ↑ w/ exercise
 Opening snap
 high-pitched early diastolic sound at apex
 from fused leaflet tips;
 MVA proportional to S2– OS interval
 tighter valve →↑ LA pressure → shorter interval
 Loud S1 (unless MV calcified)

69. Diagnostic studies
 ECG: left atrial enlargement (“P mitrale”), AF, RVH
 CXR:
 dilated LA (straightening of left heart border, double density on right, left mainstem
bronchus elevation)
 Echo:
 estimate pressure gradient,
 RV-systolic pressure,
 valve area,
 valve echo score (0–16, based on leaflet mobility &
thickening, subvalvular thickening
 exercise TTE if discrepancy between sx and severity of MS
at rest;
 TEE to assess for LA thrombus before percutaneous mitral
valvuplasty
 Cardiac cath: from simultaneous PCWP & LV pressures, calculated∇
MVA; LA pressure tall a wave and blunted y descent; ↑ PA pressures

70. V
CXR in Mitral
Stenosis
• Double Right Heart border.
• Splayed carina
• Straight left heart border
• Kerley B lines
• Kerley A lines

71. MITRAL STENOSIS – MORPHOLOGY (ECHO)

72. Classification of Mitral Stenosis
Stage Mean
gradient
(mmHg)
MV area
(cm2)
PA Systolic
(mmHg)
Normal 0 4-6 <25
Mild <5 1.5-2 <30
Moderate 5-10 1-1.5 30-50
Severe >10 <1 >50

73. Treatment
 Medical:
Na restriction,
cautious diuresis,
β-blockers,
sx-limited physical stress
 Anticoagulation if
AF,
prior embolism,
LA thrombus, or
large LA
Circ 2008;118:e523

74.  Surgical
MV repair if possible, o/w replacement
 consider in sx Pts wt ≤ MVA 1.5
if percutaneous mitral vulvotomy unavailable or
contraindicated (mod. MR, LA clot), or valve
morphology unsuitable
 Pregnancy:
 if NYHA class III/IV → PMV, o/w medical Rx w/ low-
dose diuretic & βB

75. Indications for mechanical
intervention:
heart failure sx wt MVA ≤ 1.5 or
heart failure sx wt MVA > 1.5 but ↑
PASP, PCWP, or MV w/ exercise, or∇
asx Pts wt MVA ≤ 1.5 and PHT (PASP
> 50 or 60 mmHg wt exercise) or
new-onset AF

77. Harrison, pp. 2115

78. Tricuspid Regurgitation
Etiology:
 Congenital
Ebsteins anomaly
 Rheumatic
 Right ventricular dilatation
Secondary to cardiomyopathy
Secondary to pulmonary hypertension
 Intrinsic valve disease
Endocarditis
Carcinoid syndrome

79. Clinical Features
 Systolic waves on JVP (time with carotid
pulse) therefore not v waves.
 RV+
 S3 + pasnsystolic murmur in 4th
intercostal
space
 Pulsatile liver
 Ascites
 Peripheral oedema

80. Tricuspid Regurgitation
Management
 Medical
 Valve ring

81. Mitral Valve Prolapse (MVP)

82. PATHOLOGY OF
MITRAL VALVE
PROLAPSE

83. Definition and Etiology
 Bulging of MV leaflet ≥2 mm above mitral
annulus in parasternal long axis echo view
 Leaflet redundancy from myxomatous
proliferation of spongiosa of MV apparatus
 Prevalence 1–2.5% of gen. population,
females > males; and prevalence of 5%
(OHCM, 2015)
 most common cause of MR
NEJM 1999;341:1

84. Occurrence
 Occurs alone or with; ASD, PDA,
Cardiomyopathy, Turner’s syndrome,
Marfan’s syndrome, WPW,
osteogenesis imperfecta.

85. Clinical manifestations
 usually asymptomatic
 Or
atypical chest pains
Palpitations
Symptoms of autonomic dysfunction;
○ Anxiety, panic attack, syncope

86. Physical exam
 High-pitched, midsystolic click +/- mid-
to-late systolic murmur
 ↓LV volume (standing) → click earlier; ↑ LV
volume or afterload → click later, softer
Complications:
 Mitral regurgitation
 Cerebral emboli,
 Arrythmias
 Sudden death

87. Diagnostic studies
 Echo is diagnostic
 ECG; may show inferior T-wave
inversion

89. Treatment
 Β-blockers for palpitations & chest pains
 Endocarditis prophylaxis no longer
recommended (Circ 2007:116:1736)
 Aspirin or anticoagulation if prior neurologic
event or A-fib
 Surgery in case of severe MR.

91. Prosthetic Heart Valves
 Mechanical (60%)
○ Bileaflet (eg, St. Jude Medical); tilting disk; caged-
ball
○ Characteristics: very durable (20–30 y), but
thrombogenic and require anticoagulation∴
consider if age 65 y or if anticoagulation already
indicated (JACC 2010;55:2413)

92.  Bioprosthetic (40%)
Bovine pericardial or porcine heterograft (eg,
Carpentier-Edwards), homograft
Characteristics: less durable, but minimally
thrombogenic
 consider if age 65 y, lifespan 20 y, or
contraindication to anticoagulation

93. Physical examination
 • Normal: crisp sounds, soft murmur
during forward flow (normal to have
small )∇
 • Abnormal: regurgitant murmurs, absent
mechanical valve closure sounds

94. Anticoagulation
 Warfarin
low-risk mech AVR: INR 2–3 (consider 2.5–3.5 for 1st
3 mo)
mech MVR or high-risk mech AVR: INR 2.5–3.5
high-risk bioprosthetic: INR 2–3 (and consider for 1st
3 mo in low-risk)
○ high-risk features: prior thromboembolism, AF, ↓EF,
hypercoagulable
 ASA (75–100 mg
indicated for all Pts with prosthetic valves;
avoid adding to warfarin if h/o GIB, uncontrolled HTN,
erratic INR, or 80 y
Circ 2008;118:e523

95. Correction of
overanticoagulation
 Risk from major bleeding must be weighed
against risk of valve thrombosis
 Not bleeding & INR 5: withhold warfarin, do
not give vit K, serial INRs✓
 Not bleeding & INR 5–10: withhold warfarin,
vit K 1–2.5 mg PO, serial INRs✓
 Bleeding or INR 10: FFP low-dose (1 mg) vit
K IV
Circ 2008;118:e626

96.  Endocarditis prophylaxis
Indicated for all prosthetic valves to ↓ risk of
infective endocarditis during transient bacteremia
 Complications
Structural failure
Paravalvular leak
Infective endocarditis
Embolization
Bleeding (from anticoagulants)
Hemolysis

98. What to remember
 AR & MR cause ventricular dilatation
 The duration of diastolic murmurs indicates the
severity of AR and MS.
 Intervention for AS is based on the combination
of severity with symptoms
 Intervention in AR & MR is based on symptoms
&/or evidence of left ventricular dysfunction
 The primary investigation for all valvular heart
disease is echocardiography

99. Systolic Murmurs

100. MURMURS AND THE
CARDIAC CYCLE
Aortic stenosis
Mitral Regurgitation
1 2
1 2
Mitral valve prolapse with
late regurgitation
1 2

101. Aortic stenosis vs Mitral regurgitation
Pulse BP HS Murmur Rad RV Apex
AS
Slow
rising
Low
pulse
pressure
A2 ▼
3+, 4+
Ejection Carotid N Hypertrophy
MR
Good
Volume
Normal P2▲, 3+ Pansystolic Axilla + Dilated

102. Diastolic murmurs

103. Aortic regurgitation
1 2
Mitral Stenosis
1 2
OS

104. Mitral Stenosis vs Aortic Regurgitation
Pulse BP HS Murmur Rad RV Apex
AR
Collapsing
↑pulse
Pressure
↓diastolic
pressure
A2 ▼
3+
Early
diastolic
LSE N Dilated
MS
Small
Volume
(AF)
Normal
1st
▲
P2 ▲ Mid/late
Diastolic
Axilla ++ Tapping
1st
sound

106. Asante