1. Valvular Heart Disease
ADRIEL E. GUERRERO, MD, FPCP, FPCC
Training Officer
Section of Cardiology, Dept of Medicine
The Medical City

2. Mitral Stenosis

3. Diagnostic Features of MS@
2/3 are females; Pure MS are generally rheumatic
History:
Exertional Dyspnea, PND, Orthopnea and Hemoptysis
PE:
Opening snap, loud S1, diastolic rumble at the apex
ECG and Chest Xray:
Evidence of left atrial enlargement with normal left ventricular size; RVH in later stages
2DECHO

4. Chest Xray MS

5. Common Etiologies of MS
Rheumatic Heart Disease
Congenital Heart disease
Congenital MS
Lutembachers syndrome (MS and ASD)
Mitral Annular Calcification (elderly)

7. Mitral Stenosis@ Pathophysiology Obstruction to LV filling
Increase LA pressure
RV Failure

8. Natural History of MS Pulmonary Hypertension Thrombi and Emboli
Fibrous thickening of alveolar and pulmo capillary walls
Thrombi and Emboli
Left atrial appendage
Increased: AF, older patients, reduced CO
Pulmonary Infections, IE,

9. Natural History of Mitral Stenosis
MS - blue
MR - purple

10. Differential Diagnosis of MS
Atrial Septal Defect
RVE and accentuated pulmo markings
Widely split S2 (fixed)VS Opening snap; diastolic flow across the TV
No LAE
Left Atrial Myxoma
Obstructing LA emptying, tumor-plop
Mitral Regurgitation
Systolic murmur; LVH
Aortic Regurgitation (Austin Flint)
Apical middiastolic murmur of AR. Becomes louder on handgrip and decreases with amyl nitrate 

11. Treatment of MS
Penicillin Prophylaxis of B-hemolytic Streptococcal Infections to prevent Rheumatic Fever and IE
Sodium restriction, oral diuretics
Oral Anticoagulation (Warfarin)
INR target (embolization, permanent AF)
Heart Rate Controlling drugs
To lengthen diastolic LV filling
Digitalis in Atrial Fibrillation; Beta-blockers in sinus rhythm
Nondihydropyridine Calcium Antagonists

12. Mitral Valvotomy
Indicated in symptomatic patients with isolated MS (<1.0 cm2/m2)
Ideal for mobile, thin leaflets with no or little calcium without extensive subvalvular thickening and with no or mild MR
Open valvotomy – mortality rate is 2%
50% of all patients require reoperation by 10 years.
Pregnant – carried out if pulmonary congestion occurs despite intensive medical treatment

13. Mitral Valve Replacement
MS with significant MR
Distorted valves from previous transcatheter or operative manipulation
Operative Mortality is 6%
Long term complications of valve replacement
Overall 10 year survival is 70%
Poor Recovery
Old patients
Marked disability
Depressed Cardiac index

14. Mitral Stenosis

15. Percutaneous Trans-septal Mitral Commissurotomy

16. Star Edwards Caged Ball Valve

17. Medtronic Hall Valve (Bjork-Shiley)

18. St Jude Bileaflet Valve

19. Carpentier Edwards Porcine Valve

20. Carpentier Edwards Pericardial Valve

21. Mitral Regurgitation Frequent in males History: PE:
Easy Fatigue then exertional Dyspnea
PE:
Characteristic holosystolic murmur at the apex with radiation to the axilla

22. Common Etiologies of MR
MV leaflet abnormality
Rheumatic heart disease
Myxomatous alteration (including MVP)
Infective Endocarditis
Mitral annulus dilatation of any cause
Dilated Cardiomyopathy
IHD with dilated LV
Ruptured chordae tendinae
Trauma
Myocardial Infarction
Papillary muscle disorder
Ischemic Heart Disease

23. Mitral Regurgitation

24. NORMAL

25. Pathophysiology of Mitral Regurgitation

26. Pathophysiology of Mitral Regurgitation

27. Pathophysiology of Mitral Regurgitation

28. Laboratory Examination
La enlargement; RAE maybe present if pulmonary HPN is severe
Atrial Fibrillation
LVH
ECG
2DECHO – most accurate non-invasive technique
CXR – LAE and LVE

29. Medical Treatment for MR
Restrict Physical activities
Reduce sodium intake and enhance sodium excretion (diuretics)
Increase forward cardiac output
Vasodilators (ACEI) and digitalis
Anticoagulants and leg binders to decrease likelihood of venous thrombi and pulmonary emboli
Endocarditis prophylaxis

30. Surgical Treatment of MR
Non-surgical candidates: asymptomatic, or exercise limited to strenuous exertion, normal LV function
Surgery for severe MR even if asymptomatic or when LV dysfunction is progressive (declining <60%) and/or LV ESD on echo is >45mm
MV replacement for markedly shrunken, deformed, calcified leaflets
MV repair (reconstruction) with annuloplasty
Lessens problem on long term anticoagulation and thromboembolism
For ruptured chordae, annular dilatation and IE
Not suitable for Mr due to myxomatous degeneration and patients with calcified annulus

31. Natural History of Unoperated MR

32. Late Survival Rates after Surgical Correction in MR (pre-op EF)

33. Mitral Valve Prolapse
Barlow’s syndrome, floppy-valve syndrome, systolic click-murmur syndrome, billowing mitral leaflet syndrome
Excessive or redundant mitral leaflet tissue. Posterior MV leaflet is more affected than the AMVL
May lead to excessive stress on the papillary muscles leading to dysfunction. Rupture of chordae tendineae with progressive annular dilatation and calcification
Ventricular arrythmias

35. Clinical Features Females (14-30 years old)
Clinical course is often benign
Increased familial incidence – autosomal dominant
Most common cause of isolated severe MR requiring surgical treatment in North America
Arrythmias (PVCs, SVTs, VTs) – palpitations, lightheadedness and syncope. Sudden death is rare
Chest pain substernal, prolonged, unrelated to exertion

36. Mitral Valve Prolapse
Mismatch between elongated MV and LV cavity

37. Laboratory Exams ECG – non specific STTW changes, PVCs
Echo – demonstrates systolic displacement of MVL and quantifies Mitral Regurgitation and LV function

38. Treatment of MVP IE prophylaxis
Beta-blockers sometimes relieve chest pain
For severe symptomatic MR, MV repair or rarely replacement is indicated
Antiplatelets for patients with TIA, anticoagulation if recurrent TIAs

40. Survival Rates of MVP patients at baseline risk factors
Primary Risk Factors
Mod-severe MR; EF <50%
Secondary Risk Factors
Mild-mod MR; LA > 40
Flail leaflet; AF; age > 50

41. Aortic Stenosis 80% with symptomatic AS are males
Age-related degenerative calcific AS – most common cause of AS in Adults

42. Common Etiologies of AS
Valvular (90% of all cases)
Rheumatic heart disease
Degenerative calcification (elderly)
Bicuspid AV stenosis/ Congenital heart disease
Subvalvular (9%)
Hypertrophic Obstructive Cardiomyopathy (HOCM)
Discrete
Supravalvular (<1%)
Infancy

43. NORMAL AORTIC VALVE

44. Aortic Stenosis - Rheumatic

45. Aortic Stenosis - Degenerative

46. Aortic Stenosis - Bicuspid

47. Pathophysio of AS

48. Pathophysio of AS

49. Aortic Stenosis History: PE Cardinal symptoms
Exertional Dyspnea
Angina Pectoris
Syncope PE
Carotid upstroke slowly rising and reduced in amplitude in severe cases; Systolic ejection murmur radiating to the carotid arteries

50. Laboratory Exam LV hypertrophy is the key finding ECG
2DECHO – estimate valve area, LV size and function
Cardiac catheterization
Presence or absence of concomittant CAD

51. Natural History of Severe AS
Death most commonly occurs in the 7th and 8th decade
Average time from onset of symptoms to death:
Angina – 3 years
Syncope – 3 years
Heart Failure – 1.5 – 2 years
Sudden death 10-20% in AS patients 60 years old and above

52. Medical Treatment for AS
Severe AS (<0.5 cm2/m2)Avoid strenuous physical activities even if asymptomatic
Sodium restriction
Cautious administration of diuretics and digitalis in CHF
Nitroglycerin to relieve angina
Statins (HMGCoA reductase inhibitors) slows down progression of calcification (?)
No effect on long term survival

53. Surgery in Aortic Stenosis
Indications for Surgery
Severe Aortic Stenosis ( < 0.6 cm2/m2)
Symptomatic with LV dysfunction (LV Ejection Fraction <50%)
Expanding poststenotic aortic root (even if asymptomatic)
Those who undergo CABG even if asymptomatic
Operative risk of Aortic Valve Replacement in asymptomatic severe AS is 4%. In frank CHF – 15 – 20%
10 year survival rate of patients with AVR = 60%
30% of bioprosthesis fail in 10 yrs
Mechanical prosthesis – hemorrhage fm anticoagulation

54. Management Strategy for Severe Aortic Stenosis

55. Percutaneous Balloon Aortic Valvuloplasty
Preferred in children and young adults with congenital, noncalcific AS
High “restenosis” rate in calcific AS
“bridge to operation”

56. Percutaneous Transcatheter Placement of AV prosthesis

57. Percutaneous Transcatheter Placement of AV prosthesis

60. Aortic Regurgitation Etiology
Primary Valve Disease
Rheumatic – 2/3 of patients
Infective Endocarditis
Trauma
Bicuspid valve
Primary Aortic Root Disease
Degenerative heart disease
Syphilis
Marfan’s syndrome
Ankylosing Spondylitis
Aortic Aneurysm with dissection
Systemic hypertension
Giant Cell arteritis

61. Pathophysio of AR

62. Aortic Regurgitation History: PE:
Easy fatigue then exertional dyspnea (diminished cardiac reserve) – orthopnea, PND and excessive diaphoresis
PE:
Wide pulse pressure with bounding pulses
Diastolic decresendo murmur at the base of the heart
Midsystolic ejection murmur at base of the heart
Austin Flint murmur – soft, low pitched rumbling middiastolic bruit at the apex

63. Peripheral Signs of Chronic AR
Corrigan’s pulse: Pulses with abrupt distension and quick collapse; water hammer pulse
De Musset’s sign: head bobbing
Traube’s sign: Pistol shot sound on the femoral artery
Duroziez’s sign: Systolic murmur heard over the femoral artery when compressed proximally
Muller’s sign: systoic pulsation of the uvula
Quincke’s sign: Capillary pulsation
Hill’s sign: Popliteal cuff SBP > brachial cuff SBP by 60mmHg

64. Differential Diagnosis of a Bounding Pulse
Cardiac Causes
Aortic Regurgitation
Patent Ductus Arteriosus
Non-Cardiac Causes
Arteriovenous Fistula
Fever
Thyrotoxicosis
Pregnancy

65. Symptomatology in AR
Symptoms depend on the onset of AR (acute/chronic)
Compensatory mechanisms
LV dilatation
Laplace Law ( myocardial wall tension = intracavitary pressure x LV radius)
Deterioration of LV function precedes the development of symptoms
Chronic Severe AR may have a long latent period. Patients remain asymptomatic for as long as years.

66. Laboratory Exam LV Hypertrophy
2DECHO + myocardial contractility and function
Cardiac catheterization and angiography
Magnitude of AR and status of LV function

67. Survival without Surgery in Chronic AR

68. Medical Treatment of AR
Salt restriction
Diuretics
Vasodilators (ACEI)
Nitrates not as helpful in relieving angina
Syphilitic aortitis – penicillin tx

69. Surgical Treatment of AR
Definitive treatment
Should be done before development of Heart Failure
Operation should be carried out even in Asymptomatic patients with progressive LV dysfunction and a left Ventricular Ejection Fraction < 55% or a LV end-systolic volume > 55 mL/m2 ( 55/55 rule)
AVR – mechanical or bioprosthesis
Operative mortality for isolated AVR is 4.3%
Patients with marked LVE and dysfunction
OR mortality 10%
Late operative mortality 5% per year

70. Post-operative Survival in AR

71. Post-operative Survival in AR

72. Tricuspid Stenosis

73. Treatment of TS Medical Tx Surgical Tx
Intensive salt restriction, diuretic tx
Surgical Tx
Definitive tx
Diastolic pressure gradient >4 mmHg
Tricuspid orifice < 1.5 to 2.0 cm
Open heart repair/prosthesis (preferably large bioprosthetic valve)

74. Tricuspid Regurgitation

75. Treatment Considerations in TR
Isolated TR, in the absence of Pulmo HPN, is well tolerated and does not require operation
Functional TR (secondary to PHPN with MV disease) resolves with effective correction of the MV disease)
- annuloplasty
TVR for severe valve deformity

76. Pulmonic Valve Disease
Pulmonic Regurgitation – most common acquired abnormality of the PV secondary to dilatation of the PV ring as a consequence of PHPN
Graham Steell murmur (high pitched decresendo, diastolic blowing murmur along the left sternal border- like AR)
Of little hemodynamic significance.

77. Ex.1 Patient has MS mild, AS severe, MR mild
Four Guidelines to Follow in Assessing Patients with Multiple Valvular Abnormalities
Guideline 1: Determine the Predominant Lesion
A. The most severe lesion is usually the predominant lesion
Ex.1 Patient has MS mild, AS severe, MR mild
Ans. AS is the dominant lesion
B. The lesion that causes the most corresponding chamber enlargement is usually the predominant lesion
Ex.2 Patient has AR moderate, MS moderate, Severely dilated LV, slightly dilated LA
Ans. AR is the predominant lesion

78. Guideline No. 2: Left-sided lesions are more important that right-sided lesions. Therefore tailor your treatment more for the left-sided lesion.
Guideline No. 3: Significant stenotic lesions (MS or AS) should be given more serious attention compared to regurgitant lesions (MR or AR)
Guideline No. 4: In severe valvular disease, surgical correction of the mechanical defect should be given prime consideration. Response to medical treatment is poor.

79. THANK YOU!!!