1. Valvular Disorders & Infecive Endocarditis1

2. Normal Valve Function Prevent backward flow of blood
Permit forward flow of blood

3. Abnormal valve function
Allows backward flow
valve is “leaky;” “regurgitant;” “incompetent”
Reduces cardiac output while increasing workload
results in inefficient pumping; greater volume of blood needs to be pumped with each beat to maintain cardiac output
“volume load”
Typically causes dilatation of the cardiac chamber
Backwards jet causes turbulence that is audible as murmur

4. Abnormal valve function
Prevents forward flow
valve does not open well
Greek stenōsis, a narrowing
Reduces cardiac output while increasing workload
Heart must develop more pressure to move blood
“pressure load”
usually results in hypertrophy of proximal (“upstream”) chamber (LA in MS, LV in AS)
acceleration of blood through tight valve causes turbulence that is audible as a murmur

5. Valvular Aortic Stenosis
failure of valve to open normally during systole, requiring LV to develop excess pressure to overcome increased resistance
pressure gradient between LV and aorta may be as much as 100 mm Hg
causes concentric hypertrophy
symptoms of exertional chest pain, syncope, dyspnea
mandate valve replacement to prevent sudden death

6. A.S : Etiology

7. Grades of AS Normal valve area 3-4 cm2 Mild AS >1.5 cm2
Moderate >1.0 cm2
Severe AS when area ¼ normal
<1 cm2 for large person
<0.75 cm2 for normal person

8. Clinical Presentation of Aortic Stenosis
Cardinal symptoms:
Angina
Occurs in >50% of patients, not sensitive due to prevalence of CAD
Reduced coronary flow reserve
Increased demand-high afterload
Syncope(exertional pre-syncope)
Fixed cardiac output
Vasodepressor response
CHF
Sudden cardiac death rare, <1% per year
Other signs of LV failure
Diastolic & systolic dysfunction
In earlier stages, AS presentation more subtle
Dyspnea
Decreased exercise tolerance
Rarely, AS diagnosed in the setting of GI bleeding
Heyde’s syndrome
Bleeding caused by AVM
Concurrent AS occurs at prevalence rate of 15-25%
Associated with an acquired von Willebrand syndrome due to disruption of vW multimers through a diseased AV

9. Rapid fall in survival once symptoms intervene

10. Physical Findings
S S S S2
Mild-Moderate Severe

11. Symptomatic AS- management
NO SAFE MEDICAL RX for Severe AS
Physical diagnosis straight forward
systolic crescendo-decrescendo murmur
loudest in aortic area usually (sometimes apex)
radiates to carotids
LV hypertrophy associated with gallop (S4)
Signs of critical AS
carotid upstrokes small and delayed in severe AS
loss of aortic component of S2
late peaking murmur

12. Management of Aortic Stenosis
Prognosis in asymptomatic disease excellent
Conservative approach with monitoring for symptoms recommended
When severe stenosis present-
38% of asymptomatic patients develop symptoms within 2 years
79% are symptomatic within 3 years
Once symptoms occur, AVR needed
LV dysfunction and severe AS have increased perioperative mortality with AVR
But outcomes still favorable with surgery
Nitroprusside may transiently improve cardiac function as a bridge to valve replacement
Does not supplant AVR in symptomatic patients

13. Aortic Valve Replacement
Prophylatic AVR in asymptomatic patients not routinely performed due to surgical risks
Thromboembolism, bleeding associated with anticoagulation, prosthetic valve dysfunction, and endocarditis
Occurs at a rate of 2-3% annually
Only should be considered:
If other cardiac surgery (such as CABG) planned
Severe LVH or systolic dysfunction
Women contemplating pregnancy
Patients remote from health care
Surgical valve replacement with operative morbidity and mortality of 10%
Percutaneous balloon aortic valvotomy rarely used

14. Aortic Regurgitation

15. Aortic Regurgitation: Etiology
Any conditions resulting in incompetent aortic leaflets
Congenital
Bicuspid valve
Aortopathy
Cystic medial necrosis
Collagen disorders (e.g. Marfan’s)
Ehler-Danlos
Osteogenesis imperfecta
Pseudoxanthoma elasticum
Acquired
Rheumatic heart disease
Dilated aorta (e.g. hypertension..)
Degenerative
Connective tissue disorders
E.g. ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome, Giant-cell arteritis )
Syphilis (chronic aortitis)
Acute AI: aortic dissection, infective endocarditis, trauma

16. Aortic Regurgitation: Symptoms
Dyspnea, orthopnea, PND
Chest pain.
Nocturnal angina >> exertional angina
( diastolic aortic pressure and increased LVEDP thus  coronary artery diastolic flow)
With extreme reductions in diastolic pressures (e.g. < 40) may see angina

17. Peripheral Signs of Severe Aortic Regurgitation
Quincke’s sign: capillary pulsation
Corrigan’s sign: water hammer pulse
Bisferiens pulse (AS/AR > AR)
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

18. Aortic Regurgitation: Physical Exam
Widened pulse pressure
Systolic – diastolic = pulse pressure
High pitched, blowing, decrescendo diastolic murmur at LSB
Best heard at end-expiration & leaning forward
Hands & Knee position
S S S1

19. Aortic Regurgitation: Natural History
Asymptomatic %/Y
Normal LV function (~good prognosis)
Progression to symptoms or LV dysfunction < 6
Progression to asymptomatic LV dysfunction < 3.5
75% 5-year survival
Sudden death < 0.2
Abnormal LV function
Progression to cardiac symptoms
Symptomatic (Poor prognosis)
Mortality > 10
TX: Medical  Surgery BEFORE LV dysfunction

20. Aortic Regurgitation
Loss of cardiac output backwards from aorta into LV
congenital, endocarditis, age, aortic disease, collagen vascular, syphillis
Early diastolic, decrescendo murmur best heard at LLSB with diaphragm
subtle, have pt lean forward, breathe out
associated with wide pulse pressure

21. Mitral Stenosis Almost always rheumatic in origin
>40% of cases of RHD result in mitral stenosis
Women affected more than men (2:1)
Presentation years after the initial episode of rheumatic fever
If infected at a young age, latent period is a few years
Murmur may be subtle, but high flow states cause increased pressure gradient, pulmonary edema
classic presentation is during vaginal delivery. Tachycardia, straining, volume increase cause pulmonary edema
Patients eventually have exertional dyspnea, atrial fibrillation (often with thromboembolism), chest pain

22. Mitral Stenosis Turbulent, high velocity flow occurs during diastole
murmur is therefore a DIASTOLIC, low frequency rumble heard at apex with stethoscope bell, patient in L lateral decubitus
requires quiet concentration, palpate carotid to time systole/diastole
Always look for MS in patient with new Atrial fibrillation
rate control, anticoagulation crucial

23. Mitral Stenosis Pathophysiology
Normal valve area: 4-6 cm2
Mild mitral stenosis:
MVA cm2
Minimal symptoms
Mod mitral stenosis
MVA cm2 usually does not produce symptoms at rest
Severe mitral stenosis
MVA < 1.0 cm2

24. Mitral Stenosis Symptoms
Fatigue
Palpitations
Cough
SOB
Left sided failure
Orthopnea
PND
Palpitation
AFib
Systemic embolism
Pulmonary infection
Hemoptysis
Right sided failure
Hepatic Congestion
Edema
Worsened by conditions that  cardiac output.
Exertion,fever, anemia, tachycardia, Afib, intercourse, pregnancy, thyrotoxicosis

25. Mitral Stenosis Physical Exam
S S2 OS S1
First heart sound (S1) is accentuated and snapping
Opening snap (OS) after aortic valve closure
Low pitch diastolic rumble at the apex
Pre-systolic accentuation (esp. if in sinus rhythm)

26. Management of Mitral Stenosis
Atrial fibrillation
Prevalence >30% in symptomatic patients and associated with poorer long term outcome
Warfarin indicated:
In patients with AF and MS
Patients without history of AF but with MS and embolic CVA
In patients with prior history of AF who have mitral valve surgery, decreased postoperative AF observed if MAZE performed concominantly

28. MS Mortality Minimal sxs >80% 10 year survival
Limiting sxs, <15% 10 year survival
Untreated patients
60-70% progressive pulmonary edema
20-30% systemic embolism
10% pulmonary embolism
1-5% endocarditis/infection

29. Mitral Regurgitation
Incompetent mitral valve allows loss of stroke volume back into LA
Mitral valve prolapse most common cause
rheumatic disease and endocarditis
PE much less subtle than MS
loud pan-SYSTOLIC murmur, loudest at apex and radiating into axilla
typically soft S1
S2 obscured by murmur
presence of S3 suggests severe MR

30. Mitral Regurgitation: Etiology
Valvular-leaflets
Myxomatous MV Disease
Rheumatic
Endocarditis
Congenital-clefts
Chordae
Fused/inflammatory
Torn/trauma
Degenerative IE
Annulus
Calcification, IE (abcess)
Papillary Muscles
CAD (Ischemia, Infarction, Rupture)
HCM
Infiltrative disorders
LV dilatation & functional regurgitation
Trauma

31. MR Symptoms Similar to MS Dyspnea, Orthopnea, PND Fatigue
Pulmonary HTN, right sided failure
Hemoptysis
Systemic embolization in A Fib

32. Mitral Insufficiency: Physical Exam
Fixed mitral regurgitation
Mitral valve prolapse
S S S1
S C S2

33. Recognizing Mitral Regurgitation
ECG:
LA enlargement
Afib
LVH (50% pts. With severe MR)
RVH (15%)
Combined hypertrophy (5%)
CXR:
 LV
 LA
 pulmonary vascularity
CHF
Ca++ MV/MAC

34. MR Treatment No medical therapy Most difficult clinically
By the time symptoms occur, it may be too late
Drop in EF or development of atrial fibrillation enough to justify surgery

35. Mitral Valve Prolapse : Epidemiology
Affects 5-10% of population
Most common cause of isolated severe MR
Females >> males; Ages of 14 and 30years
Strong hereditary component (? Autosomal Dominant)
2º to failure of apposition/coaptation of the anterior and posterior mitral valve leaflets.
Results form diverse pathologic conditions, but cause is unknown in a majority of pts

36. Mitral Valve Prolapse: Symptoms
Majority are asymptomatic for entire life
Palpitations
Chest pain (atypical).
Often substernal, prolonged, poorly related to exertion, and rarely resembles typical angina
Syncope

37. Mitral Valve Prolapse: Physical Exam
S C S2
Most important finding: mid  late systolic click.
Acute tensing of the mitral valve chordae
Variable murmurs:
high pitched late systolic crescendo-decrescendo murmur,
Occasionally “whooping” or “honking” at the apex

38. Mitral Valve Prolapse: Complications
Arrhythmias (Usually PVC, PSVT>>VT)
Transient cerebral ischemic (embolic – rare)
Infective endocarditis (if assoc w/ MR)
Sudden death (rare)

39. Tricuspid and Pulmonic Valve Disorders
Etiology/Pathophysiology/Manifestations
Tricuspid stenosis (more common than regurgitation)
Result in R. atrial enlargement > inc. systemic venous pressure > atrial fibrillation, peripheral edema, ascites, etc.
Found mostly in rheumatic heart disease, IV drug users
Pulmonic stenosis
Result in R. ventricular hypertension and hypertrophy
Fatigue , loud midsystolic murmur
Uncommon valve disorders

40. Tricuspid Valve Disease
Tricuspid stenosis is rare
Associated with rheumatic heart disease
TR usually occurs secondary to:
Pulmonary hypertension
RV chamber enlargement with annular dilatation
Endocarditis (associated with IV drug use)
Injury following pacer lead placement
Other secondary causes: carcinoid, radiation therapy, anorectic drug use, and trauma
Primary causes: Marfan’s syndrome and congenital disorders such as Ebstein’s anomaly and AV canal malformation
Echo is diagnostic in most cases

41. Tricuspid Regurgitation
Severe tricuspid regurgitation is difficult to treat and carries a poor overall clinical outcome
Symptoms are manifestations of systemic venous congestion
Ascites
Pedal edema
Surgical intervention usually considered if other cardiac surgery planned
Surgical options include valvular annuloplasty or replacement
If replacement planned, bioprosthetic valve preferred

42. Other Valve disorders:
NBTE: Non bacterial thrombotic…
Thrombus on valves – Hypercoag., DIC, Malignancy, etc.
May cause strokes, sec. bacterial infection.
Libman-Sacks:
Sterile Immune complex vegetations
SLE.
Carcinoid Heart Disease:
Carcinoid tum, 5HT, seratonins etc..
Endocardial fibrosis

43. Valvular Disease Rheumatic fever Endocarditis causes regurgitation
Regurgitation frequently present acutely
Long term predominant effect is stenosis
Endocarditis causes regurgitation
Patients with valve dz should take antibiotics prior to dental work to prevent endocarditis
All patients with symptomatic valvular disease (i.e. dyspnea, chest pain, syncope) need to be evaluated for surgical correction
Some asymptomatic subjects also need correction “before it’s too late”

44. Valvular Disease General Principles
Left sided valvular disease more prone to cause serious hemodynamic problems
Regurgitation causes volume overload- eccentric hypertrophy (dilatation)
Stenotic lesions cause pressure overload on proximal chamber- concentric hypertrophy (thickened walls)
Stenotic lesions cause symptoms sooner than regurgitant lesions but respond to therapy better

45. Common Murmurs and Timing
Systolic Murmurs
Aortic stenosis
Mitral insufficiency
Mitral valve prolapse
Tricuspid insufficiency
Diastolic Murmurs
Aortic insufficiency
Mitral stenosis
S S S1

46. Surgical Intervention
*Not all types valve disease require surgical intervention
Valvuloplasty-general term valve repair, invasive/non-invasive methods
Percutaneous balloon valvuloplasty (non-invasive)
Surgery
Open commissurotomy- open stenotic valves
Annuloplasty- repair of valve’s outer ring-used for stenosis, regurgitant valve
Valve Replacement
Mechanical-need anticoagulant
Biologic-only last about 15 years

47. Prosthetic Valve Complications
Common complications include:
Structural valve deterioration
Valve thrombosis
Embolism
Bleeding
Endocarditis
Endocarditis prophylaxis required for patients with all types of prosthetic valves
Suspect valve dehiscence or dysfunction in:
Acute CHF in the immediate postop period
New cardiac symptoms
Embolic phenomena
Hemolytic anemia
New murmurs
TEE is the diagnostic procedure of choice
Postop TTE should be done 2-3 months after surgery

48. 1997 American Heart Assoc. Guidelines:
Endocarditis Prophylaxis Recommended: 1997  
High-risk category      
Prosthetic cardiac valves, including bioprosthetic and homograft valves      
Previous BE     
Complex cyanotic congenital heart disease (eg, single ventricle states, transposition of the great arteries, Tetralogy of Fallot)      
Surgically constructed systemic pulmonary shunts or conduits   
Moderate-risk category :1997     
Most other congenital cardiac malformations (other than above and below)     
Acquired valvar dysfunction (eg,RHD)      
HOCM      
MVP with valvar regurgitation and/or thickened leaflets
Memorize this table. Kidding.

49. Endocarditis Prophylaxis Not Recommended:
Negligible-risk category : 1997
(No greater risk than the general population)     
Isolated secundum atrial septal defect      
Surgical repair ofASD,VSD, or (without residua beyond 6 mo)      
Previous CABG      
MVP without valvar regurgitation1      
Physiologic, functional, or innocent heart murmurs1     
Previous Kawasaki disease without valvar dysfunction     
Previous rheumatic fever without valvar dysfunction     
Cardiac pacemakers (intravascular and epicardial) and implanted defibrillators

50. 2007: Who gets prophylaxis?
Only patients with the highest risk of adverse outcomes (heart failure, surgery, death) from endocarditis:
1. Prosthetic cardiac valve
2. Previous IE
3. Cardiac transplant recipients who develop cardiac valvulopathy
4. Congenital Heart Disease
This is the “HIGH” risk category from 1997

51. Which categories of Congenital Heart Disease?
Unrepaired cyanotic CHD
Tetralogy of Fallot, Transposition of Great Arteries, including palliative shunts and conduits
Completely repaired congenital heart defect with prosthetic material or device during 1st 6 months after surgery
Repaired CHD with residual defects at or near a prosthetic patch/device (which inhibit endothelialization)

52. What about “Moderate-Risk” Pts?
1997’s “Moderate Risk” Category NO LONGER gets prophylaxis:
MVP with regurg and/or thickened leaflets
Hypertrophic cardiomyopathy
Acquired Valvular Dysfunction (RHD)

53. Dental Procedures “If it bleeds, give prophylaxis”
High-risk pts undergoing all dental procedures that involve manipulation of gingival tissues OR periapical region of teeth OR perforation of oral mucosa
i.e. biopsies, suture removal, placing orthodontic bands
NO PROPHYLAXIS:
Xray, anesthetic injections, fluoride treatments
Shedding of deciduous teeth
Placement/adjustment of removable prosthodontic or orthodontic appliances
“quote” from Vance Fowler, IE expert at Duke, IDSA review course 9/08

54. Prophylaxis for Dental Procedures
Goal: cover Strep Viridans
Single dose, min prior to procedure PO
Amoxicillin 2g
PO, PCN-allergic
Cephalexin 2g
OR Clinda 600mg OR Azithro 500mg
**Don’t use Cephalexin if anaphylaxis, angioedema, or urticaria w/PCNs or ampicillin
IV:
Ampicillin 2gm IV/IM
OR Cefazolin 1g IV/IM OR Ceftriaxone 1g IV/IM
IV, PCN-allergic
Cefazolin 1g IV/IM
OR Ceftriaxone 1g IV/IM OR Clinda 600mg IV/IM

55. Summary: IE prophylaxis
Need high-risk pt PLUS high-risk procedure
High-risk pts:
1. Prosthetic cardiac valve
2. Previous IE
3. Cardiac transplants w/ valvulopathy
4. Congenital Heart Disease
High-risk procedures:
Dental: “If it bleeds, give prophylaxis”
Respiratory: Consider if pt will be cut or biopsied
GI/GU: never

56. No Prophylaxis Endotracheal intubation Cardiac cath/stent
Pacer/ICD implantation
EGD, Colonoscopy
Barium Enema
TEE
Incision/Bx of surgically scrubbed skin
Circumcision
Vaginal delivery
Hysterectomy

57. Endocarditis Prophylaxis : 2007

58. Endocarditis Etiology Clinical Treatment
damaged valve (RHD) exposed to bacteria in blood stream
S. viridans, S. aureus
Clinical
acute, subacute, chronic
fever, murmur, ESR
(+) blood cultures
Treatment
antibiotic according to organism
future prophylaxis for procedures

59. Endocarditis Classification
Acute
Virulent! Staph aureus, GNR
Normal valves
Acute course with rapid valve destruction, HF
Subacute (SBE)
Strep, Enterococcus, Staph epi
Underlying cardiac dz
More indolent presentation: low-grade fever, murmur
Native valve, addict, prosthetic valve, culture-neg
OLD classification is acute vs subacute; NEW is native/prosthetic...

60. Septic Emboli
Osler's Nodes: Painful, erythematous nodules associated with bacterial endocarditis.
4 P’s:
Pink
Painful
Pea-sized
Pulp of fingers/toes
Splinter Hemorrhages: in the nail bed.
Roth Spots

61. Janeway Lesions
Nontender, erythematous, hemorrhagic or pustular lesions on palms, soles

62. Petechiae Not specific for IE but common Splinter Hemorrhages
Linear, under nailbeds
Conjunctival Petechiae
Hemorrhages on eversion of eyelid
Petechiae are not specific for IE but are its most common skin manifestation. They may be present on the skin, usually on the extremities, or on mucous membranes such as the palate or conjunctivae, the latter usually as hemorrhages best seen with eversion of either upper or lower eyelids.

63. Prosthetic Valve Endocarditis
Risk of IE
1% at 12 mos, 2-3% at 60 mos post-op
EARLY: < 2 months post-op
#1 cause: Staph aureus (used to be staph epi)
Usually acquired in the hospital: direct intra-op contamination or post-op hematogenous spread
Anchoring sutures and valve ring are not yet endothelialized, so more vulnerable
LATE: > 2 months post-op
Endothelialization occurs over months, making it more difficult for bugs to adhere. Community-acquired.

64. IVDU Classic teaching: IVDU  Right-sided IE 50% Staph Aureus
But left-sided IE may actually be more common
50% Staph Aureus
15% Enterococcus
8% each: Strep, GNR (Pseudomonas or Serratia), Candida
May be polymicrobial

65. TTE vs TEE TTE: TEE: 98% Specificity for veg
Sensitivity <60%; less in obesity, COPD
Begin with TTE if pt is good candidate for imaging surface, has native valves, or has low probability of IE
TEE:
Invasive, costly
Sens 75-95%, Spec 85-98%. Neg TEE: NPV >92%
Consider for pts w/prosthetic valves, high probability of endocarditis, and to evaluate myocardial abscess, perivalvular extension

66. Diagnosis of IE Fever, new murmur or heart failure, bacteremia
Systemic findings of emboli
Neurologic impairment
ECG
New AV block or BBB suggests perivalvular invasion
CXR
Septic pulmonary emboli

67. Definite IE: 2 major, 1 major + 3 minor, or 5 minor
Major Duke’s Criteria
Definite IE: 2 major, 1 major + 3 minor, or 5 minor
(+) Blood cultures with appropriate organism
Evidence of Coxiella burnetii infection
New Valvular regurgitation
+ Echo findings

68. Minor Duke’s Criteria High-risk for IE, or h/o IVDU
Temperature > 38oC
Vascular Phenomena
Arterial embolism, septic pulm infarcts, mycotic aneurysm, intracranial hemorrhage, Janeway lesions
Immunologic phenomena
Osler’s nodes, Roth spots, GN, Rheumatoid factor
Serologic studies
Blood cultures or echo results not meeting the major criteria

69. Therapy: General comments
Prolonged IV administration of bactericidal agents(s) x 4-6 wks
Culture-negative native-valve endocarditis should be individualized and generally includes penicillin, ampicillin, ceftriaxone, or vanc, +/- aminoglycoside

70. Indications for Surgery
Refractory CHF, Severe valvular dysfunction
Uncontrolled infection
Valve perforation, dehiscence, fistula, abscess
1 embolic event with persistent large vegetation, or >1 episode of embolization
Prosthetic valve infection
Fungal IE
New heart block…
Mortality 56-86% vs 11-35% for medical vs medical/surgical tx.
Pathogens
Pseudomonas, brucella, coxiella, candida, fungi, resistent enterococci
Staph aureus prosthetic valve infection
Some authorities recommend surgery if two episodes of embolization or one episode with residual large vegetations.

71. Conclusions
Valvular heart disease associated with spectrum of presentations
Recognition prior to the onset of symptoms may be life saving
Careful physical exam almost always diagnostic

72. “Pearls”
Diastolic murmurs usually represent pathological conditions as do most continuous murmurs.
Most important issue in patient with a cardiac murmur is the presence or absence of symptoms.
Many asymptomatic children and young adults with grade 2/6 midsystolic murmurs and no other cardiac physical findings need no further cardiac evaluation
Many asymptomatic elderly patients have midsystolic murmurs related to sclerotic aortic valve leaflets, flow into tortuous, noncompliant great vessels
Such murmurs must be distinguished from murmurs caused by mild to severe valvular aortic stenosis (AS) which is prevalent in this age group.