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Overview. Clinical syndromesOverview of cardiac murmurs and maneuversLeft sided valvular lesionsAortic stenosis and sclerosisMitral stenosis Rheumatic fever prophylaxisAcute and chronic aortic regurgitationAcute and chronic mitral regurgitationRight sided valvular lesionsTricuspid valve diseaseProsthetic valvesEndocarditis prophylaxisQuestions.
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1. Valvular Heart Disease and the Cardiac Exam Charlotte Bai, M.D.
Internal Medicine Board Review
May 28, 2009
2. Overview Clinical syndromes
Overview of cardiac murmurs and maneuvers
Left sided valvular lesions
Aortic stenosis and sclerosis
Mitral stenosis
Rheumatic fever prophylaxis
Acute and chronic aortic regurgitation
Acute and chronic mitral regurgitation
Right sided valvular lesions
Tricuspid valve disease
Prosthetic valves
Endocarditis prophylaxis
Questions
3. General Appearance Marfan Syndrome
Tall, long extremities
Associated with: aortic root dilitation, MV prolapse
Acromegaly
Large stature, coarse facial features, “spade” hands
Associated with: Cardiac hypertrophy
Turner Syndrome
Web neck, hypertelorism, short stature
Associated with: Aortic coarctation, pulmonary stenosis
Pickwickian Syndrome
Severe obesity, somnolence
Associated with: Pulmonary hypertension Fredreich ataxia
Lurching gait, hammertoe, pes cavus
Associated with: hypertrophic cardiomyopathy
Duchenne type muscular dystrophy
Pseudohypertrophy of the calves
Cardiomyopathy
Ankylosing spondylitis
Straight back syndrome, stiff (“poker”) spine
Associated with: AI, CHB (rare)
Lentigines (LEOPARD syndrome)
Brown skin macules that do not increase with sunlight
Associated with: HOCM, PS
4. “Spade” hands in acromegaly
5. General Appearance- 2 Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
Small capillary hemangiomas on the face or mouth
Associated with: Pulmonary arteriovenous fistula
Lupus
Butterfly rash on face, Raynaud phenomenon- hands, Livedo reticularis
Associated with: Verrucous endocarditis, Myocarditis, Pericarditis
Pheochromocytoma
Pale diaphoretic skin, neurofibromatosis- café-au-lait spots
Associated with: Catecholamine-induced secondary dilated CM Sarcoidosis
Cutaneous nodules, erythema nodosum
Associated with: Secondary cardiomyopathy, heart block
Tuberous Sclerosis
Angiofibromas (face; adenoma sebaceum)
Associated with: Rhabdomyoma
Myxedema
Coarse, dry skin, thinning of lateral eyebrows, hoarseness of voice
Associated with: Pericardial effusion, LV dysfunction
6. Grading the Intensity of Cardiac Murmurs Grade 1
Murmur heard with stethoscope, but not at first
Grade 2
Faint murmur heard with stethoscope on chest wall
Grade 3
Murmur hears with stethoscope on chest wall, louder than grade 2 but without a thrill
Grade 4
Murmur associated with a thrill
Grade 5
Murmur heard with just the rim held against the chest
Grade 6
Murmur heard with the stethoscope held away and in from the chest wall
7. Cardiac Murmurs Most mid systolic murmurs of grade 2/6 intensity or less are benign
Associated with physiologic increases in blood velocity:
Pregnancy
Elderly
In contrast, the following murmurs are usually pathologic:
Systolic murmurs grade 3/6 or greater in intensity
Continuous murmurs
Any diastolic murmur
9. Diagnostic Testing ECHOCARDIOGRAM
Exercise testing
To assess the clinical severity of valvular heart disease
Those with inconsistent resting hemodynamics
Equivocal history of symptoms
Exercise testing in AS patients
Should be ended promptly if:
Cardiac symptoms provoked
Decrease or minimal increase (<20 mmHg) in blood pressure
Prior history of angina, congestive heart failure, or exertional syncope absolute contraindications to exercise testing
Cardiac catheterization
Usually not needed for primary evaluation
10. Aortic Stenosis Most common cause is calcific degeneration
Active disease process with risk factors of male sex, smoking, HTN, DM, older age, hypercholesterolemia
2% of the general population have bicuspid aortic valves
Symptomatic or severe AS occurs earlier (age 40-60 years)
AS less commonly from rheumatic heart disease valvulitis
Invariably MV involved first
Associated AV involvement in <1/2 patients
AV sclerosis
Valve thickening without obstruction
Present in >20% of people >65 years
Associated with 50% increased risk of MI and CV death
11. Progression of Aortic Sclerosis Hemodynamic progression usually slow
Average rate of increase in aortic jet velocity of 0.3 m/s per year
Increase in mean transaortic gradient of 7 mmHg
Decrease in AVA of 0.1 cm2 per year
Severe AS
Aortic jet velocity > 4 m/s
Mean transvalvular pressure gradient > 50 mmHg
AVA < 1.0 cm2
12. Pathophysiology of Aortic Stenosis Obstruction of LV outflow increases intracavitary systolic pressures and leads to LV pressure overload
Initial compensatory mechanism is myocardial hypertrophy with preservation of systolic function
Diastolic function impaired as a consequence of increased wall thickness and abnormal myocardial relaxation
Increased wall stress and afterload causes eventual decrease in ejection fraction
13. Pseudostenosis Occurs in patients with impaired systolic function and aortic stenosis
Unable to generate transvalvular gradient
Careful diagnostic testing with dobutamine infusion protocols can aid in differentiating between true AS and pseudostenosis
If the calculated AVA increases with augmentation of cardiac output, then pseudostenosis present
If AVA does not increase with dobutamine, then obstruction fixed and true AS present
14. Clinical Presentation of Aortic Stenosis Cardinal symptoms:
Angina
Occurs in >50% of patients, not sensitive due to prevalence of CAD
Syncope
CHF
Sudden cardiac death rare, <1% per year
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
15. 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
17. 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
18. Mitral Stenosis Usually associated with history of rheumatic fever
>40% of cases of RHD result in mitral stenosis
Women affected more than men (2:1)
Presentation 20-40 years after the initial episode of rheumatic fever
If infected at a young age, latent period is a few years
19. Clinical Presentation of Mitral Stenosis Significant MS leads to ?LA pressure and pulm HTN
Symptoms include dyspnea with ? cardiac demand
Exercise
Pregnancy
Survival excellent with asymptomatic or minimally symptomatic patients
>80% survival at 10 years
Survival in symptomatic patients much worse
10 year survival drops to 15% or lower (if pulm HTN present)
Findings consistent with severe MS:
Transvalvular diastolic pressure gradient >10 mmHg
MVA <1.0 cm2
Severe pulmonary hypertension (>60 mmHg)
20. 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
21. Mitral Valve Repair Percutaneous valvotomy
Therapeutic intervention of choice if:
LAA thrombus excluded
MR less than moderate
Valvular characteristics favorable
Pliable leaflets, minimal commisural fusion, minimal valvular or subvalvular calcification
Pulmonary HTN not contraindication to valvotomy
Major complications include: severe MR (1-8%), systemic embolization (1-3%), and tamponade (1-2%)
Periprocedural mortality- 1%
Surgical commissurotomy or MVR can be performed in unfavorable anatomy
23. Rheumatic Fever Prophylaxis Primary prophylaxis
If living in an endemic area, with pharyngitis and a +test for group A strep or positive throat culture
Given once, may be repeated as needed:
PCN G 1.2 million U IM or PCN V 500 mg TID x 10d
Azithromycin 500 mg on day 1, 250 mg daily for 4d
Secondary prophylaxis
PCN G 1.2 million units IM every 4 weeks or PCN V 250 mg PO BID or erythromycin 250 mg BID
RHD without carditis- At least 5 years or until >21 y of age
RHD with carditis, no valvular HD- At least 10 y or well into adulthood
RHD with carditis and valvular HD- At least 10 years from last episode or until patient is older than 40 years
24. Acute Aortic Regurgitation Causes of acute aortic regurgitation:
Aortic dissection
Valve distruction from endocarditis
Traumatic rupture
Classic physical exam findings may be absent in the acute presentation
Diastolic murmur may not be present due to sudden increase of LVEDP
TTE, along with TEE, cath, CT or MRI may be used for diagnosis
Surgical AV repair or replacement should be performed emergently
Afterload reducing medications and inotropes may help to acutely stabilize the patient
IABP contraindicated
25. Acute Mitral Regurgitation Most often occurs in:
Chordae tendineae rupture due to myxomatous valve disease or endocarditis
Myocardial infarction with papillary muscle dysfunction or rupture
Symptoms almost always occur
Dyspnea and pulmonary edema
Systolic function may occur normal or hyperdynamic
IABP or afterload reducing drugs to temporize
Surgical intervention for treatment
26. Chronic Valvular Regurgitation Cardiac chamber size and function have time to compensate for dysfunction
May allow patients to remain asymptomatic for a long time
Both preload and afterload increases
Once increase in cardiac output insufficient? systolic function declines ? pulmonary HTN may develop and symptoms develop
LV enlargement and progressive systolic dysfunction are associated with significant morbidity and mortality
Serial echocardiography and evaluation by a cardiologist is indicated
27. Chronic Aortic Regurgitation Occurs most often in bicuspid AV
Other causes include ascending aortic aneurysm and Marfan’s Disease
Risk factors for poorer outcome:
Age
Cardiac symptoms
Atrial fibrillation
LV enlargement
Lower LVEF
Asymptomatic patients with normal LV size and function do not require prophylatic surgery
Surgery should be considered if:
LVESD > 55 mm
Ejection fraction <60%
Symptoms develop
Oral afterload reduction (nifedipine or ACE-I) may slow rate of LV dilation
29. Chronic Mitral Regurgitation Often caused by myxomatous disease or MVP
Myxomatous mitral valve disease with progressive MR associated with poor long term outcome
Higher risk of arrhythmias and sudden cardiac death
Mitral valve prolapse occurs in ~2% of the general population
Consists of the buckling of the mid portion of the valve leaflets into the LA
Usually asymptomatic, but may be associated with palpitations or chest discomfort
Prognosis usually benign
Antibiotic prophylaxis now not indicated
30. Chronic Mitral Regurgitation Other causes include secondary or acquired leaflet dysfunction
Endocarditis
Rheumatic heart disease
Annular tethering from LV dilation
Tethering of the chordal apparatus from ischemic heart disease
Rare cause: Fenfluramine and phentermine, also associated with AI
Compensatory increase in LV chamber size initially allows for increase in total stroke volume and restoration or total forward cardiac output
31. Treatment of Chronic Mitral Regurgitation Mitral valve repair preferred over mitral valve replacement
Avoids risk of anticoagulation
Preservation of subvalvular apparatus
Better postoperative LV function and long term survival
When MR occurs in volume overloaded states, afterload reduction can be beneficial
Dilated CM
CAD
Revascularization may improve dysfunction of the papillary muscle
Biventricular pacing may improve LV geometry
33. Timing of Intervention for Left-Sided Valvular Conditions
34. 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
35. 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
36. Prosthetic Valves- Mechanical Three types:
Ball-cage valve
Single tilting disk valve
Bileaflet valve
Durable but require life long anticoagulation
For operative procedures, warfarin typically is discontinued for 48-72 hours and restarted postop as soon as possible, except for:
Mechanical mitral prosthesis
Atrial fibrillation
Prior thromboembolic events
38. Prosthetic Valves- Biological Biological Valves
Composed of autologous or xenograft biological material mounted on stents and a sewing ring
Warfarin therapy not required due to lower thromboembolic potential
Valve durability less when compared to mechanical valves
Newer stentless valves with increased longevity
39. Anticoagulation Guidelines for Mechanical Valves
40. 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
41. Valve Thrombosis Incidence with mechanical prosthesis of 2-4 % per year
Suspect in patients with new murmur, change in cardiopulmonary symptoms, or an embolic event
Diagnosis based on clinical presentation, TTE/TEE, and fluroscopy
In small thrombus, treatment with heparin may be adequate
Optimal treatment for left sided thrombosis is emergency surgery
Consider thrombolytic therapy for right sided thrombosis or if surgery cannot be performed with left sided disease
42. Endocarditis Prophylaxis