cardiac valve replacement surgery

7/28/2019 Cardiac Valve Replacement Surgery

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Cardiac Valve Replacement

Surgery

Jane Hallam

RMH


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3

ACC/AHA definition:ACC/AHA definition:

Classification of recommendationsClassification of recommendations

IIIIIbIIaI

? Class I: Conditions for which there is evidence for

and/or general agreement that a given procedure or

treatment is beneficial, useful, and effective

? Class II: Conditions for which there is conflictingevidence and/or a divergence of opinion about the

usefulness/efficacy of a procedure or treatment

Class IIa: Weight of evidence/opinion is in favor ofusefulness/efficacy

Class IIb: Usefulness/efficacy is less well established byevidence/opinion

? Class III: Conditions for which there is evidence and/or

general agreement that a procedure/treatment is not

useful/effective and in some cases may be harmful

Class:

Hirsch AT et al. Available at: http://www.acc.org/clinical/guidelines/pad/summary.pdf. Accessed March 22, 2006.


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ACC/AHA definition:ACC/AHA definition:

Level of evidenceLevel of evidence

?Level of evidence A: Data derived from multiple

randomized clinical trials or meta-analyses

?Level of evidence B: Data derived from a single

randomized trial or nonrandomized studies

?Level of evidence C: Only consensus opinion of

experts, case studies, or standard of care

A

B

C

Hirsch AT et al. Available at: http://www.acc.org/clinical/guidelines/pad/summary.pdf. Accessed March 22, 2006.


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Indications for Surgery

Aortic Valve

Stenosisresults from thickening, calcificationand/or fusion. Younger pt congenital bicuspid, older pt

degenerative changes. Impairment opening, pressureoverload, LVH, reduced ventricular compliance.

Grading - N 2.5-3.5, mild (AVA >1.5 cm2), moderate(AVA =1.01.5), severe (AVA


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Average survival symptomatic AS 2-3 yrs.

Traditional indications presence of angina, CHF, syncope,resuscitation after cardiac arrest.

Surgery in asymptomatic controversial. Presence of LVsystolic dysfunction, hypotension response exercise, VT

or LVH (>15mm), transvalvular peak gradient >50mmHg are poor prognostic signs, consider earlysurgery.

Pts undergoing CABGs with AVA


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Indications for AVR in AS

Class I1AVR is indicated for symptomatic patients with severe AS.* (Level of Evidence: B)

2AVR is indicated for patients with severe AS* undergoing coronary artery bypass graft surgery(CABG). (Level of Evidence: C)

3AVR is indicated for patients with severe AS* undergoing surgery on the aorta or other heartvalves. (Level of Evidence: C)

4AVR is recommended for patients with severe AS* and LV systolic dysfunction (ejection fraction lessthan 0.50). (Level of Evidence: C)

Class IIaAVR is reasonable for patients with moderate AS* undergoing CABG or surgery on the aorta or other heart

valves (see Section 3.7 on combined multiple valve disease and Section 10.4 on AVR in patientsundergoing CABG). (Level of Evidence: B)

Class IIb

1AVR may be considered for asymptomatic patients with severe AS* and abnormal response to exercise(e.g., development of symptoms or asymptomatic hypotension). (Level of Evidence: C)

2AVR may be considered for adults with severe asymptomatic AS* if there is a high likelihood of rapidprogression (age, calcification, and CAD) or if surgery might be delayed at the time of symptomonset. (Level of Evidence: C)

3AVR may be considered in patients undergoing CABG who have mild AS* when there is evidence, suchas moderate to severe valve calcification, that progression may be rapid. (Level of Evidence: C)

4AVR may be considered for asymptomatic patients with extremely severe AS (aortic valve area less than0.6 cm2, mean gradient greater than 60 mm Hg, and jet velocity greater than 5.0 m per second) whenthe patients expected operative mortality is 1.0% or less.(Level of Evidence: C)

Class IIIAVR is not useful for the prevention of sudden death in asymptomatic patients with AS who have none of

the findings listed under the class IIa/IIb recommendations. (Level of Evidence: B)


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Aortic Valve

RegurgitationResults from abN in AV leaflets such as post

inflammatory changes, bicuspid valve, damage fromendocarditis, or aortic root dilatation preventing

coaptation.Acute AR fr endocarditis or aortic dissection produces LV

failure, pul edema as ventricale unable to dilate tohandle fluid overload. Chronic AR pressure and volume

overload of LV, with progressive dilatation, wall stress,hypertrophy, and symptoms left heart failure. Increasedstroke volume will increase pulse pressure, increase SBPand evidence of hyperdynamic circulation.


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Class I

1AVR is indicated for symptomatic patients with severe AR irrespective of LV systolicfunction. (Level of Evidence: B)

2AVR is indicated for asymptomatic patients with chronic severe AR and LV systolicdysfunction (ejection fraction 0.50 or less) at rest. (Level of Evidence: B)

3AVR is indicated for patients with chronic severe AR while undergoing CABG or surgery onthe aorta or other heart valves. (Level of Evidence: C)

Class IIaAVR is reasonable for asymptomatic patients with severe AR with normal LV systolic

function (ejection fraction greater than 0.50) but with severe LV dilatation (end-diastolicdimension greater than 75 mm or end-systolic dimension greater than 55 mm).* (Level ofEvidence: B)

Class IIb1AVR may be considered in patients with moderate AR while undergoing surgery on the

ascending aorta. (Level of Evidence: C)

2AVR may be considered in patients with moderate AR while undergoing CABG. (Level ofEvidence: C)

3AVR may be considered for asymptomatic patients with severe AR and normal LV systolic

function at rest (ejection fraction greater than 0.50) when the degree of LV dilatationexceeds an end-diastolic dimension of 70 mm or end-systolic dimension of 50 mm, whenthere is evidence of progressive LV dilatation, declining exercise tolerance, or abnormalhemodynamic responses to exercise.* (Level of Evidence: C)

Class III

AVR is not indicated for asymptomatic patients with mild, moderate, or severe AR andnormal LV systolic function at rest (ejection fraction greater than 0.50) when degree ofdilatation is not moderate or severe (end-diastolic dimension less than 70 mm, end-

systolic dimension less than 50 mm).*(Level of Evidence: B)


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Mitral Valve Stenosis

MS is an obstruction to LV inflow at the level of the MV as a result of a structuralabnormality of the MV apparatus, which prevents proper opening during diastolicfilling of the left ventricle.

The predominant cause of MS is rheumatic carditis. In patients with MS due to rheumaticfever, the pathological process causes leaflet thickening and calcification, commissuralfusion, chordal fusion, or a combination of these processes.

Acquired causes of MV obstruction, other than rheumatic heart disease, are rare. Theseinclude left atrial myxoma, ball valve thrombus, mucopolysaccharidosis, and severeannular calcification.

The normal MV area is 4.0 to 5.0 cm2. Narrowing of the valve area to less than 2.5cm2 typically occurs before the development of symptoms. MV area greater than 1.5cm2 usually does not produce symptoms at rest. However, if there is an increase intransmitral flow or a decrease in the diastolic filling period, there will be a rise in leftatrial pressure and development of symptoms.

The first symptoms of dyspnea in patients with mild MS are usually precipitated byexercise, emotional stress, infection, pregnancy, or atrial fibrillation with a rapidventricular response. As the obstruction across the MV increases, decreasing efforttolerance occurs.


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Although MS is best described as a disease continuum, and thereis no single value that defines severity, for these guidelines, MSseverity is based on a variety of hemodynamic and natural historydata using mean gradient, pulmonary artery systolic pressure, and

valve area as follows:

Mild (area greater than 1.5 cm2, mean gradient less than 5mm Hg, or pulmonary artery systolic pressure less than 30 mmHg),

Moderate (area 1.0 to 1.5 cm2, mean gradient 5 to 10 mmHg, or pulmonary artery systolic pressure 30 to 50 mm Hg),

Severe (area less than 1.0 cm2, mean gradient greater than10 mm Hg, or pulmonary artery systolic pressure greater than 50mm Hg).


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Indications for Surgery for Mitral Stenosis

Class I1 MV surgery (repair if possible) is indicated in patients with symptomatic (NYHA

functional class IIIIV) moderate or severe MS* when 1) percutaneous mitralballoon valvotomy is unavailable, 2) percutaneous mitral balloon valvotomy is

contraindicated because of left atrial thrombus despite anticoagulation orbecause concomitant moderate to severe MR is present, or 3) the valvemorphology is not favorable for percutaneous mitral balloon valvotomy in apatient with acceptable operative risk. (Level of Evidence: B)

2 Symptomatic patients with moderate to severe MS* who also have moderate tosevere MR should receive MV replacement, unless valve repair is possible atthe time of surgery. (Level of Evidence: C)

Class IIaMV replacement is reasonable for patients with severe MS* and severe pulmonary

hypertension (pulmonary artery systolic pressure greater than 60) with NYHAfunctional class III symptoms who are not considered candidates forpercutaneous mitral balloon valvotomy or surgical MV repair. (Level of

Evidence: C)Class IIbMV repair may be considered for asymptomatic patients with moderate or severe

MS* who have had recurrent embolic events while receiving adequateanticoagulation and who have valve morphology favorable for repair. (Level ofEvidence: C)

Class III

1 MV repair for MS is not indicated for patients with mild MS. (Level of Evidence:C)


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Mitral Regurge

Common causes of organic MR include rheumatic heart disease,CAD, infective endocarditis, certain drugs, and collagen vasculardisease.

MR may also occur secondary to a dilated annulus fromdilatation of the left ventricle.

In some cases, such as ruptured chordae tendineae, rupturedpapillary muscle, or infective endocarditis, MR may be acute andsevere, resulting in cardiogenic shock and acute pul edema.

Alternatively, MR may worsen gradually over a prolonged periodof time with LV dysfunction, dilatation and ^filling pressures.

These 2 ends of the spectrum have quite different clinicalpresentations.

Ischaemic MR chronic or acute.


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Three different MV operations are currentlyused for correction of MR:

1) MV repair;2) MV replacement with preservation of part orall of the mitral apparatus; and

3) MV replacement with removal of the mitralapparatus.


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Indications for Mitral Valve Operation

Class I1 MV surgery is recommended for the symptomatic patient with acute severe MR.* (Level of Evidence: B)

2 MV surgery is beneficial for patients with chronic severe MR* and NYHA functional class II, III, or IV symptoms in theabsence of severe LV dysfunction (severe LV dysfunction is defined as ejection fraction less than 0.30) and/or end-systolic dimension greater than 55 mm. (Level of Evidence: B)

3 MV surgery is beneficial for asymptomatic patients with chronic severe MR* and mild to moderate LV dysfunction,ejection fraction 0.30 to 0.60, and/or end-systolic dimension greater than or equal to 40 mm. (Level of Evidence: B)

4 MV repair is recommended over MV replacement in the majority of patients with severe chronic MR* who require surgery,and patients should be referred to surgical centers experienced in MV repair. (Level of Evidence: C)

Class IIa1 MV repair is reasonable in experienced surgical centers for asymptomatic patients with chronic severe MR* with preserved

LV function (ejection fraction greater than 0.60 and end-systolic dimension less than 40 mm) in whom the likelihood ofsuccessful repair without residual MR is greater than 90%. (Level of Evidence: B)

2 MV surgery is reasonable for asymptomatic patients with chronic severe MR,* preserved LV function, and new onset ofatrial fibrillation. (Level of Evidence: C)

3 MV surgery is reasonable for asymptomatic patients with chronic severe MR,* preserved LV function, and pulmonaryhypertension (pulmonary artery systolic pressure greater than 50 mm Hg at rest or greater than 60 mm Hg withexercise). (Level of Evidence: C)

4 MV surgery is reasonable for patients with chronic severe MR* due to a primary abnormality of the mitral apparatus andNYHA functional class III-IV symptoms and severe LV dysfunction (ejection fraction less than 0.30 and/or end-systolic dimension greater than 55 mm) in whom MV repair is highly likely. (Level of Evidence: C)

Class IIbMV repair may be considered for patients with chronic severe secondary MR* due to severe LV dysfunction (ejection

fraction less than 0.30) who have persistent NYHA functional class III-IV symptoms despite optimal therapy for heartfailure, including biventricular pacing. (Level of Evidence: C)

Class III1 MV surgery is not indicated for asymptomatic patients with MR and preserved LV function (ejection fraction greater than

0.60 and end-systolic dimension less than 40 mm) in whom significant doubt about the feasibility of repairexists. (Level of Evidence: C)

2 Isolated MV surgery is not indicated for patients with mild or moderate MR. (Level of Evidence: C)


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Tricuspid valve disease

Tricuspid valve dysfunction can occur with normal or abnormal valves. When normaltricuspid valves develop dysfunction, the resulting hemodynamic abnormality is almostalways pure regurgitation. This occurs with elevation of RV systolic and/or diastolicpressure, RV cavity enlargement, and tricuspid annular dilatation; RV systolichypertension occurs in MS, pulmonic valve stenosis, and the various causes ofpulmonary hypertension. RV diastolic hypertension occurs in dilated cardiomyopathy,RV infarction, and RV failure of any cause. Pacemaker-induced severe TR is rare butmay require intervention.

Abnormalities of the tricuspid valve leading to TR can occur with rheumatic valvulitis,infective endocarditis, carcinoid, rheumatoid arthritis, radiation therapy, trauma (suchas repeated endomyocardial biopsies), Marfan syndrome, tricuspid valve prolapse,tricuspid annular dilatation, or congenital disorders such as Ebsteins anomaly or acleft tricuspid valve as part of atrioventricular canal malformations. Anorectic drugsmay also cause TR.

Tricuspid stenosis is most commonly rheumatic in origin. On very rare occasions,infective endocarditis (with large bulky vegetations), congenital abnormalities,carcinoid, Fabrys disease, Whipples disease, or previous methysergide therapy may beimplicated. Right atrial mass lesions represent a nonvalvular cause of obstruction tothe tricuspid orifice and may also over time destroy the leaflets and cause regurgitation.Rheumatic tricuspid involvement usually results in both stenosis and regurgitation.


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clinical features of tricuspid stenosis include a giant a wave and diminishedrate of y descent in the jugular venous pulse, a tricuspid opening snap, and amurmur that is presystolic as well as middiastolic and that increases oninspiration

clinical features of TR include abnormal systolic c and v waves in the jugularvenous pulse, a lower left parasternal systolic murmur (holosystolic or less

than holosystolic, depending on the severity of hemodynamic derangement)that may increase on inspiration (Carvallos sign), a middiastolic murmur insevere regurgitation, and systolic hepatic pulsation. In rare instances, severeTR may produce systolic propulsion of the eyeballs, pulsatile varicose veins,or a venous systolic thrill and murmur in the neck. Other associated clinicalfeatures are related to the cause of TR. Moderate or severe TR may be present

without the classic clinical features.


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Management

Class ITricuspid valve repair is beneficial for severe TR in patients with MV

disease requiring MV surgery. (Level of Evidence: B)

Class IIa1Tricuspid valve replacement or annuloplasty is reasonable for severe

primary TR when symptomatic. (Level of Evidence: C)

2Tricuspid valve replacement is reasonable for severe TR secondary todiseased/abnormal tricuspid valve leaflets not amenable to

annuloplasty or repair. (Level of Evidence: C)Class IIbTricuspid annuloplasty may be considered for less than severe TR in

patients undergoing MV surgery when there is pulmonary hypertensionor tricuspid annular dilatation. (Level of Evidence: C)

Class III1Tricuspid valve replacement or annuloplasty is not indicated in

asymptomatic patients with TR whose pulmonary artery systolicpressure is less than 60 mm Hg in the presence of a normal MV. (Levelof Evidence: C)

2Tricuspid valve replacement or annuloplasty is not indicated in patientswith mild primary TR. (Level of Evidence: C)


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Pulmonary Valve

StenosisPulmonary valve is the least likely valve to be affected by acquired heart disease,virtually all cases of pulmonary valve stenosis are congenital in origin.

Symptoms are unusual in children or adolescents with pulmonary valve stenosiseven when severe.

Adults with long-standing severe obstruction may have dyspnea and fatigue

secondary to an inability to increase cardiac output adequately with exercise.Exertional syncope or light-headedness may occur in the presence of severepulmonic stenosis with systemic or suprasystemic RV pressures, withdecreased preload or dehydration, or with a low systemic vascular resistancestate (such as pregnancy). However, sudden death is very unusual. Eventually,with long-standing untreated severe obstruction, TR and RV failure mayoccur. it appears that congenital mild pulmonary stenosis is a benign disease

that rarely progresses, that moderate or severe pulmonary stenosis can beimproved with either surgery or balloon valvotomy at very low risk, and thatpatients who undergo surgery or balloon valvotomy have an excellentprognosis and a low rate of recurrence.

Thus, the goal of the clinician is to ascertain the severity of the disease, treatthose in whom it is moderate or severe, and infrequently follow up on those

with mild disease


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Pulmonary Regurgitation

Pulmonary valve regurgitation is an uncommoncongenital lesion seen occasionally with what has beendescribed as idiopathic dilation of the pulmonary arteryor with connective tissue disorders. In this condition,

the annulus of the pulmonary valve dilates, whichcauses failure of the leaflets to coapt during diastole. Pulmonary regurgitation also commonly occurs after

successful repair of tetralogy of Fallot.

Most physicians would perform pulmonary valvereplacement in patients with NYHA class II or IIIsymptoms and severe pulmonary regurgitation, but notfor asymptomatic patients.


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Valve types

Bioprosthetic/Tissue

No lifetime warfarin

Less durability

Mechanical valve

Need for warfarin

Better durability


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Need for anticoagulation

Systemic embolization (predominantly cerebrovascular

events) occurs at a frequency of approximately 0.7 to 1.0

percent per patient per year in patients with mechanical

valves who are treated with warfarin.

In comparison, the risk is 2.2 percent per patient per

year with aspirin and 4.0 percent with no anticoagulation.

Patients with mitral valve prostheses are at

approximately TWICE the risk as those with aortic valve

prostheses


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cardiac valve replacement surgery

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