Valvular Heart Disease 2

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Valvular Heart Valvular Heart Disease Disease Allan B. Ruales, M.D., Allan B. Ruales, M.D., FPCP, FPCC FPCP, FPCC

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Valvular Heart Disease

Transcript of Valvular Heart Disease 2

  • Valvular Heart DiseaseAllan B. Ruales, M.D., FPCP, FPCC

  • Aortic StenosisOccurs in 25% of all pxs with chronic VHD80% of adult pxs with valvular AS are maleEtiology : congenital (bicuspid), rheumatic, degenerative

  • Aortic StenosisRheumatic almost always associated with rheumatic involvement of mitral valve. Favored if associated with severe ARDegenerative calcific known as senile or sclerocalcific AS, most common cause in North America and Western Europe. 30% of persons >65 years old exhibit aortic valve sclerosis with systolic murmur but without obstruction, while 2% exhibit frank stenosis

  • Other forms of Left ventricular outflow tract obstructionHypertrophic cardiomyopathy subaortic obstructionDiscrete congenital subvalvularSupravalvular above the valve

  • PathophysiologySystolic pressure gradient between LV & aortaIf experimental severe obstruction is produce suddenly LV will dilate with reduction of stroke volume.Usually obstruction is gradual, with maintenance of normal CO by concentric hypertrophy, a compensatory mechanism to reduce the systolic stress developed by the myocardium

  • PathophysiologyLarge transaortic valvular gradient may exist for many years without reduction of CO or LV dilatation until decompensation occursCritical obstruction : gradient >50 mmHg or aortic orifice area
  • PathophysiologyLate in the course CO & gradient declines with elevation of LA, PA, and RV pressureHypertrophied LV muscle elevates oxygen requirement to cause ischemia with or without coronary arterial narrowingAS intensifies severity of accompanying MR

  • SymptomsRarely symptomatic until valve orifice is
  • SymptomsAngina develops later and reflects an imbalance between increased oxygen requirement & reduce availabilityExertional syncope fixed CO will cause a decline in arterial pressure as a result of vasodilation of exercising muscles

  • SymptomsHeart failure symptoms in late stagesCoexisting MS will mask clinical findings by AS because the reduced CO induced by MS will lower the gradient across the AV.

  • Physical FindingsRhythm is usually sinus until late in the course, AF should suggest associated mitral valve disease Systemic BP usually normal but late in the course, stroke volume declines and pressure may fall with narrow pulse pressurePulse rises slowly to a delayed sustained peak, pulsus parvus et tardus

  • Physical Findingsa wave in JVP is accentuated due to diminished distensibility of RV cavity caused by bulging, hypertrophied IVSLV impulse is hyperdynamic & displaced laterallySystolic thrill at base of heart, jugular notch, and carotid arteries, its absence suggest a mild AS (except in pxs with emphysema, thick chest wall, thoracic deformity, or heart failure

  • AuscultationCongenital noncalcific AS (children & adolescent) early systolic ejection sound (OS of aortic valve)Ejection sound disappears when valve becomes calcified and rigid

  • AuscultationS2 can be synchronous or paradoxic depending on severity. Loud A2 pliable valves. S4 at apex reflects LV hypertrophy and elevated LV end-diastolic pressure. S3 occurs when LV dilatesMurmur ejection systolic crescendo-decrescendo, low-pitched, rough and rasping in character, loudest at base, most commonly at 2nd right intercostal space radiating to the carotids

  • Laboratory ExaminationECG LV hypertrophy, its absence does not exclude severe obstruction. LA enlargement should suggest associated mitral valve disease

  • Laboratory ExaminationChest Xray maybe normal for many years because the initial response is concentric LVH. Some rounding of cardiac apex, critical AS is associated with post stenotic dilatation of ascending aorta. Absence of valvular calcification in an adult suggests that severe valvular AS is not present. Late stages shows LV enlargement, pulmonary congestion, enlargement of LA, PA and RV.

  • EchocardiographyLV hypertrophy with multiple, bright echoes within aortic root (calcification)LV dilatation & reduced systolic shortening reflects LV dysfunctionDoppler will estimate transvalvular gradientIdentify other lesions

  • CatheterizationPxs with clinical signs of AS and symptoms of myocardial ischemia (suspected with associated CAD)Pxs with multivalvular diseaseYoung, asymptomatic pxs with noncalcific congenital AS to define severity of obstruction to LV outflowPxs with suspected LV outflow in sub- or supravalvular regions

  • Natural HistoryPxs with severe AS death most commonly in 7th and 8th decadeAverage time to death : angina 3 years, syncope 3 years, dyspnea 2 years, congestive heart failure 1.5 to 2 years

  • Natural History>80% who died had symptoms
  • TreatmentModerate or severe AS periodic follow-upAsymptomatic severe AS avoid strenous activityHeart failure digitalis glycosides, sodium restriction, and cautious use of diuretics (avoid volume depletion since this may cause reduction of CO)

  • SurgeryAVR recommended in symptomatic pxs with critical AS, in asymptomatic pxs with severe AS exhibiting LV dysfunctionOperative risk for pxs without heart failure : 4%Long-term postoperative survival correlates inversely with preoperative LV dysfunctionPxs with LV dysfunction has poor prognosis when treated medicallyCABG with AVR for AS with CAD pxs

  • Surgery10-year survival 60%Bioprosthetic valves 30% will fail in 10 years requiring re-replacement30% with mechanical valves develop significant bleeding complications secondary to use of anticoagulants

  • Percutaneous Balloon Aortic ValvuloplastyPrefered procedure in children and young adults with congenital & noncalcific ASHigh restenosis rate in calcific valvesIn pxs too ill or frail to undergo surgeryIn pxs with life-threatening AS with advanced extracardiac diseaseBridge to operation pxs with severe LV dysfunction

  • Aortic RegurgitationEtiology primary valve disease or primary aortic root diseasePrimary valve disease males : with pure or predominant valvular AR

  • Aortic Regurgitation females : pxs with AR and associated mitral valve disease 2/3 of pxs : rheumatic in origin Other causes : IE, Prolapse of aortic valve, congenital fenestration, blunt chest trauma

  • EtiologyPrimary Aortic Root Disease marked aortic dilatation Cystic medial necrosis of ascending aorta in Marfan syndrome Idiopathic dilatation of aorta Osteogenesis imperfecta

  • Etiology Severe Hypertension Retrograde dissection of aortic annulus Syphilis Ankylosing rheumatoid spondylitis

  • PathophysiologyTotal stroke volume (effective forward stroke volume + regurgitant volume) increasedEntire LV stroke volume is ejected into a high-pressure zone (aorta)Increased LV end diastolic volume (increased preload) major hemodynamic compensation for AR

  • PathophysiologyDilatation of LV eject a larger stroke volume without increasing the relative shortening of each myofibril

  • Pathophysiology

    LV dilatation will increase LV systolic tension required to develop a level of systolic pressure Laplaces law (myocardial wall tension is the product of intracavitary pressure and LV radius)

  • PathophysiologyAs LV function deteriorates end-diastolic volume rises & forward stroke volume & EF declineThickening of LV wall also occurs in chronic AR autopsy will show large heart >1 kgEffective forward CO is normal or slightly reduced at rest and fails to rise normally on exertion

  • PathophysiologySigns of LV dysfunction reduction of EFAdvanced stages elevation of LA, PA wedge, PA, and RV pressures and lowering of forward CO at restMyocardial ischemia elevation of oxygen requirements by both LV dilatation & elevated LV systolic tension, and reduced supply when arterial pressure is subnormal reducing coronary perfusion pressure

  • HistoryFamily history Marfan syndromeCompatible with IE, or Ankylosing spondylitisAsymptomatic for 10 15 yearsEarly complaint of awareness of heartbeat on supine position, sinus tachycardia or PVCs with palpitations and head pounding during exertion or emotionExertional dyspnea first symptom of diminished cardiac reserve

  • Other SymptomsOrthopnea, PND, and excessive diaphoresisChest pain not necessary with CADCongestive hepatomegaly and ankle edema lateAcute, severe AR Pulmonary edema and/or cardiogenic shock

  • Physical FindingsJarring of entire body & bobbing motion of head with each systoleAbrupt distention & collapse of large arteriesDetect conditions predisposing to AR Marfan syndrome, rheumatoid spondylitis, & VSD

  • Arterial PulseCorrigans pulse water-hammer pulse, rapidly rising and suddenly collapsing arterial pulse during late systole & diastoleQuinckes pulse capillary pulsations, alternate flushing & paling of skin at root of nail while pressure is applied to tip of nail

  • Arterial PulseTraubes sign booming, pistol-shot sound heard on auscultation over femoral arteriesDuroziezs sign to-and-fro murmur audible if femoral artery is lightly compressed with stethoscope

  • Arterial PulseWidened pulse pressure elevation of systolic and depression of diastolic pressureSeverity of AR is not always directly correlated with pulse pressure

  • PalpationLV impulse heaving & laterally displaced inferiorly, with systolic expansion and diastolic retraction of apex.Diastolic thrill palpable along left sternal border

  • PalpationSystolic thrill palpable in jugular notch & transmitted along carotid arteries : not necessary coexisting AS but markedly increased blood flow across aortic orificeCarotid arterial pulse bisferiens : two systolic waves

  • AuscultationAbsent A2, audible S3 with systolic ejection sound, occasional S4Murmur high-pitched, blowing, decrescendo diastolic heard best 3rd ICS along left sternal border. Brief in mild AR, becoming louder & longer as severity increases

  • AuscultationPrimary valvular AR murmur is louder at left than right sternal borderAneurysmal dilatation of aortic root louder at right sternal border

  • AuscultationMidsystolic ejection murmur heard best at base & transmitted to carotid arteries. (Not to be confused with AS) Higher pitched, shorter, & less rasping than the murmur of AS

  • AuscultationAustin Flint murmur soft, low-pitched, rumbling middiastolic bruit heard best at apex : produced by displacement of anterior mitral leaflet by the AR streamMurmur of AR intensified by isometric exercise and reduced by inhalation of amyl nitrite

  • Laboratory ExaminationECG normal for mild AR, for severe chronic AR LV hypertrophy with strain Chest X-ray Apex displaced downward & to the left. Moderately dilated ascending aorta & knob for primary valve disease, aneurysmal dilated aorta for AR cause by primary disease of aortic wall

  • EchocardiographyUseful in determining the cause of AR detect dilatation of aortic annulus, thickening & failure of leaflet coaptationDoppler is very sensitive in detecting AR and helpful in assessing the severitySerial study is valuable in evaluating LV performance and to detect progressive myocardial dysfunction

  • Cardiac Catheterization and AngiographyAccurate confirmation of magnitude of regurgitation and status of LV functionCondition of coronary arteries may be evaluated preoperatively

  • TreatmentSurgery principal treatment of AR carried out before developing heart failureTiming of operation pxs with chronic AR usually do not become symptomatic until after the development of myocardial dysfunction, and surgery often does not restore normal LV function

  • SurgeryPxs with severe AR careful clinical follow-up and noninvasive testing with echocardiography every 6-month intervals to determine the optimal time of surgeryAfter the onset of LV dysfunction but prior to the development of severe symptoms

  • SurgeryIn asymptomatic pxs with progrssive LV dysfunction (LVEF55ml/sq m, 55/55 rule)Repair or AVR with or without aortic graft mechanical or bioprosthesisOverall operative mortality for isolated AVR 4.3%

  • Acute Aortic RegurgitationMost common causes IE, aortic dissection, traumaLV has no time to dilate stroke volume declines and ventricular diastolic pressure rises markedly, pulse pressure is often not markedly widened, physical signs of severe chronic AR is absent. Mitral valve will close prematurely so that S1 is soft or absent. Diastolic murmur of AR is brief.

  • Acute Aortic RegurgitationPxs will present with pulmonary congestion & edema with hypotensionPrompt surgical treatment is required

  • Tricuspid StenosisGenerally rheumatic in origin and more common in womenDoes not occur as an isolated lesionUsually associated with MSSignificant TS occurs in 5 to 10% of pxs with severe MSCommonly associated with some degree of TR

  • PathophysiologyDiastolic pressure gradient between RA & RV which is augmented when transvalvular blood flow increases during inspirationGradient >4mmHg will elevate RA pressure to result in systemic venous congestion (ascites & edema)

  • SymptomsDevelopment of MS precedes TS, pxs initially have symptoms of pulmonary congestion (improvement would raise the possibility that TS is developing)Little dyspnea for degree of hepatomegaly, ascites, and edemaFatigue secondary to low CO

  • Physical FindingsSevere TS marked hepatic congestion resulting in cirrhosis, jaundice, malnutrition, anasarca, and ascitesCongestive hepatomegaly & splenomegalyDistended jugular veins with giant a waves if sinus in rhythm with slow y descentOS of tricuspid valve with diastolic rumbling murmur along left lower sternal margin and xiphoid process (augmented during inspiration)

  • Laboratory ExaminationECG RA enlargement (tall, peaked P waves in II, and prominent, upright P in V1Chest X-ray prominent RA with less evidence of congestionEchocardiography thickening of tricuspid valve. Doppler will estimate the gradient

  • TreatmentIntensive salt restriction and diureticsSurgical relief of TS is carried out at the time of mitral operation (moderate to severe TS with gradient >4 mmHg and orifice < 1.5 to 2 sq cm)Repair or replacement (bioprosthetic valve)

  • Tricuspid RegurgitationMost commonly is functional and secondary to marked dilatation of RV & tricuspid annulus

  • Tricuspid Regurgitation Etiology RV enlargement secondary to inferior wall infarct with RV involvement, late stages of heart failure due to RHD or CHD with severe pulmonary HPN, IHD, cardiomyopathy, and cor pulmonale Organic TR Rheumatic fever, infarction of RV papillary muscles, tricuspid valve prolapse, carcinoid heart disease, endomyocardial fibrosis, IE, & trauma

  • Clinical FeaturesSystemic venous congestion & reduction of COMarked hepatomegaly, ascites, pleural effusions, edema, systolic pulsations of liver, positive hepatojugular refluxProminent RV pulsation along left parasternal region with a blowing holosystolic murmur along lower left sternal margin (intensified during inspiration and reduced on strain of Valsalva maneuver)

  • Laboratory ExaminationECG will show changes characteristic of lesion responsible for the enlargement of the RVChest X-ray enlargement of RA and RVEchocardiography will demonstrate the RV dilatation and status of the tricuspid leaflets. Doppler will estimate the severity of TR & PA pressure

  • TreatmentIsolated TR with no pulmonary HPN (e.g. IE or trauma) usually well tolerated and does not require operation

  • TreatmentTreatment of underlying cause of heart failure usually reduces severity of functional TRIn pxs with mitral valve disease & TR secondary to pulmonary HPN & massive RV enlargement effective surgical correction of mitral valvular abnormality will result in lowering of PA pressures and gradual disappearance of TR, or repair, or replacement

  • Pulmonic Valve DiseasePulmonic valve least affected by rheumatic fever, and uncommonly the seat of IEPulmonic regurgitation most common acquired abnormality of pulmonic valve secondary to dilatation of pulmonic ring secondary to severe pulmonary HPN

  • Pulmonic RegurgitationGraham Steell murmur high-pitched, decrescendo, diastolic blowing murmur along left sternal borderLittle hemodynamic significance unless serious pulmonary HPN is also present

  • Valve ReplacementOperative results dependent on : pxs myocardial function & general medical condition on operation technical ability of operative team & quality of postoperative care durability, hemodynamic characteristics, and thrombogenecity of the prosthesis

  • Late Complications of valve replacementParavalvular leakageThromboemboliBleeding due to anticoagulantsMechanical dysfunction of the prosthesisIE

  • Bioprosthetic or Artificial Mechanical Valve?Similar considerations mitral or aortic positions, stenotic, regurgitant or mixed lesionsMechanical on lifetime anticoagulants (hazard for hemorrhage)

  • Bioprosthetic or Artificial Mechanical Valve?Primary advantage of bioprosthesis reduced thromboembolic complication (except for pxs with chronic AF)

  • Bioprosthetic or Artificial Mechanical Valve?Major disadvantage of bioprosthesis mechanical deterioration (results in need to replace in 30% of pxs by 10 years and in 50% by 15 years)

  • Bioprosthetic or Artificial Mechanical Valve?Bioprosthesis is not use in pxs 65 years old, in women who expect to become pregnant, pxs in whom anticoagulation is contraindicatedMechanical prosthesis (St. Jude or other double-disk tilting valve) preferable in pxs without contraindications to anticoagulants and