Valvular Heart Disease and the Cardiac Exam

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Valvular Heart Disease and the Cardiac Exam Outline

Va V lvular Heart Disease and the Cardiac Exam 2009

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

General Appearance  Marfan Syndrome  Fredreich ataxia – Tall, long extremities – Lurching gait, hammertoe, pes – Associated with: aortic root cavus dilitation, MV prolapse – Associated with: hypertrophic  Acromegaly cardiomyopathy – Large stature, coarse facial  Duchenne type muscular features, “spade” hands dystrophy – Associated with: Cardiac – Pseudohypertrophy of the hypertrophy calves  Turner Syndrome – Cardiomyopathy – Web neck, hypertelorism, short  Ankylosing spondylitis stature – Straight back syndrome, stiff – Associated with: Aortic (“poker”) spine coarctation, pulmonary – Associated with: AI, CHB (rare) stenosis  Lentigines (LEOPARD  Pickwickian Syndrome syndrome) – Severe obesity, somnolence – Brown skin macules that do – Associated with: Pulmonary not increase with sunlight hypertension – Associated with: HOCM, PS

“Spade” hands in acromegaly

General Appearance- 2  Hereditary hemorrhagic  Sarcoidosis telangiectasia (Osler- – Cutaneous nodules, erythema Weber-Rendu) nodosum – Small capillary hemangiomas – Associated with: Secondary on the face or mouth cardiomyopathy, heart block – Associated with: Pulmonary  Tuberous Sclerosis arteriovenous fistula – Angiofibromas (face; adenoma  Lupus sebaceum) – Butterfly rash on face, – Associated with: Raynaud phenomenon- hands, Rhabdomyoma Livedo reticularis  Myxedema – Associated with: Verrucous endocarditis, Myocarditis, – Coarse, dry skin, thinning of Pericarditis lateral eyebrows, hoarseness of voice  Pheochromocytoma – Associated with: Pericardial – Pale diaphoretic skin, effusion, LV dysfunction neurofibromatosis- café-au-lait spots – Associated with: Catecholamine-induced secondary dilated CM

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 wal  Grade 3 – Murmur hears with stethoscope on chest wal , louder than grade 2 but without a thril  Grade 4 – Murmur associated with a thril  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 wal

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 fol owing murmurs are usual y pathologic: – Systolic murmurs grade 3/6 or greater in intensity– Continuous murmurs– Any diastolic murmur

Maneuver Hemodynamic Effect Murmur Effect Normal respiration Transient ↑ in venous fil ing ↑ right-sided murmurs during inspiration Passive leg elevation ↑ venous return (transient ↑ ↑ right-sided murmurs, in LV size and preload) ↓murmur of HOCM and MVP Stand to squat ↑ venous return (transient ↑ ↑ right-sided murmurs, in LV size and preload) ↓murmur of HOCM and MVP Squat to stand ↓ venous return (transient ↓ ↑ murmur of HOCM, moves in LV size and preload) midsystolic click of MVP closer to S1 and ↑ MVP murmur, ↓ AS murmur Valsalva ↓ venous return (transient ↓ ↑ murmur of HOCM, moves in LV size, preload, and midsystolic click of MVP closer relative systemic hypotension) to S1, and ↓ murmur of MVP Isometric handgrip exercise ↑ afterload ↑ murmur of MR and VSD, ↓the murmur of HOCM, ↓AS murmur Inhaled amyl nitrate ↓ afterload ↓ murmur of MR and VSD, no change in AS murmur

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 – Usual y not needed for primary evaluation

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

Progression of Aortic Sclerosis  Hemodynamic progression usual y 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

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 wal thickness and abnormal myocardial relaxation  Increased wal stress and afterload causes eventual decrease in ejection fraction

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

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

Management of Aortic Stenosis  Prognosis in asymptomatic disease excel ent  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 stil favorable with surgery  Nitroprusside may transiently improve cardiac function as a bridge to valve replacement – Does not supplant AVR in symptomatic patients

Bonow et al. J Am Col Cardiol 2006; 47: 2141-51

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% annual y– 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 bal oon aortic valvotomy rarely used

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

Clinical Presentation of Mitral Stenosis  Significant MS leads to ↑LA pressure and pulm HTN Symptoms include dyspnea with ↑ cardiac demand – Exercise– Pregnancy  Survival excel ent with asymptomatic or minimal y 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)

Management of Mitral Stenosis  Atrial fibril ation – 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

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

Bonow et al. J Am Col Cardiol 2006; 47: 2141-51

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 mil ion 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 mil ion 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 wel into adulthood  RHD with carditis and valvular HD- At least 10 years from last episode or until patient is older than 40 years

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

Acute Mitral Regurgitation  Most often occurs in: – Chordae tendineae rupture due to myxomatous valve disease or endocarditis – Myocardial infarction with papil ary 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

Chronic Valvular Regurgitation  Cardiac chamber size and function have time to compensate for dysfunction – May al ow 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

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

Bonow et al. J Am Col Cardiol 2006; 47: 2141-51

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  Usual y asymptomatic, but may be associated with palpitations or chest discomfort  Prognosis usual y benign Antibiotic prophylaxis now not indicated

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 initial y al ows for increase in total stroke volume and restoration or total forward cardiac output

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 papil ary muscle  Biventricular pacing may improve LV geometry

Timing of Intervention for Left-Sided Valvular Conditions Aortic Stenosis Mitral Stenosis Chronic Severe AR Chronic Severe MR Intervention: Intervention: Intervention: Intervention: AVR Percutaneous valvotomy if Surgical AVR with aortic root Surgical mitral valve repair if anatomy amenable and replacement if needed anatomy amenable. <moderate MR, and no LAA Otherwise, MVR clot. Otherwise, open commissurotomy or MVR IF: IF: IF: IF: Patient is symptomatic (NYHA Patient has moderate or more Patient is symptomatic (NYHA Patient is symptomatic (NYHA class II or greater, angina due severe MS (MVA < 1.5 cm2) class II or greater) class II or greater) to AS, or syncope) OR OR OR OR Pulmonary hypertrension at EF <60% EF <60% Patient has symptomatic rest (PAP > 60 mmHg) OR OR severe AS and needs other OR ESD > 55 mm ESD > 45 mm cardiothoracic surgery (i.e. Abnormal hemodynamic CABG) OR OR response to exercise: Abnormal hemodynamic Pulmonary hypertension or PAP > 60 mmHg response to exercise atrial fibril ation Mean gradient > 15 mmHg PAP increase by 25 mmHg OTHERWISE OTHERWISE OTHERWISE OTHERWISE Depending on the severity of Clinical evaluation at least Repeat TTE at least yearly, Repeat TTE yearly, repeat AS, at least annual clinical annual y, depending on the repeat clinical evaluation at clinical evaluation biannual y evaluation with TTE to monitor severity of the mitral stenosis least biannual y depending on for symptom onset the severity of the LV dilitiation

Tricuspid Valve Disease  Tricuspid stenosis is rare – Associated with rheumatic heart disease  TR usual y occurs secondary to: – Pulmonary hypertension – RV chamber enlargement with annular dilatation – Endocarditis (associated with IV drug use) – Injury fol owing 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

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

Prosthetic Valves- Mechanical  Three types: – Bal -cage valve – Single tilting disk valve – Bileaflet valve  Durable but require life long anticoagulation For operative procedures, warfarin typical y is discontinued for 48-72 hours and restarted postop as soon as possible, except for: – Mechanical mitral prosthesis – Atrial fibril ation – Prior thromboembolic events

Ball-cage valve Single tilting disk valve Bileaflet valve

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

Anticoagulation Guidelines for Mechanical Valves Bonow et al. J Am Col Cardiol 2006; 47: 2141-51

Prosthetic Valve Complications  Common complications include: – Structural valve deterioration – Valve thrombosis – Embolism – Bleeding – Endocarditis  Endocarditis prophylaxis required for patients with al 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

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 smal 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

Endocarditis Prophylaxis 2007 AHA Prevention of Infective Endocarditis Guidelines