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Transcript
Valvular Heart Disease Jay L. Rubenstone, D.O., F.A.C.C 1 Normal Structure Mitral Valve 2 Cross sectional Area 4-6cm² Anterior and Posterior Leaflets Chordae Tendineae Papillary Muscles Mitral Stenosis Etiology & Pathology Rheumatic Fever- 99% Other – – – – – – 3 Congenital Carcinoid Lupus Amyloid Infective Endocarditis Mucopolysaccharide Disease Stenotic Pathology Etiology & Pathology – – 4 Commissural Cuspal Chordal Mixed 30% 15% 10% Remaining Valve becomes funnel shaped or “fish mouthed” Thickened immobile leaflets or chordal structures Stenotic Pathology Debate: – – 5 Smoldering rheumatic process or Constant blood flow trauma leading to valve fibrosis and thickening Pathophysiology Mild MS- orifice <2 cm² Critical MS- <1 cm² – – – – – 6 A-V pressure gradient >20mmHg Increased LA Pressure Increase Pulmonary Venous + Capillary Pressures Increase Pulmonary Artery Systolic Pressure Decrease RV Function (when PAS>30-60mmHg) Pathophysiology Pulmonary HTN – 7 Passive Backward Transmission Of Incr. LA pressure Pulmonary Arteriolar Constriction Organic Obliterative Changes in Pulmonary Vascular Bed RV Failure History 8 Exertional Dyspnea Cough/Wheezing Orthopnea/PND/CHF Hemoptysis-Rupture of Pulmonary VeinBronchial Vein Shunts History Chest Pain-Increase RV Pressures or Unknown Etiology Systemic Emboli (LA clots) – – 9 Increased LA size, Decreased C.O., Atrial Fib, IE Significantly decreased w/anticoagulation Physical Exam Auscultation 10 O.S. Diastolic Rumble Assoc Murmur of MR Loud S1-thickened leaflets Increased P2-pulmonary hypertension Decreased B/P if C.O. decreased Prominent a wave if sinus rhythm present Physical Exam 11 Mitral Facies-pink, purple facial patches due to decrease CO and systemic vasoconstriction Hepatomegally Edema Ascites Hydrothorax With Right Heart Failure Diagnosis ECG – Left Atrial Abnormality – – 12 P wave becomes bifid and greater than 0.12 sec in duration in V1 and Lead II RVH- right axis deviation R wave > S wave in V1 Diagnosis Chest X-ray – – – Echo- Cornerstone of Diagnosis – – – 13 Dilated LA, RA, RV Elevated Left Main stem Bronchus Interstitial Edema Thickened Calcified Leaflets Doming of Leaflets on Opening Bernoulli equation Diagnosis – Cardiac Catherization Gorlin 14 Equation 15 Natural History 16 Asymptomatic for 15-20yrs following Rheumatic Fever Additional 5-10 yrs for progression from mild to severe stenosis Stenosis progression approximately .09 cm²/yr Natural History Presurgical Survival Rates – – – 17 NYHA Class II 80%-10yrs Class III 38%-10yrs, 62% 5yrs Class IV 15%-5yrs Management-Medical 18 Endocarditis Prophylaxis Activity Limitation Diuretics- Decrease Na Intake Heart Rate Control for A-fib or Sinus Rhythm Anticoagulation Percutaneous Balloon Angioplasty 19 Moderate-Severe MS Mild MS- if Pulmonary Artery Pressures or Wedge Pressure Elevate with Exercise Valve Replacement Indications – – – – Mortality – 20 Combined MS/MR <1.5 cm²-NYHA III or IV <1 cm² Class II if Pulmonary Artery Pressure >70mmHg 3-8% Valve Type-Prosthetic or Bioprosthetic Mitral Regurgitation Etiology – – – – – – Rheumatic Heart Disease Infective Endocarditis Collagen Vascular Disease Cardiomyopathy Ischemic Heart Disease Mitral Valve Prolapse-most common cause for valve surgery in US 21 Pathophysiology Decreased Impedance to Ventricular Emptying Determinants of Regurgitant Flow – – – 22 Instantaneous Size of MV Orifice Dependent on Preload, After load, LV Contractility, LV Size LA-LV Pressure Gradient dependent on Systemic Vascular Resistance, LV Pressure, & LV Size Pathophysiology LV Compensation – – – – – 23 Increased End Diastolic Volume Increased Wall Tension Increased Preload Increased LV Emptying Normal Ejection Fraction should be Super Normal >65% to maintain forward cardiac output and B/P Pathophysiology LV Decompensation – – – – 24 Increase End Systolic Volume Increased End Diastolic Volume Leads to Annulus Dilatation (MR begets MR) Decreased Ejection Fraction and Stroke Volume Pathophysiology Ejection Fraction in Mitral Regurgitation >65% normal in compensated MR – 50-65% mild impairment – 40-50% moderate-severe impairment – <35% advanced impairment As ejection fraction decreases operative risk increases. – 25 History 26 Shortness of Breath Exertional Dyspnea Congestive Heart Failure Right Heart Failure Significant symptoms in chronic MR usually do not develop until LV decompensation occurs. History Medical Treatment Survival – – – 27 80% 5yr 60% 10yr 30-45% 5yr if MR severe Diagnosis Physical Exam – – ECG – – – LA abnormality LVH RVH Chest X-ray – 28 Holosystolic Murmur Increase Carotid Impulse Increase LA, LV, RV, Interstitial Edema Diagnosis Echo – – 29 Transesophageal superior to transthoracic Evaluation of Chamber Sizes, Regurgitant Jet, Leaflets Management of Acute MR Medical – After load Reduction (Nitropresside & Intra aortic balloon pump) – 30 Decrease impedance to LV ejection Decrease regurgitant volume into left atrium Inotropic Support (Dobutamine)-if LV function reduced Management of Acute MR Surgical Intervention – – – – 31 Progressive LV Failure or Hemodynamic Deterioration CHF Hypertension Valve Disruption Management of Chronic MR Medical – – – – – 32 Digoxin Diuretics* After load Reduction Anticoagulation in A-fib Endocarditis Prophylaxis Management of Chronic MR Surgical – Indications Asymptomatic Class I – Severe MR Class II, III, or IV – – 33 EF < 60% or LV Systolic Diameter >45mm generally considered for surgery unless EF <30% Valve Repair vs. Replacement Mitral Valve Prolapse 34 Systolic Click-Murmur Syndrome Barlow’s Syndrome Billowing Mitral Valve Syndrome Floppy Valve Syndrome Myxomatous Valve Syndrome Parachute Valve Mitral Valve Prolapse Over diagnosed – – – 35 2.4% of population Females>Males 2:1 Severe MR- Elderly Male>Young Female MVP Etiology 36 Primary Valvular most frequent Connective Tissue Diseases Hyperthyroidism Myotonic Dystrophy Periarteritis Nodosa Von Willebrands MVP Pathology 37 Myxomatous Proliferation and Degeneration of Valve Leaflets Increased Quantity of Acid Mucopolysaccharide in Middle Layer of Valve Tissue MVP History 38 Most are asymptomatic throughout life Chest pain, fatigue, anxiety Orthostasis-questionable autonomic dysfunction Arrhythmia-SVT, PACs, PVCs Symptoms of MR if present Physical Examination Body type – Auscultation – 39 Asthenic, low weight body habitus, straight back syndrome Systolic click- multiple, non-ejection (after carotid upstroke) due to tensing of elongated chordae and prolapsing valve Physical Examination Auscultation – – 40 Murmur- mid to late crescendo progressing to holosystolic if MR becomes severe Click and murmur move closer to S1 during strain phase of valsalva, sudden standing, and Amyl Nitrate Diagnosis ECG and Chest X-ray – Echo – – – – 41 Normally unremarkable Billowing of one or both leaflets into the left atrium during systole at least 2mm Parasternal long axis view for diagnosis Associated MR Leaflet thickness Natural History 42 Progressive MR in 15% over 10-15 yrs Infective Endocarditis Cerebral Emboli-tearing of endothelial covering of myxomatous valve with platelet activation Sudden Cardiac Death-V fib, increased Q-T interval (not well established) MVP Management 43 Endocarditis prophylaxis if MR present Holter monitor-beta blocker for ectopy? Aspirin if focal neurological events present MR-treat like any other MR, valves usually amenable to repair *MVP is usually a benign disease* Aortic Valve Normal Structure 44 Valve sits at the base of Aortic Root Three Leaflets (cusps)-non coronary, right coronary, left coronary Cusps give rise to ostea of right coronary artery and left main coronary artery Normal cross-sectional area 3-4cm² Aortic Stenosis Etiology and Pathology 45 Valvular Supravalvular Subvalvular Hyperthrophic Cardiomyopathy Congenital Aortic Stenosis Unicuspid – Bicuspid – – – Adult Presentation Chronic turbulent flow Leads to fibrosis, rigidity, calcification Tricuspid – 46 Presents less than one year of age Leaflets of unequal size Acquired Aortic Stenosis Rheumatic – – Degenerative or Senile – – – – – 47 Rare Usually mitral valve also involved Most common cause of adult AS Most common cause of valve replacement Years of normal mechanical stress leads to calcium deposits on leaflets Inflammatory or Infectious component?? >age 65 2% frank AS, 30% Aortic Sclerosis Is this atherosclerotic disease? 48 Degenerative A.S. accelerated in diabetes and hyperlipidemia. Associated with tobacco use and HTN. Potentially treated with HMGcoA agents? 49 Hemodynamics Critical (Surgical) AS – – Moderate AS – 50 1-1.5cm² Mild AS – Peak systolic pressure gradient > 50mmHg in the presence of normal cardiac output Valve area <0.7-0.8cm² 1.5-2cm² Aortic Sclerosis History Long latent period of increasing obstruction Symptoms usually begin in 5th or 6th decade Angina in 2/3 of patients – – – – 51 Hypertrophied myocardium Increased ventricular systolic pressure All of which increase myocardial oxygen consumption Oxygen supply-demand imbalance leads to subendocardial ischemia History Syncope – – – Dyspnea (CHF) – – 52 Reduced cerebral perfusion Vasodilatation in the presence of fixed cardiac output leads to hypotension Baroreceptor-vasodepression due to high LV systolic pressure Particularly with exertion due to fixed cardiac output Pulmonary Venous HTN can lead to CHF Diagnosis Physical Examination – Systolic Murmur – Pulses Parvus 53 Diamond-Shaped, harsh, left sternal boarder to right intercostal spaces, neck and apex Late peak, obliteration of S2, consistent with bedside Dx of Critical AS Delayed and Prolonged Carotid Impulse Diagnosis ECG – Chest X-ray – – Concentric LVH Calcification of Aortic Valve Echo – 54 Classic LVH Bernoulli (continuity) equation-calculation of LVAortic pressure gradient and valve area Diagnosis Cardiac Catherization – 55 Gorlin Equation Natural History Asymptomatic latent period With moderate-severe AS valve area can decrease on average 0.12cm² per year *Angina, syncope or CHF – – 56 Average 1-3 year survival 50% Sudden cardiac death rare Medical Management 57 Endocarditis Prophylaxis Limit Physical Activity Watch Beta Blockers and Diuretics *Treatment of Critical AS in viable candidates is surgery Surgery (Valve Replacement) Indications – – Symptomatic Patients -valve area 0.7-0.8cm² or less Asymptomatic Patients-progressive LV dysfunction (EF <35%) or hypotensive response to mild exercise 58 Delaying surgery in asymptomatic patients with good exercise tolerance is controversial Surgery (Valve Replacement) Results – – – – 59 Effective prosthetic valve area not normal Surgery replaces Critical AS with Non-critical AS Symptoms can persist if valve-patient mismatch occurs 10 year survival –85% Aortic Regurgitation Etiology and Pathology Valvular – Rheumatic-Fibrotic Retraction of Leaflets – – – – – – 60 Ankylosing Spondylitis, Behcets, Psoriatic Arthritis, Giant Cell Arteritis Degenerative AS-75% w/AR Infective Endocarditis-Leaflet Destruction Trauma-ascending aortic tear Bicuspid aortic valve-prolapse or incomplete closure Myxomatous Degeneration-like MVP Appetite suppressant drugs-serotonin related valve deposits Etiology and Pathology Aortic Root Disease-More common than primary valvular. Root Dilatation leads to non-coaptation of leaflets. – – – – – 61 Degenerative-Hypertensive Aortic Dilatation Cystic Medial Necrosis-Classic Marfans Syndrome Aortic Dissection Syphilitic Aortitis Rheumatic Disease-same as valvular History Acute AR – – Chronic AR – – – 62 LV cannot accommodate acute regurgitant volume can lead to cardiovascular collapse Gradual LV enlargement-eccentric hypertrophy Exertional dyspnea, orthopnea, PND, CHF Presents 4th or 5th Decade 63 Physical Examination Diastolic Murmur – – – – 64 Left sternal boarder Decrescendo, high pitched Best heard Sitting Up, End Expiration Longer murmur equals worse AR Physical Examination de Mussett’s Sign (head bobbing) Corrigan’s Pulse “water hammer” – Bisferiens-pulse – Pistol shot sounds over femoral pulse Duroziez’s Sign – 65 2 peaks Traube’s Sign – Abrupt Distention with Quick Collapse Murmur over femoral pulse with compression Physical Examination Quinckes Sign – Muller’s Sign – Systolic pulsations of uvula Hill’s Sign – 66 Capillary pulsations Popliteal pulse exceed brachial pulse by > 60mmHg Physical Examination Korotkoff Sounds – – 67 Can persist to 0mmHg Wide Pulse pressure Diagnosis ECG – Chest X-ray – 68 Cardiomegaly predominantly inferior and leftward Echo – LVH Can aid in detecting etiology, quantifying degree of regurgitation, and assessing LV size and function Cardiac Catheterization Natural History Acute AR – – – Chronic AR – – – 69 Cardiovascular collapse Inotrophic agents and vasodilators Prompt surgical intervention 75% Five Year Survival 50% Ten Year Survival Progressive downhill course of CHF, Episodic Pulmonary Edema, Sudden Cardiac Death Medical Treatment Acute AR – As above Chronic AR – Asymptomatic Mild-Moderate 70 Follow by Echo Yearly Endocarditis Prophylaxis for all AR May not require medical treatment Medical Treatment Symptomatic Moderate-Severe AR – – – – – – 71 Limit exertional activity Aggressively treat B/P Diuretics Salt Restriction Digoxin Vasodilators (Nifedipine?) Surgical Treatment Indications – – 72 Defer surgery for chronic severe AR if good exercise tolerance, EF greater than 50%, end systolic diameter < 50 mmHg, and end diastolic diameter < 70 mmHg Be aware that progressive decline in LV function or size increases surgical morbidity and mortality Surgical Treatment Mortality – – 73 3-8% perioperative 5-10% late mortality with significant preop LV dysfunction