Valvular Regurgitation Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE) Assistant Professor of Physician Assistant Studies Radiologic and Imaging Sciences - Echocardiography Grand Valley State University, Grand Rapids, Michigan raaymasu@gvsu.edu du Basic Principles Etiology Congenital Acquired abnormalities Fluid Dynamics of Regurgitation Characterized Regurgitant orifice area High-velocity regurgitant jet Proximal flow convergence area Downstream flow disturbance Increased antegrade flow volume Fluid Dynamics of Regurgitation Regurgitant orifice characterized by high-velocity laminar jet Related to instantaneous pressure difference (∆P=4v2) Upstream side of regurgitant acceleration proximal to regurgitant orifice PISA Narrowest segment of the regurgitant jet occurs just distal to the regurgitant orifice reflects regurgitant orifice area Vena Contracta Fluid Dynamics of Regurgitation Size, Shape and Direction of Regurgitant Jet Size Affected by physiologic and technical factors Regurgitant volume Driving pressure Size and shape of regurgitant orifice Receiving chamber constraint Influence of coexisting jets or flowstreams Ultrasound system gain Depth Signal strength Fluid Dynamics of Regurgitation Size, Shape and Direction of Regurgitant Jet Shape and Directions Affected by Anatomy and orientation of regurgitant orifice Driving force across the valve Size and compliance of receiving chamber Volume Overload Total Stroke Volume Total volume of blood pumped by the ventricle in a single beat Forward Stroke Volume Amount of blood delivered to the peripheral circulation Regurgitant Volume Amount of backflow across the abnormal valve Volume Overload Chronic valvular regurgitation Results in progressive volume overload of the ventricle Volume overload in LV results in LV chamber enlargement with normal wall thickness (total LV mass is increased) Important clinical feature: • An irreversible decrease in systolic function can occur in absence of symptoms Detection of Valvular Regurgitation 2D imaging Indirect evidence Chamber dilation and function Color flow imaging Flow disturbance downstream form regurgitant orifice Sensitive (90%) when correct settings are utilized Specific (nearly 100%) compared with angiography True positives and false positives False positives due to mistaken origin or timing False negatives due to low signal strength or inadequate images Detection of Valvular Regurgitation Continuous-wave Doppler ultrasound Identification of high velocity jet through regurgitant orifice Advantage: Beam width is broad at the level of the valves when studied from an apical approach Valvular Regurgitation in Normal Individuals Physiologic Small degree of regurgitation in normal individuals No adverse implications Typically Spatially restricted to area immediately adjacent to valve closure Short in duration Represents on a small regurgitant volume May be detected in 70 – 80% mitral May be detected in 80 – 90% tricuspid May be detected in 70 – 80% pulmonary May be detected in 5% aortic (increases with age). • Clinical significance of AI is unknown Approaches to Evaluation of the Severity of Regurgitation Semi-quantitative measures Mild, moderate or severe utilizing Color jet area Vena contracta width Pressure half-time (for aortic insufficiency) Distal flow reversals Approaches to Evaluation of the Severity of Regurgitation Quantitative measures Regurgitant volume (RV) Retrograde volume flow across the valve Expressed either as • Instantaneous flow rate in ml/sec • Averaged over the cardiac cycle in ml/beat Calculated by • PISA • Volume flow rates across the regurgitant and competent valve (Spectral Doppler Technique) • 2D total left ventricular stroke volume minus Doppler forward stroke volume Regurgitant fraction RF = RV/SV total Regurgitant orifice area Effective Regurgitant Orifice Area (EROA) Application of continuity equation “what flows in must flow out” Based on theory of conservation of mass May be calculated utilizing Spectral Doppler technique Application of the PISA method Spectral Doppler Method Spectral Doppler Technique Regurgitant volume through an incompetent valve is equal to the flow at the regurgitant orifice Stroke volume may be calculated from the CSA and the VTI RVol = EROA x VTIRJ RVol = Regurgitant volume (cc) EROA = Effective regurgitant orifice area (EROA) VTIRJ = Velocity time integral of the regurgitant jet (cm) Rearrange equation EROA = RVOL/VTIRJ Non-dynamic Spectral Doppler Technique “Step by Step” 1. 2. 3. 4. 5. Calculate stroke volume (SV) through LVOT Calculate stroke volume (SV) through MV Calculate the regurgitant volume (cc) Measurement of VTI of regurgitant signal Calculate the effective regurgitant area (cm2) Non-dynamic Spectral Doppler Technique “Step by Step” 1. Calculate stroke volume (SV) through LVOT Measure LVOT diameter from PLAX Inner edge to inner edge CSA = 0.785 x D2 Measure the LVOT VTI from apical long axis or apical four chamber anterior tilt SV (cc) = CSA (cm2) * VTI (cm) Spectral Doppler Technique “Step by Step” 2. Calculate the stroke volume through the mitral valve Measure the mitral valve annulus Measure mitral annulus VTI Apical four chamber at mid-diastole: inner edge to inner edge CSA = 0.785 x D2 PW Doppler at the level of the annulus SV (cc) = CSA (cm2) * VTI (cm) Spectral Doppler Technique “Step by Step” 3. Calculate the regurgitant volume R Vol(MR) = SV (MV) – SV (LVOT) 4. Measurement of VTI of regurgitant signal Optimize CW Doppler spectrum of regurgitant signal Spectral Doppler Technique “Step by Step” 5. Calculate the effective regurgitant orifice area (EROA in cm2) EROA = RVol(MR) ÷ VTI(MR) Spectral Doppler Technique Limitations Accuracy of measurements Inadequate spectral Doppler envelope for mitral regurgitation VTI measurement Significant learning curve May be considered time consuming and tedious Spectral Doppler Technique Clinical Significance of the EROA and Mitral Regurgitation Color Doppler Imaging Jet Area Screening for significant flow often based on flow disturbance in receiving chamber Size of flow disturbance evaluated in at least two views Important to evaluate color flow disturbance based on cardiac cycle timing Size of jet relative to receiving chamber provides qualitative index of regurgitant severity on scale of 0(mild) - 4+(severe) Color Doppler Imaging Color Doppler Imaging Aortic Regurgitation Best evaluated from PLAX approach Shorter distance from transducer to flow region of interest: better signal to noise ratio Multiple flow directions within jet Color Doppler Imaging - Mmode Evaluation of exact timing of flow In relation to QRS and valve opening and closure Higher sampling rate Vena Contracta Narrowest diameter of the flow stream Reflects diameter of regurgitant orifice Relatively unaffected by instrument settings Recommended Perpendicular to jet width Zoom mode Narrow sector and depth Non-dynamic Proximal Isovelocity Surface Area Method (PISA) Proximal Isovelocity Surface Area Basic Principle Based on conservation of energy PISA measurement analogous to calculation of stroke volume proximal to a stenotic valve Variation of continuity equation Flow rate proximal to a narrowed orifice is the product of the hemispheric flow convergent area and the velocity of that isovelocity shells Expressed by Q = 2r2Vr Q = flow rate 2r2 = area of hemispheric shell (cm2) Vr = velocity at the radial distance – r(cm/s) Non-dynamic Proximal Isovelocity Surface Area Basic Principle Continuity principle: blood flow passing through a given hemisphere must ultimately pass through he narrowed orifice Flow rate through any given hemisphere must equal the flow rate through the narrowed orifice 2r2Vr = A0*V0 • A0 = area of the narrowed orifice (cm2) • V0 = peak velocity through the narrowed orifice (cm/s) Rearrange the equation • A0 = (2r2Vr )/V0 Non-dynamic Proximal Isovelocity Surface Area Basic Principle Continuity principle: blood flow passing through a given hemisphere must ultimately pass through he narrowed orifice Flow rate through any given hemisphere must equal the flow rate through the narrowed orifice 2r2Vr = A0*V0 • A0 = area of the narrowed orifice (cm2) • V0 = peak velocity through the narrowed orifice (cm/s) Rearrange the equation • A0 = (2r2Vr )/V0 Proximal Isovelocity Surface Area (PISA) Application in Calculation of Effective Orifice Area (EROA) Regurgitant valve acts as the narrowed orifice Peak velocity is equivalent to the peak velocity of the regurgitant jet Utilizing Doppler colorflow radius and velocity at the radial distance can be identified Proximal Isovelocity Surface Area (PISA) Application in Calculation of Effective Orifice Area (EROA) Adjustment of Nyquist limit enlarges size of shell for more accurate measurement Shift baseline to downward typically 20 to 40 cm/sec The surface area of a hemisphere is calculated by the formula: Surface area = 2πr2 Multiplication of aliasing velocity with surface area yields regurgitant volume Non-dynamic Proximal Isovelocity Surface Area Effective Regurgitant Orifice Area (ROA) EROA = RVmax /VMR RVmax : Regurgitant Volume (cm3) VMR : Velocity of mitral regurgitation (cm/sec) Non-dynamic Steps for Obtaining PISA Regurgitant Orifice Area 1. Zoom mitral valve 2. Decrease color scale to identify surface of hemisphere shell 3. Note alias velocity – color bar (Valiasing) 4. Measure alias from orifice to color change (r) 5. Regurgitant volume RVmax = 2 r2 x Valiasing 6. Measure peak mitral regurgitant velocity (VMR) 7. Effective Regurgitant Orifice Area EROA = RVmax/VMR Steps for Obtaining PISA Regurgitant Orifice Area Surface area = 2r2 2(0.67 cm)2 = 2.80 cm2 Regurgitant Volume Flow Rate RVmax=Surface Area* Valiasing 2.80 cm2 * 26 cm/sec = 72.8 cm3/sec Effective Regurgitant Orifice Area EROA = RVmax/VMR (72.8 cm3/sec) / (66.2 cm/sec) = 1.1 cm2 0.67cm Simplified Method for Calculation of the Mitral Regurgitant Volume May be employed when appropriate CW jet is unable to be obtained (i.e. eccentric jet) Based on premise: Ratio of maximum MR velocity to VTI MR is equal to a constant of 3.25 Regurgitant volume = (2r2Valiasing)/3.25 2r2 = area of hemispheric shell derived from the radius [r] (cm2) Valiasing = aliased velocity identified as the Nyquist limit (cm/s) 3.25 constant Clinical Significance of the PISA Radius and Valvular Regurgitation Proximal Isovelocity Surface Area – EROA MV Considerations Assumption is made that RVmax and VMR occur at the same position in the cardiac cycle PISA is larger in large volume sets and smaller in smaller volume sets Also changes size in accordance with color Doppler scale PISA should be recorded in a view parallel to flow stream typical apical four chamber If PISA is hemi-elliptical or if valve is nonplanar, alternate approach or alternate corrections PISA Limitations Nonoptimal flow convergence Phasic changes Eccentric jets Interobserver variability Isovelocity surface not always hemisphere PISA model is a sphere. Mitral regurgitant orifice may be irregular Multiple regurgitant jets May not be able to completely envelope the mitral regurgitation trace Mitral flow rate will vary throughout systole PISA – EROA Limitations Nonoptimal flow convergence Suboptimal Flow Convergence Suboptimal Flow Convergence Flow: not symmetric Perforated mitral leaflet - TEE Continuous Wave Doppler Approach Signal intensity Proportional to number of blood cells contributing to regurgitant signal Compare retrograde to antegrade flow intensity Weak signal = mild regurgitation Strong signal = severe regurgitation Intermediate signal = moderate regurgitation Continuous Wave Doppler Approach Antegrade flow velocity Regurgitation results in increase in antegrade flow across the incompetent valve Greater the severity of regurgitation; the greater the antegrade flow velocity • Consideration of co-existent stenosis Continuous Wave Doppler Approach Time course (shape) of mitral regurgitant velocity curve Dependent on time-varying pressure gradient across regurgitant orifice Related to pressure gradient Normal LV systolic pressure = 100 – 140 mmHg Normal LA systolic pressure = 5 – 15 mmHg Difference therefore: 85 – 135 mmHg • MR velocity is typically 5 – 6 m/sec Continuous Wave Doppler Approach Time course (shape) of mitral regurgitant velocity curve Normal LV systolic function: • Rapid acceleration to peak velocity • Maintenance of high velocity in systole • Rapid deceleration prior to diastolic opening of the mitral valve Increase in left atrial pressure results in late systolic decline in the instantaneous pressure gradient Continuous Wave Doppler Approach Shape of aortic regurgitant curve Dependent on time course of diastolic pressure difference Normal low end-diastolic pressure Aortic end-diastolic pressure is normal (high pressure difference) Slow rate of pressure decline Acute AI results in more rapid velocity decline in diastole Continuous wave Doppler across AV Decel = 270 cm/sec Decel >500 cm/sec With permission, Dunitz 2000 Distal Flow Reversals Severe atrioventricular valve regurgitation may result in Flow reversal of veins entering atrium Flow reversal in hepatic vein due to severe tricuspid regurgitation Flow reversal in pulmonary veins on TEE due to severe mitral regurgitation Distal Flow Reversals Severe semilunar valve regurgitation may result in Flow reversal of associated vessel Abdominal flow reversal in diastole due to severe aortic regurgitation. Note moderate aortic regurgitation is limited to descending thoracic aorta Aortic Regurgitation Aortic Valve Diastole: free margins of the cusps coapt tightly preventing the backflow of blood into the ventricle. “Y” shape in PSAX (sometimes referred to as inverted Mercedes-Benz sign) Systole: cusps open widely in a triangular fashion, with flexion occurring at the base. Semi-lunar valve Aortic Cusps Three Cusps named for the corresponding origins of the coronary arteries. Folds of endocardium with a fibrous core attached to the aortic wall rather than the ventricular wall. Base of the cusps is thicker and cusps themselves are thin and translucent. Crescent and pocket shaped. Equal in size. Aortic Cusps Free edge of each cusp curves upward from commissure and form a slight thickening at tip called Arantius nodule. When valve closes: three nodes meet in center, allowing coaptation to occur along three lines. “Y” shape in diastole. Behind each cusp is its associated Sinus of Valsalva. Aortic Cusps Sinotubular junction Sinus of Valsalva Sinuses represent out-pouchings in the aortic root directly behind each cusps. Function to support the cusps during systole and provide reservoir of blood to augment coronary artery flow during diastole. Sinus and its corresponding cusp share the same name. Noncoronary sinus is posterior and rightward just above the base of the interatrial septum. M-mode Normal AV – Coaptation Point In Center Of Aortic Root Parasternal Views Apical views Aortic valve in the far field Poor resolution of anatomic details PARALLEL to flow Best view for measuring velocities across valve AR jet AS jet Subcostal view Often the view that “saves” the study Non-coronary cusp is intersected by the interatrial septum Short axis Subcostal view - Non-coronary cusp intersected by Interatrial septum TEE views Anterior root is at the bottom of the screen (reverse parasternal LAX view) Leaflet at top of screen usually noncoronary (can be left coronary cusp) Leaflet at bottom of screen is right coronary cusp TEE - 137º Non-dynamic Aortic Cusps – Lambl’s Excrescences Thin, delicate filamentous strands that arise from ventricular edge of aortic cusps. Normal variants. Seen increasingly with advancing age and improved image quality. Aortic Cusps – Lambl’s Excrescences Originate as small thrombi on endocardial surfaces Have the potential to embolize to distant organs 10-56 Feigenbaum 21-9 Lambl TEE Feigenbaum Aortic Insufficiency Presence of AI should be assessed by Doppler Flail AV leaflet will always produce AI Direction of regurgitant jet may or may not produce MV or septal fluttering Use TEE of abscess detection Aortic Regurgitation History Exertional dyspnea Fatigue Palpitations Chest pain (angina) Dizziness Syncope (uncommon) Congestive Heart Failure (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea) Right heart failure (e.g., jugular venous distention, hepatomegaly, peripheral edema, ascities, anasarca) Aortic Insufficiency Complications Chronic AI; Initially patients may appear asymptomatic and may later develop signs of CHF Patients with bicuspid valve are at higher risk for endocarditis LV volume overload (similar to MR) Diastolic murmur at left sternal border (LSB) and apex (Austin-Flint murmur- diastolic rumble) Acute AI; sudden onset of CHF may occur because the LA does not have time to enlarge Aortic Insufficiency Etiology • Inflammatory • Structural • Genetic • Stress Aortic Insufficiency (AI) Inflammatory Rheumatic Fever Ankylosing Spondylitis Rheumatoid Arthritis Systemic Lupus Erythematosus Syphilus Phen-fen Aortic Insufficiency (AI) Structural Atherosclerosis Bicuspid or unicuspid aortic valve Aortic dissection Aortic valve prolapse Infective endocarditis Ventricular septal defect (perimembranous, outlet) Sinus of Valvsalva aneurysm Trauma Catheter balloon valvuloplasty Dilated root and effacement sinotubular junction Non-dynamic Preserved root - dilated ascending aorta Non-dynamic Aortic Valve Prolapse Best seen in parasternal long axis Disruption of commissural support Dissection Dilatation Perimembranous VSD Myxomatous or congenitally abnormality Aortic Valve Prolapse Right Coronary Cusp Non-dynamic Severe AR filling LVOT Non-dynamic Bicuspid Aortic Valve 10-47 Feigenbaum Quadracusp Aortic Valve http://video.google.com/videoplay?docid=-1101037639424512577# Endocarditis 19-32a Feigenbaum 19-32b Feigenbaum Rupture of Sinus of Valsalva Due to Endocarditis 13-17 Feigenbaum Endocarditis 10.33b Feigenbaum 10.33a Feigenbaum Aortic Dissection Proximal extent usually 1 cm distal to sinotubular junction Flap may extend to root Rupture into pericardial space Dissect coronary (right > left) Disrupt AV architecture Transthoracic very INSENSITIVE TEE aortic dissection disrupting commissure between right and left coronary cusps Non-dynamic TEE Long Axis View – Dissection Flap In Aortic Root Non-dynamic images Marfan’s Syndrome Connective tissue multisystemic disorder characterized by Skeletal changes (arachnodactyly, long limbs, joint laxity, pectus) Cardiovascular defects Aortic aneurysm which may dissect Mitral valve prolapse Ectopia lentis Autosomal dominant inheritance, caused by mutation in the fibrillin-1 gene (FBN1) on chromosome 15q . Marfan’s Syndrome Arachnodactyly in an 8-year-old girl with Marfan’s syndrome Marfan Syndrome 20.22b Feigenbaum 20.22a Feigenbaum Marfan’s Syndrome 10.31b Feigenbaum Aortic Insufficiency (AI) Stress Systemic hypertension (dilated root due to hypertension is the most common cause of AI) Renal failure Type A Aortic Dissection 20.30b Feigenbaum 20.30a Feigenbaum “Renal” Heart 22.7 Feigenbaum Aortic Insufficiency (AI) M-Mode, 2D Criteria and Doppler Criteria AI - M-Mode Criteria MV fluttering in early diastole Austin-Flint murmur Diastolic septal fluttering depends on direction of jet Chronic AI Increased LV size with minimal LVH Normal or hyperdynamic LV systolic function In decompensated state, LV systolic function may be depressed. Presence of “B” bump (Increased LV end diastolic pressure) associated with acute AI. Premature AV opening in acute AI Aortic Insufficiency 2D Criteria Valve Anatomy Flail, Bicuspid, Endocarditis, Prolapse Chronic AI; enlarged LV cavity with minimal LVH – normal or hyperdynamic LV function unless decompensated Ascending aorta size usually increased; identify aortic aneurysms (ascending, arch, descending) Reverse doming of anterior mitral valve leaflets is associated with severe AI Non-dynamic Aortic Insufficiency Doppler Criteria Evidence of diastolic turbulence beginning at aortic valve closure Patients with severe aortic insufficiency may demonstrate a reversed diastolic flow by PW Doppler in the abdominal or thoracic aorta. Color flow mapping of flow disturbance into LV may disclose severity. Color flow may be useful in quantitating severity based on width of flow disturbance to width of LVOT in parasternal long-axis view. Aortic Insufficiency Doppler Criteria Doppler cursor is parallel to flow, “Normal” peak velocity of an aortic regurgitant jet is 3.0 to 5.0 m/s Due to the pressure difference between the aorta and LV during diastole. Spectral Doppler display signal intensity Should be considered in evaluating the degree of AI. Compare the forward aortic flow with the signal strength of the AI jet. Aortic Insufficiency 10.5 Feigenbaum Aortic Insufficiency Aortic Valve Prolapse - 2D Criteria Parasternal long-axis view: posterior placement of aortic leaflet(s) into LVOT during diastole. May be noted in association with MV or TV prolapse. Right coronary cusp prolapse may occur with membranous ventricular septal defect. M-Mode is not diagnostic; may see echo in LV outflow tract during diastole. Sinus of Valsalva aneurysm Non-dynamic Aortic Insufficiency - Flail Aortic Leaflet 2D Criteria In PLAX, loss of leaflet coaptation and erratic echoes in LVOT PSAX-Ao may disclose leaflet(s) involved. Perforations in leaflets Aortic ring abscess due to endocarditis Flail Aortic Leaflets - M-Mode Criteria Course flutter of closed aortic leaflets during diastole. Erratic systolic motion of closed aortic leaflet(s). When AI is present, associated diastolic fluttering of MV and/or septum. Enlarged LV chamber with hyperdynamic LV systolic function. Premature closure of AV in acute AI. Left Ventricular Response Chronic volume overload Progressive dilation and increased sphericity of LV Initially LV systolic function remains normal Stroke volume is ejected across the aortic valve into the high-impedence systemic vasculature therefore not hyperdynamic Long asymptomatic period Chronic gradual increasing AI LV remains compliant in diastole: end-diastolic pressure remains normal Over time LV systolic dysfunction occurs in presence of significant regurgitation Diastole Systole LV Dysfunction Secondary to AI 10-35 Feigenbaum Left Ventricular Response Acute Aortic Regurgitation Short interval from set of volume overload to clinical presentation Volume overload is poorly tolerated due to the normal left ventricular size and the constraining effects of the pericardium. Mitral regurgitation Left ventricular pressure increases rapidly. Premature closing of MV, which can be recorded using M-mode imaging. Acute AI Usually caused by endocarditis Disruption or destruction of aortic leaflets and/or aortic dissection Annular and/or root dilation Acute AI Acute AI may also be caused by: Trauma Effect of AI on mitral valve 10.030 Feigenbaum Severity of Aortic Regurgitation Severity of Aortic Regurgitation Semi-quantitative measurement No gold standard Invasive measurement is qualitative Ventricular opacification following aortic root injection with IV dye Severity of Aortic Regurgitation Size of the color flow jet Length of jet dependent on ultrasound machine settings Gain Pulse repetition frequency Transmission frequency Length of jet dependent on ventricular compliance Severe AR - broad jet extends into LV cavity Severity of Aortic Regurgitation Width of jet compared to LVOT diameter Measured in parasternal long axis view Or in TEE longitudinal plane <25% - mild AR 25-40% moderate >40% severe Mild AR - jet ratio <25% Severe AR - jet ratio >60% Grading Aortic Regurgitation by Regurgitant Jet Area/LVOT Area (PLAX) 10.44a Feigenbaum 10.44b 10.44c ≥ 65% Regurgitant Jet Area/LVOT Area (PLAX) 10.36 Feigenbaum View Dependent Color Flow Doppler Evaluation Both Images Obtained From Same Patient 10.48b Feigenbaum 10.48a Feigenbaum Severity of Aortic Regurgitation Short axis area of regurgitation Dependent on level of short axis image Short axis of the LVOT, not aortic sinuses Color M-mode Continuous wave Doppler across AV Deceleration slope of AR spectral envelope Pressure gradient = 4 V 2 Fall in velocity during diastole related to decrease in pressure gradient Flat slope indicates no change in gradient during diastole = mild AR Deceleration Slope Grading of AR (AI) <200 cm2/sec = mild 200 - 350 cm2/sec = moderate >350 cm2/sec = severe Pressure half time also may be used Dependent on ventricular compliance Eccentric jets may be difficult to assess Diastolic Reversal of Flow Sample volume in descending thoracic aorta from suprasternal notch Also in abdominal aorta from subcostal position Reversal of flow in diastole from abdominal aorta Indications for Surgery AR Symptoms End-systolic internal dimension > 55 mm May not be applicable in women - use smaller LVIDD Fall in ejection fraction Diastolic dimension > 70 mm associated with sudden death Mitral Regurgitation Mitral Valve Apparatus Left atrial wall Mitral annulus Anterior and posterior leaflets Chordae Papillary muscles Left ventricular myocardium underlying the papillary muscles Mitral Regurgitation Occurs during systole, which at normal heart rates constitutes approximately 1/3 of the cardiac cycle. Mitral Regurgitation Hemodynamically significant mitral regurgitation results in volume overload. Subsequent left ventricular dilation and left atrial dilation. Consequentially there is elevation of left atrial pressure, which is transmitted in pulmonary congestion. Mitral Regurgitation Signs and Symptoms Shortness of breath, especially with exertion or when lying down Fatigue, especially during times of increased activity Cough, especially at night or when lying down Heart palpitations — sensations of a rapid, fluttering heartbeat Swollen feet or ankles Heart murmur Excessive urination Mitral Regurgitation- Acute Acute severe mitral regurgitation often results in acute pulmonary congestion. Left atrial size is normal. Left ventricular sysotolic function is hyperdynamic Most common cause of acute MR: Rupture of chordae tendineae due to mitral valve prolapse Acute ischemia Infarction Infective endocarditis Mitral Regurgitation-Chronic Chronic mitral regurgitation may be tolrated for decades Left ventricular size is dilated, left ventricular function is hyperdynamic early, may be normal or depressed with longstanding regurgitation, enlarged LA Etiology Myxomatous valve disease Annular dilatation Mitral Regurgitation Etiologies Rheumatic mitral valve disease Mitral valve prolapse Myocardial infarction (papillary muscle dysfunction) Ruptured chordae tendineae Flail mitral leaflet Mitral valve vegetations Dilated cardiomyopathies Left ventricular outflow tract obstructions Use of certain appetite suppressants Calcification of the mitral annulus Tumors of the mitral valve Annular Dehiscence Radiation damage Rheumatic Heart Disease Non-dynamic Mitral Valve Prolapse Non-dynamic Mitral Valve Prolapse 11.72a-72b Feigenbaum Mitral Valve Prolapse 11.80a Feigenbaum Mitral Valve Prolapse Ruptured Papillary Muscle Due to Coronary Artery Disease 15.44 Feigenbaum Ruptured Chordae Tendineae Standard real-time B-scan Duplex scan: color Doppler superimposed on real-time B-scan Diagnosis: Severe mitral regurgitation due to flail posterior MV leaflet. Underlying pathology: Mitral valve prolapse with ruptured chordae tendinae. Data source : Arizona Society of Echocardiography Image Library Flail Mitral Leaflet Rupture of the supporting apparatus of the mitral valve allowing the tip of the leaflet to project into the left atrium in systole The most frequent etiologies are : Chordal rupture complicating mitral valve prolapse syndrome Infective endocarditis Papillary rupture caused by acute myocardial infarction. Primary degeneration of the chordae is a cause of spontaneous rupture. 11.81b Feigenbaum Flail Mitral Leaflet Yale Atlas of Echo- Flail Mitral Valve Mitral Valve Vegetations/Infections Mitral Valve Vegetations/Infections Mitral vegetations Found on the upstream side of valves such as the left atrium in mitral valvular vegetation. Mitral Regurgitation 13.3a & b Feigenbaum Dilated Cardiomyopathies Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Idiopathic Hypertrophic Subaortic Stenosis (IHSS) IHSS Appetite Suppressants Common name: Fen-Phen (fenfluramine, phentermine, dexfenfluramine) Use of Fenfluramine or dexfenfluramine for more than four months may have an increased risk of valvular heart disease. Fenfluramine and dexfenfluramine are no longer marketed in the U.S. as of 1997 and have no current FDA labels. Calcification of the Mitral Annulus Mitral annulus area normally is smaller in systole than in diastole. Increased rigidity of the annulus impairs systolic contraction of the annulus leading to mitral regurgitation. Appearance on 2D imaging as area of increased echogenicity on left ventricular side of annulus immediately adjacent to attachment point of the posterior leaflet. Commonly seen in elderly subjects and in younger patients with renal failure or hypertension. 11.89 Feigenbaum Tumor of mitral valve/Papillary Fibroelastoma Unlike vegetations: fibroelastomas are more often found on the down stream side of the valve Usually of no clinical significance but may cause mitral regurgitation 21.6 Feigenbaum Annular Dehiscence Infrequent sequela of blunt trauma. Presumed mechanism Sudden dramatic increase in pressure against a closed mitral valve resulting in tearing of the posterior leaflet from the mitral valve annulus 19.31b Feigenbaum Radiation Damage Note Pathologic echo density of the anterior mitral leaflet Reduced mobility of the portion of the mitral valve Increased echo densities in the aortic valve, Which is also a consequence of radiation therapy in these two relatively young patients. 11.095a Feigenbaum Mitral Regurgitation Jets Central Bileaflet prolapse Rheumatic disease Peripheral Vegetations Unicuspid prolapse Flail Mitral Regurgitation Color Doppler is primary tool for detection and quantification Recognition of expected timing of regurgitation is critical. Mitral Regurgitation Doppler evaluation of mitral regurgitation Not all color Doppler signals appearing within the LA represent mitral regurgitation Mitral Regurgitation Normal posterior motion of the blood pool caused by mitral valve closure. Pulmonary Vein Flow 11.40 Feigenbaum Mitral Regurgitation Reverberation from aortic flow 11.39 Feigenbaum Mitral Regurgitation Characteristics of True Mitral Insufficiency/Regurgitation Evidence of proximal flow acceleration (proximal isovelocity surface area (PISA) Flow conforms to the appearance of a true “jet” or ejection flow with a vena contracta Downstream (left atrial) appearance is consistent with a volume of blood being ejected through a relatively constraining orifice Mitral Regurgitation Characteristics of True Mitral Insufficiency/Regurgitation (cont.) Flow signal is appropriately confined to systole Color Doppler signals are appropriate in color for the anticipated direction and/or reveal the appropriate variance or turbulence encoding PW and CW Doppler confirms origin, timing and direction of blood flow Mitral Regurgitation Physiologic Spacially restricted to the area immediately adjacent to valve closure Short in duration Represents only a small regurgitant volume When meticulously sought MR can be detected in 70%-80%. Determination of Mitral Regurgitation Severity Determination of Mitral Regurgitation Color Flow Doppler Size of the flow disturbance relative to the chamber receiving the regurgitant jet in at least two views. Severity scale of 0(mild) to 4+(severe) Limitation: Variation with technical and physiological factors Continuous Wave-Doppler Signal intensity Shape of velocity curve Limitation: Qualitative Vena Contract Width Width of regurgitant jet at origin Limitation: Small values, careful measurement needed Determination of Mitral Regurgitation …continued PISA Calculation of RV (regurgitant volume) and ROA (regurgitant orifice area) Less accurate with eccentric jets Volume Flow at Two Sites Calculation of RV (regurgitant volume) and ROA (regurgitant oriface area). Limitation: Tedious Distal Flow Reversals Pulmonary Vein reversal in Doppler Limitation: Qualitative, affected by LA pressure Continuous Wave Signal intensity Proportional to the number of blood cells contributing to the regurgitant signal Weak signal reflects mild regurgitation, whereas a signal equal to intensity to the antegrade (forward) flow reflects severe regurgitation Time course (shape) of the velocity curve Acute MR: increase in end-systolic left atrial pressure results in last-systolic decline in the instantaneous pressure gradient. Waveform appears more early slanted “V” than an equal “V”. Vena Contracta 11.42 Feigenbaum Distal Flow Reversals Significant volume of flood is displaced by the regurgitant resulting in flow reversal seen in the pulmonary veins entering the left atrium Reversal of normal patterns of systolic inflow of pulmonary veins. Determination of Mitral Regurgitation PISA (Proximal Isovelocity Surface Area) The highest velocity of blood flow occurs proximal to the valve plane Series of isovelocity “surfaces” leading to the high velocity jet in the regurgitant orifice Decision Making Repair or Replacement Most important factor: left ventricular size and function Progressive dilatation, an end-systolic dimension of greater than 45 mm or any reduction of left ventricular function may prompt surgical intervention regardless of symptomatic status. Posterior leaflet prolapse and annular dilatation are most amendable to repair, others require more complex procedures with lower likihood of successful repair. Intraoperative Evaluation of Mitral Repair Transesophageal Echo is used during operations. Baseline images are obtained in the operating room to reconfirm regurgitant severity. After valve repair, the patient is weaned from cardiopulmonary bypass and valve anatomy and regurgitation is re-evaluated. Intraoperative Evaluation of Mitral Repair If significant residual mitral regurgitation is present, Second bypass pump may be done to allow a second attempt at repair or mitral valve replacement. Complications may include: Left ventricular outflow tract obstruction Functional mitral stenosis Worsening of left ventricular systolic function. Actually young hairy man. Antibiotics prior to dental cleanings is no longer indicated in patients with mitral valve prolapse. Tricuspid Regurgitation Anatomy of the Tricuspid Valve Anatomy of the Tricuspid Valve Atrioventricular valve that prevents backflow of blood from the right ventricle into the right atrium. Composed of: tricuspid annulus leaflet tissue chordae tendinae papillary muscles Tricuspid Annulus Make-up of the tricuspid valve is similar to mitral valvular composite but is less strong Shape is roughly triangular Largest valvular orifice of the heart Tricuspid Valve Leaflets Three leaflets of the tricuspid valve Named based upon the physical location in relation to the right ventricular walls Anterior Medial Inferior (posterior) Leaflets composed of collagenous material surrounded by endocardium Basal zones are thicker than the tips, which possess indentations or commissures, which attach to chordae tendinea Chordae Tendinae Support the leaflets and prevent them from prolapsing during systole Strong, fibrous, collagenous structures which arise from papillary muscles and insert on the ventricular side of the valve leaflets Primary Secondary Tertiary Papillary Muscles Two major papillary muscles Less prominent than those of the left ventricle Named for their location within the ventricle Anterior papillary muscle Largest Located on the anterolateral wall of the ventricle Supplies chordae to the anterior leaflet Posterior (sometimes called inferior) Located on the inferoseptal wall Muscle is smaller and frequently has two or three head Supplies chordae to the inferior leaflet Unique Feature of the Right Ventricle Medial or septal leaflet receives its chordae directly from the ventricular septum, found only in the RV Normal Valve Area of the Tricuspid Valve 7-9 2 cm Tricuspid Valve Views RVIT Apical 4 PSAX-Ao Subcostal Long Axis M-Mode Tricuspid Valve Transesophageal Echocardiogram 110 degree view at the base of the heart 12.24 Feigenbaum M-Mode Tricuspid Valve Tricuspid Regurgitation Disorder involving backflow of blood From the right ventricle to the right atrium during contraction of the right ventricle. May be acute, chronic, or intermittent The most common cause of tricuspid regurgitation Not damage to the valve itself Enlargement of the right ventricle, which may be a complication of any disorder that causes right ventricular failure Tricuspid Regurgitation Common abnormality in the adult population Caused by two general mechanisms Functional Anatomic Functional (secondary) – Structurally Normal Tricuspid Valve Pulmonary hypertension due to left heart failure Cor pulmonale Primary pulmonary hypertension Right heart pathological conditions Pulmonic stenosis, Eisenmenger’s syndrome Constrictive pericarditis Anatomic (primary) – Abnormal Tricuspid Apparatus Rheumatic heart disease Infective endocarditis Tricuspid valve prolapse Tricuspid annular dilatation/calcification Ruptured chordae tendinae Papillary muscle dysfunction Carcinoid syndrome Ebstein’s anomaly Catheter induced (e.g. pacemaker wire) Prosthetic heart valve Systemic lupus erythematosus Trauma Tumor Orthotopic heart transplantation Endomyocardial fibrosis Physiologic Symptoms Usually well tolerated Weakness Fatigue Congestive heart failure Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Pulmonary edema Tricuspid Valve Prolapse Tricuspid Regurgitation Complications Severe right heart failure Renal failure when severe congestion is present Chest X-Ray Right atrial enlargement Right ventricular enlargement Left heart enlargement http://www.yale.edu/imaging/findings/enlarged_heart/index.html Suggests functional tricuspid regurgitation Pulmonary congestion Suggests functional tricuspid regurgitation Pulmonary artery dilatation Suggests functional tricuspid regurgitation Prominent superior vena cava/right innominate vein Cardiac Catheterization Right ventriculography to determine presence and severity Increased right atrial pressure and right ventricular diastolic pressure Kussmaul’s sign Increased right atrial pressure with inspiration Treatment None Tricuspid regurgitation may be well tolerated for years Endocarditis prophylaxis Digitalis/diuretics Vasodilators in patients with pulmonary hypertension Anticoagulation Right heart failure Treatment Tricuspid valve excision Drug addition with infective endocarditis Annuloplasty Carpentier ring Kay ring Dural ring Tricuspid valve replacement Usually with a tissue valve to reduce the risk of thrombus formation M-Mode Criteria of Tricuspid Regurgitation Right ventricular overload pattern Increased D-E amplitude of the anterior tricuspid valve leaflet Increased E-F slope of the anterior leaflet of the tricuspid valve leaflet B “bump” or “notch” of the anterior tricuspid valve leaflet indicated increased right ventricular end-diastolic pressure (≥9 mmHg) Color M-mode may be useful in determining the presence, timing and duration of tricuspid regurgitation when combined with PISA 2D Criteria for Tricuspid Regurgitation Anatomic basis for the presence of tricuspid regurgitation Tricuspid valve vegetation, ruptured chordae tendinae Right atrial dilatation with systolic expansion Right ventricular diastolic expansion Right ventricular dilatation Right ventricular volume overload pattern 2D Criteria for Tricuspid Regurgitation continued D-shaped left ventricle during ventricular diastole indicating a right ventricular diastolic volume overload Globular (spherical)-shaped right ventricle which may form the cardiac apex Dilated tricuspid valve annulus (≥3.0 cm in systole, ≥3.2 cm in diastole) indicates severe tricuspid regurgitation 2D Criteria for Tricuspid Regurgitation continued Dilated inferior vena cava with lack of inspiratory collapse (normal 1.2 to 2.3 cm) Dilated hepatic veins (normal: 05 to 1.1 cm) Dilated superior vena cava/innominate vein Systolic bowing of the interatrial septum toward the left atrium Systolic reflux of saline contrast into the inferior vena cava and hepatic vein may indicate significant tricuspid regurgitation May also be visualized by color flow Doppler Determine right atrial dimension, area and volume Determine right ventricular end diastolic, end systolic dimensions, volumes and ejection fraction PW Doppler - Inflow Up to 93% of normal patients appear to have tricuspid regurgitation; calculate the duration and length of the regurgitant Increased tricuspid E velocity may indicate significant tricuspid regurgitation Laminar tricuspid regurgitation flow may denote significant regurgitation Associated with lack of tricuspid valve leaflet coaptation Important to Note Tricuspid regurgitation is a volume overload of the right heart Most common etiology of tricuspid regurgitation is pulmonary hypertension due to left heart pathology 90% incidence when systolic pulmonary artery pressure is >40 mmHg Classic clinical triad of prominent jugular distension, holosystolic murmur at the lower sternal border increasing with inspiration and a pulsatile liver is present in only 40% of patients with severe tricuspid regurgitation Myxomatous, redundant appearance of the involved tricuspid valve leaflet(s) Tricuspid annular dilatation (normal 2.2 cm ± 0.3) – apical four chamber Important to Note - Continued Tricuspid regurgitation is the most common physiologic regurgitation Normal tricuspid valve apparatus Normal chamber dimensions Peak tricuspid regurgitation (2.0 m/s ± 0.2) Small regurgitant jet area are indicators of physiologic flow Significant Tricuspid Regurgitation Regurgitant jet area ≥0.9 cm2 Right atrial area ›30 cm2 Proximal jet jet width ≥0.8 cm Systolic flow reversal in the hepatic veins Paradoxical septal motion Diastolic septal flattening Inferior vena cava diameter ≥2.1 cm Lack of inferior vena cava respiratory variation Secondary Effects of TR Moderately severe tricuspid regurgitation. Dilated right ventricle and diastolic flattening of the ventricular septum consistent with a right ventricular volume overload. 12.33 Feigenbaum Mild Tricuspid Regurgitation Apical four-chamber view recorded in a patient with mild to moderate tricuspid regurgitation. Note the color Doppler signal filling approximately 25% of the right atrium Dilated Cardiomyopathy 12.30a Feigenbaum 12.30b Feigenbaum Flail Tricuspid Leaflet Due to Trauma (MVA) 12.31a Feigenbaum 12.31b Feigenbaum Marfan Syndrome • Myxomatous changes • Tricuspid valve with pronounced bileaflet prolapse (small arrows) • Incidental note: • Prominent Eustachian valve (EV) 12.32 Feigenbaum Carcinoid Heart Disease Presence of Carcinoid Tumors Found predominantly in the gastrointestinal tract Tumors produce vasoactive substances that ultimately cause endothelial damage to the right side of the heart Primary tumors can be small, with hepatic metastases noted in most patient who demonstrate cardiac involvement Involvement of the heart occurs late in the progression of the disease in nearly half of those with carcinoid syndrome Carcinoid heart disease. Insert shows pulmonary stenosis. The leaflets of the tricuspid valve are thickened. The valve is predominantly incompetent and causes pulmonary regurgitation. Fibrous plaques are deposited on the lining of the right ventricle and pulmonary trunk. Carcinoid Heart Disease Clinical Symptoms Episodes of facial flushing with stimuli Abdominal pain Diarrhea Renal and hepatic failure Hepatomegaly is usually associated with later stages of the disease Cardiac signs include Elevated venous pressure Systolic and diastolic murmurs Carcinoid Heart Disease 2D Echocardiographic Signs Distinctive and are usually restricted to the right heart Findings include: Dilation of the right ventricle with abnormal septal motion, indicative of right ventricular volume overload Thickened tricuspid valve leaflets that are retracted, with foreshortened chordae Tricuspid valve leaflets usually do not coapt completely and remain open throughout the cardiac cycle Carcinoid Heart Disease Tricuspid Doppler Signs Tricuspid regurgitation, most prevalent finding Increased diastolic velocities across the tricuspid valve Carcinoid Complete failure of coaptation of the leaflets, which results in severe tricuspid regurgitation, confirmed in an apical fourchamber view with color flow Doppler imaging 12.41 Feigenbaum Epstein’s Anomaly Congenital Anomaly Apical displacement of one or more leaflets Most often septal leaflet is involved Degree of displacement is extremely variable Epstein’s should be considered when separation between mitral and tricuspid valve is > 1cm Results in atrialization of a portion of the right ventricle. Normal Ebstein’s Anomaly Note: apical displacement of the septal leaflet Epstein’s Anomaly • Marked distortion of right ventricular and right atrial geometry. • The approximate position of the mitral anulus is noted by the broad arrow at the lower right. • Septal leaflet of the tricuspid valve: apically displaced from the anulus by approx 3 cm • Lateral leaflet is tethered to the right ventricular wall along much of its length (small arrows). • Also pathologically elongated. 12.43 Feigenbaum Pacemakers Stiffer, larger diameter leads used for implantable defibrillators may interrupt normal coaptation to a greater degree Typically does not result in significant TR Fibrosis combined with pacemakers may result in more significant regurgitation Pacemakers • Pacemaker wire has restricted motion of the tricuspid valve • Moderate tricuspid regurgitation Non-dynamic Bi-Ventricular Pacemaker Pulmonic Valve Pulmonic Valve Similar to aortic valve Trileaflet Inserted into pulmonary artery annulus distal to the right ventricular outflow tract Pulmonic Valve Views PSAX-Ao RVOT Subcostal Short-Axis Etiology of Pulmonic Regurgitation Pulmonary hypertension Causing regurgitation secondary to dilatation of the valve ring Most common Referred to as high pressure pulmonary disease Infective endocarditis Second most common cause Rheumatic heart disease Myxomatous degeneration Etiology – Cont. Idiopathic dilatation of the pulmonary artery Connective tissue disorders (e.g. Marfan’s syndrome) Congenital abnormalities e.g. tetralogy of Fallot, ventricular septal defect, valvular pulmonic stenosis, congenital agsence of the pulmonic valve Iatrogenic Post surgical repairs for congenital heart disease Etiology – Cont. Pulmonary artery catheter Carcinoid heart disease Syphilis Tuberculosis Chest trauma Prosthetic heart valve Physiologic History/Physical Examination May tolerated for years w/o difficulty Severe hemodynamic changed due solely to pulmonary regurgitation is rare Dyspnea Fatigue Palpable right ventricular impulse along left sternal border Right heart failure e.g. jugular venous distention, hepatomegaly, peripheral edema, ascites, anasarca Complication Right heart failure Treatment Pulmonary regurgitation is generally well tolerated Endocarditis prophylaxis Digitalis (right heart failure) Valvuloplasty/valve replacement M-Mode Criteria Right ventricular dilatation Right ventricular volume overload pattern Right ventricular dilatation with paradoxical septal motion Fine diastolic flutter of the tricuspid valve Diastolic flutter of the pulmonic valve Premature opening of the pulmonic valve due to severe acute pulmonary regurgitation Defined as pulmonic valve opening on or before the QRS complex Evidence of pulmonary hypertension 2D Criteria Anatomic basis for the presence of pulmonary regurgitation Evidence of pulmonary hypertension Common cause Right ventricular dilatation Right ventricular volume overload pattern Right ventricular dilatation with paradoxical septal motion Right ventricular diastolic expansion D-shaped left ventricle due to right ventricular volume overload Pulmonary valve ring/artery dilatation Right atrial dilation Pulsed Wave Doppler Up to 87% of normal patients appear to have pulmonary regurgitation Length and duration of the regurgitant jet differentiate between true and physiologic regurgitation <1 cm in length and non-holodiastolic in duration with normal pulmonary artery pressures implies physiologic regurgitation Peak velocity across the RVOT is increased with significant pulmonary regurgitation Increased RVOT velocity time integral (VTI) with significant pulmonary regurgitation Color Flow Doppler Holodiastolic flow reversal in main pulmonary artery and its branches may indicate severe pulmonary regurgitation Continuous Wave Doppler Compare the pulmonary regurgitation Doppler spectral display with the pulmonic outflow Doppler spectral display strength Steep slope with cessation of flow at or before end diastole may indicate severe pulmonary regurgitation Shortened pressure half-time Pulmonary Regurgitation Severity Scales PW and Color Physiologic Normal pulmonic valve and pulmonary artery Normal chamber dimensions Normal pulmonary artery pressures <1 cm in length and not holodiastolic in duration Borderline 1 to 2 cm in length and holodiastolic in duration Clinically significant > 2 cm in length with a peak velocity ≥1.5 m/sec and holodiastolic in duration Pulmonary Regurgitation Severity Scale CW Spectral Strength of Regurgitant Jet Grade 1+ (mild) Spectral in tracing stains sufficiently for detection, but not enough for clear delineation Grade 2+ (moderate) Complete spectral tracing can just be seen Grade 3+ (moderate severe) Distinct darkening of spectral tracing is visible but density is less than antegrade flow Grade 4+ (severe) Dark-stained spectral training Important to Note Significant pulmonary hypertension is a right heart pressure overload The velocity of pulmonic regurgitation varies with respiration When determining the mean pulmonary artery pressure and pulmonary artery end diastolic pressure, 3 to 5 beats should be averaged Eccentric Jet PI Parasternal short-axis view recorded at the base of the heart in a patient with minimal pulmonary valve insufficiency originating at the lateral aspect of the cusp commissure. Because this jet originates immediately adjacent to the aorta (Ao), it could be confused for an aorta-pulmonary fistula. Note, however, the exclusively diastolic flow, which would not be expected in the presence of the true shunt. 12.13 Feigenbaum Mild Pulmonic Insufficiency/Regurgitation 12.14a Feigenbaum Moderate Pulmonic Insufficiency/Regurgitation 12.14b Feigenbaum Severe Pulmonic Insufficiency/Regurgitation 12.14c Feigenbaum Sources Azis F, Baciewicz F. (2007). Texas Heart Institute Journal. 34(3) 366-8. Feigenbaum H, Armstrong W. (2004). Echocardiography. (6th Edition). Indianapolis. Lippincott Williams & Wilkins. Goldstein S., Harry M., Carney D., Dempsey A., Ehler D., Geiser E., Gillam L., Kraft C., Rigling R., McCallister B., Sisk E., Waggoner A., Witt S., Gresser C.. (2005). Outline of Sonographer Core Curriculum in Echocardiography. Otto C. (2004). Textbook of Clinical Echocardiography. (3rd Edition). Elsevier & Saunders. Reynolds T. (2000). The Echocardiographer's Pocket Reference. (2nd Edition). Arizona. Arizona Heart Institute.