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Evaluation of Diastolic Dysfunction by Echocardiography
Brandon Kuebler, MD Pediatric Cardiology Fellow Wednesday, February 09, 2011
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Assessment of Diastolic Ventricular Function
Defining diastole Methods to assess diastole Patterns of diastolic disease Age-related changes
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When does diastole occur?
Is it around tea time? No Required for every heart beat Systole Diastole
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Phases of Diastole Isovolumetric relaxation Rapid filling Diastasis
E-wave 2/3 LV filling Diastasis Atrial contraction A-wave 1/3 LV filling
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Factors Affecting Diastole
Ventricular function AV valve function Rate of relaxation Ventricular compliance Atrial systolic function Preload Heart rate and rhythm
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Pulmonary Venous Inflow
Apical 4-chamber view Identify RUPV or LUPV inflow parallel to beam Pulsed-wave sampling 1-2 cm distal to orifice Alternatives views: Parasternal Suprasternal Subcostals Place Apical 4 w PW in Distal PV
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Pulsed-wave Pulmonary Vein Inflow
Identify peak S and D velocities Measure atrial reversal (AR) duration AR presence is variable. It is indicative of abnormal elevated LA pressure in a neonate, but may be normal in a child with more compliant pulmonary veins. The duration of flow reversal is more helpful in relation to atrial systole
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Note: S-wave may be biphasic owing to differences of atrial relaxation and mitral valve annular displacement Should take the highest of the peaks
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Mitral Inflow Apical 4-chamber view
Align Doppler beam to be parallel to mitral inflow Pulsed-wave sampling at tips of MV leaflets Decreased velocity if sampled within LA
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Pulsed-wave Mitral Valve Inflow
Peak E and A velocities, ratio E/A Mitral A-wave duration (to compare with PV AR duration) Mitral deceleration time(from peak of E-wave to base) Mitral Doppler VTI (and valve area)
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Mitral Valve Doppler Evaluation
In a 5 chamber view Continuous-wave across tips of MV through LVOT Obtain mitral inflow & LV outflow Measure Isovolumetric Relaxation Time (IVRT)
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Tissue Doppler Measures displacement of myocardium while avoiding blood flow detection throughout the cardiac cycle For our purposes: Mitral valve annular junction Septal annular junction Tricuspid annular junction Mitral and tricuspid data is relatively volume load independent, including respiratory cycle
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TDI Methodology Using Doppler pulsed cursor, 3-5 mm
Set Nyquist limits to cm/s Using lowest wall filter Set dynamic range to 30-35db Sweep speed of mm/s
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TDI Pulsed-wave Ea ( or E´), Aa ( or A´), Sa ( or S´) waves
IVRT and Isovolumetric Contraction Time (IVCT) Important to maintain a parallel line of annular motion with the imaging beam
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Color M-mode Flow Propagation
Estimate of ventricular filling to correlate with LV relaxation, even at increased LA pressures Not affected by preload Varies with changes of lusitropic conditions Correlates in ischemic heart disease
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Color M-mode Flow Propagation
In apical 4 chamber view Align M-mode cursor through LV apex and orifice of MV Apply Color Doppler Switch to M-mode acquisition Decrease Nyquist limit until color inflow shows line of aliasing
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Color M-mode Flow Propagation
Demonstrated by Garcia et al., JACC 1999, that in both dogs with occluded IVC and in adults undergoing CABG, under partial CPB, measures were not affected Although, MV E waves and associated measures were impacted by each scenario In dogs, under various doses of dobutamine and esmolol, there were expected changes of Vp correlating to measured changes of LVEDp
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Calculations using Vp Border et al, JASE 2003 20 pts age 6.6yrs ± 6yrs
Indicated L heart cath w/o MV stenosis/arrhythmia Found E/ Vp > 2.0, LVEDp >15mmHg Sensitivity 100% Specificity 77% PPV: 70% NPV: 100%
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Calculations using Vp(FPV)
Gonzalez-Vilchez, JACC 1999 Adults in ICU w Swan’s 20 test, 34 study patients Estimated PCWP = 4.5(103/[2•IVRT]+FPV)-9 Simplified to: 103/[2•IVRT]+FPV Value ≥5.5, correlates to PCWP > 15mmHg (r=0.89)
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Calculations using Vp
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Use of TDI and Color M-mode in Infants
Study by Larrazet et al, Pediatric Critical Care Medicine, 2005 Studied infants 3-8 months of age, immediately post-operatively for VSD/AVCD repair w LA line in place For LA pressure > 10mmHg E/Ea > 15 – Sensitivity 94%, Specificity 72% E/Vp >2.0 – Sensitivity 83%, Specificity 89%
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LA Volume In adults, atrial dilation has correlated as a risk for first CV event (a-fib, stroke, CHF) Defined as: women ≥ 30cm2/m2, men ≥ 33cm2/m2 Not routinely measured in children, but recent norms established 8/3π[(A1)(A2)/(L)] obtained from Apical 2 & 4 chamber views
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LA Volume in Children Data collected by 3D Echo and separated by BSA
m2 : mL/m2 m2 : mL/m2 m2 : mL/m2 m2 : mL/m2 >1.5m2 : mL/m2 No normative values for RA established in kids
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Tricuspid and Right Heart Evaluation
Usual measures performed on MV, are influenced by variable preload through the respiratory cycle. With inspiration amongst children Peak E may increase by 26% Peak A may increase by 20%
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Tricuspid and Right Heart Evaluation
SVC inflow invariably does not have AR amongst healthy children AR-wave usually seen with: Right atrial hypertension Tricuspid stenosis Reversal with ventricular systole Significant tricuspid regurgitation Loss of AV-synchrony Restrictive physiology Decreased flow of systemic veins or TV inflow with Exhalation seen with Tamponade MV E-wave decreases by >25% during onset of INhalation
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Tricuspid and Right Heart Evaluation
In a restrictive, non-compliant RV, which acts essentially as a conduit for the PA Forward flow may be seen in PA with atrial systole Only in settings with low PVR or absence of distal stenoses May be seen in those with history of Tetralogy or Pulmonary valve abnormalities
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Classification of Diastolic Dysfunction
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Classification of Diastolic Dysfunction
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Abnormal LV Relaxation
The ability of the LV myocardial filaments to actively uncouple after systole, is delayed Ventricular compliance is unaffected IVRT is prolonged, as time needed to decrease LV pressure < LA pressure is extended
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Abnormal LV Relaxation
LA-LV pressure difference in early diastole narrowed – max E-wave velocity decreased LV relaxation is slower, so E-wave is prolonged A-wave increased as a compensatory to complete LV filling Insert fig 8.14 Insert fig 8.15
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Abnormal LV Relaxation
Infamous “L-wave” seen in MV inflow pattern Described by Keren in 1986 Presence of LA-LV pressure gradient in diastasis Occurs with MARKEDLY delayed LV relaxation
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Abnormal LV Relaxation … and LA Hypertension
Also called “Pseudonormalization” Result of worsened ventricular compliance with transmitted increase of atrial pressure Ultimately, relative pressure difference between LA-LV is similar to normal, just at higher pressure Pulmonary vein inflow pattern helpful to distinguish this from normal
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Abnormal LV Relaxation … and LA Hypertension
TDI has been shown to be relatively independent of preload Abali et al, JASE 2005, studied 100+ adult males after 500mL blood donation, found no differences in TDI measures or Color M-mode, Vp Eidem et al, JASE 2005, found that children with chronic LV preload (VSD’s) and preserved systolic and diastolic function, did not have changes in TDI Those with chronic afterload (AS) demonstrated decreases of TDI measures
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Abnormal LV Relaxation … and LA Hypertension
Nagueh et al, JACC 1997 125 adults, 60 cathed for PCWP, separated Normal from Impaired Relaxation from Pseudnormalized (EF low in this group) Found E/Ea >10 correlated to PCWP of >12mmHg Sensitivity 91%, Specificity 81%
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Nagueh et al, JACC 1997 Could predict mean PCWP= 1.24(E/Ea ) +1.9
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TDI in Pseudonormalization
Nagueh et al, JACC 1997, 30;
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Color M-mode in Pseudonormalization
Helpful to differentiate normal MV inflow patterns from ‘pseudonormalization’ Decreased rate of flow propagation (Vp) correlate with delayed relaxation, even with elevated LA pressure Measures are preload independent Measure of MV peak E velocity to rate of flow propagation, E/ Vp > 2.0 predicts LVEDp >15mmHg (sensitivity 100%, specificity 77%)
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Restrictive Physiology/Decreased Ventricular Compliance
Ventricle is significantly stiff, non-compliant, that with small increases of volume, pressures increase disproportionately On MV inflow, the E-wave is accelerated with short deceleration time due to rapid rise of ventricular pressure and the end of inflow A-wave is remarkably small, if not absent all together, as atrial systole minimally generates a pressure gradient across the AV valve Instead prolonged reflux in PV observed
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Restrictive Physiology/Decreased Ventricular Compliance
IVRT shortened due to atrial hypertension with early opening of MV and ventricular filling
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Measures through childhood
Infants Very limited early diastolic flow Significant contribution from atrial systole Limited tolerance to changes in preload Improved compliance around 2 months Childhood Limited variability of measures (Inflow/TDI) through childhood and adolescence Noted changes with increasing IVRT likely associated with age-related decreased HR
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Tables of normative values for children are available
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Tables of normative values for children are available
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Let’s apply our data 52.4 cm/s 57.0 cm/s
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Let’s apply our data 144 cm/s 2.0 72 cm/s 130 108 ms 90 ms
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Let’s apply our data 13.1 cm/s 11
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Vs= Vp x Li Vs = strength of early filling
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Vs Strength of Filling In a recent article by Stewart et al., JACC Imaging 2011 Found that in addition to a decreased filling velocity (Vp) with diastolic dysfunction, the velocity further slowed closer to the MV than the apex (Li) Vs= Vp x Li Found this measure to have better correlation to gold-standard than Vp alone Would like to see used with other measures to further strengthen accuracy and separation of abnormal states
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Looking at Vp 69 cm/s E/Vp= 2.0
Estimated PCWP = 4.5(103/[2•IVRT]+FPV)-9 4.5(103/[2•60]+69)-9 = 15 mmHg Simplified version = 103/[2•IVRT]+FPV 103/[2•60]+69 = 5.2
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To summarize our non-invasive data
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E/Vp= 2.0
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So by our echo data… RESTRICTIVE PHYSIOLOGY
I would classify this patient as having RESTRICTIVE PHYSIOLOGY
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He just so happened to have been cathed just before I obtained these measures… I did not know these results
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Disease states Hypertrophic cardiomyopathy Chronic disease states
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HOCM Abnormalities of E/Ea, color M-mode flow propagation, and diastolic strain rates have correlated with abnormal relaxation and predict LV filling pressures. TDI (DTI) has been found to be predictive of adverse outcomes E/Ea >12 predicted risk for SCD, Cardiac Arrest, and VT Those without, events had range Those with symptoms had ratio higher compared to those without (11.9 vs 8.1)
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Distinguishing HOCM from Athletic Heart
Diastolic TDI annular patterns, IVRT, and LA volume have identified HOCM in absence of pathologic changes Early diastolic TDI velocities (Ea) Athletes: normal to increased HOCM: consistently decreased, often Ea/Aa <1.
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Children with Chronic Dz’s
Renal failure Those on dialysis had changes on echo compared to normal controls: Increased LV mass with preserved systolic function Evidence of diastolic dysfunction: higher E’s, lower Ea’s and therefore increased E/Ea ratios Obesity Demonstrated changes with Ea (↓) and Aa (↑) velocities where the ratio Ea/Aa was < controls Demonstrated changes with strain rate imaging also noted
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Children with Chronic Dz’s
Obstructive sleep apnea Evidence of diastolic dysfunction correlated with severity of sleep apnea Measures improved with effective therapies Anthracycline toxicity Demonstrated changes with Ea (↓) and Aa (↑) velocities, Ea/Aa ratio is ↓↓↓ Persists over time, even without evidence of systolic dysfunction
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Congenital Heart Disease
Aortic Stenosis Measures are more pronounced in more severe disease Does not resolve immediately with relief of obstruction Changes/improvement correlate more with degree of ventricular hypertrophy
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Congenital Heart Disease
Single ventricles Demonstrated impaired relaxation, decreased peak E velocities, presence of mid-diastolic filling waves, decreased E/A velocity ratio Different pulmonary venous inflow patterns due to different sources of pulmonary antegrade blood flow In well functioning single ventricles, biphasic pulmonary venous inflow still seen (mid-systolic peak, and late diastolic peak)
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Congenital Heart Disease
Single ventricles With decrease ventricular systolic function Decreased systolic flow in PV Increased late diastolic flow in PV Seems to correlate with changes in EF Serial studies in HLHS No differences in early stages within 1st year of life Need more longitudinal studies
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Congenital Heart Disease
TGA Atrial Switches (Senning/Mustard) Found to have decrease IVCT, and sensitive to changes of systemic RV dysfunction in adolescents and young adults Measures of TDI are lower than normals, as expected More data needed for the population, esp Arterial Switches
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References Frommelt, P. (2009). Diastolic Ventricular Function Assessment. In WW Lai, LL Mertens, MS Cohen, T Geva (Eds), Echocardiography in Pediatric and Congenital Heart Disease (1st Edition, p95-118). Hoboken, USA: Wiley-Blackwell. Garcia MJ, et al. Color M-mode doppler flow propagation velocity is a preload insensitive index of left ventricular relaxation: animal and human validation. JACC 2000; 35: Nagueh SF, et al. Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. JACC 1997; 30: Eidem BW, et al. Impact of chronic left ventricular preload and afterload on doppler tissue imaging velocities: a study in congenital heart disease. J Am Soc Echocardiogr 2005; 18: Larrazet F, et al. Tissue doppler echocardiographic and color M-mode estimation of left atrial pressure in infants. Pediatr Crit Care Med 2005; 6: Gonzalez-Vilchez F, et al. Combined use of pulsed and color M-mode doppler echocardiography for the estimation of pulmonary capillary wedge pressure: an emperical approach based on an analytical relation. JACC 1999; 34: Border WL, et al. Color M-mode and doppler tissue evaluation of diastolic function in children: simultaneous correlation with invasive indices. J Am Soc Echocardiogr 2003; 16: Abali G, et al. Which doppler parameters are load independent? A study in normal volunteers after blood donation. J Am Soc Echocardiogr 2005; 18: Stewart KC, et al. Evaluation of LV diastolic function from color M-mode echocardiography. J Am Coll Cardiol Img 2011; 4:
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