Presentation on theme: "Antoine Hage, M.D Director, Solid Organ Transplant Cardiology"— Presentation transcript:
1 Role of the Echocardiogram in the Assessment of Pulmonary Hypertension and the Right Ventricle Antoine Hage, M.DDirector, Solid Organ Transplant CardiologyCo-Director, Pulmonary Hypertension ProgramCedars Sinai Heart InstituteClinical Professor of Medicine/ CardiologyDavid Geffen School of Medicine at UCLA
2 Role of Echocardiography in Pulmonary Hypertension: Overview Definition and classificationRole of ECHO inDiagnosis (allows identification of patients for whom RHC is required)Screening high risk patient populationsEvaluation of Structure/ Morphology/ Function/ Hemodynamics of RV and PA (CHD)Determining etiology / PH group (PAH vs PVH) and secondary causesRisk stratification (Evaluation of functional and hemodynamic impairment)Formulating therapeutic options, monitoring disease stability and response to therapy (longitutudinal F/U)Prognostic evaluation
3 Hemodynamic Definition of PH/PAH Mean PAP ≥25 mm HgMean PAP ≥25 mm Hg plus PCWP/LVEDP ≤15 mm HgPAHDoppler echo is the best noninvasive method to evaluate PAP, and should be used in all patients suspected to have PAH. Cardiac cath is mandatory for the final diagnosis of PAHThe hemodynamic working definition of PAH listed here is derived from the 2009 Proceedings of the 4th World Symposium on PH. In the new recommendations, exercise and PVR criteria have been eliminated.An accurate PCWP can be difficult to obtain in patients with PH and enlarged pulmonary arteries.If PCWP is elevated despite multiple attempts, especially if blood obtained in the wedge position is not fully saturated, direct measurement of LVEDP should strongly be considered so as not to misdiagnose patients who have PAH.In a recent retrospective study of 4300 patients undergoing simultaneous right and left catheterization, 53% meeting criteria for PAH on the basis of a PCWP <15 had a LVEDP >15 (even among patients being evaluated specifically for PH)Refs: Badesch et al. JACC 2009;126:in press. Halpern SD, Taichman DB. Chest, Mar 24. [Epub ahead of print].ACCF/AHA CECD includes PVR >3 Wood UnitsBadesch D et al. J Am Coll Cardiol. 2009;54:S55-S66.McLaughlin VV et al. J Am Coll Cardiol. 2009;53:
4 Clinical Classification of Pulmonary Hypertension (Dana Point 2008) PAHIdiopathic PAHHeritable (BMPR2, ALK1, Endoglin)Drug- and toxin-inducedPersistent PH of newbornAssociated with:CTDHIV infectionportal hypertensionCHDschistosomiasischronic hemolytic anemia1’. PVOD and/or PCHPH Owing to Left Heart DiseasesSystolic dysfunctionDiastolic dysfunctionValvular disease3. PH Owing to Lung Diseases and/or HypoxiaCOPDILDOther pulmonary diseases with mixed restrictive and obstructive patternSleep-disordered breathingAlveolar hypoventilation disordersChronic exposure to high altitudeDevelopmental abnormalities4. CTEPH5. PH With Unclear Multifactorial MechanismsHematologic disorders (MPD, splenectomy,..)Systemic disorders (sarcoidosis, LAM,..)Metabolic disorders (e.g Thyroid disorders,.. )Others (e.g Renal failure/ dialysis, fibrosingmediastinitis,..)The clinical classification of pulmonary hypertension,updated at the 4th World symposium, is represented here.PAH is represented in the first subgroup. Pulmonary veno-occlusive disease and pulmonary capillary hemangiomatosis are housed within this classification, but in a separate group, distinct from but very close to Group 1 (now called Group 1-prime).Of note, left heart disease (Category 2) probably represents the most frequent cause of PH. Therefore, it is critically important in the diagnostic work-up to distinguish right heart form left heart disease.The predominant cause of PH in Category 3 is alveolar hypoxia as a result of lung disease, impaired control of breathing, or residence at high altitude.Patientswith suspected or conﬁrmed CTEPH (Category 4) should be referred to a center with expertise in the management of this disease.Group 5 comprises several forms of PH for which the etiology is unclear or multifactorial.Simmoneau G et al. J Am Coll Cardiol. 2009;54:S43-S54.Simonneau G et al. J Am Coll Cardiol. 2009;54;S43-S54.
5 When to Suspect and Screen for PAH Family history6% - 12% prevalence of positive family history. If BMPR2 present, 20% chance of developing PAH.Autosomal dominant, incomplete penetrance, genetic anticipationConnective tissue diseaseLimited and diffuse scleroderma: 8%- 30%CREST: up to 20% - 25%Systemic lupus erythematosus: 4% - 14%Rheumatoid arthritis up to 21%Congenital Heart DiseaseReversal of left-to-right shuntVentricular septal defect, patent ductusarteriosus, atrialseptal defectPortal hypertensionNearly 10% have elevated right ventricular systolic pressure by echo and RHC.4% have severe PAH to contraindicate liver transplantationDeep venous thrombosis/history of pulmonary embolismUp to 3-4% of survivorsAppetite suppressant or stimulant use1/20000 of Fen Phen users more than 3 monthsMethamphetamine useHIV0.5% (1/200) patients.Sickle cell disease, hemodialysis patients, etc
6 Echocardiography in Pulmonary HTN Echocardiography is an integral part of the assessment of a patient with PH, Often the first test to detect PHEvaluates cardiac structure, function and hemodynamicsRules out congenital heart diseases and shunts*Provides a reasonably accurate estimate of pulmonary artery pressuresGuides diagnosis and therapyHelps determine prognosis: Many Echo parameters are prognostic indicators:RV size and function (eg,TAPSE, S’, FAC, MPI/TEI index)Pericardial effusionEstimate of CO/CI and RA pressure (hemodynamics)* May need TEE
7 Role of Echocardiography in the Screening of Patients at Risk of Developing PH/ PAH The substantial time delay from symptom onset to definite diagnosis in PAH remains an unresolved issue. This has relevant clinical implications, especially when considering the better prognosis and response to treatment with early detection of the disease (WHO class I or II, 6-min walk distance > 450 m, normal or mildly increased B-type natriuretic peptide, no evidence of right-heart failure). Regular echocardiographic screening of patients at high risk for PAH or with unexplained symptoms of fatigue or dyspnea is essential and provides an overall good sensitivity and specificity.1
8 When to Suspect and Screen for PAH Family history/ Heritable PAHConnective tissue diseaseCongenital Heart DiseasePortal hypertensionDeep venous thrombosis/ history of pulmonary embolismHIV patientsAppetite suppressant or stimulant use (Methamphetamine)Sickle cell disease, hemodialysis patients/fistula, sarcoidosis, post-splenectomy etc.
9 Echocardiographic Criteria Corresponding to Various Levels of Likelihood of Presence of Pulmonary HypertensionPeak tricuspid jet velocity m/secEstimated sPAP mm HgOther echo signs of PH present*PH ( grade of evidence)< 2.8<36NoUnlikely (I-B)Yes*Possible (IIa- C)Possible (IIa-C)#> 3.4> 50Yes/NoLikely (I-B)* Eg, if RV morphology and function and/or systolic time intervals such as PAAT, or mid systolic deceleration of right ventricular ejection (notching) are suggestive of PH, such diagnosis shouldbe considered “possible” even if Doppler estimate of sPAP is within normal range .# TRV > 2.8 m/Sec corresponds to TIPG > 31 mm Hg, suggest PH except in elderlyor very obese patientsGalie N, et al: EurRespir J. 2009; 34;
10 Screening Patient Groups at Risk of Developing PAH Yearly echocardiography is recommended in patientsAt risk for heritable PAHWith CTD, especially patients with sclerodermaSome recommend echo Q 2 years if normal BNP and :DLCO > 70% andFVC% /DLCO% < 1.6With sickle cell diseaseEchocardiography should be considered, in patients with PH-suggestive symptomsAfter pulmonary embolismWith HIV infectionWith portal hypertensionWith prior appetite suppressant useWith sarcoidosisAfter splenectomy
11 Limitations of Echocardiography in PAH1,2 Experienced technicians and interpreting physicians are essentialConsistency of skilled technicians/readersApplies to all imaging modalitiesImages can be limited in some patient populationsThe RV, the chamber of highest concern in PAH, is the least emphasized on the “standard” echocardiography examTR jet may be absent in some patients, thus precluding PASP assessmentMay overestimate or underestimate actual pulmonary arterial pressureCan estimate LVEDP (PCWP) or CO/CI, but may prove impracticalCI, cardiac index; CO, cardiac output; LVEDP, left ventricular end diastolic pressure; PASP, pulmonary arterial systolic pressure; PCWP, pulmonary capillary wedge pressure; RV, right ventricle; TR, tricuspid regurgitation.1. Cheitlin et al. Circulation. 1997;95: McGoon et al. Chest. 2004;126:14S-34S.
12 ECHO FEATURES OF PULMONARY ARTERIAL HYPERTENSION Right atrial enlargementRight ventricular enlargement/dilatation - D-shaped LV on short axisRight ventricular hypertrophySignificant tricuspid regurgitation – (TR jet estimated RVSP is 4V2 + RAP)Right ventricular dysfunctionPulmonary regurgitation - PR jet estimated mPA and PAEDPReduced RV outflow tract velocity, short acceleration timeDilated IVC not collapsing with respiration (if patient not ventilated)Patent foramen ovale (bubble contrast used)Pericardial effusionDilated pulmonary arteries
13 Echocardiographic Findings that Increase Clinical Suspicion of PVH Absence of right heart chamber enlargement or pericardial effusionEvidence of left atrial enlargementPresence of left ventricular hypertrophyImpaired diastolic relaxation indicesElevated left ventricular filling pressures as determined by E/e’ratio >15 (most reliable predictor of LA pressure >15 mmHg)Extent of functional MR and size of mitral valve regurgitant orificeat rest or during exercise (predictor of increased PA and pulmonaryedema in ischemic heart disease and probably in HFpEF)Modest elevation of pulmonary pressures (i.e., 60’s rather than >80’s)
14 Findings that Increase the Clinical Suspicion of PVH Age (elderly)Female genderObesitySystemic Htn (particularly if not optimally controlled) and LVHDiabetes mellitusCoronary artery diseaseObstructive sleep apneaAtrial fibrillationEKG findings:Lack of right axis deviationLack of right atrial enlargement or RVHEvidence of left atrial enlargementEvidence of left ventricular hypertrophyChest X-ray findings:Pulmonary vascular congestion/ Kerley B linesPulmonary edemaPleural effusion
15 Progression of RV Dysfunction in PAH Champion H C et al. Circulation 2009;120:
16 Role of Echo in Diagnosis of PH and Assessment of PA / RV Hemodynamics
18 Mean Pulmonary Artery pressure The most reproducible method to estimate mean PA pressure is based on the mean Doppler gradient of the tricuspid regurgitant (TR) signalMEAN RV-RA SYSTOLIC GRADIENT. Aduen et al recently proposed a novel and simple method to estimate mPAP on the basis of the ad- dition of RAP to the RV-RA mean systolic gradient obtained by tracing the TRv profile. This method was validated in 102 patients, compar- ing it with simultaneous right-heart catheterization; it showed great re-liability (mean difference with invasively obtained pressures, 1.6 mm Hg; median absolute percentage difference, 18%) and accuracy in diagnosing PH (area under the curve, 0.92; 95% confidence inter- val, ). The addition of saline contrast did not improve accuracy. This method appears straightforward and could easily be incorporated into a standard echocardiographic exam, allowing a reliable estimation of mPAP.Mean PA Mean systolic EstimatedPressure RV-RA gradient RA pressure=+Aduen JF, et al. J Am Soc Echocardiogr : 22;
19 Pulmonary Artery Mean and Diastolic Pressures mPAP= 79 – 0.45x (PAAT)= x (130)=79-59= 20 mm Hg=79 – 0.45x (PAAT)= x (70)= 79 – 32= 47 mm HgPA Diastolic Pressure[PADP = 4 x (end-diastolic pulmonaryregurgitant velocity)² + RA pressure]Mean PA PressuremPAP = 1/3(SPAP) + 2/3(PADP)Or 4 x (early PR velocity)² + estimated RA pressureOr: 0.61 xsPAP + 2 mm Hg ( Chemla’s Equation)Or: x (PAAT)Or: 90 – (0.62 x PAAT)Or mPAP= 80 – 0.5 x (PAAT)Or: RAP + VTI of TR jetDerivation of mPAP by pulsed Doppler echocardiography. A, Positioning of the pulsed Doppler echocardiography sample volume in the main PA. B and C, Case of a patient without (B) and with (C) severe PAH. PAAT is the time in milliseconds from the beginning of the Doppler envelop to the peak of the signal, as shown by the dotted lines (time is in the horizontal axis). On the basis of the formula shown, the mPAP can be estimated, although for heart rates <60 beats/min or >100 beats/min, this has not been validated. In addition to the shortening of the PAAT in severe PAH, the decreased compliance of the PA and the transmission of a reflective wave of blood result in a characteristic midsystolic interruption of flow, as indicated by the arrows. AoV = aortic valve; mPAP = mean pulmonary artery pressure; PA = pulmonary artery; PAAT = pulmonary artery acceleration time; PAH = pulmonary artery hypertension.CHEST. 2011;139(5):
20 Pulmonary Acceleration Time PV AccT 72 msmPA = 47 mm HgMean PA pressure = 79 - (0.45 x AT)
21 PA in Pulmonary vascular disease Before and after therapy.CTEPH- Before PTESame pt After PTE
22 Right Atrial Pressure Estimate: IVC and Hepatic Vein Right atrial (RA) pressure estimate should not not be based on an arbitrary value, but rather based on 2D and Doppler imaging of the IVC and hepatic veins*Modified from Garvan Kane*Hepatic veins > 11 mm is abnormal
23 Right Atrial Pressure Estimate: IVC and Hepatic Vein American Society of Echocardiography Recommends:3mmHg, IVC diameter <21mm w/ >50% collapse8mmHg, IVC normal in diameter w/ <50% collapse15mmHg, IVC diameter >21mm w/ >50% collapse20mmHg, IVC dilatation with <50% collapse2D and M-Mode examples of dilated IVC without collapse. On right, a dilated Hepatic Vein (normal value 5-11 mm.)Some use the following RA estimates:American Society of Echocardiography Recommends:3mmHg, IVC diameter <21mm w/ >50% collapse8mmHg, IVC normal in diameter w/ <50% collapse15mmHg, IVC diameter >21mm w/ >50% collapse20mmHg, IVC dilatation with <50% collapse
24 Right Atrial Pressure Estimate: Hepatic Vein Flow in PAH Patients Systolic filling fraction: Vs/ (Vs + Vd) < 55% sensitive and specific for increased RA pressureAbnormal: A wave is larger than systolic S waveAbnormalThe example on the right shows low systolic filling fraction and increased A wave (compared to S wave.)AAADSSDDNormal: Systolic predominance in hep. vein flowAbnormal: Vs/Vd< 1 (eg; High RA pressure)
25 How should you define mild, moderate, and severe PH? Not by RVSPNot by the ratio of RVSP to systemic BPDefine PH severity bythe degree of:RV dilatationRV dysfunctionRA pressure elevationDecrease in cardiac indexModified from Garvan Kane
26 Right Ventricular Afterload RESISTANCEPVR: mean PAP – PCWP = TPGFlow (CO) COReflects the arterial load to steady flowDoppler correlate:Peak TR pressure gradient / RVOT TVI(although does not incorporate LV filling pressure)Modified from Garvan Kane
27 PVR PVR = [(TRV/TVIRVOT) x 10] + 0.16 (Abbas Formula)* = (3.9 / 10.2) x ; = 0.38 x ; == 3.98 WUPVRc = (RVSP – E/e’) / VTIRVOT (Corrected Dahiya equation)#*Abbas, AE et al. JACC :#Dahiya, A et al . Heart :
29 Right Ventricular Afterload Compliance / CapacitanceCan be estimated by SV / Pulse Pressure (by cath or ECHO)May be as (more) important in PH as resistancePulsatile component of pressure and flow is 30-50% of power transferred from RV to pulmonary bedLess than 1.0 is abnormal and < 0.8 mL/mm Hg predicts mortality in PAH patientsPVCAP = Stroke Volume = LVOT Area x TVIPA Pulse Pressure* (TR Vmax2 – PRendV2)PVCAP = Pulmonary vascular capacitance* PA systolic – PA diastolicMahapatra, S et al. J. Am Soc Echocardiogr, 2006, 19:
30 Indirect Echocardiographic Findings in PH Mean PA pressure := 79 - (0.45x PAAT)Or = 90 – (0.62 x PAAT)Or =80 – 0.5 x (PAAT)PV AccT 72 ms= 47 mm HgRVOT Acceleration time < 90 msec“Flying W” sign by M-Mode (mid-systolic notching)Dilated Coronary SinusDecreased PV acceleration time in patient with PH. Dilated coronary sinus in a patient with Carcinoid Heart Disease.Reynolds, BS, RDCS, Terry. The Echocardiographer’s Pocket Reference. Arizona: Print.
31 Echocardiographic Features of PAH Left:RVE/RAE . Apex forming RVUpper right LPAXLower right : Septal flattening. Short axis, parasternal
32 RV Apical 4 Chamber view: Obtain apical long axis views optimized to visualize RV RV centricLV centricCan be obtained by sliding the transducer to a more lateral position than the standard Apical-4.
33 RA / RV Morphology in PAH RV Dilatation / LV CompressionFlattening / D-shaped SeptumRAE / IAS DisplacementApex-forming RV
34 RV size: Qualitative “Eyeball” Estimate Mild RVENormalNormalRV Similar to LV/ Shares apexRV 2/3 size of LVSevereRVEModerateRVEVery large RV/ Apex formingD shaped septumRV Larger than LV
35 Quantitative Estimate of RV Size Length (> 86 mm*)Mid diameter (> 35 mm*)Basal diameter (>42 mm*)RV area > 28 cm2** Measures indicate dilatationRV end-diastolic diameter has been identifiedas a predictor of survival in patients withchronic pulmonary diseaseTipsMeasure at end diastole from an RVfocused apical 4-chamber viewOptimize image to have maximumdiameter without foreshortening theventricleRudski,LG et al. J. Am Soc Echocardiogr :RVH: RV thickness > 0.5 cmLA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.Voekel et al. Circulation. 2006;114:Images courtesy of Kirk Spencer, MD, and Lissa Sugeng, MD, MPH, University of Chicago.
36 RV measurements in 2DRV end-diastolic diameter has been identified as a predictor of survival in patients with chronic pulmonary diseaseRV Enlargement:RVD1 > 42 mm orRVD2 > 35 mm orRV Length > 79 mmRV Area > 28 cm2RV dimesnsions mesaured in the Apical-4 view. The RV wall dimension measured in the subcostal view.RVH: RV thickness > 0.5 cmJ Am Soc Echocardiogr 2010;23:
37 Septal Flattening- Eccentricity Index Eccentricity Index : D1/D2 > 1In Diastole= volume overloadIn Systole= volume and pressure overloadE.I = 40/25 = 1.6 (D1/D2)
38 Pericardial Effusion: A bad Sign in PH Associated with greaterdisease severityIncreases mortality riskLikely reflects high venouspressure and poor lymphatics drainage rather than a risk of cardiac tamponade
39 Echo and RV Function 3D ECHO might become gold standard No other valid quantitative assessment of RV functionSubjective evaluationTricuspid annular plane systolic excursion (TAPSE)Tricuspid annulus TDI velocities (S’)RIMP (Tei Index)RV area fractional shorteningDp/dtRV longitudinal strain measurementMeasurement of cardiac output
40 Echo measures of RV Function: TAPSE Simple, reproducibleRepresents longitudinal functionCorrelates well with radionuclide angiography in determining RV systolic function. Relatively load dependent.Normal > 20 mm.TAPSE < 18 mm has negative prognostic implicationsAngle and load dependentTo execute:In Apical-4 chamber view, place M-Mode cursor through the lateral tricuspid annulusMeasure excursion from end-diastole toend-systoleAverage over 3 beatsOff-axis views tend to overestimate TAPSE (as with the apex-forming RV)J Am Soc Echocardiogr 2010;23: , Heart 2006;92:i19-i26 doi: /hrt
41 Echo Measures of RV Function: TV annular velocity (S’) by TDI MPI=(TCO-ET)/ETSimple, sensitive, reproducibleGood indicator of basal free wall functionBy TDI, several indices of RV function can be obtained from a single cardiac cyclePeak velocitiesIsovolumic parametersTei indexAngle dependantRelatively independent of loading conditionsCorrelated with RVEF by first pass radionuclide ventriculographyNormal > 10 cm/sNormal MPI by TDI < 0.55Our lab prefers this method of obtaining MPI since it is usually very simple to obtain a quality TDI, and multiple other measurements can also be made at the same time.
42 The RV Index of Myocardial Performance (RIMP) Global Indicator of Systolic and Diastolic Function.Needs the measurementsof 2 different cardiac cycles(tricuspid inflow and RVoutflow by PW Doppler)Normal values below 0.4(mean 0.28)Relatively independent of HRand from loading conditionsPrognostic in PHMay get pseudonormalizedwith high RVDP/ RAPFigure 6. The RV myocardial performance index (MPI). E indicates the rapid filling velocity; A, atrial filling velocity; IVCT, isovolumic contraction time; IVRT, isovolumic relaxation time; and ET, ejection time.Haddad F et al. Circulation 2008;117:Tei C, et al: J Am Soc Echocardiogr. 1996; 9:
44 Dp/dt Rate of rise of LV or RV pressure Normal dp/dt> 400 mm Hg/sec
45 Role of ECHO in Therapy, Longitudinal F/U and Prognosis
46 Prognostic Parameters and Determinants of Risk in PAH LOWER RISKDETERMINANTS OF RISKHIGHER RISKNoClinical evidence of RV failureYesGradualProgression of symptomsRapidII, IIIWHO classIVLonger (>400 m)6MWDShorter (<300 m)Peak VO2>10.4 mL/kg/minCPETPeak VO2<10.4 mL/kg/minMinimal RV dysfunctionEchocardiographyPericardial effusion, significant RV enlargement/dysfunction; RA enlargement(TAPSE in ESC guidelines)RAP <10 mm Hg; CI >2.5 L/min/m2HemodynamicsRAP >20 mm Hg; CI <2.0 L/min/m2Minimally elevatedBNPSignificantly elevatedSyncope is poor prognostic sign added in the ESC guidelinesMcLaughlin VV et al. J Am CollCardiol. 2009;53:
47 Prognostic Value of Echo Parameters of RV Function 47 pts with PAH2-year survival = 88 % if TAPSE > 18 mm2-year survival = 50 % if TAPSE < 18 mmForfia PR – Am J RespirCrit Care Med 2006; 174:Prognostic Value of MPIMeluzin J – Eur J Echocardiogr 2003; 4:Prognostic Value of MPIYeoTc – Am J Cardiol 1998; 81:Tei, C- JASE 1996; 9:Van Wolferen, SA et al. Eur Heart J (2007) 28, 1250–1257
48 Kaplan-Meier Survival Curves for Echocardiographic Predictors of Outcomes 81 pts prostacyclinevs placeboF/U 36 months, 20 deaths, 21 transplantationsRight atrial area > 20 cm2, abnormal; > 27 cm2 associated with poor prognosisEccentricity index > 1 abnormal; > 1.7 carries poor prognosisRaymond, R. J. et al. J Am CollCardiol 2002;39:
49 Suggested Assessments and Timing for Follow-ups in patients with PAH: ESC Guidelines
51 Determining PH Type on Basis of ECHO Caution is needed in distinguishing PAH from PH related to diastolic abnormalities solely on the basis of ECHOFeatures of “diastolic dysfunction”, e.g., delayed relaxation pattern and reduced e’ (mitral annular tissue velocities), may occur in PAH ( secondary to bad RV)Pulmonary vascular resistance (PVR) calculations by ECHO do not take into account left atrial pressure- they do not distinguish PAH from PVH.
52 Left-sided vs. Right-sided Origin of Pulmonary Hypertension Left-Sided Origin of PHRight-Sided Origin of PH2-D Echocardiographic Findings:LVH, LAENormal LV size, normal LA sizeVariable LV functionNormal LV functionNormal RV sizeRV dilation (ratio of RV:LV size >1)No interventricular septal bowingRight to left interventricularseptal bowingAtrial septum neutral or bowed to rightAtrial septum bowed to leftNormal or mildly reduced RV functionMild to severe RV dysfunctionNo pericardial effusionMild to moderate pericardial effusionDoppler Findings:≥2+ mitral valve disease (MR or MS)Minimal or no MR or MSGrade II or III diastolic dysfunctionNormal diastolic function or grade I diastolicdysfunction (E:A reversal)Variable TRVariable TR (TR severity > MR severity)Absence of notched pattern in Doppler signal obtained from RVOTNotched Doppler signal in RVOTVariable PASP (typically <70 mm Hg)Variable PASP (typically ≥70 mm Hg)
53 EchocardiographicParameters for the Assessment of Pulmonary Hypertension/ Right Ventricle Size and surface areas of both atria.Bi-ventricular size and systolic /diastolic function (RV), presence of RVH, CMY, any valvular abnormality (MS, MR, AS etc..), pericardial effusion or intracardiacshunt:Subjective “eyeball” assessment of RV function ( good vs mild, moderate or severe RV dysfunction)Percent Fractional Area Change (% FAC)Tricuspid Annular Plane Systolic Excursion (TAPSE)Eccentricity Index / D-shaping of the IVSRV Myocardial Performance Index (MPI) or Tei indexTDI systolic velocity of the RV lateral annulus (S’), (and short IVRT on RV TDI)Pulmonary artery pressure estimation / Hemodynamics:Pulmonary Artery Acceleration Time (PAAT) and presence/ timing of NotchingPulmonary artery pressures (Systolic, Diastolic, Mean) , Resistance and CapacitanceRA pressure ( IVC size and collapse)Assessment of C.O ( LVOTdiameter and time-velocity integral of aortic flow by PW Doppler)Bubble study (CHD, PFO)3D echocardiography, myocardial deformation techniques (strain imaging or speckle-tracking techniques derived from tissue Doppler ultrasonography) if availableBP should be reported on echo , as well as systolic and diastolic functiona and any valvular abnormality.ECCENTRICITY INDEX ( NORMAL =1) : SYSTOLIC >1= RV pressure overload: DIASTOLIC>1= RV volume overloadTei index relatively independent from loading conditions. Represents global estimate of RV function, independent of geometric assumtions. Normal 0.28 by PULSED DOPPLER MPI Abnormal >0.4 Prolonged in PAHLimited by mode of calculation based on 2 different cardiac cycle measurement.Can be obtained by tissue doppler imaging (TDI) which has advantage of obtaining both measurement during same cardiac cycle. Tissue Doppler MPI Abnormal > 0.55
54 Role of ECHO in PH: Summary ECHO is an essential tool and plays a key role the initial and subsequent evaluation of a patient with PH. Despite its limitations, it remains the most clinically useful nonivasive test for the assessment of the pulmonary circulationECHO Provides a reasonably accurate estimate of the RV / PA pressures and hemodynamics .The prognostic value of the echocardiographic parameters discussed here are well established, and the regular assessment of these, as part of a goal-oriented therapy, is critical to monitor the progression of PH and the response of patients to PAH specific therapy, independent of clinical and RHC data
55 Acknowledgements Lauren Skinner, RDCS: Sonographers RDCS: Partners Preparation and acquisition of many of the slidesSonographers RDCS:Yvonne GolombLiliana (Lily) MirandaCarol MortierYousef KohenPartnersJon Kobashigawa, M.DJaime Moriguchi, M.DMichele Hamilton, M.DJignesh Patel, M.DBabakAzarbal, M.DMichelle Kittleson, M.DDavid Chang, M.D
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