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Antoine Hage, M.D Director, Solid Organ Transplant Cardiology

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1 Role of the Echocardiogram in the Assessment of Pulmonary Hypertension and the Right Ventricle
Antoine Hage, M.D Director, Solid Organ Transplant Cardiology Co-Director, Pulmonary Hypertension Program Cedars Sinai Heart Institute Clinical Professor of Medicine/ Cardiology David Geffen School of Medicine at UCLA

2 Role of Echocardiography in Pulmonary Hypertension: Overview
Definition and classification Role of ECHO in Diagnosis (allows identification of patients for whom RHC is required) Screening high risk patient populations Evaluation of Structure/ Morphology/ Function/ Hemodynamics of RV and PA (CHD) Determining etiology / PH group (PAH vs PVH) and secondary causes Risk 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 Hg Mean PAP ≥25 mm Hg plus PCWP/LVEDP ≤15 mm Hg PAH Doppler 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 PAH The 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 Units Badesch 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)
PAH Idiopathic PAH Heritable (BMPR2, ALK1, Endoglin) Drug- and toxin-induced Persistent PH of newborn Associated with: CTD HIV infection portal hypertension CHD schistosomiasis chronic hemolytic anemia 1’. PVOD and/or PCH PH Owing to Left Heart Diseases Systolic dysfunction Diastolic dysfunction Valvular disease 3. PH Owing to Lung Diseases and/or Hypoxia COPD ILD Other pulmonary diseases with mixed restrictive and obstructive pattern Sleep-disordered breathing Alveolar hypoventilation disorders Chronic exposure to high altitude Developmental abnormalities 4. CTEPH 5. PH With Unclear Multifactorial Mechanisms Hematologic 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 history 6% - 12% prevalence of positive family history. If BMPR2 present, 20% chance of developing PAH. Autosomal dominant, incomplete penetrance, genetic anticipation Connective tissue disease Limited and diffuse scleroderma: 8%- 30% CREST: up to 20% - 25% Systemic lupus erythematosus: 4% - 14% Rheumatoid arthritis up to 21% Congenital Heart Disease Reversal of left-to-right shunt Ventricular septal defect, patent ductusarteriosus, atrialseptal defect Portal hypertension Nearly 10% have elevated right ventricular systolic pressure by echo and RHC. 4% have severe PAH to contraindicate liver transplantation Deep venous thrombosis/history of pulmonary embolism Up to 3-4% of survivors Appetite suppressant or stimulant use 1/20000 of Fen Phen users more than 3 months Methamphetamine use HIV 0.5% (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 PH Evaluates cardiac structure, function and hemodynamics Rules out congenital heart diseases and shunts* Provides a reasonably accurate estimate of pulmonary artery pressures Guides diagnosis and therapy Helps determine prognosis: Many Echo parameters are prognostic indicators: RV size and function (eg,TAPSE, S’, FAC, MPI/TEI index) Pericardial effusion Estimate 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 PAH Connective tissue disease Congenital Heart Disease Portal hypertension Deep venous thrombosis/ history of pulmonary embolism HIV patients Appetite 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 Hypertension Peak tricuspid jet velocity m/sec Estimated sPAP mm Hg Other echo signs of PH present* PH ( grade of evidence) < 2.8 <36 No Unlikely (I-B) Yes* Possible (IIa- C) Possible (IIa-C)# > 3.4 > 50 Yes/No Likely (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 should be 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 elderly or very obese patients Galie N, et al: EurRespir J. 2009; 34;

10 Screening Patient Groups at Risk of Developing PAH
Yearly echocardiography is recommended in patients At risk for heritable PAH With CTD, especially patients with scleroderma Some recommend echo Q 2 years if normal BNP and : DLCO > 70% and FVC% /DLCO% < 1.6 With sickle cell disease Echocardiography should be considered, in patients with PH-suggestive symptoms After pulmonary embolism With HIV infection With portal hypertension With prior appetite suppressant use With sarcoidosis After splenectomy

11 Limitations of Echocardiography in PAH1,2
Experienced technicians and interpreting physicians are essential Consistency of skilled technicians/readers Applies to all imaging modalities Images can be limited in some patient populations The RV, the chamber of highest concern in PAH, is the least emphasized on the “standard” echocardiography exam TR jet may be absent in some patients, thus precluding PASP assessment May overestimate or underestimate actual pulmonary arterial pressure Can estimate LVEDP (PCWP) or CO/CI, but may prove impractical CI, 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.

Right atrial enlargement Right ventricular enlargement/dilatation - D-shaped LV on short axis Right ventricular hypertrophy Significant tricuspid regurgitation – (TR jet estimated RVSP is 4V2 + RAP) Right ventricular dysfunction Pulmonary regurgitation - PR jet estimated mPA and PAEDP Reduced RV outflow tract velocity, short acceleration time Dilated IVC not collapsing with respiration (if patient not ventilated) Patent foramen ovale (bubble contrast used) Pericardial effusion Dilated pulmonary arteries

13 Echocardiographic Findings that Increase Clinical Suspicion of PVH
Absence of right heart chamber enlargement or pericardial effusion Evidence of left atrial enlargement Presence of left ventricular hypertrophy Impaired diastolic relaxation indices Elevated 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 orifice at rest or during exercise (predictor of increased PA and pulmonary edema 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 gender Obesity Systemic Htn (particularly if not optimally controlled) and LVH Diabetes mellitus Coronary artery disease Obstructive sleep apnea Atrial fibrillation EKG findings: Lack of right axis deviation Lack of right atrial enlargement or RVH Evidence of left atrial enlargement Evidence of left ventricular hypertrophy Chest X-ray findings: Pulmonary vascular congestion/ Kerley B lines Pulmonary edema Pleural 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

17 Estimating Pulmonary Artery Pressures by Echo
TR PR TR TR Mean Diast 2* SPAP = 4TR Vmax2 + RAP TR Vmax= Peak TR velocity Diast PA = 4PRend Vmax2 + RAP PRend Vmax= End PR velocity Mean PA = TR Vmean+ RAP Or = 4PR Vmax2 + RAP PR Vmax= Peak PR velocity TR Vmean=from VTI Modified from Garvan Kane

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) signal MEAN 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 Estimated Pressure 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 Hg PA Diastolic Pressure [PADP = 4 x (end-diastolic pulmonary regurgitant velocity)² + RA pressure] Mean PA Pressure mPAP = 1/3(SPAP) + 2/3(PADP) Or 4 x (early PR velocity)² + estimated RA pressure Or: 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 jet Derivation 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 ms mPA = 47 mm Hg Mean PA pressure = 79 - (0.45 x AT)

21 PA in Pulmonary vascular disease
Before and after therapy. CTEPH- Before PTE Same 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% collapse 8mmHg, IVC normal in diameter w/ <50% collapse 15mmHg, IVC diameter >21mm w/ >50% collapse 20mmHg, IVC dilatation with <50% collapse 2D 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% collapse 8mmHg, IVC normal in diameter w/ <50% collapse 15mmHg, IVC diameter >21mm w/ >50% collapse 20mmHg, 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 pressure Abnormal: A wave is larger than systolic S wave Abnormal The example on the right shows low systolic filling fraction and increased A wave (compared to S wave.) A A A D S S D D Normal: Systolic predominance in hep. vein flow Abnormal: Vs/Vd< 1 (eg; High RA pressure)

25 How should you define mild, moderate, and severe PH?
Not by RVSP Not by the ratio of RVSP to systemic BP Define PH severity by the degree of: RV dilatation RV dysfunction RA pressure elevation Decrease in cardiac index Modified from Garvan Kane

26 Right Ventricular Afterload
RESISTANCE PVR: mean PAP – PCWP = TPG Flow (CO) CO Reflects the arterial load to steady flow Doppler 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 WU PVRc = (RVSP – E/e’) / VTIRVOT (Corrected Dahiya equation)# *Abbas, AE et al. JACC : #Dahiya, A et al . Heart :

28 PA – W Sign

29 Right Ventricular Afterload
Compliance / Capacitance Can be estimated by SV / Pulse Pressure (by cath or ECHO) May be as (more) important in PH as resistance Pulsatile component of pressure and flow is 30-50% of power transferred from RV to pulmonary bed Less than 1.0 is abnormal and < 0.8 mL/mm Hg predicts mortality in PAH patients PVCAP = Stroke Volume = LVOT Area x TVI PA Pulse Pressure* (TR Vmax2 – PRendV2) PVCAP = Pulmonary vascular capacitance * PA systolic – PA diastolic Mahapatra, 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 Hg RVOT Acceleration time < 90 msec “Flying W” sign by M-Mode (mid-systolic notching) Dilated Coronary Sinus Decreased 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 RV Upper right LPAX Lower right : Septal flattening. Short axis, parasternal

32 RV Apical 4 Chamber view: Obtain apical long axis views optimized to visualize RV
RV centric LV centric Can 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 Compression Flattening / D-shaped Septum RAE / IAS Displacement Apex-forming RV

34 RV size: Qualitative “Eyeball” Estimate
Mild RVE Normal Normal RV Similar to LV/ Shares apex RV 2/3 size of LV Severe RVE Moderate RVE Very large RV/ Apex forming D shaped septum RV 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 dilatation RV end-diastolic diameter has been identified as a predictor of survival in patients with chronic pulmonary disease Tips Measure at end diastole from an RV focused apical 4-chamber view Optimize image to have maximum diameter without foreshortening the ventricle Rudski,LG et al. J. Am Soc Echocardiogr : RVH: RV thickness > 0.5 cm LA, 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 2D RV end-diastolic diameter has been identified as a predictor of survival in patients with chronic pulmonary disease RV Enlargement: RVD1 > 42 mm or RVD2 > 35 mm or RV Length > 79 mm RV Area > 28 cm2 RV dimesnsions mesaured in the Apical-4 view. The RV wall dimension measured in the subcostal view. RVH: RV thickness > 0.5 cm J Am Soc Echocardiogr 2010;23:

37 Septal Flattening- Eccentricity Index
Eccentricity Index : D1/D2 > 1 In Diastole= volume overload In Systole= volume and pressure overload E.I = 40/25 = 1.6 (D1/D2)

38 Pericardial Effusion: A bad Sign in PH
Associated with greater disease severity Increases mortality risk Likely reflects high venous pressure 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 function Subjective evaluation Tricuspid annular plane systolic excursion (TAPSE) Tricuspid annulus TDI velocities (S’) RIMP (Tei Index) RV area fractional shortening Dp/dt RV longitudinal strain measurement Measurement of cardiac output

40 Echo measures of RV Function: TAPSE
Simple, reproducible Represents longitudinal function Correlates well with radionuclide angiography in determining RV systolic function. Relatively load dependent. Normal > 20 mm. TAPSE < 18 mm has negative prognostic implications Angle and load dependent To execute: In Apical-4 chamber view, place M-Mode cursor through the lateral tricuspid annulus Measure excursion from end-diastole to end-systole Average over 3 beats Off-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)/ET Simple, sensitive, reproducible Good indicator of basal free wall function By TDI, several indices of RV function can be obtained from a single cardiac cycle Peak velocities Isovolumic parameters Tei index Angle dependant Relatively independent of loading conditions Correlated with RVEF by first pass radionuclide ventriculography Normal > 10 cm/s Normal MPI by TDI < 0.55 Our 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 measurements of 2 different cardiac cycles (tricuspid inflow and RV outflow by PW Doppler) Normal values below 0.4 (mean 0.28) Relatively independent of HR and from loading conditions Prognostic in PH May get pseudonormalized with high RVDP/ RAP Figure 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:

43 RV FAC (Fractional Area Change) / Apex-forming RV
RV FAC%= 100x RVarea diastole – RVareasystole / Rvareadiastole / 27.2 = 20%

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 RISK DETERMINANTS OF RISK HIGHER RISK No Clinical evidence of RV failure Yes Gradual Progression of symptoms Rapid II, III WHO class IV Longer (>400 m) 6MWD Shorter (<300 m) Peak VO2>10.4 mL/kg/min CPET Peak VO2<10.4 mL/kg/min Minimal RV dysfunction Echocardiography Pericardial effusion, significant RV enlargement/dysfunction; RA enlargement (TAPSE in ESC guidelines) RAP <10 mm Hg; CI >2.5 L/min/m2 Hemodynamics RAP >20 mm Hg; CI <2.0 L/min/m2 Minimally elevated BNP Significantly elevated Syncope is poor prognostic sign added in the ESC guidelines McLaughlin VV et al. J Am CollCardiol. 2009;53:

47 Prognostic Value of Echo Parameters of RV Function
47 pts with PAH 2-year survival = 88 % if TAPSE > 18 mm 2-year survival = 50 % if TAPSE < 18 mm Forfia PR – Am J RespirCrit Care Med 2006; 174: Prognostic Value of MPI Meluzin J – Eur J Echocardiogr 2003; 4: Prognostic Value of MPI YeoTc – 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 placebo F/U 36 months, 20 deaths, 21 transplantations Right atrial area > 20 cm2, abnormal; > 27 cm2 associated with poor prognosis Eccentricity index > 1 abnormal; > 1.7 carries poor prognosis Raymond, R. J. et al. J Am CollCardiol 2002;39:

49 Suggested Assessments and Timing for Follow-ups in patients with PAH: ESC Guidelines

50 Role of Echo in Determination of PH Group

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 ECHO Features 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 PH Right-Sided Origin of PH 2-D Echocardiographic Findings: LVH, LAE Normal LV size, normal LA size Variable LV function Normal LV function Normal RV size RV dilation (ratio of RV:LV size >1) No interventricular septal bowing Right to left interventricularseptal bowing Atrial septum neutral or bowed to right Atrial septum bowed to left Normal or mildly reduced RV function Mild to severe RV dysfunction No pericardial effusion Mild to moderate pericardial effusion Doppler Findings: ≥2+ mitral valve disease (MR or MS) Minimal or no MR or MS Grade II or III diastolic dysfunction Normal diastolic function or grade I diastolic dysfunction (E:A reversal) Variable TR Variable TR (TR severity > MR severity) Absence of notched pattern in Doppler signal obtained from RVOT Notched Doppler signal in RVOT Variable 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 IVS RV Myocardial Performance Index (MPI) or Tei index TDI 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 Notching Pulmonary artery pressures (Systolic, Diastolic, Mean) , Resistance and Capacitance RA 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 available BP 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 overload Tei 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 PAH Limited 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 circulation ECHO 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 slides Sonographers RDCS: Yvonne Golomb Liliana (Lily) Miranda Carol Mortier Yousef Kohen Partners Jon Kobashigawa, M.D Jaime Moriguchi, M.D Michele Hamilton, M.D Jignesh Patel, M.D BabakAzarbal, M.D Michelle Kittleson, M.D David Chang, M.D

56 THANK YOU Any questions?

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