Role of Stress Echo in Valvular Heart Disease. Satoshi Nakatani Osaka University Graduate School of Medicine Osaka, Japan
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1 Role of Stress Echo in Valvular Heart Disease Satoshi Nakatani Osaka University Graduate School of Medicine Osaka, Japan
2 Exercise echocardiography Dobutamine echocardiography
3 Usefulness of exercise echo in VHD (Lancellotti P, EHJ CVI 2016;17:1191) 76 yo male At 33 yo, abnormal ECG pointed At 63 yo, exertional dyspnea occurred Diagnosed as idiopathic DCM by cath and myocardial biopsy and B-blocker started Repeated admissions due to HF symptoms EF 19%, +1-2 Mr, +1Tr, TRPG 16 mmhg What is the cause of HF symptoms?
4 pre 15W 30W 45W dyspnea SPAP 15 mmhg 35 mmhg 40 mmhg 66 mmhg BP 100/56 116/68 128/70 154/76 HR Ex-induced PH and increase in MR may be causes of HF symptoms. Indications of intervention for MR Appearance of symptoms in asymptomatic patient Primary MR Poor prognosticators Dynamic PH (SPAP Limited CR (<5% increase in EF, <2% increase in GLS) Limited RVCR (TAPSE <19 mm) Secondary MR Increase in MR (increase in ERO 2 ) Dynamic
5 Indications of intervention for MS Exercise stress echo mpg >15 mmhg on exertion SPAP >60 mmhg on exertion Dobutamine stress echo (if the patient cannot exercise) mpg >18 mmhg 62 yo female At 58 yo, diastolic heart murmur pointed Diagnosed as MS (MVA = 1.6 cm 2 ) At 60 yo, exertional dyspnea occurred MVA = 1.6 cm 2 (planimetry), 1.4 cm 2 (PHT), cm 2 (continuity equation) mpg = 6 7 mmhg TRPG = 19 mmhg
6 Echo at rest pre 25W 50W 75W mpg 6 mmhg 13 mmhg 21 mmhg 20 mmhg TRPG 24 mmhg 53 mmhg 59 mmhg 60 mmhg Surgery was recommended.
7 Indications of intervention for AR Appearance of symptoms in asymptomatic patient Limited CR (<5% increase in EF) ) Dynamic MR However, there is limited evidence. Indications of stress echo in AS Asymptomatic severe AS Low-flow, low-gradient AS With reduced EF (classical LFLG AS) Pseudo-severe AS True-severe AS With preserved EF (paradoxical AS)
8 Indications of intervention for asymptomatic severe AS Appearance of symptoms Ex-induced hypotension Increase in mpg -20 mmhg) Limited CR (<1.4% increase in GLS*) Induced PH (SPAP >60 mmhg) (*, Donal E, EHJ CVI 2011;12:235) Low-flow, low-gradient AS AVA <1.0 cm 2, mpg <40 mmhg, LVEF <50% True severe AS Severe AS Low SV due to LV systolic dysfunction low PG Pseudo severe AS Moderate AS Low SV due to LV systolic dysfunction cannot open AV small AVA and low PG Paradoxical low-flow, low-gradient AS EF >50% but low SV (SVi <35 ml/m 2 ) DSE
9 Dobutamine stress echo in AS Start from 5 /kg/min Increase DOB by 5 /kg/min every 5 min until 20 /kg/min % increase in SV 20% contractile reserve (+) mpg 2 severe AS mpg < 2 moderate AS % increase in SV <20% contractile reserve (-) Severe calcification severe AS Mild calcification moderate AS CT score is helpful. CT score>1650 u, JACC2012;60: yo male Prior MI, chronic HF, post CRT-D implantation LVEDD = 72 mm, LVESD = 66 mm, EF = 25% AVA = 0.68 cm 2, mpg = 28 mmhg, SVi = 29 ml/m 2 Mild MR, mild AR Pseudo-severe AS or true-severe AS?
10 Echo at rest Dobutamine stress echo Pre 5 g/kg/min 10 g/kg/min 20 g/kg/min SV (ml) ET (ms) Flow rate (ml/s) mpg (mmhg) AVA (cm2) SV = (63 45) / 45 = 40% >20% Flow reserve (+) AVA at peak DSE = 0.94 <1.0 cm 2 True-severe AS TAVI was performed.
11 After TAVI AVA: from 0.68 to 1.17 cm 2 LVEDD: from 72 to 65 mm, LVESD: from 66 to 57 mm, EF: from 25 to 31% NYHA class: from III to I 70 yo female (A case when I was young ) History of present illness Exertional dyspnea starting 9 yrs ago. Diagnosed as HHD at 8 yrs ago by cath and biopsy. Repeated admission due to CHF. Had nocturnal dyspnea recently. Past medical history Hypertension since 50 y/o, DM, hyperlipidemia PCI to mid LAD in 5 yrs ago with residual stenosis at Dx br ECG Atrial fibrillation with wide QRS complex (CLBBB)
12 70 yo female with LV dysfunction EF = 17% AV PG = 30 mmhg AVA = 0.73 cm 2 Low dose DSE Rest 5 g/kg/min 10 g/kg/min 20 g/kg/min HR BP 102/54 95/66 101/55 90/49 AVA (cm 2 ) Peak PG (mmhg) TVI (cm) TVI x HR No LV flow reserve!
13 Intraoperative finding No calcification, pliable cusps! TTE TEE is important. If no CR, you cannot determine the severity. Look at the valve closely or use CT. Assess the grade of calcification and pliability of cusps.
14 Limited CR (flow reserve) Limited CR is due to: Afterload mismatch Associated CAD Myocardial damage due to prior MI or myocardial fibrosis Limited CR is seen in 1/3 of patients and is associated with high operative mortality (6 33%) with AVR. However, limited CR does not predict absence of LV function improvement after AVR. Projected AVA (AVA at flow rate of 250 ml/s) should be calculated to differentiate pseudo-severe AS and true-severe AVA proj = Projected AVA AVA Q x (250 Q rest ) + AVA rest (Q = SV / LVET) AVA proj = AVA at normal flow rate (250 ml/s), AVA rest = AVA at rest, AVA = absolute changes in AVA during DSE, Q rest = mean transvalvular flow rate at rest, Q = absolute changes in mean transvalvular flow rate during DSE. Projected AVA AVA proj = 1.02 cm 2 AVA (cm 2 ) Concerns: Slope determination from only 4 points. Accuracy of Q (esp. ET) Are you confident with this measurement? (Blais C, Circulation 2006;113:711)
15 Simplified projected AVA AVA proj = AVA peak AVA rest Q peak -Q rest x (250 Q rest ) + AVA rest (Q = SV / LVET) AVA proj = AVA at normal flow rate (250 ml/s), AVA rest = AVA at rest, AVA peak = AVA at peak, Q rest = mean transvalvular flow rate at rest, Q peak = mean transvalvular flow rate at peak Calculation of projected AVA and simplified projected AVA should be carefully performed. Concerns: Slope determination from only 2 points. Accuracy of Q (esp. ET) (Clavel MA, JASE 2010;23:380)
16 Indications of stress echo in VHD Identify patients in need of intervention Severe VHD without symptoms Truly asymptomatic or not? Non-severe VHD with symptoms Stress echo Hemodynamic disturbances or not? (Ex-induced hypotension, arrhythmia, PH) Intervention VHD with low flow Truly severe or not?
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