EACVI/ASE CLINICAL RECOMMENDATIONSThe Clinical Use of Stress Echocardiography inNon-Ischaemic Heart Disease: Recommendationsfrom the European Association of CardiovascularImaging and the American Society ofEchocardiographyPatrizio Lancellotti, MD, PhD, FESC (Chair), Patricia A. Pellikka, MD, FASE (Co-Chair),Werner Budts, MD, PhD, Farooq A. Chaudhry, MD, FASE, Erwan Donal, MD, PhD, FESC,Raluca Dulgheru, MD, Thor Edvardsen, MD, PhD, FESC, Madalina Garbi, MD, MA,Jong Won Ha, MD, PhD, FESC, Garvan C. Kane, MD, PhD, FASE, Joe Kreeger, ACS, RCCS, RDCS, FASE,Luc Mertens, MD, PhD, FASE, Philippe Pibarot, DVM, PhD, FASE, FESC, Eugenio Picano, MD, PhD,Thomas Ryan, MD, FASE, Jeane M. Tsutsui, MD, PhD, and Albert Varga, MD, PhD, FESC, Li e ge, Belgium; Bariand Pisa, Italy; Rochester, Minnesota; Leuven, Belgium; New York, New York; Rennes, France; Oslo, Norway; London,UK; Seoul, South Korea; Atlanta, Georgia; Toronto and Qu e bec, Canada; Columbus, Ohio; S ao Paulo, Brazil; andSzeged, HungaryA unique and highly versatile technique, stress echocardiography (SE) is increasingly recognized for its utility in theevaluation of non-ischaemic heart disease. SE allows for simultaneous assessment of myocardial function andhaemodynamics under physiological or pharmacological conditions. Due to its diagnostic and prognostic value,SE has become widely implemented to assess various conditions other than ischaemic heart disease. It has thusbecome essential to establish guidance for its applications and performance in the area of non-ischaemic heartdisease. This paper summarizes these recommendations. (J Am Soc Echocardiogr 2017;30:101-38.)Keywords: Cardiomyopathy, Congenital heart disease, Heart failure, Pulmonary hypertension, Stress echocardiography, Stress test, Valvular heart disease ge Hospital,From the Department of Cardiology, University of Lie ge, Belgium (P.L., R.D.); Gruppo VillaGIGA-Cardiovascular Sciences, LieMaria Care and Research, Anthea Hospital, Bari, Italy (P.L.); Division ofCardiovascular Ultrasound, Department of Cardiovascular Medicine, MayoClinic, Rochester, Minnesota (P.A.P., G.C.K.); Congenital and StructuralCardiology University Hospitals Leuven, Leuven, Belgium (W.B.);Echocardiography Laboratories, Mount Sinai Heart Network Icahn School ofMedicine at Mount Sinai, Zena and Michael A. Wiener Cardiovascular e and Henry R. Kravis Center for CardiovascularInstitute and Marie-Jos eHealth, New York, New York (F.A.C.); Service de Cardiologie, CHU RENNES Rennes-1, Rennes, France (E.D.); Department ofet LTSI U 1099 – UniversiteCardiology, Oslo University Hospital, Rikshospitalet and University of Oslo,Oslo, Norway (T.E.); King’s Health Partners, King’s College Hospital NHSFoundation Trust, London, UK (M.G.); Cardiology Division, Yonsei UniversityCollege of Medicine Seoul, Seoul, South Korea (J.W.H.); Echo Lab,Children’s Healthcare of Atlanta, Emory University School of MedicineAtlanta, Georgia (J.K.); Echocardiography, The Hospital for Sick Children, bec Heart & LungUniversity of Toronto, Toronto, Canada (L.M.); Que bec,Institute/Institut Universitaire de Cardiology et de Pneumologie de QueDepartment of Cardiology, Laval University and Canada Research Chair in bec, Canada (P.P.); Institute of ClinicalValvular Heart Disease, QuePhysiology, National Research Council, Pisa, Italy (E.P.); Ohio State o PauloUniversity, Columbus, Ohio (T.R.); Heart Institute – University of Sa o Paulo, Brazil (J.M.T.); and theMedical School and Fleury Group, S aDepartment of Medicine and Cardilogy Center, University of Szeged, r 13, Szeged, Hungary (A.V.).Dugonics teThis article has been co-published in the European Heart Journal – CardiovascularImaging.Attention ASE Members:The ASE has gone green! Visit www.aseuniversity.org to earn free continuingmedical education credit through an online activity related to this article.Certificates are available for immediate access upon successful completionof the activity. Nonmembers will need to join the ASE to access this greatmember benefit!Reprint requests: Patrizio Lancellotti, MD, PhD, FESC (Chair), Department of ge Hospital, GIGA-Cardiovascular Sciences, Lie ge,Cardiology, University of LieBelgium (E-mail: email@example.com).The following authors reported no actual or potential conflicts of interest relative tothis document: Patrizio Lancellotti, MD, PhD, FESC, Patricia A. Pellikka, MD,FASE, Raluca Dulgheru, MD, Thor Edvardsen, MD, PhD, FESC, Madalina Garbi,MD, MA, Jong Won Ha, MD, PhD, FESC, Joe Kreeger, ACS, RCCS, RDCS,FASE, Luc Mertens, MD, PhD, FASE, Eugenio Picano, MD, PhD, Thomas Ryan,MD, FASE, Jeane M. Tsutsui, MD, PhD, Albert Varga, MD, PhD, FESC.The following authors reported relationships with one or more commercial interests: Werner Budts, MD, PhD received research support from Occlutech, St.Jude Medical, Actelion, and Pfizer; Farooq A. Chaudhry, MD, FASE consultedfor Lantheus and GE, received a restricted fellowship grant from Bracco, andresearch grants from Bracco and GE; Erwan Donal, MD, PhD, FESC received aresearch grant from GE; Garvan C. Kane, MD, PhD, FASE consulted for PhilipsHealthcare; Philippe Pibarot, DVM, PhD, FASE, FESC received research grantsfrom Edwards Lifesciences, Cardiac Phoenix, and V-Wave Ltd.0894-7317/ 36.00Published on behalf of the European Society of Cardiology. All rights reserved.Ó The Author 2016. For permissions please email: 1016/j.echo.2016.10.016101
102 Lancellotti et alAbbreviationsACC American College ofCardiology American HeartAssociationAHAAR aortic regurgitationAS aortic stenosis aortic valve areaAVAAVR aortic valve replacement congenital heartdiseaseCHD continuous waveCWEACTS European associationof cardiothoracic surgery ejection fractionEFEOA effective orifice areaESC European society ofcardiologyHAPE high altitudepulmonary edema hypertrophiccardiomyopathyHCMLF low flowLG low gradientLV left ventricleLVOT left ventricle outflowtract left ventricle outflowtract obstructionLVOTOMR mitral regurgitationMS mitral stenosis pulmonary arterialhypertensionPAHPAP pulmonary arterypressurePH pulmonary hypertension patient–prosthesismismatchPPM pulmonary vascularresistancePVRQ flow rateRV right ventricle right ventricularoutflow tractRVOTRVFAC right ventricularfractional area changeSPAP systolic pulmonaryartery pressureSE Stress echocardiographyTAPSE tricuspid annularplane systolic excursionTR tricuspid regurgitationJournal of the American Society of EchocardiographyFebruary 2017TABLE OF CONTENTSIntroduction 102Stress EchocardiographyMethods 102Haemodynamic Effects ofMyocardial Stressors103Exercise 103Dobutamine103Vasodilators 103Stress Echocardiography Protocols 103Treadmill 103Bicycle 103Dobutamine107Vasodilators 107Image Acquisition 108Interpretation of the Test 108Safety 109Diastolic Stress Echocardiography 109Interpretation and Haemodynamic Correlation 111Impact on Treatment 112Hypertrophic Cardiomyopathy 112Impact on Treatment 113Heart Failure with Depressed LVSystolic Function and Nonischaemic Cardiomyopathy 113Differentiating Non-ischaemicfrom Ischaemic Cardiomyopathy 114Cardiac ResynchronizationTherapy 115Response to Therapy 116Native Valve Disease 116Mitral Regurgitation 116Primary MR 117Secondary MR 117Impact on Treatment 117Aortic Regurgitation 117Severe Aortic Regurgitationwithout Symptoms 118Non-severe Aortic Regurgitation with Symptoms 118Impact on Treatment 118Mitral Stenosis 118Severe Mitral Stenosis withoutsymptoms 118Non-severe Mitral Stenosiswith Symptoms118Impact on Treatment 119Aortic Stenosis 119Asymptomatic Severe AorticStenosis 119Impact on Treatment 119Low-flow, Low-gradient AS 119Low-flow, Low-gradient ASwith Reduced LV EjectionFraction 119Impact on Treatment 122Low-flow, Low-gradient ASwith Preserved EjectionFraction 122Multivalvular Heart Disease 123Post Heart Valve Procedures123Aortic and Mitral ProstheticValves 123Mitral Valve Annuloplasty 124Pulmonary Hypertension and Pulmonary Arterial Pressure Assessment 125Pulmonary Artery Pressurewith Exercise inNormal Individuals126Screening for Susceptibility forHigh Altitude PulmonaryOedema and ChronicMountain Sickness 126Screening for PH in Patients atHigh Risk for PulmonaryArterial Hypertension 126SE in Patients with Established PH 127Athletes’ Hearts 127Congenital Heart Disease 127Atrial Septal Defect127Tetralogy of Fallot128Treated Coarctation of the Aorta 128Univentricular Hearts 128Systemic Right Ventricle 128Training and Competencies 129Summary and Future Directions129Reviewers 129Supplementary data131INTRODUCTIONStress echocardiography (SE) has most frequently been applied to theassessment of known or suspected ischaemic heart disease.1,2 Stressinduced ischaemia results in the development of new or worseningregional wall motion abnormalities in the region subtended by a stenosed coronary artery; imaging increases the accuracy of the stress electrocardiogram for the recognition of ischaemia and high-risk features.However, ischaemic heart disease is only one of the many diseasesand conditions that can be assessed with SE. In recent years, SE hasbecome an established method for the assessment of a wide spectrumof challenging clinical conditions, including systolic or diastolic heart failure, non-ischaemic cardiomyopathy, valvular heart disease, pulmonaryhypertension (PH), athletes’ hearts, congenital heart disease (CHD),and heart transplantation.3,4 Due to the growing body of evidencesupporting the use of SE beyond the evaluation of ischaemia, itsincreasing implementation in many echocardiography laboratoriesand its recognized diagnostic and prognostic value, it has thus becomeessential to establish guidance for its applications and performance.This paper provides recommendations for the clinical applications ofSE to non-ischaemic heart disease. When clinically indicated, ischaemiacan also be assessed in conjunction with assessments of non-ischaemicconditions, but it is not the focus of this document.STRESS ECHOCARDIOGRAPHY METHODSSE provides a dynamic evaluation of myocardial structure and function under conditions of physiological (exercise) or pharmacological
Journal of the American Society of EchocardiographyVolume 30 Number 2(inotrope, vasodilator) stress. The images obtained during SE permitmatching symptoms with cardiac involvement. SE can unmask structural/functional abnormalities, which—although occult in the restingor static state—may occur under conditions of activity or stress, andlead to wall motion abnormalities, valvular dysfunction, or other haemodynamic abnormalities.5-8Exercise is the test of choice for most applications. As a general rule,any patient capable of physical exercise should be tested with an exercise modality, as this preserves the integrity of the electromechanicalresponse and provides valuable information regarding functional status.Performing echocardiography at the time of exercise also allows links tobe drawn among symptoms, cardiovascular workload, wall motion abnormalities, and haemodynamic responses, such as pulmonary pressureand transvalvular flows and gradients. Exercise echocardiography canbe performed using either a treadmill or bicycle ergometer protocol.Semi-supine bicycle exercise is, however, technically easier than uprightbicycle or treadmill exercise, especially when multiple stress parametersare assessed at the peak level of exercise.Pharmacological stress does not replicate the complex haemodynamic and neurohormonal changes triggered by exercise. This includes psychological motivation and the response to exercise of thecentral and peripheral nervous systems, lungs and pulmonary circulation, right ventricle (RV) and left ventricle (LV), myocardium, valves,coronary circulation, peripheral circulation, and skeletal muscle.9-11Dobutamine is the preferred alternative modality for the evaluationof contractile and flow reserve. Vasodilator SE is especiallyconvenient for combined assessment of wall motion and coronaryflow reserve, which may be indicated in dilated non-ischaemic cardiomyopathy and hypertrophic cardiomyopathy (HCM).12,13A flexible use of exercise, dobutamine, and vasodilator stressesmaximizes versatility, avoids specific contraindications of each, andmakes it possible to tailor the appropriate test to the individual patient(Table 1).9HAEMODYNAMIC EFFECTS OF MYOCARDIAL STRESSORSAll SE stressors have associated haemodynamic effects. As a commonoutcome, they result in a myocardial supply/demand mismatch andmay induce ischaemia in the presence of a reduction in coronary flowreserve, due to epicardial stenoses, LV hypertrophy, or microvascular disease.10 Exercise and inotropic stressors normally provoke a generalized increase of regional wall motion and thickening, with an increment ofejection fraction (EF) mainly caused by a reduction of systolic dimensions.ExerciseDuring treadmill or bicycle exercise, heart rate normally increasestwo- to three-fold, contractility three- to four-fold, and systolic bloodpressure by 50%,11 while systemic vascular resistance decreases. LVend-diastolic volume initially increases (increase in venous return) tosustain the increase in stroke volume through the Frank–Starlingmechanism and later falls at high heart rates. For most patients,both duration of exercise and maximum workload and achievedheart rate are slightly lower in the supine bicycle position, due primarily to the development of leg fatigue at an earlier stage of exercise.Then, for a given level of stress in the supine position, the enddiastolic volume and mean arterial blood pressure are higher. Thesedifferences contribute to a higher wall stress and an associated increase in myocardial oxygen demand and filling pressures comparedwith an upright bicycle test.11 In response to exercise, there is a variable increase in pulmonary artery pressure (PAP), for which the de-Lancellotti et al 103gree depends on the intensity of test. Coronary blood flow alsoincreases three- to five-fold in normal subjects,14 but much less ( 2fold) in one-third of patients with non-ischaemic dilated or HCM.In the presence of a reduction in coronary flow reserve, the regionalmyocardial oxygen-supply mismatch determines subendocardialmyocardial ischaemia and regional dysfunction, which can beobserved in 10–20% of patients with angiographically normal coronary arteries and either dilated or HCM.DobutamineDobutamine acts directly and mainly on b-1 adrenergic receptors of themyocardium, producing an increase in heart rate and contractility. Theincrease in the determinants of myocardial oxygen consumption is substantial: heart rate increases two- to three-fold, end-diastolic volume 1.2fold, and systolic arterial pressure 1.5- to 2-fold. Myocardial contractility(measured as elastance) increases over four-fold in normal subjects andmuch less so (less than two-fold) in patients with dilated cardiomyopathy.15 The activation of b-2 adrenergic receptors by dobutamine contributes to the mild decrease in blood pressure common at higherdobutamine dose, through a vasodilatatory effect. During dobutamineinfusion, LV end-systolic volume decreases to a greater extent than LVend-diastolic volume while the cardiac output increases as a result ofincreased heart rate and stroke volume. Compared with exercise, thereis a lesser recruitment of venous blood volume with dobutamine, so thatLV volumes and wall stress increase less with dobutamine.VasodilatorsVasodilator SE can be performed with dipyridamole, adenosine, or regadenoson, all using the same metabolic pathway, increasing endogenous adenosine levels (dipyridamole), increasing exogenousadenosine levels (adenosine), or directly acting on vascular A2A adenosine receptors (with higher receptor specificity for regadenoson andless potential for complications). These vasodilatators produce a smalldecrease in blood pressure, a modest tachycardia, and a minor increase in myocardial function.12,13 In the presence of a criticalepicardial stenosis or microcirculatory dysfunction, vasodilatoradministration results in heterogeneity of coronary blood flowbetween areas subtended by stenosed vs. normal coronary arteries,a supply–demand mismatch, and a decrease in subendocardial flowin areas of coronary artery stenosis via steal phenomena.STRESS ECHOCARDIOGRAPHY PROTOCOLSTreadmillThe advantage of treadmill exercise echocardiography is the widespread availability of the treadmill system and the wealth of clinicalexperience that has accumulated with this form of stress testing(Supplementary data online 1). Commonly used treadmill protocolsare the Bruce and modified Bruce protocols. The latter has with twowarmup stages, each lasting 3 min. The first is at 1.7 mph and a 0%grade, and the second is at 1.7 mph and a 5% grade.BicycleBicycle ergometer exercise echocardiography may be performed withthe patient upright or on a special semi-recumbent bicycle, which mayhave left lateral tilt to facilitate apical imaging. The patient pedalsagainst an increasing workload at a constant cadence (Figure 1).The workload is escalated in a stepwise fashion while imaging is performed. Successful bicycle stress testing requires the patient’s
SE indicationSE queryType of stressSequence ofimage acquisitionLevels of imageacquisitionSE resultSE reportDiastolic stress echoDiastolicdysfunction 6 SPAPincrease as reasonfor HF symptoms andsignsExercisePW Doppler E and A, PWTissue Doppler e0 †, TRCW Doppler for SPAPBaseline, lowworkload, peakexerciseE/e0 increase 6SPAP increaseDiastolic icdysfunction/dynamicMR/inducibleischaemia as reasonfor symptoms, or toplan treatment/lifestyle adviceExerciseCW Doppler LVOT velocity,TR CW Doppler forSPAP, PW Doppler E andA, PW Tissue Doppler e0 ,colour flow Doppler forMR, LV views for RWMABaseline, lowworkload, peakexercise, fortreadmill,immediately postexerciseLVOTO 6 SPAP increaseE/e0 increase 6 SPAPincreaseMR appearance/increaseRWMAExertion-induced LVOTODiastolic dysfunctionDynamic MRInducible ischaemiaDilated cardiomyopathyContractile reserve,inducible ischaemia,diastolic reserve,SPAP change,dynamic MR,pulmonarycongestionExerciseLV views, PW Doppler Eand A, PW tissueDoppler e0 , TR CWDoppler for SPAP,Colour flow Doppler forMR, lung imagesBaseline, lowworkload, peakexerciseContractility increaseNo contractility increaseE/e0 increase 6 SPAPincreaseRWMALung cometsMR increase/decreaseContractile reserveNo contractile reservePulmonary congestionDynamic MR/functionalMRInotropic reserveNo inotropic reserveCRT responderInotropic reserve,inducible ischaemiaDobutamineLV viewsBaseline, lowdose 6 high doseContractility increaseNo contractility increaseRWMAContractile reserveNo contractile reserveInducible ischaemiaInotropic reserve,viability in paced areaDobutamineLV viewsBaseline, low doseContractility increaseNo contractility increaseEF increase, paced areaviabilityInotropic reserveNo inotropic reserveCRT responderSevere AS with nosymptomsExerciseLV views, colour flowDoppler for MR, TR CWDoppler for SPAP, AVCW Doppler, LVOT PWDopplerBaseline, lowworkload, peakexerciseSymptoms 6 LVEF drop/no increase a/oGLS 6 RWMA 6 SPAPincrease 6 MRappearance/increase 6 gradientincreaseSevere AS with symptoms/pulmonary hypertension/dynamic MR/nocontractile reserve/inducible ischaemia/non-compliant valveNon-severe AS withsymptomsExerciseAV CW Doppler, LVOT PWDoppler, LV views,Colour flow Doppler forMRBaseline, lowworkload, peakexerciseGradient increase no/minAVA increase 6 LVEFdrop/no increase a/oGLS 6 RWMA 6 MRappearance/increase 6 SPAPincreaseNon-compliant valve/nocontractile reserve/inducible ischaemia/dynamic MR/pulmonaryhypertensionDiastolic function104 Lancellotti et alTable 1 Targeted parameters to be assessed during ortic stenosisJournal of the American Society of EchocardiographyFebruary 2017Native valve disease
AV CW Doppler, LVOT PWDoppler, LV viewsBaseline, low doseDobutamineLVOT PW Doppler, AV CWDoppler, LV viewsBaseline, low doseExerciseLVOT PW Doppler, AV CWDoppler, LV viewsBaseline, low workloadSevere MR with nosymptomsExerciseLV views, TR CW Dopplerfor SPAPNon-severe MR withsymptomsExerciseChange in MR severitywith exertion 6 SPAPincreaseLow–flow, low-gradientASPrimary mitralregurgitationSecondary mitralregurgitationAortic RegurgitationMitral stenosisMultivalvular diseaseNo/min SVincrease 6 LVEF drop/noincrease a/oGLS 6 gradientincrease 6 no/min AVAincreaseNo flow reserve/no LVcontractile reserve/truesevere ASBaseline, low workload,peak exerciseSymptoms, SPAPincrease, LV EF failure toincreaseSevere MR withsymptoms/pulmonaryhypertension/nocontractile reserveColour flow Doppler forMR, LV views, TR CWDoppler for SPAPBaseline, low workload,peak exerciseMR increaseNo MR increaseSevere MR with symptomsSymptoms unrelated withMRExerciseColour flow Doppler forMR, TR CW Doppler forSPAP, LV viewsBaseline, low workload,peak exerciseMR increase 6 SPAPincreaseMR decreaseDynamic MR, assessseverityFunctional MRSevere AR with nosymptomsExerciseLV viewsBaseline, low workload,peak exerciseSymptomsEF failure to increaseSevere AR with symptoms/no LV contractile reserveNon-severe AR withsymptomsExerciseLV views, Colour flowDoppler for MR, TR CWDoppler for SPAPBaseline, low workload,peak exerciseRWMA 6 SPAPincrease 6 MRappearance/increaseInducible ischaemia/pulmonary hypertension/dynamic MRSevere MS with nosymptomsExerciseTR CW Doppler for SPAPBaseline, low workload,peak exerciseSymptoms 6 SPAPincreaseSevere MS with symptoms/pulmonary hypertensionNon-severe MS withsymptomsExerciseTR CW Doppler for SPAP,MV CW Doppler formean gradientBaseline, low workload,peak exerciseMV gradientincrease 6 SPAPincreaseSevere MSDobutamineMV CW Doppler for meangradientBaseline, low doseDiscordance inbetween symptomsand severity of valvediseaseExerciseCombination on the abovedepending oncombination of featuresat baselineBaseline, low workload,peak exerciseRe-evaluate symptoms/severity of valve diseaseSymptoms due or not tovalve diseaseStenosis/PPM with orwithout low flowExerciseAV CW Doppler, LVOT PWDoppler, TR CW Dopplerfor SPAP, LV views,Colour flow Doppler forMRBaseline, low workload,peak exerciseSymptoms 6 gradientincrease no/min EOAincrease 6 SPAPincrease 6 RWMA 6 MRappearance/increaseSignificant stenosis orPPM/inducibleischaemia/dynamic MRDobutamineAV CW Doppler, LVOTDoppler, LV viewsBaseline, low doseJournal of the American Society of EchocardiographyVolume 30 Number 2DobutaminePost valve proceduresAortic valve prosthesisLancellotti et al 105(Continued )
SE indicationMitral valve prosthesisMitral valve annuloplastySE queryStenosis/PPMIatrogenic MSSequence ofimage acquisitionLevels of imageacquisitionExerciseTR CW Doppler for SPAP,MV CW Doppler formean gradientBaseline, low workload,peak exerciseDobutamineMV CW Doppler for meangradientBaseline, low workloadExerciseTR CW Doppler for SPAP,MV CW Doppler formean gradientBaseline, low workload,peak exerciseDobutamineMV CW Doppler for meangradientBaseline, low workloadType of stressSE resultSE reportSymptoms 6 gradientincrease 6 SPAPincreaseSignificant stenosis or PPMGradient increase 6 SPAPincreaseIatrogenic MS106 Lancellotti et alTable 1 (Continued )Pulmonary hypertensionPulmonary hypertensionSymptoms and SPAPon exertionExerciseTR CW Doppler for SPAP,RV viewsBaseline, low workload,peak exerciseSPAP increaseRegrade severityCor pulmonale*RV contractile reserveand SPAPExerciseRV views, TR CW Dopplerfor SPAPBaseline, low workload,peak exerciseRV contractility increaseRV contractile reserveAssess response toexercise andsymptomsExerciseLV views, LVOT CWDoppler for LVOTO, TRCW Doppler for SPAP,Colour flow Doppler forMR, lung imagesBaseline, low workload,peak exerciseRWMALVOTOPathologic SPAP increaseMR appearance/increaseLung cometsInduced ischaemiaLVOTOPulmonary hypertensionDynamic MRPulmonary congestionSPAP and RVcontractile reserveExerciseTR CW Doppler, RV viewsBaseline, low workload,peak exerciseSPAP increaseRV contractility increaseRegrade severityRV contractile reserveAthlete’s heartSymptomatic athleteCongenital heart diseaseAtrial septal defectDobutamineRV viewsBaseline, low workloadRV contractility increaseRV contractile reserveRV and LV contractilereserveExerciseRV views, TAPSE, PWTissue DopplerBaseline, low workload,peak exerciseRV/LV contractilityincreaseRV/LV contractile reserveAortic coarctationAssessment of severityand of LV contractilereserveExerciseDescending aorta CWDoppler, LV viewsBaseline, low workload,peak exerciseGradient increaseLV contractility increaseRegrade severityLV contractile reserveUniventricular heartsAssessment ofcontractile reserveand haemodynamicconsequences ofexerciseExerciseVentricular views, colourflow Doppler to detectatrio-ventricular valveregurgitation, CWDoppler to measuregradientsBaseline, low workload,peak exerciseContractility increaseOther abnormalitiesContractile reserveDescribe and gradeAR, aortic regurgitation; AV, aortic valve; CW, continuous wave; EF, ejection fraction; LV, left ventricle; LVOTO, LV outflow tract obstruction; MR, mitral regurgitation; MS, mitral stenosis;MV, mitral valve; PW, pulse wave; RV, right ventricle; RWMA, regional wall motion abnormality; PPM, prosthesis–patient mismatch; SPAP, systolic pulmonary artery pressure; TAPSE,tricuspid annular systolic plane excursion; TR, tricuspid regurgitation.*Cor pulmonale refers to the altered structure (e.g. hypertrophy or dilatation) and/or impaired function of the RV that results from pulmonary hypertension.† 0e often refers to averaged septal and lateral velocities, though either septal or lateral velocity can be used since the goal is to determine the change from rest to exercise.Journal of the American Society of EchocardiographyFebruary 2017RV contractile reserveTetralogy of Fallot
Journal of the American Society of EchocardiographyVolume 30 Number 2Lancellotti et al 107Figure 1 Exercise echocardiography protocol and parameters that can be assessed at each stage. bpm, beats per minute; LV, leftventricle; LVOT, LV outflow tract; MR, mitral regurgitation; E/e0 , ratio of early transmitral diastolic velocity to early TDI velocity of themitral annulus; RWM, regional wall motion; RV, right ventricle; SPAP, systolic pulmonary artery pressure; W, watts; rpm, rotations perminute. Valve refers to aortic or mitral valve.Figure 2 Diagnostic end-points, causes of test cessation and definition of abnormal stress test. Asterisk indicates specific targetedfeatures relates to cut-off values associated with poor outcome in defined population (i.e. 50 mmHg intraventricular obstruction).NS, non-sustained; SVT, sustained ventricular tachycardia.cooperation to maintain the correct cadence and coordination toperform the pedalling action. Causes of test cessation and definitionof abnormal stress test are listed in Figure 2.DobutamineFor detection of inotropic response in HF patients, stages of 5 min areused, starting from 5 up to 20 mg/kg/min (Figure 3). To fully recruitthe inotropic reserve in patients with HF and under b-blocker therapy,doses up to 40 mg/kg/min may be required. Atropine coadministration is associated with higher rate of complications in those with a history of neuropsychiatric symptoms, reduced LV function, or smallbody habitus.9 In assessment of the patient with possible severe aorticvalve stenosis, the maximal dose is usually 20 mg/kg/min; higherdoses are less safe and probably unnecessary. The dobutamine infusion is started as usual at 5 mg/kg/min but titrated upward in stepsof 2.5–5 mg/kg/min every 5–8 min. After each increment in dobutamine dose, a period of 2–3 min before starting the image acquisitionwill allow the haemodynamic response to develop.VasodilatorsAdministration of dipyridamole (0.84 mg/kg over 6 min or the samedose over 10 min, or an initial dose of 0.56 mg/kg over 4 min sometimes followed by 4 min of no dose and additional 0.28 mg/kg over2 min), adenosine (140 mg/kg/min over 4–6 min to a maximum of60 mg), or regadenoson (0.4 mg over 10 s) is performed withoutthe administration of atropine.
108 Lancellotti et alJournal of the American Society of EchocardiographyFebruary 2017Figure 3 Dobutamine echocardiography protocol. A low-dose test is recommended in patients with low-flow, low-gradient aorticstenosis and reduced LVEF. In patients with heart failure that are receiving beta-blocker therapy, high doses up to 40 mg/kg/min(without atropine) of dobutamine are often required. AVA, aortic valve area; LV, left ventricle; LVOT, LV outflow tract; RWM, regionalwall motion; SV, stroke volume. Valve refers to aortic or mitral valve.Image AcquisitionThe echocardiographic imaging acquisition protocol of choice variesaccording to the objectives of the test and the stressor used (Tables 1and 2). Several parameters can be assessed, including ventricular andvalvular function, valvular and subvalvular gradients, regurgitantflows, left and right heart haemodynamics including systolic pulmonary artery pressure (SPAP), ventricular volumes, B-lines (also calledultrasound lung comets, a sign of extravascular lung water), andepicardial coronary flow reserve.When either treadmill or upright bicycle exercise is performed,most protocols rely on post-exercise imaging, which is generallylimited to apical, parasternal and/or subcostal views. It is imperativeto complete post-exercise imaging as soon as possible since wall motion changes, valve gradients, and pulmonary haemodynamicsnormalize quickly during recovery. To accomplish this, the patient ismoved immediately from the treadmill to an imaging table and placedin the left lateral decubitus position so that imaging can be completedwithin 1–2 min. However, when the LVOT gradient is assessed in athletes or HCM patients, it may be more relevant to obtain this measurement with the patient in the upright position, since cardiacsymptoms in these patients are noted most com
TABLE OF CONTENTS Introduction 102 Stress Echocardiography Methods 102 Haemodynamic Effects of Myocardial Stressors 103 Exercise 103 Dobutamine 103 Vasodilators 103 Stress Echocardiography Proto-cols 103 Treadmill 103 Bicycle 103 Dobutamine 107 Vasodilators 107 Image Acquisition 108 InterpretationoftheTest 108
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