Dr CHARALAMPOS KAVVOURAS MD, Msc

ACHD Consultant Liverpool Heart and Chest Hospital, UK

Disclosures

No conflict of interest regarding this talk

Stress Test

Exercise stress testing preserve the integrity of the electromechanically response and provides valuable information regarding functional status

Provides links among

Symptoms

Cardiovascular workload

Wall motion abnormalities

Hemodynamic responses

Types of Exercise

Treadmill stress Echocardiography

Higher maximum heart rate (2-3 times the baseline)

Increase in BP

Increase in LV contractility

Functional aerobic capacity well defined

Bicycle Stress

Higher Blood pressure in supine position

Shorter duration of exercise /and lower HR due earlier leg fatigue

Allows better images and Doppler assessment

Pharmacological Stress

Dobutamine is a useful agent for evaluation of contractility and flow reserve (contraindicated in HCM)

Dodutamine HR X2-3 and Contractility >X4, mild BP increase ,causes less recruitment of venous blood volume

(LV volumes and wall stress less than exercise )

Vasodilator stress agents (dipyridamole, adenosine, regadenoson) are useful for wall motion abnormalities and coronary flow reserve

Contractile reserve LVEF >5% or GLS>2%

Flow reserve forward stroke volume > 20%

Dobutamine echocardiography protocol.

END POINTS Diagnostic end points

Max dose /workload

Target Heart rate

Obvious ECG changes

Obvious Echo changes

Severe Chest pain

Causes of test cessation

Intolerable symptoms

Muscular exhaustion

Hypertension >220mmHg systolic

Hypotension >40mmHg baseline

Arrhythmias/Frequent ectopics

(SVT /AF/NSVT/VT )

Positive test >1 criteria

Angina ,dyspnea, pre-syncope Ischemia >2mm ST depression or elevation Arrhythmia VT/AFib New regional wall motion abnormalities

Anatomical lesion Interventions Residual lesions

ASD

Surgical or percutaneous closure with a device

Residual shunt across the atrial septum

RV dilatation

RV dysfunction

Pulmonary hypertension

VSD

Surgical closure

Residual VSD

Aortic valve regurgitation

Tricuspid valve regurgitation

LV dilatation

LV dysfunction

Pulmonary hypertension

PDA

PDA closure either surgical or or with a device

percutaneous

LV dysfunction

Pulmonary hypertension

AVSD

ASD/VSD Closure

AV valve repair

Residual shunts across ASD/VSD

LV dysfunction

Pulmonary hypertension

AV valve regurgitation

LVOT Obstruction

TOF

Initial palliation and then

VSD closure

RV outflow tract muscle bundles resection

Patch enlargement of the RV outflow tract

Pulmonary valve replacement

Residual shunt across the VSD

Right Ventricle outflow tract or conduit

obstruction / stenosis

Pulmonary regurgitation /stenosis

Tricuspid regurgitation

Pulmonary hypertension

Aortic regurgitation

TGA

Palliation before repair (Atrial septostomy via

transcatheter approach )

Surgical repair before 1980 with an Atrial switch(

Mustard or Senning procedure)

Surgical repair after 1980 Arterial switch

Rastelli procedure

Atrial switch :

Baffle stenoses or leaks

Systemic RV systolic +/- diastolic dysfunction

Tricuspid (systemic AV valve) abnormalities

Subpulmonic LV systolic function

Arterial switch

Neoaortic valve regurgitation

Coronary ischemia

LV systolic dysfunction

Rastelli procedure

RV-PA conduit stenosis/regurgitation

ccTGA

No surgical repair is required unless other

congenital anomalies exists also

Systemic RV systolic dysfunction

Systemic Tricuspid valve regurgitation

Aortic regurgitation

Subpulmonic LV systolic dysfunction

Pulmonary hypertension

Single ventricle

Fontan operation

atriopulmonary Fontan,

lateral tunnel Fontan,

extracardiac Fontan

AV valve regurgitation

Ventricular systolic function

Outflow tract obstruction

Semilunar valve regurgitation

Coarctation of the aorta

Ebstein anomaly

No surgical repair is required in all patients.

Surgical approaches may include tricuspid valve

replacement , tricuspid valve repair ( Cone

reconstruction)

Tricuspid regurgitation

RV dysfunction

LV dysfunction

Congenital aortic valve disease

Balloon valvuloplasty

Surgical valvotomy

Aortic valve replacement

Ross procedure

Aortic valve stenosis/regurgitation

LV dysfunction

Recurrent subaortic obstruction

Pulmonary valve disease

Balloon pulmonary valvuloplasty

Surgical valvotomy

RV systolic dysfunction

Pulmonary regurgitation

Tricuspid regurgitation

Coarctation aorta

Surgical options include end-to-end anastomosis,

subclavian flap aortoplasty, bypass conduit or

patch plasty at the site of coarctation or

Balloon angioplasty and stent implantation

Aortic recoarctation( Conduit stenosis/obstruction)

LV systolic dysfunction

Coronary ischemia

Atrial septal defect

Chronic volume overload of the right ventricle

SE testing is feasible to evaluate the RV performance in both open and closed atrial septal defect

RV performance indirectly relates to SPAP at maximal exercise.

Increased SPAP at rest is associated with a worse outcome inpatients with closed atrial septal defects.

Ventricular septal defect

In patients with repaired VSD, chest pain may be related to the previous scar from the sternotomy or it can related to other musculoskeletal reasons. It can also be due to LV dysfunction.

SE is a valuable diagnostic tool to differentiate between the causes.

In cases of a residual small left-to-right shunt, chronic left ventricle volume overload may occur which can lead to chest pain.

Tetralogy of Fallot

Exercise echocardiography to study the RV and LV contractile reserve.

RV function can be studied measuring RVFAC, TAPSE and tissue Doppler velocities.

SE can also identify increased pressure gradients in patients with RV-PA conduits

RV dysfunction by stress echocardiography could be helpful at determining optimal timing for pulmonary valve replacement

Transposition of great arteries

Chronic systemic pressure load on the RV might lead to ventricular dysfunction, progressive TR, and HF

The evaluation of systolic performance is particularly difficult since no standardized methods have been established for systemic RV

SE may provide information about myocardial contractile reserve and the behaviour of the TR during stress

Univentricular hearts Assess Systemic LV

Assess Systemic RV

Doppler assessment of regurgitant or obstructive valvular and vascular lesions as exercise increases may be beneficial for surgical planning.

Treated coarctation of the aorta Subclinical hypertension.

Exercise-induced systemic arterial hypertension (defined as a peak systolic blood pressure >200 mmHg) was predictive of chronic hypertension in adults after coarctation repair.

Exercise testing can also be used to assess dynamic residual gradients after repaired CoA

ALCAPA

Incidence of 0.008%

Coronary steal phenomenon resulting in severe myocardial ischemia and dysfunction.

SE can be utilized to identify any systolic and diastolic dysfunction of the LV before and after surgery.

VALVULAR HEART DISEASES

Severe valve disease without symptoms

Non-severe valve disease with symptoms

Valve disease with low flow state.

VALVE DISEASES IN ACHD Repaired VSD TR/MR/AR

Repaired ASD TR

Repaired TOF PR /TR/AR

Repaired AVSD LAVVR /RAVVR

Ross Procedure AR/AS PR/PS

Ebstein anomaly TR

TGA(atrial switch) TR

TGA (arterial switch) AR/PR

VALVULAR HEART DISEASES.

ESC /ACC guidelines consider aortic valve replacement (AVR) class I indication, level of evidence B, in patients with severe AR and symptoms revealed by exercise testing

The increase in MR severity (≥1 grade),dynamic PH (SPAP ≥ 60 mmHg),the absence of contractile reserve (<5% increase in EF or <2% increment in global longitudinal strain) and a limited RV contractile recruitment (quantified by tricuspid annular plane systolic excursion (TAPSE) <19 mm) are all parameters of poor prognosis.

In patients with asymptomatic severe AS, exercise SE may uncover the development of symptoms, necessitating consideration for AVR. Increase in mean gradient is considered an indication for early elective AVR (Class IIb recommendation, level of evidence C in ESC guidelines) in asymptomatic patients with severe AS.

Pulmonary hypertension and pulmonary arterial pressure assessment

There are no validated diagnostic criteria for PH during exercise.

The term exercise-induced pulmonary hypertension should generally be avoided.

Careful attention to study quality, including signal acquisition and measurement, is needed to prevent overestimation or underestimation of PAP.

TRV is higher in 5-10% of normal outliers, patients over 50 years of age, obese individuals, and elite athletes.

Except in the above-stated conditions, TRV >3.1 m/sec and estimated PAP >43 mmHg may be abnormal and prompt further evaluation.

PH during stress echocardiography may be seen in pathologic conditions such as high-flow states, HFpEF, and valvular heart disease.

PH seen during stress echocardiography is most commonly due to left heart disease.

PH during stress echocardiography may be seen in patients at risk of or with subclinical PAH.

Congenital heart disease Indications for SE

ASD/VSD

Chest pain

SPAP

RV Contractile reserve

Diastolic function

Tetralogy Fallot

RV systolic and diastolic function

Evaluation of RV to pulmonary artery conduit

PR Severity

Optimal time for PVR

Transposition of great arteries

Myocardial Dysfunction

Baffle Stenosis

Single ventricle

Systolic and diastolic ventricle dysfunction

Assessment of contractile reserve

AV valve regurgitation

Valvular diseases

Severe valvular disease without symptoms

Non severe valvular disease with symptoms

Change of valvular severity with exertion+/- SPAP increase

ALCAPA

Myocardial Ischemia

Coarctation aorta

Assessment of blood pressure response

Gradient across repaired CoA

Assessment of LV contractile reserve

Pulmonary hypertension

Exercise induced PH / SPAP on exertion

RBHT Data 2013/2017 215 patients with congenital heart diseases

Stress echocardiography was normal in 78% and abnormal in 22%.

A positive SE was reported in 48/215 patients (22%).

commonest findings

New onset RWMA (n= 19, 35%)

Worsening valvular haemodynamic (n= 16, 22 %)

Worsening symptoms (n=6, 15%)

Increased gradient across the previous repaired coarctation (n=4, 20%)

Exercise induced PHT (n=3, 6%).

Condition Number of patients

Valve

Stenosis

Regurgitation

64

42

22

Transposition of great arteries (arterial switch) 38

TGA –Atrial switch

Mustard

Senning

ccTGA

20

16

4

2

Single ventricle

4

Coarctation 8

Ventricular septal defect 11

ALCAPA 10

ASD 10

Repaired AVSD 5

In all 48 patients after SE

optimize medical therapy due to stress induced symptoms

To predict the development symptoms or LV dysfunction in asymptomatic patients

In patients with mild or moderate valvular disease SE useful in elucidating the cause of symptoms.

Risk stratification

Help to define optimal time of intervention

CONCLUSION Stress echo is an emerging technique in patients with CHD.

The indications for the use of SE in patients with congenital heart disease are continuously evolving.

SE can be used in a consecutive manner for the assessment of a certain patient for

diagnosis,

risk stratification,

follow-up,

evaluation of treatment.

Following a negative study, patients can be reassured of the low-likelihood of a major adverse cardiovascular event.

THANK YOU