Courtesy to Dr Saadia Arshad

1. Stress echocardiography
Sadia Arshad

2. What is stress??

3. STRESS
• Any stimulus, (as fear or pain), that disturbs or
interferes with the normal physiological equilibrium
of an organism
The Random House College Dictionary

4. Common Types of Stress Tests
• Routine Treadmill (ETT)
• Exercise Echocardiography
• Exercise Nuclear Stress
• Dobutamine Echocardiography
• Dobutamine Nuclear Stress
• Adenosine Nuclear Stress
• Persantine Nuclear Stress
• Uncommonly with transespophageal atrial pacing
• Ergonovine
• Adjuncts are atropine and handgrip

5. TREADMILL

6. Patients Appropriate for Routine ECG Stress Test
without Imaging
• Patient can exercise for 6 or more minutes
• No history of diabetes
• No history of coronary revascularization
• No history of myocardial infarction
• Normal baseline ECG

7. • The potential for using echocardiography for this purpose was
first reported in 1979 when two groups of investigators
demonstrated the proof of concept
• Mason and colleagues used M-mode echocardiography to
study 13 patients with coronary artery disease and 11 age-
matched control subjects during supine bicycle exercise
• Stress-induced wall motion changes were detected in 19 of 22
segments supplied by stenotic coronary arteries
• Although this was the first demonstration of transient
ischemia being detected with ultrasound, the inherent
limitations of the M-mode technique were apparent

8. • That same year, Wann and co-workers applied an early two-
dimensional, 30-degree sector imaging system to
demonstrate inducible wall motion abnormalities during
supine bicycle exercise and subsequent improvement of the
wall motion response after revascularization.
• These early studies were limited by image quality and a
reliance on videotape analysis, factors that would slow the
growth of the field in its early years.

9. Indications

10. • Induces ischaemia via
– Increased HR, BP & contractility
• Preferred agent if
– History of asthma or COPD
– Critical carotid stenosis
– Women with intermediate predictors
– ECG changes LBBB LVH Resting ST/T changes

12. Contraindications
• Ventricular arrhythmias
• Recent myocardial infarction (1-3 days)
• Unstable angina
• Hemodynamically significant left ventricular
outflow tract obstruction
• Severe aortic stenosis
• Aortic aneurysm or aortic dissection
• Systemic hypertension

13. • Common protocols include treadmill or bicycle
(upright or supine) with immediate post stress
imaging.
• Imaging needs to be aquired immediately, otherwise
wall motion may terminate in up to a few minutes
• The best post exercise image is compared side by
side to the baseline images.

14. Advantages Disadvantages
Treadmill Widely available
High workload
Post stress images
Mild ischemia may
revert
Upright bicycle Imaging during
exercise
Technically difficult
Supine bicycle Imaging during
exercise
Dopplers readily
available
Low workload
Dobutamine Continuous imaging Side effects
Dipyridamole Continuous imaging Side effects

17. Different Degrees of Coronary Blood
Flow
0.0
0.5
1.0
1.5
2.0
2.5
3.0
3.5
4.0
4.5
mg/miin/g
Baseline Adeno Dipy Dobuta Exercise
Blood Flow

18. ISCHEMIA

20. Three States of the Sodium Channel
and the Normal Sodium Current (INa)
Ca++
out
in
out
in
Na+
/Ca++
Exchanger
Ca++
Ca++
Ca++
Ca++
Na+
Na+
Na+
Na+
Na+
Na+
Na+
Resting
Closed
Na+
Activated Inactivated
Na+
Na+
Na+
Ca++
Ca++
0
Late
Peak
Sodium
Current
[Na]
140 mM ~ 10mM

21. Ischemia Induced Effects on Late INa
and
Intracellular Calcium
Ca++
Na+
/Ca++
Exchanger
Ca++
Na+
Na+
Na+
Na+
Na+
Na+Na+
Na+
Na+
Na+
Ca++
Ca++
Ca++
Ca++
Ca++Ca++ Ca++
Ca++
Ca++
Ca++
Ca++
Excess Calcium:
• Electrical instability
• Contractile dysfunction
• ECG changes
0
Late
Peak
out
in
out
in
Na+
Na+
Na+
Na+
Ca++
Ca++
Impaired
Inactivation
Ca++
Sodium
Current

22. Cellular Mechanism of Ischemia
Consequence(s) of Mechanical Dysfunction
Mechanical Dysfunction
• Abnormal Contraction and RelaxationAbnormal Contraction and Relaxation
• ↑↑ Diastolic TensionDiastolic Tension
↑ O2 Consumption
(to maintain tonic contraction)
↓
↑ ATP Hydrolysis
↑ Diastolic Wall Tension (Stiffness)Diastolic Wall Tension (Stiffness)
↑↑ OO22 DemandDemand↓↓ OO22 SupplySupply
↑ Extravascular Compression
↓
↓ Blood Flow to Microcirculation
(↓ O2 delivery to Myocytes)
Modified from: Belardinelli et al. Eur Heart 8 (Suppl. A):A10-A13, 2006

23. • Dobutamine is a synthetic catecholamine that has been
developed as a positive inotropic agent for short-term
intravenous administration.
• The predominant mechanism of action, augmentation of
myocardial contractility, is mediated through β1-adrenergic
receptor stimulation.

24. • Although referred to as a selective β1-adrenergic receptor
agonist, dobutamine has mild β2- and α1-adrenergic receptor
agonist effects.
• Because the β2- and α1-adrenergic agonist effects are
relatively balanced, the net effect on the systemic vasculature
is minimal in most patients.
• Direct linear correlations exist among the dose of
dobutamine, the plasma concentration, and hemodynamic
effects.

25. • Cardiac output increases as a result of ↑heart rate and stroke
volume.
• Half life 2 minutes/steady state 10 minutes
• Must be administered by continuous intravenous infusion. It is
rapidly metabolized in the liver to inactive metabolites
• Atropine needed concurrently to increase HR 36% of time

27. Interpretation

30. • Normal LV wall motion becomes hyperdynamic on stress.
• Worsening of wall motion abnormalities or development of
new ones is hallmark of stress induced ischemia.
• Improvement of existing wall motion abnormalities indicates
viable myocardium
• In 10% of cases an akinetic myocardial segment becomes
dyskinetic during stress echo this change was not found to
have a diagnostic or prognostic implication.

31. ADJUNCTIVE CRITERIA
• LV cavity dilatation.
• Decrease in global systolic function.
• Diastolic dysfunction
• New or worsening MR.

33. WMA grading
• 1. Normal
• 2. Hypokinetic , marked reduction in endocardial motion and
thickening
• 3. Akinetic virtual absence of inward motion and thickening
• 4. dyskinetic/paradoxical wall motion during systole.

34. False –
Suboptimal stress
Delayed post treadmill imaging
Single vessel disease
Lcx disease
Moderate stenoses (50-70%)
Concentric LVH
Significant MR/AR
False+
Hypertensive response
HCM
Microvascular disease
LVH
Syndrome X
DM
Myocarditis
Epicardial spasm
Tethering
Abnormal IVS motion(LBBB/RV
pacing /post OP

35. DSE
• Sensitivity 85%
1 Vessel 60-70%
Better for ≥70% leisons
≥2 vessel 90%
• Specificity 85%

36. Advantages of Stress Echocardiography
Compared to Nuclear Stress Testing
• Higher Specificity
• Visualization of cardiac valves
• Evaluate for presence of pericardial effusion
• Ability to measure RV Systolic Pressure
• More accurate assessment of LV ejection fraction
• Doppler interrogation to determine Diastolic Function
• Lower Cost
• Lack of Radiation Exposure

37. Factors decreasing sensitivity of exercise stress
echocardiography
• Ischemic myocardium can resume function in as little as 10
seconds after exercise so the “ischemic moment” can be
missed if images are obtained too long after exercise
completed
• Small vessels may not create large enough of an ischemic
zone to generate a wall motion abnormality that is detectable
• Suboptimal visualization of endocardium

40. VIABILITY

41. • Viability
• Stunning
– Prediction of viability after acute MI
– Clinical relevance
– Compare with other non invasive techniques
• Hibernation
•Predicting viability in CAD+CHF
•DSE in the setting of BB

42. Viable myocardium
• Myocardial segments characterized by reduced function at
rest but potentially recoverable either:
• spontaneously (stunned)
Or
• with revascularization (hibernating)

43. Myocardial Stunning
• Persistant contractile dysfunction with delayed recovery after
transient ischemia despite adequate reperfusion
• Prolonged functional depression requiring ≥ 24 hours for
recovery
• Develops on reperfusion even after brief periods of coronary
occlusion which are insufficient to cause myocardial necrosis

44. • Likely causes are cellular Ca overload, free radical generation
and neutrophil accumulation.
• Seen during reperfusion s/p MI, Unstable ACS and exercise
induced ischemia.

45. Myocardial hibernation
• Chronic depression of myocardial function which exhibits
complete or partial recovery of function after
revascularisation
• Association with severe CAD
• Originally thought to be due to ↓ myocardial blood flow.
• Now realised to be multifactorial:
– Repeated ischemia in collaterall dependant myocardium
– ↓ coronary perfusion pr in post stenotic bed
– Ischemia induced changes in gene expression (preconditioning)

46. • In contrast to stunning, is associated with loss of contractile
matreial and severely ↓ residual coronary flow reserve,
affective ability to respond to ionotropic stimulus.
• It is an unstable state , not the successful adaptation to
ischemia once thought.Stunning and hibernation frequently
co exist and contribute to CHF
• Nesto et al were the first to demonstrate response of LV to
ionotropic stimulus (epi or PVC) during LHC as an index of
viability.

47. Methods of detecting Viability
• Metabolic activity
FDG
• Myocardial perfusion
PET Rubidium /NH3
Myocardial contrast echo
• Cellular membrane integrity
TC99
TL201
• Contractile reserve
DSE
MRI

49. Response of dysfunctional myocardium to
dobutamine
• Bifasic response
• Worsening of function
• Sustained reponse
• No change

50. Determinants of contractile reserve of viable
myocardium
• Severity of coronary stenosis
• Coronary reserve
• Collateral supply
• Metabolism
• Tethering

53. Stress Echo Limitations
• Technical quality of images
– COPD
– Obesity
• Timing of acquisition of images
• Learning curve
• Operator dependent
• Reproducibility

54. • THANK YOU