stress echocardiography
DESCRIPTION
Courtesy to Dr Saadia ArshadTRANSCRIPT
Stress echocardiography
Sadia Arshad
What is stress??
STRESS
• Any stimulus, (as fear or pain), that disturbs or interferes with the normal physiological equilibrium of an organism
The Random House College Dictionary
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
TREADMILL
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
• 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
• 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.
Indications
• 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
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
• 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.
Advantages DisadvantagesTreadmill Widely available
High workloadPost stress imagesMild ischemia may revert
Upright bicycle Imaging during exercise
Technically difficult
Supine bicycle Imaging during exerciseDopplers readily available
Low workload
Dobutamine Continuous imaging Side effects
Dipyridamole Continuous imaging Side effects
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
ISCHEMIA
Three States of the Sodium Channel and the Normal Sodium Current (INa)
Ca++
outin
out
in
Na+/Ca++
Exchanger
Ca++
Ca++
Ca++
Ca++
Na+
Na+
Na+
Na+Na+
Na+
Na+
RestingClosedRestingClosed
Na+
ActivatedActivated InactivatedInactivated
Na+
Na+
Na+ Ca++
Ca++
0
Late
Peak
SodiumCurrent
[Na]140 mM ~ 10mM
Ischemia Induced Effects on Late INa and
Intracellular Calcium
Ca++
Na+/Ca++
Exchanger
Ca++Ca++
Na+
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
Excess Calcium:• Electrical instability• Contractile dysfunction• ECG changes
0
Late
Peak
out
in
outin
Na+
Na+
Na+
Na+ Ca++
Ca++
ImpairedInactivation
ImpairedInactivation
Ca++Ca++
SodiumCurrent
Cellular Mechanism of Ischemia
Consequence(s) of Mechanical DysfunctionMechanical 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 Demand Demand OO22 Supply Supply
Extravascular Compression
Blood Flow to Microcirculation( O2 delivery to Myocytes)
Modified from: Belardinelli et al. Eur Heart 8 (Suppl. A):A10-A13, 2006
• 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.
• 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.
• 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
Interpretation
• 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.
ADJUNCTIVE CRITERIA
• LV cavity dilatation.
• Decrease in global systolic function.
• Diastolic dysfunction
• New or worsening MR.
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.
False –Suboptimal stressDelayed post treadmill imagingSingle vessel diseaseLcx diseaseModerate stenoses (50-70%)Concentric LVHSignificant MR/AR
False+Hypertensive responseHCMMicrovascular disease
LVHSyndrome XDMMyocarditis
Epicardial spasmTetheringAbnormal IVS motion(LBBB/RV
pacing /post OP
DSE
• Sensitivity 85% 1 Vessel 60-70% Better for ≥70% leisons ≥2 vessel 90%
• Specificity 85%
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
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
VIABILITY
• 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
Viable myocardium
• Myocardial segments characterized by reduced function at rest but potentially recoverable either:
• spontaneously (stunned)
Or
• with revascularization (hibernating)
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
• Likely causes are cellular Ca overload, free radical generation and neutrophil accumulation.
• Seen during reperfusion s/p MI, Unstable ACS and exercise induced ischemia.
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)
• 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.
Methods of detecting Viability • Metabolic activity FDG• Myocardial perfusion PET Rubidium /NH3
Myocardial contrast echo• Cellular membrane integrity TC99
TL201• Contractile reserve
DSE MRI
Response of dysfunctional myocardium to dobutamine
• Bifasic response
• Worsening of function
• Sustained reponse
• No change
Determinants of contractile reserve of viable myocardium
• Severity of coronary stenosis
• Coronary reserve
• Collateral supply
• Metabolism
• Tethering
Stress Echo Limitations
• Technical quality of images– COPD– Obesity
• Timing of acquisition of images
• Learning curve
• Operator dependent
• Reproducibility
• THANK YOU