Patients Appropriate for Routine ECG Stress Testwithout 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 wasfirst reported in 1979 when two groups of investigatorsdemonstrated the proof of concept• Mason and colleagues used M-mode echocardiography tostudy 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 22segments supplied by stenotic coronary arteries• Although this was the first demonstration of transientischemia being detected with ultrasound, the inherentlimitations of the M-mode technique were apparent
• That same year, Wann and co-workers applied an early two-dimensional, 30-degree sector imaging system todemonstrate inducible wall motion abnormalities duringsupine bicycle exercise and subsequent improvement of thewall motion response after revascularization.• These early studies were limited by image quality and areliance on videotape analysis, factors that would slow thegrowth of the field in its early years.
• 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 ventricularoutflow tract obstruction• Severe aortic stenosis• Aortic aneurysm or aortic dissection• Systemic hypertension
• Common protocols include treadmill or bicycle(upright or supine) with immediate post stressimaging.• Imaging needs to be aquired immediately, otherwisewall motion may terminate in up to a few minutes• The best post exercise image is compared side byside to the baseline images.
Three States of the Sodium Channeland the Normal Sodium Current (INa)Ca++outinoutinNa+/Ca++ExchangerCa++Ca++Ca++Ca++Na+Na+Na+Na+Na+Na+Na+RestingClosedNa+Activated InactivatedNa+Na+Na+Ca++Ca++0LatePeakSodiumCurrent[Na]140 mM ~ 10mM
Ischemia Induced Effects on Late INaandIntracellular CalciumCa++Na+/Ca++ExchangerCa++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 changes0LatePeakoutinoutinNa+Na+Na+Na+Ca++Ca++ImpairedInactivationCa++SodiumCurrent
Cellular Mechanism of IschemiaConsequence(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 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
• Dobutamine is a synthetic catecholamine that has beendeveloped as a positive inotropic agent for short-termintravenous administration.• The predominant mechanism of action, augmentation ofmyocardial contractility, is mediated through β1-adrenergicreceptor stimulation.
• Although referred to as a selective β1-adrenergic receptoragonist, dobutamine has mild β2- and α1-adrenergic receptoragonist effects.• Because the β2- and α1-adrenergic agonist effects arerelatively balanced, the net effect on the systemic vasculatureis minimal in most patients.• Direct linear correlations exist among the dose ofdobutamine, the plasma concentration, and hemodynamiceffects.
• Cardiac output increases as a result of ↑heart rate and strokevolume.• Half life 2 minutes/steady state 10 minutes• Must be administered by continuous intravenous infusion. It israpidly metabolized in the liver to inactive metabolites• Atropine needed concurrently to increase HR 36% of time
• Normal LV wall motion becomes hyperdynamic on stress.• Worsening of wall motion abnormalities or development ofnew ones is hallmark of stress induced ischemia.• Improvement of existing wall motion abnormalities indicatesviable myocardium• In 10% of cases an akinetic myocardial segment becomesdyskinetic during stress echo this change was not found tohave 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 andthickening• 3. Akinetic virtual absence of inward motion and thickening• 4. dyskinetic/paradoxical wall motion during systole.
Advantages of Stress EchocardiographyCompared 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 stressechocardiography• Ischemic myocardium can resume function in as little as 10seconds after exercise so the “ischemic moment” can bemissed if images are obtained too long after exercisecompleted• Small vessels may not create large enough of an ischemiczone to generate a wall motion abnormality that is detectable• Suboptimal visualization of endocardium
• 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 atrest but potentially recoverable either:• spontaneously (stunned)Or• with revascularization (hibernating)
Myocardial Stunning• Persistant contractile dysfunction with delayed recovery aftertransient ischemia despite adequate reperfusion• Prolonged functional depression requiring ≥ 24 hours forrecovery• Develops on reperfusion even after brief periods of coronaryocclusion which are insufficient to cause myocardial necrosis
• Likely causes are cellular Ca overload, free radical generationand neutrophil accumulation.• Seen during reperfusion s/p MI, Unstable ACS and exerciseinduced ischemia.
Myocardial hibernation• Chronic depression of myocardial function which exhibitscomplete or partial recovery of function afterrevascularisation• 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 contractilematreial and severely ↓ residual coronary flow reserve,affective ability to respond to ionotropic stimulus.• It is an unstable state , not the successful adaptation toischemia once thought.Stunning and hibernation frequentlyco exist and contribute to CHF• Nesto et al were the first to demonstrate response of LV toionotropic stimulus (epi or PVC) during LHC as an index ofviability.