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Stress Test Lecture
- 1. Cardiac Stress Testing Corinne Jackson, MD August 7, 2014
- 2. Objectives Indications Limitations Guidelines Value of results
- 3. Introduction Chest pain: 6 million visits per year 2/3 undergo cardiac eval 15-20% ACS Remaining possible ACS Cost: $10-12 billion
- 4. Clinical Case 50 y/o female with diabetes, HTN, smoker Nonspecific substernal chest pain Slight dyspnea, no diaphoresis or N/V ECG nonspecific t wave flattening x 2 30 min apart Normal cardiac markers What to do?
- 5. Another case 45 y/o male with chest pain while working outside No PCP BP 180/95
- 6. Last one 69 yo male with HTN, hyperchol, DM with onset of CP after emotional phone call Stress test at outside hospital 4 months ago normal ECG unchanged Negative biomakers
- 7. Next steps History Typical or atypical Risk factors Traditional less important Risk level Low, Intermediate, High Which study to order
- 8. CAD Likelihood Nature of anginal symptoms Prior CAD Sex Age Traditional risk factors
- 9. Angina Deep Poorly localized Exertion / emotional stress Relief with nitro / rest Anginal equivalents
- 10. Weak stories Pleuritic Lower/middle abdominal pain Pain localized at fingertip Reproducible pain Very brief Radiation to lower extremities
- 11. Risk factors Weakly predictive in acute setting Family history
- 12. TIMI Risk Classification Age >65 >3 risk factors Known CAD >2 anginal episodes in the past 24 hours ASA use within 7 days ST segment deviation of 0.05mV or more Elevated cardiac marker
- 14. Current Guidelines AHA/ACC Low risk patients who are pain free No recurrent symptoms No ischemic ECG changes Normal serial markers over 6-8 hours Stress in observation unit or outpatient
- 15. Types of Stress Testing ECG exercise treadmill test Exercise Stress Echo Dobutamine Stress Echo Nuclear stress Test
- 16. Sensitivity and Specificity Sensitivity Percentage of patients with a disease who will have abnormal test Specificity Percentage of patients without disease who will have normal test results
- 17. Pretest Probability False-positives False-negatives
- 18. Stress Exercise Pharmacologic Dobutamine Adenosine Regadenoson (Lexiscan) Dipyridamole
- 19. Imaging Technique ECG Echo Nuclear Imaging Tc-99m sestamibi Tc-99m-tetrofosmin Thallium
- 20. Exercise ECG Sensitivity 68% Specificity 77%
- 22. ETT Selection Low to intermediate risk patients Ability to exercise No significant baseline ECG changes HD stable No arrhythmia Negative cardiac markers
- 23. ETT Not useful WPW Paced > 1 mm ST segment depression Complete LBBB Dig effect
- 24. ETT Absolute Contraindications AMI High risk UA Uncontrolled dysrhythmias Severe AS Active endocarditis Symptomatic HF Acute PE/DVT Myo/pericarditis Acute aortic dissection
- 25. ETT Relative Contraindications Left main disease Moderate valvular stenosis Electrolyte abnormalities Recent stroke /TIA HTN >200/110 High degree AV block Tachy/brady dysrhythmias HCOM Wellens syndrome
- 26. Limitations Severe PAD COPD Degenerative arthritis Amputation General debilitation Mental health/cognitive impairment
- 27. ETT Procedure Bruce Modified Bruce protocol
- 28. ETT End Points Symptom-limited Ischemia > 0.10mV horizontal ST depression or elevation Decreased blood pressure during exercise > 10mmHg systolic
- 29. ETT Results Positive > 0.10mV horizontal ST depression Negative No exercise-induced abnormalities at 85% MPHR Nondiagnostic <85% MPHR with no ECG evidence of ischemia
- 30. ETT Benefits Simplicity Lower cost
- 31. ETT drawbacks Sensitivity Pretest probability Women Young patients
- 32. Stress Echocardiogram Exercise or pharmacologic stress Combines ECG stress with imaging at rest and after stress Sensitivity 80% Specificity 84%
- 33. Stress Echocardiography Images synched to QRS complex Normal: increased contractility Positive: regional wall motion abnormalities
- 34. Stress Echo Indications Inability to exercise Baseline ECG alterations
- 36. Dobutamine Contraindications Recent MI/UA Aortic stenosis Cardiomyopathy Atrial tachycardias with uncontrolled vent response Uncontrolled HTN Thoracic Aortic Aneurysm LBBB
- 37. Stress Echo Pros Noninvasive No radiation exposure Structural and functional data Possible alternative diagnosis
- 38. Stress Echo Limitations Operator dependent Reader dependent Cannot detect subendocardial ischemia Timing Increased cost
- 39. Nuclear Stress Test IV radioactive tracer Rest Stress – usually pharmacologic SPECT or PET
- 40. Coronary Vasodilators Dipyridamole Adenosine Regadenson
- 41. Adenosine/Dipyridamole Contraindications Active bronchospasm Allergy >1 degree AVB SBP <90 Caffeine/aminophylline COPD (relative) Sick sinus syndrome (relative)
- 42. Regadenoson Contraindications 2 degree AVB Sinus node dysfunction Acute myocardial ischemia
- 43. Myocardial Perfusion Imaging Thallium 201 Technetium 99m sestamibi Technetium 99m tetrofosmin SPECT
- 44. Nuclear stress test indications Inability to exercise Baseline ECG abnormalities Intermediate risk patients with TIMI score of 4
- 45. MPI benefits Improved sensitivity (89%) and specificity (75%) Widely available Compatible with exercise, dobutamine, and vasodilators
- 46. MPI Drawbacks Radioisotope Radiation Cost Long protocol Reader dependent
- 47. Cardiac CTA High sensitivity Radiation exposure No information on myocardial perfusion
- 48. Recent Negative Stress Test Consider alternative diagnosis Repeat ETT limited value “Warranty period” Plaque rupture
- 49. Case conclusions
- 50. Clinical Case 50 y/o female with diabetes, HTN, smoker Nonspecific substernal chest pain Slight dyspnea, no diaphoresis or N/V ECG nonspecific t wave flattening x 2 30 min apart Normal cardiac markers What to do?
- 51. Another case 45 y/o male with chest pain while working outside No PCP BP 180/95
- 52. Last one 69 yo male with HTN, hyperchol, DM with onset of CP after emotional phone call Stress test at outside hospital 4 months ago normal Negative biomarkers ECG unchanged
- 53. Summary Indications for different stress test modalities Consider your pretest probability Familiarity with guidelines It’s all about the story
Editor's Notes
- Guideline of ACC/AHA
- ACS diagnosed by positive ECG findings and/or positive cardiac marker Rate of d/c for patients with ACS is 4% (risk highest in women and those with atypical pain); also overreliance on past studies in a common reason for missed/delayed diagnosis
- On and off for a couple days – sharp – worse with movement; no radiation; lasted for 1 hour or two then goes away on own Good story or bad story? Risk factors? FH?
- Substernal pressure – feels funny left arm, sweaty, dyspneic, felt better when I rested Good story for CP? Does not chol, normal BP, +smoker Risk factors? What do want to do?
- Deep pain – felt better when I took that they gave me nitro Had some on and off pain Negative biomarkers
- Nature of symptoms, HPI important. Clinical gestalt – pretty good predictive value Age most important and outweighs all other risk factors male >55 Female >65
- Or in other words – what is a good story? Chest /arm/shoulder/epigastric discomfort Anginal equivalents – dyspnea, n/v, diaphoresis, unexplained fatigue
- Pts that did not read the text books But 1 in 20 pts diagnosed with mi can have atypical features
- Framingham Risk Factors (first degree relative, male sex, advanced age, hypertension, smoking, dm, hyperlipidemia and family history) But a/w worse outcomes family history – inc risk of 30 day events, even greater with siblings
- Thrombolysis in Myocardial Infarction Used in ACS/UA 2010 Candian medical association journal Diagnostic accuracy of the TIMI risk score in patients with chest pain in the emergency department: a meta-analysis10 prospective cohort studies (with a total of 17 265 patients) Of patients with a score of zero, 1.8% had a cardiac event within 30 days (sensitivity 97.2%, 95% CI 96.4–97.8; specificity 25.0%, 95% CI 24.3–25.7; positive likelihood ratio 1.30, 95% CI 1.28–1.31; negative likelihood ratio 0.11, 95% CI 0.09–0.15). Meta-regression analysis revealed a strong linear relation between TIMI risk score (p < 0.001) and the cumulative incidence of cardiac events. Out of every 1000 pt 20 will experience a cardiac event within 30 days
- Excluded from guidelines – low likelihood CAD Eval for other causes – esophageal spasm, gastritis, PUD, dissection, neuropsychiatric symptoms
- Prefer 24 hours but up to 72 hours; recommend ASA and possible nitrates No RCT to support this Controversy in low risk chest pain: dependent on finding CAD that is amenable to revascularization. Exceedingly low in low risk pts
- Likelihood signs and symptoms represent ACS from obstructive CAD (contingent on likelihood of having CAD) diagnostic test you must consider this – why it is not helpful in very low risk or very high risk Negative stress test result in pt with high pretest prob – inc likelihood of false negative Positive stress test in a pt with a low pretest prob – inc false positive (increased in women, esp. young women)
- Mean numbers Sensitivity ranging from 23-100% and specificities 17-100% Marked differences in characteristics of populations studies, differences in definition of presence and severity of disease Limited by gold standard of angiography – work up bias (pts selected for cath are more likely to have obstructive CAD (inflates sensitivity and deflates specificity)
- Exercise increases oxygen demand from working muscle – to meet demands -> inc CO by increasing stroke volume and HR Myocardial oxygen uptake increase during exercise (linear relationship with coronary blood flow) Pts with obstructive CAD cannot provide adequate coronary blood flow to the affected myocardium during exercise causing ischemia St depression during demand induced subendocardial ischemia doe not localize area of myocardium Bicycle – better for orthopedic or balance problems – sitting or supine used to increased myocardial oxygen demand
- Most likely adequate exercise if can walk .5 min on flat ground and up 1-2 flights of stairs
- Dysrythmias with uncontrolled rate Wellens syndrome: T wave abnormality in precordial lead (v2, v3 +/- V4): specific for obstructive LAD lesion; high risk for anterior wall MI and death Type 1: deeply symmetric t waves; type 2: biphasic T waves with terminal T wave inversion Stress testing may precipitate AMI
- Initial warm up period followed by progressive graded exercise and recovery period Bruce protocol – incline and speed of treadmill increased every 3 minutes thru seven stages Starts 1.7mph at 10% incline; 3 min 2.5mph and incline 12%, similar increases every 3 minutes Modified – treadmill horizontal with first few intervals increased slope only Bruce protocol developed for middle age men – may not be optimal for elderly, obese and deconditioned – the large increments in aerobic requirements of successive stages leads to premature termination Various protocols reduces large workload changes between stages Assumption 85% MPHR (220-age in men ; 210-age in women) to diagnose ischemia has been challenged – tailor to pt’s true maximum exercise capacity Quantifying has a MET (metabolic equivalent) – superior format Abnormal chronotropic response predictive of cardiac events and death – inability to reach age predicted maximum heart rate or use the chronotopic index which takes into account resting heart rate
- STE Moderate to severe angina, fatigue, dyspnea,pt asks to stop CNS symptoms
- 60-70% sensitivity (although some studies as low as *23) Women: baseline ECG alterations, labile ST segment changes, breast artifact, lower exercise capacity, and false positive - women tend to have ischemia from vascular dysfunction (coronary endothelial and/or microvascular dysfunction) in absence of CAD Young patients – low CAD risk and no drug use - concern re: low positive predicative value (those that test positive who actually have disease) - majority of positive results are false - consider cost versus low likelihood of detection - excluding metabolic syndrome/multiple risk factors
- Low risk patient with negative stress echo less than 1% AMI/cardiac death within 1 year
- Myocardial contractility normally increases with exercise Ischemia causes hypo kinesis, a kinesis, or dyskinesis
- Direct iontrope and chronotrope that Increases myocardial oxygen demand in a way similar to exercise
- LBBB – can cause artifactual perfusion defects
- Real time anatomic and physiologic info PE (right heart strain), valvular disease, cardiomyopathy, ventricular aneurysm, and pericardial disease
- Adjacent wall segments = false + and – Wall thickening dependent on imaging technique Timing= Transient wall abnormality as resolve quickly COPD / obesity can = poor images
- Tracer distributed to coronary circulation Uptake occurs in proportion to regional myocardial blood flow Can do rest with pain – immediate Single photon emmision computed tomography
- Induces maldistribution of coronary perfusion Increase blood flow and cause vasodilatation in normal coronaries with little to no increase in stenotic arteries
- Aminophylline – competitive inhibitor of adenosine and can decrease vasodilatory effects Caffeine can block effects – withhold for 24 hours
- Thallium 201 potassium analogue that relies on uptake by viable myocardium Technetium (lipophilic cation that relies on negatively charged mitochondrial membrane SPECT= single photon emission CT Taken up myocardium and distributed in proportion to tissue perfusion Con of radiation exposure
- Sensitivity 89% and specificity 75% Rest spect imaging – neg low incidence of cardiac event/death High incidence of cardiac event after abnormal scan
- Reader dependent – decreased detection of subendocardial perfusion defect; motion artifact; scatter from gut and biliary activity; attenuation artifact (breat/subdiaphragmatic) Asses relative perfusion – decreased sensitivity for left main and 3 vessel disease
- Absence of CAD makes ACS unlikely – presence of such does not imply pain was cardiac in origin
- Up to 40% may be panic attack / somatoform disorder Careful reexamination for undetected cardiac disease Recent negative stress test can be useful without too much emphasis; should not prevent eval in pt with concerning story or EKG finings Positive stress : inc likelihood of acute event Negative stress still has 6 mo incidence ACS of 14% (stress test occurs prior to plaque rupture) – unpredictable and occurs in previous nonobstructive lesions No studies on warranty period – output stress test = normal stress MPI – overall cardiac event rate of 0.6% per year (predictor of event – h/o CAD< increased age, diabetes) Study in 2010 retrospective chart rev 20% pt presented with neg stress within last 3 years had significant CAD; 47% of which stress test was performed within 6months and 23% was performed within one month Another study revealed that it did not affect disposition decisions Serial cath - luminal diameter in normal arteries decreased by <3% per year; minor irregularities progressed at 6% per year. BUT plaque rupture occurs at non-flow-limiting lesions so estimates not absolute indicator of ACS
- TIMI risk score is 1 for >3 risk factors ETT – negative sent home for f/u
- Susternal pressure – feels funny left arm, sweaty, dyspnic, felt better when I rested Good story for CP? Smoker Does not chol, normal BP, no family history Risk factors? Timi 0-1 What do want to do? Ett positive- admitted for further w/u - cath with stent
- Deep pain – felt better when they gave me nitro Had some on and off pain Negative biomarkers Timi risk score of 3 (age, risk factors, ASA use) Admitted to cardiology – cath – medical managment
- Treadmill- no significant baseline ecg changes, ability to exercise, low to intermediate risk Echo – obesity, large breast size Nuclear – ecg changes, inability to exercise Start the work up – finish it ???Stress testing is useful in low and intermediate prevalence; high prevalence – stress will not lead to inclusion or exclusion of CAD More useful in confirming CAD than excluding it