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
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
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
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
32. Stress Echocardiogram
Exercise or pharmacologic stress
Combines ECG stress with imaging at rest and after
stress
Sensitivity 80%
Specificity 84%
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
