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ACS – a simplified approach

ACS – a simplified approach. Shawn Dowling. Case #1. 68F. Known CAD (CABG 10 yrs ago). L RSCP over past few weeks. States RSCP same as prior & but brought on by walking one to two blocks & relieved with rest. What are the 3 features of typical CP?

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ACS – a simplified approach

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  1. ACS – a simplified approach Shawn Dowling

  2. Case #1 • 68F. Known CAD (CABG 10 yrs ago). L RSCP over past few weeks. States RSCP same as prior & but brought on by walking one to two blocks & relieved with rest. • What are the 3 features of typical CP? • What kind of angina is this (stable or unstable)? • What Class of Angina? • You get ready to tell Bryan about the cardiac RF and he tunes out and ignores you..why?

  3. Typical CP • RSCP • Brought on by exertion/stress • Relieved with rest/NTG

  4. Stable angina • Angina brought on by exertion and relieved with predictable measures (rest, NTG) • Unstable angina/ACS • New onset angina w/i past 2/12 and at least CCS III • Rest angina lasting >20 min & presenting w/i one week of angina • Change from baseline

  5. Pathophysiology of Stable and Unstable Plaques Thin fibrous cap Thrombus Thick fibrous cap Smooth muscle cells Lipid rich coreof McDonalds Media Unstable plaque Stable plaque What is an ACS? How does it relate to this?

  6. Why distinguish between stable angina and UA/ACS? • Stable Angina: • Typically represents a stable, fixed lesion that has had time to develop collaterals, Sx reflect inadequate myocardial O2 supply • Unstable angina/ACS • Represents an acute plaque rupture and thrombosis

  7. Terminology • Acute Coronary Syndromes is the preferred terminology to refer a spectrum of disease related to myocardial ischemia (stable angina) Unstable Angina NSTEMI STEMI +/- abN ECG, -ve markers +/- abN ECG, +ve markers STE on ECG, +ve markers

  8. What are some secondary causes of MI? (I.e. myocardial ischemia not secondary to coronary artery plaque rupture)

  9. Secondary Causes of MI • Exclude secondary causes (10-15% ) • Coronary vasospasm • Anemia • Hypoxemia • Uncontrolled HTN • Arrhythmias • Heart Failure • Infection • Drugs: i.e. cocaine • Thyrotoxicosis  Supply of Myo02  Demand of Myo02

  10. What are some features of the character of Chest Pain that make you worry? • What about reproducible chest wall pain? • What about response to NTG?

  11. Goodacre et al. How Useful are Clinical Features in the Diagnosis of Acute, Undifferentiated Chest Pain? Academic Emergency Medicine, vol. 9, no. 3, 2002. Features Predictive of AMI: Thanks Adam

  12. Goodacre et al. How Useful are Clinical Features in the Diagnosis of Acute, Undifferentiated Chest Pain? Academic Emergency Medicine, vol. 9, no. 3, 2002. Features Predictive of ACS: Thanks Adam

  13. Case #1’s ECG

  14. What percentage of people will have a normal ECG and have an ACS? • How about non-specific ST-T changes? • What carries a higher mortality past 60 days • STE or STD?

  15. ECG changes

  16. GUSTO 2B: ST DepressionA High Risk Finding ST  P  0.001 ST  T-wave inversion CM Gibson 2002

  17. Case # 2 • 71M. L precordial CP, radiating to L arm/jaw, x 25 minutes (about 1H ago). Onset with exertion, relieved with rest and taking his wife’s NTG. • Cardiac RF: smoker, DM, HTN • ECG – NSST changes • Trop was already sent off b4 you saw the pt. • Who is going to wait for the 6, 8 or 10H trop?

  18. Case #3 • 75M. Known CAD, MI last year. EMS bringing pt in for abdo pain (sharp, RUQ). They patch in and fax ECG- ? STEMI.

  19. Do you call the cath lab?

  20. You get his most recent ECG from 6 months ago and it is completely unchanged • Prior ECHO reports shows LV aneurysm secondary to prior MI.

  21. Not all STE is STEMI • Retrospective EKG review of 902 adult pts in ED admitted to CP centre • Acute MI cause of ST elevation in only 15% of all pts • Other 85% had alternative diagnosis • LVH (25%) • LBBB (15%) • BER (12%) • RBBB (5%) • Undefined BBB (5%) • LV aneurysm (3%) • Pericarditis (1%) • Ventricular paced Rhythm (1%) • Undefined ST elevation in 17% Brady WJ. AM J Emerg Med 2001; 19:25-28 Thank Mark

  22. What percentage of patients are d/c’d home with MI or ACS? • Do these patients have a worse outcome?

  23. 10 689 patients • Data collected for 30d (hospitalised patients) or at 24 to 72hrs for non-hospitalised patients (repeat assessment, ECG, CK-MB’s)

  24. Final Diagnosis 894 (8.5%) AMI 972 (9%) unstable angina 21% non-ischemic cardiac problem 55% non-cardiac

  25. 22 missed unstable angina (2.26%) • MC diagnosis; • stable angina, atypical chest pain • 19 missed AMIs (2.1% of 894) • MC diagnosis; • non-cardiac chest pain, pulmonary conditions and stable angina

  26. Factors associated with non-hospitalisation for patients with missed ACI • female • <55 yoa • non-white • chief complaint of SOB • normal ECG • 30d adjusted risk of mortality 1.7 times higher if not hospitalised (95% CI 0.7 to 5.2- NS)

  27. Conclusion: • Rate of missed MI’s is low, but the patients that are missed ? higher MR

  28. Case #4 • 75M. Hx of CAD. • Presents with rest angina x 30 minutes. • Any reliable tool to risk stratify this patients likelihood of a poor outcome in 14 days? • Which historical features and investigations do you need to know?

  29. Hx Age >65 Smoker, DM, HTN Known stenosis > 50% Uses ASA Presentation ECG – no ST deviation Enzymes + Only 1 episode of angina in 24H His story…

  30. Risk of all-cause mortality, MI or recurrent angina requiring re-vascularization • TIMI score >4 considered high risk ACS

  31. Caveats and Critique • tested on admitted patients with unstable angina/NSTEMI • Validation Phase not prospective • cohort who qualified for enrolment in a phase III study (?generalisabilty to all-comers with chest pain) • CKMB was the marker in TIMI but now use Troponin without study to prove similarly predictive Thanks Adam

  32. Case # 5 • 57F. DM, high chol, smoker. L precordial CP, rads to shoulder. Lasting 35 minutes now and associated with nausea & diaphoresis. VSS. • What is the first thing you want to do (cannot answer ABC’s)?

  33. What percentage of patients with an AMI will have a clearly diagnostic ECG at presentation (STE or STD) • 50%

  34. TroponinT • Highly cardiac specific • Not found in serum of healthy volunteers (as opposed to CK, CK-MB) • Following myocardial injury, troponin is leaked into serum

  35. Troponin Sensitivity

  36. Onset of elevation • 3-6H • Peak • 12-18H • Remain elevated for • 5-7 days

  37. What causes an increased TnT? CARDIAC Ischemia/ infarction Cardiomyopathy Pericarditis/Myocarditis Cardiac contusion Hypertensive emergencies Pulmonary embolus Renal failure Electrical injury Sepsis Troponin T

  38. UA/NSTEMI 9/00 TROPONINS T AND IAS PREDICTORS OF MORTALITY Cardiac Mortality Total Mortality 6.9 6.4 7 6 5.0 5 4 3.3 3 2.0 1.7 2 1 0 PTS 1993 1057 RR 1641 792 RR Trop. Neg Pos Neg Pos No. Trials 6 7

  39. Case #6 • 89M. Hx of ESRD (MWF dialysis). RSCP today x 30 min. The usual trifecta – DM, HTN, high chol. • ECG: NSST • Trop-0.13, Cr-250 • CCU resident (not fellow) says his trop is just up cuz of his Cr – can go to the hospitalist. • What do you think?

  40. Over 7000 pts enrolled in GUSTO IV trial • These were all patients that were suspected of having an ACS: required >5 min of angina + at least 0.5mm STD or +ve trop (>0.1) • Looked at short-term outcomes (death or MI at 30 days) based on 1) Trop >0.1 and trop >0.03, 2) Quartiles of Creatinine Clearance

  41. Conclusion • 581 pts had outcome (renal failure, elevated trop + MI or death) • 305 had non-fatal MI • 71 had fatal MI • 205 died w/o evidence of MI • Regardless of degree of renal failure, elevated troponins predict short term mortality and MI’s in RF pts

  42. Case #8 • 74F. HTN, high chol, ex-smoker. RSCP x 3 days, LBBB (old). • Told to come in by FP on call b/c trop 0.38. • Waited in the WR for 6 hours b/c she did not mention her CP – simply said she was to come in b/c of abnormal blood test. Repeat trop 0.39. • How do you want to treat her?

  43. Cardiology Trials Generalizations • All pts receive ASA & heparin • Nitrates, β-blockers, CCB’s use at discretion of treating physicians • UA/NSTEMI definitions require at least one objective finding (ECG changes, elevated cardiac markers) therefore most studies on relatively high risk pts • Often use composite E.P. (re-infarction, death, need for urgent re-vascularization) • Renal failure often an exclusion criteria Thanks Moritz

  44. Treatment • Prior to current medical management, MR rate and re-infarction rate were 17% and 47% at 3 months • Now, 3month MR are in the range of 10-12% post MI

  45. Treatment Strategies • Anti-ischemic • Increase supply: Oxygen, nitrates • Decrease demand: β-B’s, morphine, ACE-I’s • Anti-platelet • ASA, clopidogrel, GPIIb/IIIa inhibitors • Anti-thrombotic • Medical: UFH, LMWH, thrombolytics • Invasive: PTCA, CABG • Anti-inflammatory • Statins

  46. Oxygen • Give it • Definitely if sats <90%, likely to everyone • Animal data shows that it decreased infarct size(110) • Small human study that showed it resulted in ECG changes(111) • According to AHA - give it

  47. Nitrates • Two major studies (GISSI-3 and ISIS-4) • no reduction in MR • Meta-analysis of more than 80,000 patients showed a MRof 7.7% in the control group, versus 7.4% in the nitrate group – not s.s. • Use for Tx of Sx, but if BP low – save the BP for mortality reducing interventions

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