1. Acute Coronary Syndrome Update
Charles Shoalmire, MSN, RN, ACNP-BC

2. Objectives
At the conclusion of this activity, participants will be able to:
Recognize ST elevation MI
Differentiate current subtypes of acute coronary syndrome (ACS)
Discuss appropriate initial treatment algorithm for different subtypes of ACS

3. Definition of Acute Coronary Syndrome
Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non–ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. In terms of pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery.

4. Defintion of Acute Coronary Syndrome
In some instances, however, stable coronary artery disease (CAD) may result in ACS in the absence of plaque rupture and thrombosis, when physiologic stress (eg, trauma, blood loss, anemia, infection, tachyarrhythmia) increases demands on the heart. The diagnosis of acute myocardial infarction in this setting requires a finding of the typical rise and fall of biochemical markers of myocardial necrosis in addition to at least 1 of the following:
Ischemic symptoms
Development of pathologic Q waves
Ischemic ST-segment changes on electrocardiogram (ECG) or in the setting of a coronary intervention

5. Universal Definition of MI
ESC/ACCF/AHA/WHF Expert Consensus Document (2012) divides myocardial infarction into five different subtypes:
ST Elevation Myocardial Infarction—STEMI—Type I
Non-ST Elevation Myocardial Infarction—NSTEMI—Type I
Type II
Type III
Type IV
Type V

6. Review of ECG Interpretation

7. Characteristics of STEMI (Type I)
Plaque rupture
Intraluminal coronary artery thrombus formation
Associated ECG changes
Spontaneous MI related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection – with associated thrombus leading to decreased distal flow and ensuing myocyte necrosis.
This may be – on occasion associated with non-occlusive CAD

8. STEMI on ECG

9. STEMI ECG Criteria
≥ 2 mm of ST segment elevation in 2 contiguous precordial leads in men (1.5 mm for women)
≥ 1mm in other leads (2 contiguous)
An initial Q wave or abnormal R wave develops over a period of several hours to days.
Within the first 1-2 weeks (or less), the ST segment gradually returns to the isoelectric baseline, the R wave amplitude becomes markedly reduced, and the Q wave deepens. In addition, the T wave becomes inverted.

10. STEMI ECG Criteria
In addition to patients with ST elevation on the ECG, two other groups of patients with an acute coronary syndrome are considered to have an STEMI:
those with new or presumably new left bundle branch block
those with a true posterior MI
An elevation in the concentration of troponin or CK-MB is required for the diagnosis of acute MI

11. STEMI ECG Criteria
Anterior STEMI: ST elevation in the precordial leads + I and aVL (LAD territory)
Posterior STEMI: reciprocal ST depressions in V1-V3 (ST elevation in post leads), may have component of inferior ischemia as well (ST elevations in II, III and aVF)
Often occurs w/ inferior MI (L Cx)
Inferior STEMI: ST elevation in II. III and aVF (+ ST elevation in R-sided precordial leads), reciprocal changes in I and aVL (R coronary or L Cx)

12. STEMI

13. ECG Challenge
50 year old male with no known past medical history presents to the ED with new onset left-sided chest pain for one hour.

14. Characteristics of NSTEMI (Type I)
Evidence of necrosis consistent with acute ischemia
A rise and/or fall of cardiac enzyme (specifically troponin I) plus any ONE of these findings meets MI requirements:
Symptoms of ischemia
New (or presumed new) significant ST-segment/T-wave changes OR a new LBBB
Pathological Q waves
Radiologic evidence of loss of viable myocardial tissue at the cellular level OR new regional wall motion abnormality
Intracoronary thrombus by angiography or autopsy
Thygesen, K., Alpert, J. S., Jaffe, A. S., Simoons, M. L., Chaitman, B. R., & White, H. D. (2012). Third universal definition of myocardial infarction. Circulation, pp doi //cur,0b013e3182e1058

15. Pathologic Q Waves
Any Q-wave in leads V2–V3 ≥ 0.02 s or QS complex in leads V2 and V3
Q-wave ≥ 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4–V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4–V6; II, III, and aVF)
R-wave ≥ 0.04 s in V1–V2 and R/S ≥ 1 with a concordant positive T-wave in the absence of a conduction defect

16. Pathologic Q Waves

17. NSTEMI

18. NSTEMI (Type I)

19. Characteristics of Type II
Instance of myocardial injury with necrosis when a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand
Coronary endothelial dysfunction
Coronary artery spasm
Coronary embolism
Tachy-/brady-arrhythmias
Anemia
Respiratory failure
Hypotension
Hypertension with our without LVH

20. Characteristics of Type III
Cardiac death with symptoms suggestive of ischemia and presumed new EKG ischemic changes or new LBBB
Death occurred before cardiac enzymes were obtained or before the values had increased

21. Characteristics of Type IVa
MI associated with PCI defined by an elevation of cTn values of >5X 99th percntile URL in patients with a normal baseline cTn
>20% if the baseline value is elevated and are stable or falling in addition:
Symptoms of MI
New ECG changes or new LBBB
Aniographic evidence of loss of patency
Imaging demonstration loss of viable myocardium or new regional wall motion abnormality

22. Characteristics of Type IVb
MI associated with stent thrombosis detected by angiography or autopsy in the setting of MU with a rise and or fall of cardiac enzymes

23. Characteristics of Type V
MI associated with CABG
Defined by elevation of cardiac biomarker >10x 99th percentile URL in patents with normal baseline values in addition:
New pathological Q waves or new LBBB
Angiographic evidence of new graft or new native coronary artery occlusion
Imaging evidence of loss of viable myocardium or new regional wall motion abnormality.

24. Characteristics of Unstable Angina
The traditional term of unstable angina was first used 3 decades ago and was meant to signify the intermediate state between myocardial infarction and the more chronic state of stable angina.
Unstable angina is considered to be an acute coronary syndrome in which there is no release of the enzymes and biomarkers of myocardial necrosis.

25. Selecting the Appropriate Algorithm
STEMI – preferred treatment in a center with PCI capability:
PTCA with a target door to wire time <90 minutes.
Fibrinolics are an acceptable choice
Medical management for certain patient populations
NSTEMI – primary PCI is acceptable
Medical management is an acceptable choice

26. Non-Pharmacologic Interventions
Percutaneous transluminal coronary angioplasty (PTCA)
Intra-aortic balloon pump
Coronary artery bypass graft (CABG)

27. Pharmacologic Interventions STEMI
Fibrinolytics
Unfractionated heparin
Dual platelet inhibition
Beta blockade
ACE inhibition for LV dysfunction
Consideration of minerocorticoid receptor antagonism for LV dysfunction, e.g. EF < 40%
Spironolactone or Inspra (epleronone)
Statin

28. Non-Pharmacologic Interventions NSTEMI
Percutaneous transluminal angioplasty
Coronary artery bypass grafting

29. Pharmacologic Interventions NSTEMI
Dual platelet inhibition
Aspirin and Plavix or other thienopyridine
Beta blockade
Nitrates
ACE inhibition for LV dysfunction
Consideration of minerocorticoid receptor antagonism for LV dysfunction, e.g. EF < 40%
Spironolactone or Inspra (epleronone)
Statin
Fractionated or unfractionated heparin

30. Treatment of USA
For all practical purposes, the treatment algorithm for NSTEMI is appropriate for unstable angina

31. Conclusion and Questions
Five different categories of MI
Differences on ECG, lab values, etc.
Priority acute treatment for STEMI
Priority acute treatment for NSTEMI
Questions?