Lecture overview on the diagnosis and management of acute coronary syndrome.

1. Acute Coronary Syndrome
Brian Wells, MD, MS, MPH

2. Review of Coronary Anatomy
• Left Main
– Left Anterior
Descending (LAD)
– Circumflex (Cx)
• Right Coronary Artery
– Posterior Descending
Artery (PDA)

3. Volume-rendered (VRT) Imaging

4. Blood Supply to the Heart

5. Anatomic Variations
• Be aware they exist, but this is beyond the
scope of today’s lecture
Ramus intermedius (RI) is a variant
coronary artery resulting from
trifurcation of the left main
coronary artery. It is present in
~20% (range 15-30%) of the
population
Single coronary artery: All
coronaries arise from the left cusp
with a single origin and there is a
retro-aortic (benign) course of the
RCA (RC)
Malignant LM: Axial MIP image
reveals a malignant LM taking origin
from the right cusp and coursing
between the aorta and the
pulmonary artery which can be
subjected to compression during
heavy exercise and cause sudden
death

6. Ischemic-Type Chest Pain
• Pressure sensation,
fullness or squeezing
retro-sternally
• Radiation of chest pain
into the jaw/teeth,
shoulder, arm, and/or
back
• Associated dyspnea or shortness of breath
• Associated epigastric discomfort with or
without nausea and vomiting

7. Presentations of Angina
• Among patients considered to have angina,
there are three presentations of angina
that suggest an ACS:
– Rest angina, which is usually more than 20
minutes in duration
– New onset angina that markedly limits
physical activity
– Increasing angina that is more frequent, longer
in duration, or occurs with less exertion than
previous angina

8. Anginal Equivalents
• Most commonly found in patient with
diabetes and in women
• Include
– Exertional dyspnea
– Fatigue
– Nausea
– Vomiting

9. What about Atypical Chest Pain?
• Reduces like likelihood that symptoms represent
myocardial ischemia or injury
• Per guidelines of the ACC and AHA, the following are not
characteristic of myocardial ischemia
– Pleuritic pain (sharp/knife-life pain associated with
respiration or cough)
– Primary or sole pain in the middle or lower abdomen
– Pain localized with one finger, particularly over the left
ventricular apex
– Pain reproduced with movement or palpation
– Constant pain persisting for many hours
– Very brief episodes of pain that last a few seconds or
less

10. What is Acute Coronary Syndrome (ACS)?
• Umbrella term for the clinical
signs and symptoms of myocardial
ischemia:
–Unstable angina
–Non–ST-segment elevation
myocardial infarction
–ST-segment elevation myocardial
infarction.

11. Everything Results From A “Flow
Problem”

12. Unstable Angina
• Blood clots that block an artery partially or
totally are what causes unstable angina.
• Occurs at rest and usually lasting >20
minutes
• New onset angina that limits activity
• Increasing angina: Pain that occurs more
frequently, lasts longer periods or is
increasingly limiting the patients activity

13. The Cardiac Cycle

14. ECG Paper
• Standardized paper
• Speed 25 mm/sec (1 small square = 0.04
seconds; large square = 0.2 seconds)
• Amplitude 1 mV (10 mm to 1 mV)

15. NSTEMI
• NSTEMI is a clinical syndrome with
symptoms of myocardial ischemia not in
association with persistent
electrocardiographic (ECG) ST elevation or
ST elevation equivalents. There may be ST
depressions or non-specific EKG changes.
This is subsequent release of biomarkers.

16. STEMI
• STEMI is a clinical syndrome defined by
characteristic symptoms of myocardial
ischemia in association with persistent
electrocardiographic (ECG) ST elevation
and subsequent release of biomarkers of
myocardial necrosis.

17. NSTEMI v. STEMI

18. Distinguishing Types
• The 12 lead EKG and serum biomarkers distinguish the
types of ACS
– Unstable angina: Normal cardiac biomarkers (troponin
and CK-MB) without characteristic EKG changes (non-
specific changes or normal)
– NSTEMI: Positive biomarkers without ST elevations or
ST-elevation equivalents (although ST depression and
non-specific changes can be seen)
– STEMI: Positive biomarkers and ST-segment elevation
in two or more contiguous leads; ST-elevation
equivalents including a new LBBB or a posterior MI
(tall R waves and ST depressions in V1-V3)

19. What Qualifies as ST elevation?
• The joint European Society of Cardiology,
American College of Cardiology Foundation, the
American Heart Association, and the World
Heart Federation (ESC/ACCF/AHA/WHF)
committee for the definition of MI established
specific ECG criteria for the diagnosis of ST
elevation MI:
– New ST segment elevation at the J point in
two contiguous leads with the cut-points: >0.1
mV in all leads other than leads V2-V3.
– For leads V2-V3, the following cut points
apply: ≥0.2 mV in men ≥40 years, ≥0.25 mV in
men <40 years, or ≥0.15 mV in women.

20. Don’t Be Tricked!
• Remember for real life and the boards
– STEMI is NOT the only cause of ST-elevation
segments.
– Consider acute pericarditis, left ventricular
aneurysm, takotsubo (stress) cardiomyopathy,
coronary vasospasm, or normal variant (early
repolarization)

22. Localization and Changes

23. Anteroseptal STEMI

25. ECG Evolution of Q-wave MI
• Usual ECG evolution of a Q-wave MI; not all of the
following patterns may be seen; the time from
onset of MI to the final pattern is quite variable
and related to the size of MI, the rapidity of
reperfusion (if any), and the location of the MI.
1. Normal ECG prior to MI
2. Hyperacute T wave changes - increased T wave
amplitude and width; may also see ST elevation
3. Marked ST elevation with hyperacute T wave
changes (transmural injury)
4. Pathologic Q waves, less ST elevation, terminal T
wave inversion (necrosis)
a. Pathologic Q waves are usually defined as
duration ≥ 0.04 s or ≥ 25% of R-wave
amplitude)
5. Pathologic Q waves, T wave inversion (necrosis and
fibrosis)
6. Pathologic Q waves, upright T waves (fibrosis)

26. Cardiac Biomarkers
• Troponin values within the normal range (using current
methodologies) likely come from a mixture of truly normal
individuals with detectable values and some with
comorbidities reflected by low but detectable values. (See
'Normal range' above.)
• Troponin elevations (above the 99th percentile) can be
due to structural heart disease in the absence of any
acute process.
• The diagnosis of an acute myocardial infarction depends
on observation of a rise and/or fall of blood biomarkers,
particularly troponins, with at least one value above the
99th percentile, in addition to clinical information or
electrocardiographic changes. The more sensitive the
assay, the more important it is to determine a change in
troponin level for confirmation of myocardial infarction.

27. Cardiac Biomarkers
• Cardiac troponins are recommended in preference to CK-MB for
diagnostic and prognostic purposes; it is unnecessary to obtain both
values. Cardiac troponins I and T are equally useful.
• For the diagnosis of myocardial infarction after coronary artery
bypass graft surgery (CABG), a 10-fold or greater increase from
baseline in biomarkers along with ancillary criteria, such as new Q
waves, is needed. Myocardial infarction after CABG is associated
with an increase in mortality.
• There is a delay in the rise of biomarkers after an acute myocardial
infarction (MI). In patients who have an acute ST elevation
myocardial infarction (STEMI), reperfusion therapy should not await
the results of cardiac biomarkers. In patients without diagnostic ST
segment elevation, serial biomarker testing is performed after four or
more hours if the initial values are indeterminate, the
electrocardiogram (ECG) remains nondiagnostic, and clinical
suspicion remains high.

29. Serum Markers in ACS

30. Estimating Risk in UA and NSETMI
• Score 0-2
– Stress testing
and angiography
if testing shows
ischemia
• Score 3-4 or
recurrent angina,
elevated biomarkers
or previous
revascularization
– Early
angiography
• Score 5-7
– Early
angiography

31. Therapy
• With STEMI, PCI is preferred with a door-
to-balloon goal of <= 90 minutes
• Stent thrombosis may occur 24 hours to 1
year after placement and usually presents
as recurrent angina, sudden death, or MI.
– To prevent this, start ASA and a
thienopyridine (clopidogrel or prasugrel),
continue dual therapy for 1-12 months with a
bare-metal stent with ASA afterward
– DES – Clopidogrel for 12 months or longer.

32. Cath Lab

41. What if PCI is not available?
• Administer tPA for large MI or previous
streptokinase use (90 minute patency better with tPA
than SK; roughly equal at 24 hours)
• Contraindications or cautions:
– Previous ICH (absolute contraindication)
– Ischemic stroke within the last 3 months except acute ischemic
stroke within 3 hours (absolute contraindication)
– Malignant intracranial neoplasm (absolute contraindication)
– Aortic dissection or active bleeding excluding menses (absolute
contraindication)
– Major surgery within 3 weeks (relative contraindication)
– BP >180/110 (relative contraindication)
– Pregnancy (relative contraindication)
– Concurrent warfarin therapy (relative contraindication)
– Active peptic ulcer disease (relative contraindication)

42. When is CABG the answer?
• STEMI in the presence of:
– Failure of fibrinolysis or PCI
– Cardiogenic shock
– Left main or left main equivalent disease
– Two- or three-vessel disease involving the LAD
and a reduced LVEF

43. Remember for Exams
• Choose transfer for PCI instead of thrombolytic therapy for
STEMI only if transfer and PCI can be done within 90 minutes
– Real world: The Danish DANAMI-2 trial (2003) suggested
that transferring patients for primary PCI is associated
with better outcomes than local thrombolysis if the transfer
time is less than three hours
• Do not choose thrombolytic therapy for patients with NSTEMI
or for asymptomatic patient with onset of pain <24 hours
• Reperfusion arrhythmias following thrombolytic therapy,
typically manifested as transient accelerated idioventricular
arrhythmia, do not require additional antiarrhythmic therapy
– AIVR appears similar to ventricular tachycardia with wide
QRS complexes (QRS >120) and a regular rhythm. It can
most easily be distinguished from VT in that the rate is less
than 120 and usually less than 100 bpm.

44. Drug Therapy
Therapy
Aspirin If CI, use clopidogrel, except if CABG is likely
Clopidogrel Use for UA, NSTEMI, and STEMI, and for PCI with stent placement
IV Beta blockers for acute care Decreased mortality evident by day 1; Avoid in pulmonary edema and/or
cardiogenic shock, SBP <90, HR <50, or second degree AV block
Calcium Channel Blockers (not
nifedipine)
Use in patient with contraindications to B-blockers and in those with continued
angina despite B-blockers and nitrates
IV Nitroglycerin Pain due to ongoing ischemia relived with nitro; routine recommendation for most
MI’s 24-48 hours; Use except with suspected RV infarction
LMWH or UFH Use for all cases of ACS
Bivalrudin Alternative to UFH/LMWH, especially in patients undergoing PCI
Fondaparinux Alternative to UFH/LMWH
Glycoprotein IIb/IIIa antagonists Considerations
ACE Inhibitors Within 24 hours of MI or MI + CHF with EF <40%; Can use ARBs as an alternative
Statins Prognosis improves in post-MI; Use within 24-96 hours
Cardioselective B-blockers Use within 3-21 days, continue indefinitely
Eplerenone Use for severe LV dysfunction after MI; Do not select spironolactone as its
effectiveness in patients with acute MI is unknown

45. • In summation…

46. Follow-up Care
• Mechanical complications (VSD, papillary muscle
rupture, LV free wall rupture) may occur 2-7 days
after an MI.
– Emergency echocardiography is the initial
diagnostic study
– Patients with VSD or papillary muscle rupture develop
abrupt pulmonary edema or hypotension and a loud
holosystolic murmur
– LV free wall rupture causes sudden hypotension or
cardiac death associated with PEA

47. Follow-up Care
• Cardiac catheterization is indicated for
patients with postinfarction angina or the
following post-MI stress test results:
– Exercise-induced ST-segment depressions or
elevations
– Inability to achieve 5 METs during testing
– Inability to increase systolic BP by 10-30
mmHg
– Inability to exercise (arthritis)

48. When To Place an ICD?
• ICDs are indicated in patients meeting the
following criteria:
– >40 days since MI
– >3 months since PCI or CABG
– EF <30%