1. Acute Coronary Syndrome and Coronary Artery Disease
Garrett Preston Clark, D.O.

2. What is ACS? Includes clinical presentations that cover the following range of diagnoses:
Unstable angina
Non–ST-elevation myocardial infarction (NSTEMI)
ST-elevation myocardial infarction (STEMI)

3. What is ACS?
Unstable angina & NSTEMI  unstable plaques w/ nonocclusive thrombosis
STEMI  thrombotic occlusion of epicardial coronary artery

4. ACS / CAD
Spontaneous and cocaine-related coronary artery dissection are unusual causes of ACS
Still, should be included in your differential especially when a younger female or cocaine user is being evaluated.

5. Other considerations for ACS:
Marfan syndrome
Kawasaki disease
Takayasu arteritis
Cystic medial necrosis with aortic root dilatation
Aneurysm formation
Dissection into the coronary artery

6. ACS / CAD Higher incidence in males in all patients <70 y/o
Incidence of angina occurs equally 15 years postmenopause
Women more likely to have coronary events without typical symptoms

7. ACS Risk Factors: Male gender Diabetes mellitus (DM) Smoking history
Hypertension
Increased age
Hypercholesterolemia
Hyperlipidemia
Prior CVA
Inherited metabolic disorders
Methamphetamine use
Occupational stress
Connective tissue disease

8. ACS  Whats In Your Diff ?
Anxiety Aortic Stenosis Asthma Cardiomyopathy, Dilated Esophagitis Gastroenteritis Hypertensive Emergencies Myocardial Infarction Myocarditis Pericarditis and Cardiac Tamponade Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum Pulmonary Embolism

9. Alternative diagnoses to cardiac ischemia for patients with chest pain
Non-ischemic cardiovascular
Aortic dissection*
Myocarditis
Pericarditis
Chest wall
Cervical disc disease
Costochondritis
Fibrositis
Herpes zoster (before the rash)
Neuropathic pain
Rib fracture
Sternoclavicular arthritis
Gastrointestinal
Biliary
Cholangitis
Cholecystitis
Choledocholithiasis
Colic
Esophageal
Esophagitis
Spasm
Reflux
Rupture*
Pancreatitis
Peptic ulcer disease
Nonperforating
Perforating*
Pulmonary
Pleuritis
Pneumonia
Pulmonary embolus*
Tension pneumothorax*
Psychiatric
Affective disorders (eg, depression)
Anxiety disorders
Hyperventilation
Panic disorder
Primary anxiety
Somatiform disorders
Thought disorders (eg, fixed delusions)

10. WHAT’S HAPPENING? Disease process includes:
A chronic phase of atherosclerosis  modification of the blood vessel wall
Development of an atherosclerotic plaque
Thin fibrous cap of extracellular matrix proteins is formed over a lipid core (rich in foam cells & comprised of cholesteryl esters & tissue factor)
Thickened intima.
Rupture of the fibrous cap  thrombosis & partial or total occlusion of the vessel

14. Whoop, THERE IT IS:

15. OUCH !

16. ACS  The Meat & Potatoes Part I: Unstable Angina
The ACC/AHA guidelines state that UA and NSTEMI differ primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury.

17. ACS  The Meat & Potatoes Part I: Unstable Angina
Unstable angina is considered in patients with ischemic symptoms suggestive of an ACS and no elevation in troponins or CK-MB, with or without ECG changes indicative of ischemia.

18. ACS  The Meat & Potatoes Part I: CLASSIFICATIONS OF UNSTABLE ANGINA
New onset exertional angina
Rest angina
Early post-MI angina
Postrevascularization angina
Periprocedural
Late

19. New onset angina: CLASSIFICATIONS OF UNSTABLE ANGINA
If occurring only after heavy physical exertion, patients have a prognosis similar to patients with chronic stable angina
New angina occurring after minimal exercise or at rest, has a poorer prognosis.

20. Rest angina: CLASSIFICATIONS OF UNSTABLE ANGINA
Patients at increased risk if:
Prolonged
Associated with transient ST segment changes >0.05 mV

21. Early post-MI angina: CLASSIFICATIONS OF UNSTABLE ANGINA
Chest pain occurring within 48 hours after an acute MI
Associated with high risk without immediate intervention
GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) IIb trial 
Refractory ischemia was associated with an approximate doubling of mortality among patients with ST-segment elevation and a near tripling risk among those without ST elevation.
Circulation 1998 Nov 3;98(18):

22. GUSTO IIb TRIAL: Global Use of Strategies to Open Occluded Coronary Arteries
Occurrence of refractory ischemia was associated with a higher 30 day mortality compared to responsive ischemia or no ischemia.

23. Postrevascularization & Periprocedural angina: CLASSIFICATIONS OF UNSTABLE ANGINA
Postrevascularization  Angina occurring after PCI or CABG
Periprocedural  Ischemic chest pain within 48 hours after stenting.

24. LATE: CLASSIFICATIONS OF UNSTABLE ANGINA
Delayed onset of angina
May reflect restenosis after PCI, graft stenosis after CABG, or progression of native disease
Patients usually progress to return of effort angina

25. ACS  The Meat & Potatoes Part II: Non–ST-elevation myocardial infarction (NSTEMI)
UA & NSTEMI often indistinguishable at time of initial evaluation
Most patients present with chest pain and ST segment depression
ST seg depression is an unfavorable predictor
Increased incidence of left main or three vessel disease compared to those without ST segment depression

26. ACS  The Meat & Potatoes Part II: Non–ST-elevation myocardial infarction (NSTEMI)

27. ACS  The Meat & Potatoes Part II: Non–ST-elevation myocardial infarction (NSTEMI)
Absence of Q waves suggests a high rate of spontaneous reperfusion
May occur after percutaneous coronary intervention (PCI) or CABG

28. Braunwald classification
Classification of UA which included patients with NSTEMI since troponins were not measured:
Class I — New onset, severe, or accelerated
Class II — Angina at rest and subacute (no anginal episodes within the preceding 48 hours)
Class III — Angina at rest and acute (angina within the preceding 48 hours)

29. Braunwald classification
Clinical circumstances:
Class A — Secondary UA (in the setting of anemia, infection, fever, etc)
Class B — Primary UA
Class C — Post

30. Braunwald classification
Intensity of treatment:
No or minimal treatment
Symptoms occurring in the setting of standard medical therapy
Symptoms occurring despite maximally tolerated doses of beta blockers, nitrates, and calcium channel

31. Goldman risk score for chest pain:

32. ACS Risk Factors Reinforcement:
Male gender
Diabetes mellitus (DM)
Smoking history
Hypertension
Increased age
Hypercholesterolemia
Hyperlipidemia
Prior CVA
Inherited metabolic disorders
Methamphetamine use
Occupational stress
Connective tissue disease

33. ACS  The Meat & Potatoes Part III: ST-elevation (Q-wave) myocardial infarction (STEMI)
Enough Said?

34. ACS  The Meat & Potatoes Part III: ST-elevation (Q-wave) myocardial infarction (STEMI)
In 2000, the European Society of Cardiology (ESC) with the American College of Cardiology (ACC) set out to define an acute, evolving, or recent MI.

35. ESC / ACC Definitions:
Rise and gradual fall in troponin or more rapid rise and fall of biochemical markers of myocardial necrosis with at least one of the following:
    a.  Ischemic symptoms     b.  Development of pathologic Q waves     c.  ECG changes indicative of ischemia (ST segment elevation or depression)     d.  Coronary artery intervention (eg, angioplasty)
Pathologic findings of an acute MI

36. SO, WHAT’S A Q-WAVE ? ? ?
Q = 1st deflection of the QRS which is negative
When QRS complex consists soley of a Q wave, it’s called a “QS” complex
Normal Q = less than 0.03 seconds and can be common in most leads (except aVR, V1-V3)

37. Dr_Evil.jpg848 x 440 pixels - 49.0kB diary.ru/~green-filin
“Is It Evil ???”
Dr_Evil.jpg848 x 440 pixels kB diary.ru/~green-filin

38. THE EVIL Q-WAVE ! ! ! Any Q-Wave in leads V1-V3 is an Evil Q
Q’s in leads I, II, aVL, aVF, & V4-6 are considered evil if they are greater than or equal to 0.03 seconds
Evil Q’s must be greater than or equal to 1mm in depth least 2 contiguous leads to be considered for Q-wave MI and thereby, making them very evil !

39. ACS  The Meat & Potatoes Part III: ST-elevation (Q-wave) myocardial infarction (STEMI)
“Clinically significant ST segment elevation is considered to be present if it is greater than 1 mm (0.1 mV) in at least two anatomically contiguous leads, or 2 mm (0.2 mV) in two contiguous precordial leads”.

40. ACS / TREATMENT:
In the initial assessment, the following should be implemented if ACS is suspected:
Airway, breathing, and circulation assessment
12-lead ECG obtained
Crash cart nearby
Cardiac monitor attached
Oxygen given
IV access and blood work obtained (series cardiac)
Aspirin
Nitrates and morphine (unless contraindicated)

41. Lower cardiac workload = less O2 demand
ACS / TREATMENT:
Morphine reduces sympathetic stimulation caused by pain and anxiety  lowers cardiac workload
Lower cardiac workload = less O2 demand
= Patients feel better

42. ACS / TREATMENT:
Due to the lack of data, the ACC/AHA, & ACCP guidelines did not address the use of clopidogrel in patients managed without reperfusion Tx.
However, most experts give clopidogrel, 300 mg loading dose then 75 mg daily based on benefits demonstrated in non-revascularized patients with non-ST elevation syndromes.

43. Clopidogrel in Unstable angina to prevent Recurrent ischemic Events (CURE) TRIAL:
Clopidogrel  platelet ADP receptor antagonism
Something to consider if ASA sensitive
CURE Trial suggests more efficacy with ASA and Plavix combo therapy, but at a cost = increased risk of nonintracranial bleeding complications.

44. Foreign Cars May Save Your Life ! If It’s Good Enough for Bond…
x k

45. Interventions Shown To Decrease Mortality in CAD (Die Another Day 007©):
Statins
ASA
ACE Inhibitors
Beta Blockers
“SAAB”
Nitrates shown to minimize angina Sx’s, but NO conclusive evidence that show decreased mortality.

46. DON’T FORGET:
Initial EKG is often NOT diagnostic. Repeat EKG at 5 to 10 minute intervals if patient remains symptomatic & high clinical suspicion for MI
Ask about phosphodiesterase-5 inhibitors (Viagra, Levitra, Cialis). Nitrates are contraindicated if used w/in hours due to risk of severe hypotension

47. DON’T FORGET:
In the setting of an inferior wall MI, remember the possibility of right ventricular involvement. Patient dependence on preload to maintain cardiac output may result in severe hypotension w/ nitrate use.

48. ST elevation in the right precordial leads - V4, V5, and V6 indicates right ventricular involvement

49. DON”T FORGET:
About ½ the patients with LBBB & acute MI do NOT have Sx’s of chest pain w/ their ischemia
= Much less likely to receive ASA, beta blockers, and reperfusion therapy
= Not a good idea
= Beware the LBBB ! ! !

50. ACS THERAPY: Evidence Supports early aggressive strategy ASA
Beta-Blocker
ACEIs
Statin
LMW Heparin or Unfractionated
Clopidogrel (PLAVIX)

51. TEST YOUR SKILL…

52. TEST YOUR SKILL…
A 67 y/o postmenopausal woman w/ CAD, stable angina, CHF, and hyperlipidemia comes for her regular 3-month exam. Her vitals: HR: 94, RR: 18, BP: 130/70. Physical exam is WNL. Her LDL is 129, HDL is 45. Which of the following therapeutic options would you prescribe that have been shown to decrease mortality:
Atorvastatin
Digoxin
Diltiazem
Estrogen
Isosorbide mononitrate

53. TEST YOUR SKILL…
A 67 y/o postmenopausal woman w/ CAD, stable angina, CHF, and hyperlipidemia comes for her regular 3-month exam. Her vitals: HR: 94, RR: 18, BP: 130/70. Physical exam is WNL. Her LDL is 129, HDL is 45. Which of the following therapeutic options would you prescribe that have been shown to decrease mortality:
Atorvastatin
Digoxin
Diltiazem
Estrogen
Isosorbide mononitrate

54. THE END

55. References: http://www.kup.at/kup/images/browser/787.jpg
sfghed.ucsf.edu/.../ClinicImages/MI%20EKG1.1.jpg
Circulation 1998 Nov 3;98(18):