2. Non-ST Elevation Acute
Coronary Syndrom- NSTE ACS
Unstable Angina
Non-ST elevation MI
ST Elevation Myocardial Infarct
STMI
Stable Angina
Class1
Class2
Class3
Class 4
3.
4. Acute coronary syndrome is defined as
myocardial ischemia due to myocardial
infarction (NSTEMI or STEMI) or unstable angina
Unstable angina is defined as angina at rest,
new onset exertional angina (<2 months),
recent acceleration of angina (<2 months), or
post revascularization angina
6. Dx of acute coronary syndrome is based on history,
physical exam, ECG, cardiac enzymes
Patients can then be divided into several groups
Non-cardiac chest pain (i.e., Gastrointestinal,
musculoskeletal, pulmonary embolus)
Stable angina
Unstable angina
Myocardial infarction (STEMI or NSTEMI)
Other cardiac causes of chest pain (i.e., aortic dissection,
pericarditis)
8. Plaque rupture and subsequent formation of thrombus
– this can be either occlusive or non-occlusive (STEMI,
NSTEMI, USA)
Vasospasm such as that seen in Prinzmetal’s angina,
cocaine use (STEMI, NSTEMI, USA)
Progression of obstructive coronary atherosclerotic
disease (USA)
In-stent thrombosis (early post PCI)
In-stent restenosis (late post PCI
Poor surgical technique (post CABG)
9. Acute coronary syndromes can also be due to
secondary causes
Thyrotoxicosis
Anemia
Tachycardia
Hypotension
Hypoxemia
Aterial inflammation (infection, arteritis)
15. In the absence of abnormal findings on physical exam,
ECG, or enzymes, the pre-test probability of acute
coronary syndrome must be determined by the
clinician
A good history is crucial (is the chest pain typical or
atypical; what are the associated symptoms)
Determination of risk factors is also crucial (male, age
>55, smoking, DM, HTN, FamHx, hyperlipidemia,
known CAD)
16. Aspirin is an antiplatelet agent that initiates the
irreversible inhibition of cyclooxygenase,
thereby preventing platelet production of
thromboxane A2 and decreasing platelet
aggregation
Administration of ASA in ACS reduces cardiac
endpoints
17. Aspirin should be given in a dose of 75-325
mg/day to all patients with ACS unless there is a
contraindication (in which case, clopidogrel
should be given)
18. Clopidogrel is a potent antiplatelet agent
It should be administered to all patients who
cannot take ASA
The CURE trial suggests a benefit to adding
Clopidogrel to ASA/Heparin in patients going for
PCI
Give 300 mg loading dose followed by 75
mg/day
19. Clopidogrel should be administered to patients who
cannot take ASA because of hypersensitivity or
gastrointestinal intolerance
In hospitalized patients in whom an early,
noninterventional approach is planned, clopidogrel
should be added to ASA as soon as possible on
admission and administered for at least 1 month and
up to 9 months. Do not use clopidogrel if there is any
possibility patient may be candidate for CABG
20. Nitroglycerin is considered a cornerstone of anti-
anginal therapy, despite little objective evidence for its
benefit
Benefit is thought to occur via reduction in myocardial
O2 demand secondary to venodilation induced
reduction in preload as well as coronary vasodilation
and afterload reduction
Titrate to relief of chest pain; chest pain = death of
myocardial cells
No documented mortality benefit
21. Beta Blockers reduce myocardial oxygen
demand by reducing heart rate, contractility,
and ventricular wall tension
Administration of beta blockers in ACS reduces
cardiac endpoints
22. Intravenous beta blockers should be used
initially in all patients (without contraindication)
followed by oral beta blockers with the goal
being decrease in heart rate to 60 beats per
minute
A combination of beta blockers and nitrates can
be viewed as first line therapy in all patients
with ACS
23. Heparin (unfractionated heparin or UFH) has
traditionally been the mainstay of therapy in
acute coronary syndromes as its efficacy has
been documented in several large, randomized
trials
24. More recent studies indicate that low molecular
weight heparin is also effective in the reduction
of end points such as myocardial infarction or
death
Some studies report that LMWH, when used in
combination with ASA, may be superior to
continuous infusion of Heparin
25. All patients with acute coronary syndromes
should be treated with a combination of ASA
(325 mg/day) and heparin (bolus followed by
continuous infusion with goal of PTT 1-2.5X
control) or ASA and low molecular weight
heparin unless one of the drugs is
contraindicated
26. The best documented mechanism by which
these agents act is to reduce ventricular
remodeling over days to weeks after myocardial
damage. However, there is data that a mortality
benefit exists when these agents are used early
in the course of ACS
Administration of ACE-I in ACS reduces cardiac
endpoints
27. ACE-I should be administered to all patients in
the first 24 hours of ACS provided hypotension
and other clear cut contraindications are absent
28. Statins may be of benefit in ACS
Possible mechanisms include plaque
stabilization, reversal of endothelial
dysfunction, decreased thrombogenicity, and
reduction of inflammation
29. Age >65 yrs
Daily ASA Therapy (>7 days prior to event)
Symptoms of Unstable Angina
Documented CAD (stenosis > 50%)
3 or more traditional cardiac risk factors
Elevated cardiac enzymes
ECG changes
30. Score of 3 or less = low risk
Score of 4-5 = intermediate risk (use IIBIIIA)
Score of 6-7 = high risk (use IIBIIIA)
31. In the setting of STEMI primary PCI is associated
with better outcomes than thrombolysis
Emergent PCI is also indicated in the setting of a
new LBBB
32. PAMI (PTCA vs. thrombolysis)
Netherlands Trials (PTCA vs. thrombolysis)
GUSTO IIB (PTCA vs. thrombolysis)
DANAMI-2 (stenting vs. thrombolysis)
STAT (stenting vs. thrombolysis)
33. Primary PCI is indicated as an alternative to
thrombolysis when the following criteria are met:
STEMI or new LBBB
Can undergo PCI within 12 hours of the onset of symptoms
The MD doing the intervention does more than 75 PCI’s/yr
The procedure is done in a center that does more than 200
PCI’s/yr and has surgical backup
34. Good History and Physical (note time and
duration of symptoms)
Careful evaluation of ECG (compare to previous
when possible)
Check Cardiac Enzymes
Monitor on Telemetry
Oxygen
35. ASA
NTG (consider MSO4 if pain not relieved)
Beta Blocker
Heparin/LMWH
ACE-I
+/- Statin
+/- Clopidogrel (don’t give if CABG is a possibility)
+/- IIBIIIA inhibitors (based on TIMI risk score)
36. ASA
NTG (consider MSO4 if pain not relieved)
Beta Blocker
Heparin/LMWH
ACE-I
+/-Clopidogrel (based on possibility of CABG)
IIBIIIA
+/- Statin
Activate the Cath Lab!!!
45. 1. Evidence of myocardial necrosis: cardiac biomarker values (preferably
cardiac troponin [cTn]) and with at least one of the following
. Symptoms of ischemia
. New or presumed new significant ST-T changes or new LBBB
. Development of pathologic Q waves on ECG
. Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
. Identification of an intracoronary thrombus by angiography or autopsy
. Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ischemic ECG changes of new LBBB， but death occurred
before cardiac biomarkers were obtained or before cardiac biomarker
values would be increased
. Percutaneous coronary intervention (PCI)-related MI is arbitrarily de有
ned by elevation of cTn val ues (>5 x 99th percentile U RL) in patients with
nor
mal 七as巳line val ues (王99th percentile URL) or a rise of cTn val ues
46. Criteria for Prior Myocardial l nfarction
Any one of the fol lowing criteria meets the diagnosis for prior
MI
. Pathologic Q waves with or without 5ym仁tom5 in the ab5巳
nce of nonischemlc caU5巴5
. I maging evidence of a region of 1055 of viable myocardium
that i5 thinned
and fails to contract， in the absence of a noni5chemic cause.
. Pathologic 有ndings of a prior M
47. Type 1: Sponta neous Myocardial lnfarction
Type 2: Myocardial l nfarction Secondary to an Ischemic Imbalance
Type 3: Myocardial l nfarction Resulting in Death When Biomarker
Values Are Unavailable
Type 4a: Myocardia川 nfarction Related to Percutaneous Coronary
Intervention (PCI)
Type 4b: Myocardial lnfarction Related to Stent Thrombosis
Type 5: Myocardial l nfarction Related to Coronary Artery Bypass
Grafting (CABG)
62. Syndrome Stenoses
Plaque
Disruption Plaque-Associated Thrombus
Stable angina >75% No No
Unstable angina Variable Frequent Non-occlusive
Transmural MI Variable Frequent Occlusive
Subendocardial
MI
Variable Variable Widely variable
Sudden death severe Frequent Often small
63. Ischemic Heart Disease
Angina Pectoris
Chest discomfort = prolonged, recurrent, different qualities
Cause = transient myocardial ischemia( seconds to minutes)
Patterns
Stable = 75% vessel block, transient ( <15 minutes),
aggravated by exertion, relived by rest & Nitroglycerin
(VD)
Prinzmetal = coronary spasm, episodic, Typical EKG
change – ST elevation, Relived by VD but not rest
Unstable = 90% vessel block or Acute plaque change (
superimposed thrombus), prolonged ( >15 min.), not relived
by rest, VD, Pre-infarction Angina
64. Transmural
Full thickness
Superimposed thrombus in
atherosclerosis
Focal damage
Sub-endocardial
Inner 1/3 to half of
ventricular wall
Decreased circulating blood
volume( shock, Hypotension,
Lysed thrombus)
Circumferential
65. Ischemic Heart Disease
MI= Also called Heart attack
Incidence = disease of old
elderly (45% in 65 yrs. old)
young ( 10% in 40yrs. Old),
Sex = Male > Female
Ethnic = same in African & American
Risk factors
Major modifiable- DM, HTN, Smoking,
Hypercholesterolemia
HRT for Postmenopausal females – will not protect
the heart
66. Ischemic Heart Disease
MI
Pathogenesis
Coronary vessel occlusion
Atherosclerosis with thrombus = MC cause ( 90% cases)
Others = vasospasm (10%)
Most important mechanism = dynamic changes in
the plaque (rather than plaque size),
Plaque disruption PLTS aggregation thrombus
and VC (happens in minutes)
Irreversible changes = after 30 minutes of ischemia
ATP < 10% of normal
Mechanism of cell death = necrosis ( Coagulative)
68. Ischemic Heart Disease
MI -Morphology
light microscopy
First 12 hrs. after MI – no change
Up to 3 days = Coagulative necrosis, neutrophils
1-2 weeks = Granulation tissue
≥ 3 weeks = fine scar
≥ 2 months = dense scar
EM – membrane disruption and Mitochondrial densities
Special stain = TTC ( Triphenyl Tetrazolium chloride),
Detects and stains Mahogany brown with Lactate dehydrogenase
Unstained area = infarction
Mahogany brown = viable
White, glistening= scar
Most common and nonspecific change in ischemia = sub-
endocardial myocyte vacuolization
72. Ischemic Heart Disease
MI = Clinical
Silent MI = DM, Elderly, Cardiac transplantation
recipients,
Typical features = Rapid, weak pulse and sweating
profusely (diaphoretic), Dyspnea, chest pain
Lab=
Diagnostic
Best markers = Troponins ( T & I), both sensitive and
cardio – specific
Next best – CK-MB
Predictive
CRP- >3mg/l – highest risk
73. Ischemic Heart Disease
MI –Complications
In 75% of Patients with MI
Poor prognosis in = elderly, females, DM, old case of MI, Anterior
wall infarct – worst, posterior –worse, Inferior wall – best
1. Arrhythmia = Ventr. Fibrillation – MC arrhythmia lead to
sudden death in MI patients, before they reach hospital
2. pump failure – LVF, cariogenic shock, if >LV wall infarcts,
lead to death ( 70% of hospitalized MI patients)
3.Ventricular rupture = Free or lateral LV wall – MC site, later
cause false aneurysm,
4.True aneurysm = rupture is very rare
5.Pericarditis = Dressler’s syndrome ( Late MI complication)
6.Recurrence
74. Ischemic Heart Disease
Sudden cardiac death = unexpected death in one hour due
to cardiac causes with or without clinical symptoms
Cause – Atherosclerosis ( 90%), others (10%)
Romano- Ward syndrome – Long Q-T syndrome
( K+, Na+ channel defects)
Mechanism- Most likely due to arrhythmias ( VF)
Patients – young athletes, with Pul. HTN, IHD
Morphology
Prominent finding – increased heart mass
Vacuolations in Sub – endocardial myocardium
75. Ischemic Heart Disease
Chronic IHD = also called ischemic cardiomyopathy
Patients = post heart transplant receipts, previous MI or
CABG pts
Cause =compromised ventricular function
Morphology =vacuoles, Myocyte Hypertrophy
Diagnosis= by exclusion
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