This document provides an overview of a case of a 70-year-old African American female presenting with acute respiratory distress and signs of a non-ST elevated myocardial infarction (NSTEMI). It discusses her medical history of cardiovascular risk factors and presents her vital signs, physical exam findings, laboratory and imaging results supporting the diagnosis of NSTEMI. The document then outlines her pharmacological management including antiplatelet therapy, anticoagulation, beta-blockers, ACE inhibitors and statins as well as her appropriate treatment options going forward.

1. Spectrum of Myocardial
Infarction

2.  Provide brief overview of the patients case
 Discuss the disease state, presentation and
signs and symptoms
 Explain the non-pharmacological and
pharmacological management options
 Display the place in therapy of each medications
 Provide a synopsis of a major landmark trial
 Discuss the patient’s appropriate management
options
2

3. MAGN is a 70 y/o African American female who developed
acute respiratory distress while in the rehab.The patient
was found to be using her abdominal muscle to breath with
slurry speech, tachypnea, and tachycardia. Code 66 was
called after sedating the patient and she was subsequently
intubated.The patient was then sent to the CCU following
intubation due to development of acute respiratory distress
for more close monitoring.
3

4. PMH: HTN, CAD S/P CABG, PVD, DM, right foot
ulcer, osteomyelitis of the 3rd and 5th right toe.
FH: Insignificant
SH: Insignificant
NKDA
VS: Temp: 96 ° F, BP: 193/120 mm Hg, HR: 146 BPM
RR: 22 BPM, O2 Sat: 66%,Pain scale: 0/10
4

5. Physical Findings:
 ABW: 165lb (75kg), Height: 5 feet 4.96 inch, IBW: 56.9 kg, AdJBW: 64.14kg.
 Mental status: Speech clear, oriented X 3, responds appropriately to
questions
 HEENT: No nasal discharge, intubated, no airway obstruction
 Lungs: No wheezing, mild rales bilateral middle, mild rhonchi middle chest
 CV: Normal rate, normal rhythm, normal S1, normal S2, no murmur no rub
 Extremities: Good pulses in all extremities, no swelling/tenderness in the
extremities, pitting edema half way to knees
 GI: Normal BS, soft, no abdominal tenderness.
CXR: Persistent infiltration in the right lower lung zone
EKG: Unremarkable
ECHO: Moderate mitral valve regurgitation, Normal LV Ejection fraction,
Mild concentric left ventricular hypertrophy, Mild aortic valve sclerosis
without stenosis. 5

6.  Na: 142 mEq/L
 K: 4 mEq/L
 Cl: 101 mEq/L
 CO2: 27 mEq/L
 SCr: 1.2 mg/dL
 BG :196 mg/dL ↑
 HgA1C: 6.6% ↑
 CKMB: 43.5 U/L ↑
 Troponin: 5.5 ng/mL ↑
 ABG analysis pCO2: 36,
pO2: 58↓, HCO3: 28.7 ↑
 WBC: 13.7 x 10^3/mm^3 ↑
 Hgb: 10.6g/dL ↓
 Hct: 32% ↓
 Plt:363 x 10^3/mm^3
 AST: 41 U/L
 ALT: 30 U/L
6

7.  Aspirin (Ecotrin) 325mg PO QAM
 Clopidogrel(Plavix) 75mg PO QAM
 Zosyn 2.25g Q6H QD
 Ciprofloxacin 200mg Q12H QD
 Vasotec 10mg PO QAM
 Januvia 50mg PO QAM
 Lantus 10 units SQ QD
 Pepcid 20 mg PO QAM
 Glucotrol 10mg PO AC Breakfast
 Heparin 5600 units PO Q8H
 NovologTID
 Percocet 1T PO Q6H
 Tylenol 650 mg PO Q 4H
7

8. Non- ST Elevated Myocardial
Infarction
8

9.  Acute ischemic event that causes myocardial
necrosis
 Detected by elevation of serum cardiac
biomarkers and changes in ECG
 Troponin
 CK-MB
 ECG
9

10. http://www.aic.cuhk.edu.hk/web8/corona5.gif 10

11.  Gradual buildup of cholesterol
and fibrous tissues in the
arteries
 Most predominant cause of
unstable ACS is due to the
rupture of the plaque
 Plaques that occludes up to 70-
90% of the artery are more likely to
rupture
 After the plaque ruptures-
formation of a thrombi is seen
on the plaque
 Leading to the clotting cascade
 Impairment of the blood flow
and if it is long enough
 Ischemic cascade begins and
necrosis of the myocardium is seen11

12.  1 per 3 American has an underlying CVD
 Estimated that 2/3 of ACS presents as NSTEMI or
unstable angina
 NSTEMI accounts for 1.5 million hospital admission
per year
 Percentage of patients with diagnosis of NSTEMI is
increasing dramatically
 Sensitive assays for MI, available earlier
pharmacotherapy
12

13.  Common
 Deprivation of oxygen in the myocardium
 Adhesion, activation of plateletsPreventing blood
flowresulting in myocardial ischemia
 Rare
 Progressive atherosclerosis
 Recreational drug use
 Inflammation of the arteries
 Extrinsic cause
13

14. Modifiable Non-Modifiable
Diabetes Age >65 years
Obesity FHx of CAD
PVD History of Angina
Smoking Previous CVD
Hypertension Recent PCI
Dyslipidemia
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am
Coll Cardiol. 2007;50:1-157
14

15. Factors Characteristics
Chest pain Squeezing, aching,
burning, sharp pain
Prolonged
discomfort ≥ 30
minutes
Radiation to left
arm or neck is very
common
Diaphoresi
s
Classical sign and
symptom of MI
Factors Characteristics
 SOB Secondary to
diminished cardiac
output
Anxiety Displayed females,
elderly and DM
Fourth Heart Sound
(S4)
Present in ischemia
Signs of CHF Pulmonary rales
Lower extremity
edema
S3 gallop
Elevated Jugular
Venous Pressure
Sheridan PJ, Crossman DC. Critical review of unstable angina and non-ST elevation myocardial infarction. Postgrad Med J. 2002;78:717-726
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction.
J Am Coll Cardiol. 2007;50:1-157 15

16. KeyTest Characteristics
 ECG  ST-Wave depression > 0.5 mm
T-Wave Inversion > 2 mm
 ECG may be normal
 Serial tests 15-30 minute interval
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation
myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition 16

17. Key
Tests
Characteristics
CK-MB Sensitivity- 95%
False Positive can occur
Trauma
 Surgery
Cardioversion
Troponin Highly Sensitive and
specific
Confirms Diagnosis of MI
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-
elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
17

18. PROGNOSIS
 High risk of morbidity and
death from future events
 Rate of death is 4-6 times
higher compared to the
general population
 Risk of the mortality and
morbidity depends on the
patients risk factor
GOALS OFTREATMENT
 Provide early restoration of
blood flow to the infarct-
related artery to prevent
infarct expansion
 Relieve ischemia and pain
 Prevention of coronary artery
reocclusion
 Relief of ischemic chest
discomfort
 Prevention of death and other
complications 18

19. Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
19

20. Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
20

21.  Intranasal Oxygen
 Oxygen saturation is < 90%
 PCI or CABG
 Early treatment for high risk
patients
 Consider in patients with
moderate risk
 Benefit
 Results in fewer MI’s
 Less hospital readmissions
for a recurrent MI’s
 Less need for an additional
revascularization following
hospitalization
 Risk (1:1,000 patients)
 Bleeding
 Infection
 Pain at site of insertion
 Damage to the blood vessels
 Buildup of blood and fluid in
the pericardium
 Much higher in patients who
has
▪ Diabetes
▪ CKD
▪ Age > 75
Bavry DA, Kumbhan DJ, Rassi AN, et al. Benefit of early invasive therapy in acute coronary syndromes: A meta-analysis of contemporary,
randomized clinical trials. J Am Coll Cardiol 2006;48:1319–1325 21

22.  PCI -feasible and safe to do
so
 Straight, quick, and performed at
low risk
 Performed for one or stenosed
vessels
 Not for multiple stenosed vessels
▪ Greater risk of restenosis
 CABG- for multiple-vessel
stenosis
 Greater chance of achieving
full revascularization
 Choices can be institution
specific
 Easier to proceed with PCI
than to wait for an operation
Gunn J et al. Revascularization for AcuteCoronary Sundromes:PCI or CABG? Heart 2003 89: 967-970
http://0.tqn.com/f/p/440/graphics/images/en/19006.jpg 22

23. Aspirin Thienopyridine β-Blockers
Nitrates Opioids GP IIb/IIIa Receptor
Inhibitors
Calcium Channel
Blockers
ACE Inhibitors Angiotensin
Receptor Blockers
Anticoagulants Lipid Lowering
Agents
23

24. MOA Irreversibly inhibits COX-1 and 2 decrease formation of
thrombaxaneA2Inhibits platelet aggregation
Important
Pharmacokinetic
Parameter
Hydrolyzed to salicylate via liver (Active)
Half Life
 Parent drug (15-20 minutes)
T1/2= 3 hours (300-600 mg)
T1/2= 5-6 hours ( > 1000 mg)
Elimination via Urine
Clcr <10 mL/minute: Avoid use
Drug Interaction NSAID - diminish the cardioprotective effect of Salicylate
Warfarin- enhance anticoagulant effect of warfarin
(additive)
 Heparin and Anti-platelets- increase risk of bleeding
 Low dose OK
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
24

25. Guideline
Recommendation
Class 1A
Contraindications  Hypersensitivity
Active Bleeding
Severe Bleeding Risk
Dose and Duration
of therapy
 162–325 mg PO STAT on hospital day 1
75–162 mg PO QD starting day 2  indefinitely
Pt. undergoing PCI- 162–325 mg PO QD for a minimum of
30 days
Monitoring
Parameter
Clinical signs of bleeding- Melena, hematuria, bloody
stool
Upset GI
Baseline CBC and platelet count
CBC platelet count every 6 months
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
25

26. Clopidogrel (Plavix) Ticlopidine (Ticlid)
MOA  Mediate their antiplatelet effects through a
blockade of ADP P2Y12 receptors on platelets
Important
Pharmacokinetic
Parameters
Metabolized
hepatically (CYP2C19)
T1/2= 6 hours
Elimination
 Urine-50%
 Feces- 46%
Renal Impairment- No
dose adjustment
 Hepatic Metabolism
T1/2= 13 hours
Elimination
 Urine-60%
 Feces- 23%
Preferred Agent? Ticlopidine  Neutropenia
 Requires frequent monitoring of CBC
Plavix preferred
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
26

27.  Reserved for patients allergic toAspirin
 Trials shows that the addition of Plavix to Aspirin is
safe and efficacious
 CommitTrial
▪ Adding Plavix to Aspirin prevents 10 major vascular events per
1000 treated
 Patients scheduled for CABG
 Best not to administer Plavix until procedure is complete
 If Plavix is already administered
▪ Hold dose for 5-7 days prior to procedure
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
27

28. Guideline
Recommendation
Class 1A
Dose and Duration
of therapy
 300-600 mg PO STAT on hospital day 1
75 mg PO QD starting day 2
 Administer for 9 months
Aspirin allergy-Administer Indefinitely
 Post-PCI bare-metal stented patients- 1 month
Post-PCI Sirolimus/Paclitaxel stent-12 month
Contraindications  Hypersensitivity
Active Bleeding
Severe Bleeding Risk
Adverse Events Bleeding
TTP
Diarrhea
 Rash
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157 28

29. Guideline
Recommendation
Class 1A
Drug Interactions Calcium Channel Blockers- Diminish the therapeutic
effect of Plavix
PPI’s- Reduced efficacy of Plavix
Macrolide’s- Diminish the therapeutic effect of Plavix
Warfarin- Enhance the anticoagulant activity of
warfarin
Monitoring
Parameter
Clinical signs of bleeding- Melena, hematuria, bloody
stool
Upset GI
Baseline CBC and platelet count
CBC platelet count every 6 months
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
29

30.  Recommended for HIGH
risk patients
 Patient undergoing PCI
 Continued or recurrent
ischemia despite
treatment
▪ Aspirin
▪ Plavix
▪ Anticoagulant
Pharmacotherapy-A Pathophysiologic approach-Depiro’s
7th edition
30

31. Tirofiban
(Aggrastat )
Eptifibatide(Integrilin ) Abciximab (Reopro )
(NOT Recommended)
MOA  Block platelet binding of fibrinogen to the GP IIb/IIIa receptor
Pharmacokinetics T1/2=2 hours
Elimination
 Urine- 65%
Feces- 25%
T1/2=2 hours
Elimination
 Urine
Dialysis-
Contraindicated
T1/2= 30 minutes
Drug Interactions Anticoagulants
 Increased effect
Antiplatelets
 Increased effect
NSAIDS- Increase risk of bleeding
ADR Bleeding
 Acute profound thrombocytopenia
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010 31

32. Guideline
Recommendation
Class I- for patients who are undergoing PCI
Class Iib-without high-risk features or who are not
undergoing PCI
Contraindications Thrombocytopenia
Active Bleeding
Prior stroke
Monitoring
Parameter
Clinical signs of bleeding
A baseline CBC and platelet count
Daily CBC
Platelet count at 4
hours after initiation then daily
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation
myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
32

33.  Invasive strategy is
selected
 Enoxaparin, UFH,
Bivalirudin, and
fondaparinux
 If heparin continue dose
for 48 hours
 Enoxaparin or
Fondaparinux
 Administer dose for a
maximum of eight days
 Conservative strategy
 Preferred: Lovenox or
Fondaparinux
 Fondaparinux if increase risk
of bleeding
 If CABG planned
 Fondaparinux
33

34. Drug Guideline
Recommendation
Contraindication Doses
34

35. UFH LMWH Fondaparinux Bivalirudin
MOA- Potentiates
the action of
antithrombin III
 Inactivates
thrombin
Prevents the
conversion of
fibrinogen to
fibrin
 Enhances the inhibition rate of clotting protease
by inhbiting factor Xa
Pharmacokinetics T1/2= 1-2 hrs T1/2= 4.5-7
hrs
Elimination=
urine (40%)
CrCL<30=
1mg/kg SQ QD
F= 100% if SC
T1/2= 17-21
hours
CrCl<30= use
is C/I
T1/2= 25
minutes
CrCl < 30
T1/2= 57
minutes
35

36. UFH LMWH Fondaparinux Bivalirudin
Drug Interaction Aspirin- increase risk of bleeding
Antiplatelets- Increase anticoagulant effect
NSAIDS- Enhance anticoagulant effect
ADR Bleeding
Heparin Induced
Thrombocytopenia
Bleeding
Monitoring
Parameters
Clinical signs of bleeding
Baseline CBC, platelet count
Daily CBC
aPTT Q6HQ24H
36

37.  Indicated for patients with persistent ischemia,
hypertension, and symptoms of acute heart failure
 Produce venous and arterial vasodilation
 SL followed by IV after 3 doses
 NTG in all patients w/o contraindications
 SBP <90 mm Hg
 HR <50 beats/min
 Right ventricular infarction
 Sildenafil or vardenafil within 24 hours
 Tadalafil within 48 hours
37

38. Nitroglycerin
MOA Primarily reduces cardiac oxygen demand by decreasing preload or
the left ventricular end-diastolic pressure
Pharmacokinetics T1/2= 1-4 minutes
Metabolized via the liver
Drug Interactions Heparin - diminish the anticoagulant effect of Heparin
Phosphodiesterase 5 Inhibitors - enhance the vasodilatory effect
of Nitroglycerin
ADR Tachycardia, Flushing, Hypotension
Monitoring Parameters BP and HR every 2 hours
38

39. Guideline Recommendation Dose
Nitroglycerin Class 1 0.4 mg SL, repeated every 5
minutes × 3 doses
5–10 mcg/min IV infusion
titrated
Continue IV infusion for 24–
48 hours
up to 200 mcg/min until
relief of symptoms or limiting
side-effects
 headache
 SBP <90 mm Hg
Discontinue if SBP drops
>30 mm Hg below baseline
SBP
39

40.  Morphine- Class IIa recommendation
 If Nitroglycerin is not sufficient
 Produce vasodilation and reduces the heart rate and
your systolic BP to further reduce Myocardial oxygen
demand
 Alternative to nitroglycerin when nitroglycerin is
contraindicated
40

41. MOA Produce vasodilation and reductions in HR through
increased vagal tone and systolic BP to further reduce
myocardial oxygen demand
Pharmacokinetic Hepatic metabolism
F= 17-33% PO
T1/2= 2-4 hours
Excretion
 Urine- 2 to 12%
 Feces- 10%
 CrCl 10-50 mL/min- Administer 75% of the normal dose
CrCl< 10 mL/min- Administer 50% of the normal dose
Drug Interactions Alcohol- enhance CNS depression of alcohol
Thiazide diuretics- Enhance the effect of orthostatic HOTN
Succinylcholine- increase bradycardic effect of morphine
41

42. Dose 2-5 mg IV bolus dose
Can be repeated every 5-30 minutes PRN
Contraindications Hypotension
Respiratory Depression
Confusion
ADE Hypotension
Respiratory Depression
Monitoring
Parameters
Blood pressure and respiratory rate 5 minutes
after each bolus dose
42

43.  Reduces the risk of recurrent ischemia, infarct size, risk of
reinfarction in the hours and days following MI
 Selective Beta-Blockers
 Continue indefinitely
 Do not use in patients who are hemodynamically unstable
 IV route preferred over PO
 Persistent Ischemia
 Hypertension
 Tachycardia
 Goal of resting heart rate= 50-60 BPM
43

44. Metoprolol Propranolol Atenolol
MOA Selectively inhibits B1- receptorReduces heart rate,
myocardial contractility and BP Decreasing oxygen demand
Pharmacokinetics Extensively
metabolized via the
liver
F=50% Oral
T1/2=3-8 hours
Renal or hepatic
failure- No dose
adjust
Hepatic via
CYP2D6, and
CYP1A2
T1/2
 Immediate
release-3-6 hours
 Extended
Release-8-10 hours
Hepatically
metabolized
T1/2 Adults=6-7
hrs
Elimination
 50% urine
 40% urine
Adults w/ ESRD
T1/2=15-35 hrs
CrCl <15-35= Max
50mg/day
CrCl <15mL/min=
Max 50mg QOD 44

45. Drug Guideline
Recommendation
Contraindication Doses
Drug-Interactions Alpha 2-agonist-enhance rebound hypertensive effect of the
Alpha-2
Amiodarone- increase the bradycardiac effect
MAOI=Enhance orthostatic HOTN effect
45

46. Metoprolol Propranolol Atenolol
ADR Hypotension
Bradycardia
Heart block
Monitoring
Parameters
BP, RR, HR
12-lead ECG
Clinical signs of heart failure every 5 minutes during
bolus intravenous dosing
Every shift during oral administration during
Hospitalization, then BP and HR every 6 months
following hospital discharge
46

47.  Indication for use
 Patients with continuing or recurrent ischemic symptoms despite Nitrate and
Beta-Blocker therapy
 Contraindication to Beta-Blocker’s
 Preferred over Beta-Blocker
 cocaine induced ACS
 Prinzmetal angina
 Reduces coronary spasm by relaxing the smooth muscle in the arteries
 DHP’s not so much favored
 No effect on AV node No effect on heart rate
 Can increase myocardial ischemia
 Non-DHP’s Preferred
 Holds anti-ischemic effect by reducing contractility and the conduction AV
node decrease heart rate
47

48. Diltiazem Verapamil
MOA  Prevent the entry of Ca2+ into the vascular smooth
muscle and the myocardium Relaxing the vascular
smooth muscle and increase O2 delivery
Pharmacokinetics Hepatic Metabolism
 First Pass effect
F= 40 % PO
T1/2
IR= 3-4.5 hours
 XR= 6-9 hours
Renal Impairment= No
Dose adjustment
necessary
Hepatic Metabolism
 First Pass effect
F= 35 % PO
T1/2= 3-7 hours
 Hepatic
Impairment= 14-16 hours
Elimination= 70% Urine;
20% Feces.
Renal Impairment= Use
low dose
Hepatic Impairment=
Decrease dose by 70%
48

49. Diltiazem Verapamil
Drug Interactions Antifungal= Decrease metabolism of CCB
Atorvastatin= Increase serum level of both
Atorvastatin and CCB
Calcium Salts= Diminish the therapeutic effect of CCB
ADR Hypotension
Bradycardia
Heart Block
Heart Failure
Gingival Hyperplasia
Contraindications Pulmonary Edema
SBP < 100 mm HG
PR interval >0.25 sec on ECG
2nd or 3rd degree AV block
HR <60 BPM 49

50. Diltiazem Verapamil
Recommended dose 120-360 mg SR QD 180-480 mg SR QD
Monitoring
parameters
 BP and HR
Signs of heart failure on every shift
during hospitalization
Then assess every 6 months for similar
signs following discharge
Dental exam and cleaning teeth every 6
month
50

51.  Should be used in all
patients with
 Left ventricular systolic
dysfunction
▪ EF <40%
 Heart Failure
 HTN
 Cardiogenic Shock
 Started w/in 24 hours
following post-stabilization
 Shown to reduce
▪ Mortality
▪ Decrease reinfarction
▪ Prevent development of
heart failure
 Benefit: Ability to prevent
cardiac remodeling
 BP Optimal Goal: 125/75 mm
Hg
 Ideally < 130/85 mm Hg 51

52. Contraindications Drug Dose Target Dose
52

53.  Data portrays the benefit of Statin in CAD
 Low Mortality
 Less incidence of stroke
 Use statin in all patients withACS, regardless of
LDL cholesterol levels
 Goal LDL < 100 mg/dL
 Preferred <70 mg/dL
53

54. 54

55.  Cardiac Rehabillation
 Increase functional capacity
 Aerobic and weight-bearing
exercise 4 to 5 times per
week for >30 minutes
 PLUS
 Continue Antiplatelet
therapy
▪ Indefinitely
▪ 1° option-Aspirin PLUS Plavix
▪ 2° option-Clopidogrel alone
 PLUS
 Continue Beta-Blockers
▪ Indefinitely
▪ Metoprolol,Atenolol,
Propranolol
 PLUS
 Statins
▪ Indefinitely
 Adjunct
 ACE/ARB
▪ Patients who has EF <40%
▪ Heart Failure
▪ Ongoing Ischemia
55

56.  Inpatient follow up with in 1-2 weeks of
discharge
 Monitor Lipids at least every 6 months
 LDL < 70mg/dL
 Control and monitor HTN
 <130/80 mm Hg
56

57. Purpose: To evaluate the efficacy and safety of clopidogrel when used along with
aspirin in patients without ST-segment elevation, because it was seen that these
patient has a very high rates of major vascular events
Study Design: Randomized, Double blind, Placebo-Controlled trial.
Methods:
 12,562 patients were randomized
 6,259 patients received clopidogrel 300 mg followed by 75 mg PLUS
aspirin post 24 hour onset of symptoms
 6,303 patients received a placebo PLUS aspirin post 24 hour onset of
symptoms
57

58. Primary endpoint: Assess the
composite of death that
occurred from cardiovascular
causes, nonfatal myocardial
infarction, or stroke
Conclusion: Clopidogrel has
beneficial effects in patients
with acute coronary syndromes
without ST-segment elevation,
in addition also has a risk of
major bleeding among patients
treated with clopidogrel
Result
58

59.  Fish Oil
 ω- 3 Fatty Acids
▪ EPA and DHA-Abundant in fish
 Diet high in EPA & DHA or supplementation of fish oil
▪ Reduces the risk of CV mortality,
▪ Reinfarction
▪ Stroke
 Three 1 gram fish oil capsule should be consumed per
daywill provide 1 gram of ω- 3 Fatty Acid
Grupo Italiano per lo Studio dela Sopravvivenza nell’infarcto miocardio.Dietary Supplementation with n-3 fatty acids and
Vitamin E after myocardial infarction: Results of GISSI- Prevenzione trial. Lancet 1999;354:447-455
59

60.  Mainstays of therapy include risk stratification, and early
angiography and revascularization with either PCI or
CABG for patients with NSTE ACS at high risk for MI and
death
 Pharmacotherapy for acute treatment includes SL NTG,
antiplatelets, anticoagulants and B-blockers
 Ensuring selection of evidence-based therapies in all
patients without contraindications results in lower
mortality
 Pharmacists have an important role in encouraging
patient adherence and persistence to pharmacotherapy
60

61.  Severe respiratory distress
 Slurry speech and was wheezing
 Low O2 saturation (66%)
 Tachypneic and tachycardia (HR= 146 BPM)
 Elevated blood pressure (193/120 mm Hg)
 Lower extremity edema
 Troponin level: 5.5 ng/mL
 CK-MB: 43.5 U/L
 Low Hgb (9.3 g/dL) and Hct (28%)
61

62.  Previous history of CABG
 It is possible that thrombi formed, occluding the
coronary blood flow and resulting in myocardial
ischemia
 Other significant risk hypertension, diabetes
mellitus and being elderly
62

63.  Administer oxygen
 TIMI RISK: 5-Moderate
 Patient is greater than 65 years
old (71)
 She has as known history of
CAD
 The patient has been taking
aspirin for the last 7 days
 ECG revealed ST- segment
depression
 The patient has positive
biochemical markers of
infarction as seen by the
troponin level and the CK-MB
level
 Does not need to go for any sort
of early coronary angiography
and revascularization
 ECHO revealed no stenosis
63

64.  Aspirin 325 mg as a single dose
followed by aspirin 81 mg
indefinitely
 Clopidogrel (Plavix) 300-600mg via
NG-Tube as a loading dose on day 1
followed by 75 mg via NG-Tube once
daily
 atorvastatin (Lipitor) 10-80 mg/day
orally
 Metoprolol (Lopressor) 5 mg slow IV
push (Over 1-2 minutes), repeated
every five minutes for a total of 15
mg followed in 15-30 minutes by 25-
30 mg by mouth Q6H
64

65. Bavry DA, Kumbhan DJ, RassiAN, et al. Benefit of early invasive therapy in acute
coronary syndromes: A meta-analysis of contemporary, randomized clinical trials.
Am Coll Cardiol 2006;48:1319–1325
Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
Anderson JL,Adams CD,Antman EM, et al.ACC/AHA 2007 guidelines for the
management of patients with unstable angina/non-ST-elevation myocardial
infarction. J Am Coll Cardiol. 2007;50:1-157
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;October
2010.
65

66. 66