Acute Coronary Syndromes
Gobezie T.
1

Acute coronary syndromes
 Acute coronary syndromes (ACS), including unstable
angina (UA) and myocardial infarction (MI), are a form
of coronary heart disease (CHD) that comprises the
most common cause of CVD death.
 Non-ST-Segment Elevation MI (NSTEMI & UA)
 ST-Segment Elevation MI (STEMI)
 The cause of an acute coronary syndrome is
 the rupture of an atherosclerotic plaque with
subsequent platelet adherence, activation, and
aggregation, and the activation of the clotting
cascade. 2

Epidemiology (Ethiopia)
 AMI annual admissions ↑ed consistently over the
years
 mean age of these patients was 55.1 +/- 13.0 years.
 Males constituted 82% of all AMI cases
 87% (69/79) of cases were first admissions with Dx of
AMI
 90 % died in hospital.
 81% had >1major coronary risk factors excluding age
& gender. ↑ed total cholesterol & HTN commonest
risk factors, 69% & 47% of AMI respectively (Ethiop Med J.
2001 Jul;39(3):193-202) 3

Ethiology/ Pathophysiology
 Endothelial dysfunction, inflammation, and formation
of fatty streaks contribute to the formation of
atherosclerosis.
 Atheromatous plaque rupture, fissuring, or erosion of
unstable atherosclerotic plaque (in > 90% of ACS
patients).
 ↓ in myocardial oxygen supply or an ↑in myocardial
demand in absence of a coronary artery process.
 MI could also occur during revascularization
procedures.
4

Pathophysiology
 Plaque Rupture and Clot Formation
 In contrast to stable angina, an ACS results primarily
from diminished myocardial blood flow secondary to
an occlusive or partially occlusive coronary artery
thrombus.
 Acute plaque rupture platelet adhesion
activation of coagulation cascade thrombus
formation with partial (UA/NSTEMI) or total
(STEMI) occlusion of arterial lumen 5

6

ACS, Pathophysiology
Ventricular Remodeling Following an
Acute MI
 VR is a process that occurs ffowing MI.
 Characterized by left ventricular dilation and
reduced pumping function of the LV leading to
cardiac failure.
 HF represents one of the principal causes of
mortality & morbidity following MI, preventing
ventricular remodeling is an important
therapeutic goal.
 ACEIs, ARBs, βBs, & AAs, all slow or reverse VR 7

ACS, Pathophysiology
complications that may result from MI are
cardiogenic shock- most serious complication
of MI
HF, valvular dysfunction,
bradycardia, heart block, pericarditis,
stroke secondary to LV thrombus embolization,
venous thromboembolism,
LV free wall or ventricular septal rupture, LV
aneurysm formation, and
ventricular and atrial tachyarrhythmias.
8

RISK FACTORS
 Increasing age.
 Male sex.
 Smoking.
 Hypertension.
 Diabetes mellitus.
 Dyslipidemia.
 Obesity.
9

10

 Unstable angina
 Angina with at least one of the three features
• It occurs at rest, lasts >10 min
• Severe & of new onset, with in the past 4-6 wks.
• Occurs with a crescendo/ intensification/ pattern
 NSTEMI
 UA + elevated cardiac biomarkers
 STEMI: NSTEMI + ST elevaiton
 30 day mortality rate is 30 %, ½ of it occurs
before the patient reaches the hospital
11

CLINICAL PRESENTATION
Diagnosis of ACS
 General: typically in acute distress and may
develop or present with acute HF, cardiogenic shock,
or cardiac arrest.
 Symptoms
 Midline anterior chest pain/discomfort is the classical
symp of ACS
 Accompanying symp may include arm, back, or jaw pain, N,
V, or SOB
 Sudden onset and Increasing angina > 20 minutes
 Women, diabetics, & elderly are less likely to have
12

Signs
 No signs are classic for ACS.
 Patients with ACS may present with signs of acute
decompensated HF including jugular venous
distention (JVD) and an S3 sound on auscultation.
 Patients may also present with arrhythmias, and
therefore may have tachycardia, bradycardia, or heart
block.
13

Laboratory Tests
◦ Biomarkers (Troponin I or T = cTnI or cTnT)
◦ Troponin I or T at time of first assessment & repeated at least
once, 3 to 6 h later to ascertain muscle damage, confirmatory
for MI Dx.
◦ Blood chemistry (particularly K & Mg, may affect heart
rhythm)
◦ SCr & CrCl for dosing adjustments of some drugs as
well as to assess ↑ risk of morbidity and mortality.
◦ Baseline CBC & coagulation tests (aPTT and INR),
as most patients will receive antithrombotics that ↑s
risk for bleeding.
◦ glucose
◦ Fasting lipid panel (optional).
14

Risk Stratification
15
 TIMI Risk Score for NSTE-ACS
 Risk of death, MI, or urgent need for revascularization as
follows: (One point for each of seven)
 Age >65 years
 >3 CHD risk factors: (smoking, hypercholesterolemia, HTN,
DM, Fx of premature CHD death/events)
 Known CAD (50% or greater stenosis of at least one major
coronary artery on coronary angiogram)
 Aspirin use within the past 7 days
 Two or more episodes of chest discomfort within past 24
hours
 ST-segment depression 0.5 mm or greater
 Positive biochemical marker for infarction
 TIMI Risk Score (5-7 points= High, 3-4 =Medium, 0-2= Low-

Acute Coronary Syndromes:
Treatment
DESIRED OUTCOMES
The short-term goals of Rx for ACS patient are as
follows:
 Early restoration of blood flow to the infarct-related
artery to prevent infarct expansion (in case of MI) or
prevent complete occlusion and MI (in unstable
angina)
 Prevention of death and other complications
 Prevention of coronary artery reocclusion
 Relief of ischemic chest discomfort
 resolution of ST-segment and T-wave changes on the
ECG.
Long-term desired outcomes are
 control of CV risk factors,
16

General approach for ACS
 General tt measures for all STEMI & high- &
intermediate-risk NSTE-ACS patients include
 admission to hospital,
 oxygen administration (if oxygen saturation is low, <90%),
 continuous multi-lead ST-segment monitoring for
arrhythmias & ischemia,
 frequent measurement of vital signs,
 bed rest for 12 hours in hemodynamically stable patients,
 Avoidance of Valsalva maneuver, bed rest, stool softeners,
& pain relief.
17

General approach….
 STEMI,
 Reestablish coronary perfusion immediately (without
evaluation of biochemical markers).
• immediate primary PCI with balloon angioplasty or
stent placement is reperfusion treatment of choice
when patient presents within 12 hours of symptom
onset.
 STEMI is a high risk for death, and efforts to reestablish
coronary perfusion, as well as adjunctive pharmacotherapy,
should be initiated immediately.
 NSTE ACS at low risk:
 Obtain serial biochemical markers.
 High-risk NSTE ACS:
 early coronary angiography (within 24 hours) &
18

Early Pharmacotherapy for STE ACS
 In Emergency department (ED):
 Morphine PRN
 Oxygen (if SO2<90)
 sublingual ± IV NTG
 DAT: (ASA+P2Y12Is)
 Anticoagulant (UFH or enoxaparin/fondaparinux/
bivalirudin)
 β-blocker (in ED, within first 24 h)
 Fibrinolysis
19

Tt Algorism for STE MI
20

Fibrinolytic Therapy
Administer within 30 min of arrival of STE ACS
patients if
 Presenting to hospital within 12 hours of onset of chest
discomfort
 and have at least 1 mm of STE .
Fibrinolytic is preferred over primary PCI if
 no cardiac catheterization laboratory or
 there would be a delay in “door-to-primary PCI” of more than
90 minutes (of first medical contact) within the institution or
120 minutes (of first medical contact) if the patient is
transferred
21

22

23

Drug Fibrin
Specificity
Dose
Streptokinase (SK)
(Streptase)
+ 1.5 MU in 50 mls NS/D5W IV over 60 mins
Tissue
plasminogen
activator (tPA)
(Alteplase)
+++ IV Bolus: 15 mg, 0.75 mg/Kg over 30 mins
(max: 50mg), 0.5mg/Kg over 1 hr (max 35mg)
(max dose 100 mg)
Reteplase (rPA)
(Retevase)
++ 10 U IV push over 2 min, repeat after 30 min
Tenecteplase (TNK)
(TNKase)
++++ Single IV bolus given over 5 s based on
weight
< 60Kg: 30 mg IV Bolus
60-70Kg: 35 mg IV Bolus
71-80Kg: 40 mg IV Bolus
81-90Kg: 45mg IV Bolus
> 91Kg: 50mg IV Bolus
24
alteplase, reteplase, & tenecteplase are acceptable as first-line agents.

Aspirin
Early aspirin administration to all patients without
contraindications within the first 24 hours of hospital
admission is a quality care indicator.
In patients undergoing PCI, aspirin prevents acute
thrombotic occlusion during the procedure.
In patients experiencing ACS, an initial dose ≥160 mg
nonenteric aspirin is necessary to achieve rapid platelet
inhibition.
 This first dose can be chewed in order to achieve high blood
concentrations and rapid platelet inhibition.
 Although an initial dose of 160 to 325 mg is required, long-
term therapy with doses of 75 to 150 mg daily are as
effective as higher doses and, therefore, a daily
maintenance dose of 75 to 160 mg is recommended. 25

Thienopyridines.
 Should be used as soon as possible concomitantly
with aspirin to prevent subacute stent thrombosis
and longer term CV events.
 Recommended duration is 12 months following
PCI for STEMI receiving a bare metal stent or
drug-eluting stent.
 E.g: Clopidogrel, prasugrel, and ticlopidine
26

Thienopyridines.
 Clopidogrel.
 For patients with aspirin allergy,
• use 300–600 mg loading on day 1, followed by 75
mg/day, continued indefinitely.
 For patients treated with fibrinolytics and in those
receiving no revascularization,
• use 75 mg or 300 mg on day 1 followed by 75 mg/day for
up to 1 year plus aspirin 75–325 mg once daily.
 For patients undergoing primary PCI,
• Use 300–600 mg loading followed by 75 mg/day plus
aspirin 81 mg once daily.
27

Thienopyridines….new but high bleeding
risk
 Prasugrel.
 For patients undergoing PCI, give 60 mg loading dose
followed by 10 mg daily; continue for at least 12 months.
 Ticagrelor.
 For patients undergoing PCI or ischemia-guided
management, give ticagrelor 180 mg loading, followed by 90
mg BID for at least 12 months. After 1 year, administer 60
mg BID.
 Cangrelor.
 Initiate 30 mcg/kg IV bolus before PCI followed by 4
mcg/kg/min IV infusion for duration of PCI or 2 hours,
whichever is longer. To maintain platelet inhibition after
infusion, initiate oral P2Y12 treatment.
28

Glycoprotein (GP) IIb/IIIa receptor
inhibitors.
 Do not give GPIs to STEMI patients who will not undergo
PCI.
 If UFH is selected for primary PCI in STEMI, add GPIs
 to UFH (in addition to a thienopyridine and aspirin)
 to reduce likelihood of reinfarction for patients not given
fibrinolytics.
 Abciximab 0.25 mg/kg IV bolus given 10–60 min before
start of PCI, followed by 0.125 mcg/kg/min (maximum 10
mcg/min) for 12 hours.
 Eptifibatide 180 mcg/kg IV bolus, repeated in 10 min,
followed by infusion of 2 mcg/kg/min for 18–24 hours after
PCI.
 Tirofiban 25 mcg/kg IV bolus, followed by an infusion of
29

Anticoagulants
 Patients undergoing primary PCI
 UFH or bivalirudin is preferred;
 In fibrinolysis,
 UFH, enoxaparin, or fondaparinux may be
administered.
30

Anticoagulants….UFH dosing
 UFH dose for primary PCI:
 50–70 units/kg IV bolus if GPI is planned and 70–
100 units/kg IV bolus if no GPI is planned;
 give supplemental IV bolus doses to maintain the
target activated clotting time (ACT).
 UFH dose for STEMI with fibrinolytics:
 60 units/kg IV bolus (max 4000 units), followed by
continuous infusion of 12 units/kg/h (max. 1000
units/h).
 Adjust to maintain target aPTT 1.5–2 times control
(50–70 s). 31

Anticoagulants… UFH dosing
32

Dosing…for others
 Enoxaparin dose for STEMI:
 1 mg/kg SC Q 12–24 hours depending on renal function.
 For STEMI patients receiving fibrinolytics, enoxaparin 30 mg
IV bolus is followed immediately by 1 mg/kg SC Q12h if < 75
years (0.75 mg/kg SC Q12h if ≥75 years).
 Bivalirudin dose for PCI in STEMI:
 0.75 mg/kg IV bolus then 1.75 mg/kg/h continuous infusion.
 Discontinue at end of PCI or continue at 0.25 mg/kg/h if
prolonged anticoagulation is necessary.
 Fondaparinux dose for STEMI:
 2.5 mg IV bolus, followed by 2.5 mg SC daily starting on
hospital day 2. 33

Nitrates
 One SL NTG tablet (0.4 mg) should be administered
every 5 minutes for up to three doses to relieve
myocardial ischemia.
 Call a physician if no response within >5 minutes after intial
dosing
 ACEIs or βBs, should not be withheld for nitrates use
because the mortality benefit of nitrates is unproven.
 IV NTG initiated in all ACS with persistent ischemia,
HF, or uncontrolled high BP in the absence of CIs.
 IV NTG continued for approximately 24 h after ischemia
relieved
 The most significant adverse effects of nitrates are 34

β-Blockers
 A βB should be administered early in the care of
patients with STE ACS and continued indefinitely.
 Early administration of a βB within the first 24 hours
of hospitalization in patients lacking a
contraindication is a quality care indicator.
35

β-Blockers
 β1- blockade produces a reduction in heart rate,
myocardial contractility, and blood pressure,
 decreasing myocardial oxygen demand.
 the reduction in heart rate increases diastolic time,
thus improving ventricular filling and coronary artery
perfusion
 βBs reduce the risk for recurrent ischemic, infarct size,
risk of reinfarction, and occurrence of ventricular
arrhythmias in the hours and days following MI
36

β-Blockers
 although initiating IV followed by oral βBs early in the
course of STEMI was associated with a lower risk of
reinfarction or ventricular fibrillation,
 there may be an early risk of cardiogenic shock, especially in
patients presenting with pulmonary congestion or systolic
blood pressure <120 mm Hg.
 the use of βBs, particularly when administered IV,
should be limited to patients who are hemodynamically
stable and who do not demonstrate any signs or
symptoms of decompensated heart failure.
37

β-Blockers
 A βB is not appropriate for patients who present with
decompensated HF,
 But initiation of βBs can be attempted before hospital
discharge in most patients following treatment of acute
HF.
 βBs with ISA may increase Myocardial oxygen
demand, should be avoided.
38

BB…
 Target resting HR is 50–60 beats/min; initial IV
therapy may be omitted, if appropriate.
 Metoprolol 5 mg by slow (over 1–2 min) IV bolus,
repeated Q 5 min for a total initial dose of 15 mg;
follow in 1–2 hours by 25–50 mg orally every 6 hours.
 Propranolol 0.5–1 mg slow IV push, followed in 1–2
hours by 40–80 mg PO every 6–8 hours.
 Atenolol 5 mg IV dose, followed 5 min later by a
second 5 mg IV dose, then 50–100 mg PO daily
beginning 1–2 h after the IV dose.
 For at least 3 years for normal EF, indefinitely if
39

Calcium Channel Blockers
 Administration of CCBs in the setting of STE ACS is
reserved for patients who have contraindications to
βBs and is given for relief of ischemic symptoms.
 In patients prescribed CCBs for treatment of
hypertension who are not receiving βBs and who do
not have a contraindication to βBs, the CCB should be
discontinued and a βB initiated.
 Nifedipine should be avoided because it has
demonstrated reflex sympathetic activation,
tachycardia, and worsened myocardial ischemia. 40

CCBs
Guideline
Recommendations
Contraindication
s
Dose and Duration of
Therapy
NSTE-ACS class I for
patients with ongoing
ischemia who are already
taking adequate doses of
nitrates and βBs or in
patients with CIs to or
intolerance to βBs
(diltiazem or verapamil
preferred during initial
presentation if EF >
40%).
NSTE-ACS, class IIb
recommendation for
diltiazem for patients with
Pulmonary
edema, evidence
of LVD, SBP< 100
mm Hg, PR
segment to >0.24
seconds 2 or 3-
degree AV block
for verapamil or
diltiazem, pulse
rate <60
beats/min for
diltiazem or
verapamil
Diltiazem 120-360 mg
sustained release
orally once daily.
Verapamil 180-480 mg
sustained release PO
daily.
Amlodipine 5-10 mg
PO daily.
Continue as indicated
to manage angina,
HTN, or arrhythmias.
41

Early pharmacotherapy for NSTE-
ACS
 Generally similar to that of STEMI
 all patients with NSTE-ACS should be tted in the ED
with
 Morphine PRN in refractory patients
 IN Oxygen (if O2 saturation <90)
 sublingual ± IV NTG (IV in selected patients )
 DAT (Aspirin with P2y12 inhibitors)
 Anticoagulant (UFH or enoxaparin/fondaparinux/bivalirudin)
 PO β-blocker (in ED, within first 24 h) (IV in selected pnts)
 High-risk patients should proceed to early angiography and
may receive a GPI (optional with either UFH
or enoxaparin but should be avoided with bivalirudin). 42

Fibrinolytic Therapy
 is not indicated in any patient with NSTE-ACS
 because increased mortality has been reported with
fibrinolytics compared with controls in clinical trials in
(patients with normal or ST-segment depression
ECGs).
43

Aspirin
 Reduces the risk of death or developing MI by about
50% (compared with no antiplatelet therapy) in
patients with NSTE-ACS.
 Therefore, aspirin remains the cornerstone of early
treatment for all patients with ACS.
 Dosing of aspirin for NSTE-ACS is the same as that
for STEMI.
44

Anticoagulants
 Choice of anticoagulant in NSTE-ACS is guided by
risk stratification & initial treatment strategy, either
early invasive approach with early coronary
angiography & PCI or early ischemic-guided with
angiography in selected pnts
 Early invasive strategy, UFH, enoxaparin,
fondaparinux, or bivalirudin should be administered
 In initial ischemia-guided (ie, not anticipated to receive
coronary angiography and
revascularization): enoxaparin, UFH, or low-dose
fondaparinux is recommended.
 Fondaparinux is equivalent to enoxaparin with less
45

Anticoagulants
 UFH 60 units/kg IV bolus (max. 4000 units), followed
by a continuous IV infusion of 12 units/kg/h (max.
1000 units/h); titrate to maintain aPTT between 1.5
and 2 times control.
 Duration: continued for
 up to at least 48 hours for UFH,
 until the patient is discharged from the hospital (or 8
days, whichever is shorter) for either enoxaparin or
fondaparinux, or
 until the end of PCI or angiography procedure (or
up to 72 hours following PCI for bivalirudin). 46

P2Y12 Inhibitors
 In patients with initial ischemia-guided approach,
either clopidogrel (300–600 mg loading dose
followed by 75 mg daily) or ticagrelor can be used
in addition to low-dose aspirin for 12 months,
 If invasive management selected,
clopidogrel, prasugrel, or ticagrelor can be used
following PCI for at least 12 months
47

Glycoprotein IIb/IIIa Receptor
Inhibitors.
 Role of GPI is diminishing as P2Y12 is used earlier
in therapy, and bivalirudin is selected more
commonly as the anticoagulant received in early
intervention.
 For low-risk patients with conservative management
strategy, no role for routine GPIs as the bleeding risk
exceeds the benefit.
 For initial conservative strategy was selected but
experienced recurrent ischemia (chest discomfort and
ECG changes), HF, or arrhythmias after initial medical
therapy necessitating a change in strategy to
angiography and revascularization, a GPI may be
48

Nitrates
 Similar indication and dose recommendation to STE
ACS
 BBs
 Recommendations are similar to STE ACS
 Calcium Channel Blockers
 Should not be administered to most patients.
 Agent selection and indication for NSTE-ACS is
identical to STEMI
49

SECONDARY PREVENTION FOLLOWING
MI
50

SECONDARY PREVENTION FOLLOWING
MI
 The long-term goals following MI are as follow:
1. Control modifiable CHD risk factors
2. Prevent development of systolic heart failure
3. Prevent recurrent MI and stroke
4. Prevent death, including sudden cardiac death
51

Late hospital care/secondary prevention
agents for both types of MI
52
All patients (ABAS)
1. Antiplatelet (ASA indefinitely +P2Y12 inhibitors ≥ 12
months)
2. BBs (within 24 hours of ED visit) indefinitely if no CI
3. ACEIs/ARBs
4. Statins (high-intensity)
5. NTG PRN
On selected pnts
1. Aldosterone antagonists
2. Clopidogrel
3. warfarin

SECONDARY PREVENTION FOLLOWING MI
 For all ACS patients, treatment and control of
modifiable risk factors, such as HTN, dyslipidemia,
and DM, are essential.
 Pharmacotherapy that has been proven to decrease
mortality, HF, reinfarction, or stroke should be initiated
prior to hospital discharge for secondary prevention.
 following MI from either STE or NSTE ACS, patients
should receive indefinite tt with aspirin, a βB, &
ACEI.
 Selected patients also should be treated with long-
term warfarin anticoagulation.
53

Aspirin
 Aspirin ↓s risk of death, recurrent MI, & stroke
following MI.
 Aspirin prescription at hospital discharge is a quality
care indicator in MI patients
 Aspirin should be given indefinitely to all patients, or
clopidogrel to patients with a contraindication to
aspirin
 After initial dose of 325 mg, chronic tt be 75 to 81
mg/d
 Major bleeding risk from chronic aspirin therapy is
approximately 2% and is dose related.
 Other GI disturbances, including dyspepsia and
54

Anticoagulants
 Warfarin should be considered in selected patients
following an ACS,
 patients with an LV thrombus,
 patients demonstrating extensive ventricular wall-
motion abnormalities on cardiac echocardiogram,
and
 patients with a history of thromboembolic disease or
chronic atrial fibrillation.
55

βBs, Nitrates, and CCBs
 Following an ACS, all patients should receive a βB
indefinitely unless contraindicated or intolerant
 Benefit from βBs maintained for ≥≥6 years following
MI.
 βBs with intrinsic sympathomimetic activity are
generally not recommended (e.g., pindolol and
acebutolol).
 βBs should be avoided in decompensated heart failure
 initiation of βBs prior to hospital discharge is safe in
these patients once HF symptoms have resolved
 If CI to βBs, CCB be used to prevent angina
symptoms but should not be used routinely in z
56

57
TABLE: Evidence-Based β-blockersc therapy for STE and NSTE ACS
Recommendation Contraindications Dose and Duration
- STE MI and
NSTE ACS, class
I recommendation
for oral BBs in all
patients without
contraindications
in the first 24 hrs,
class IIa for IV
BBs in HTN
patients
- PR ECG segment
>0.24 sec,
- 2nd degree or 3rd
degree AV heart
block
- HR < 60 beats per
min Systolic BP <
90 mm Hg
- Shock
- Left ventricular
failure with
congestive HF
- Severe reactive
airway disease
- Target resting HR of 50–60 beats/min
- Metoprolol 5 mg slow IV push (over 1 to 2
min), repeated Q 5 min for a total of 15 mg
followed in 1 to 2 hours by 25 to 50 mg by
mouth Q 6 hours; if a very conservative
regimen is desired, initial doses can be reduced
to 1 to 2 mg
- Propranolol 0.5 to 1 mg IV dose followed in
1–2 hours by 40–80 mg by mouth Q 6 to 8
hours
- Atenolol 5 mg IV dose followed in 5 min by a
second 5 mg IV dose for a total of 10 mg,
followed in 1 to 2 hours by 50 to 100 mg by
mouth once daily
- Alternatively, initial IV therapy can be omitted

58
TABLE: Evidence-Based CCB therapy for STE and NSTE ACS
Clinical Recommendation Contraindications Dose and Duration
- STE MI class IIa recommendation
and NSTE ACS class I
recommendation for patients with
ongoing ischemia who are already
taking adequate doses of nitrates and
BBs or in patients with
contraindications to or intolerance to
BBs (diltiazem or verapamil
preferred during initial presentation)
- NSTE ACS, class IIb
recommendation for diltiazem for
patients with AMI
- Pulmonary edema
- Evidence of LVD
- Systolic BP< 100 mm
Hg
- PR ECG segment >0.24
sec
- 2nd or 3rd degree AV
heart block for
verapamil and
diltiazem,
- pulse rate < 60 beats per
min for diltiazem or
verapamil
Diltiazem 120–360 mg
sustained release orally
once daily
Verapamil 180–480
mg sustained release
orally once daily
Nifedipine 30–90 mg
sustained release orally
once daily
Amlodipine 5–10 mg
orally once daily
Continue indefinitely if
CI to oral βB persists

ACEIs/ARBs
 Benefit of ACEIs may be related with their ability to
prevent cardiac remodeling.
 The largest reduction in mortality is observed for
patients with LV dysfunction (low LVEF) or HF
symptoms.
 Because the benefits of ACEI administration have been
documented for up to 12 years following therapy for 2 to 4
years post- MI in patients with LV dysfunction, administration
should continue indefinitely.
 Angiotensin Receptor Blockers
 Candesartan & valsartan shown to improve clinical
outcomes in HF 59

Dose recommendations of ACEIs & ARBs
in MI
 Initiate ACEIs within 24 hours of presentation to
hospital.
 Captopril 6.25–12.5 mg initially; target dose 50 mg 2–3 times
daily.
 Enalapril 2.5–5 mg initially; target dose 10 mg BID.
 Lisinopril 2.5–5 mg initially; target dose 10–20 mg/daily.
 Ramipril 1.25–2.5 mg initially; target dose 5 mg BID or 10
mg/daily
 Trandolapril 1 mg initially; target dose 4 mg/daily.
 Use ARBs for patients intolerant to ACEIs.
 Candesartan 4–8 mg initially; target dose 32 mg/daily.
 Valsartan 40 mg initially; target dose 160 mg BID. 60

Aldosterone Antagonists
 Aldosterone causes vascular & myocardial fibrosis,
endothelial dysfunction, HTN, LV hypertrophy,
electrolyte abnormalities, & arrhythmias
 Consider eplerenone or spironolactone within 2
weeks following MI in certain patients
 those already receiving ACEI with EF < 40% & HF
symptoms or DM
 Dose: Eplerenone 25 mg initially; target dose 50 mg/daily.
• Spironolactone 12.5 mg initially; target dose 25–50
mg/daily.
 Monitor K+ … especially patients with renal
dysfunction 61

Lipid Lowering Agents
 Patients with CAD have LDL cholesterol:
 LDL cholesterol goal < 100 mg/dL
• < 70 mg/dL: optional goal
 All ACS patients should receive a statins:
 Simva-, atorva-, lova-, fluva-, prava-, rosuva-statin
 Statins have anti-inflammatory & anti-thrombotic
properties
 lipid lowering therapy at discharge is a quality care indicator
 High-intensity statins preferred following MI
regardless of LDL cholesterol level.
 (atorvastatin 80 mg or rosuvastatin 40 mg once daily) 62

Non-pharmacologic Therapy
 Primary Percutaneous Coronary Intervention (PCI) is
the treatment of choice for reestablishing coronary
artery blood flow when the patient presents within 3
hours of symptom onset.
 Coronary Artery By-pass Grafting (CABG): This
surgery involves an artery or vein from the patient
being implanted to bypass narrowing or occlusions on
the coronary arteries.
63

Primary PCI for STEMIs
 Early reperfusion therapy with primary PCI of the
infarct artery within 90 minutes of first medical contact
is the reperfusion treatment of choice for patients
presenting with STEMI who present within 12 hours of
symptom onset.
 For primary PCI, undergoes coronary angiography
with
 either balloon angioplasty or placement of a bare
metal or drug-eluting intracoronary stent in the
artery associated with the infarct.
64

Primary PCI for STEMIs
 Primary PCI may be associated with a lower mortality
rate than fibrinolytics,
 Why? (possibly because 90% of occluded infarct opened
with PCI vs fewer than 60 in fibrinolytics; ICH & major
bleeding risk is lower in PCI than fibrinolytics)
 better side effect profile: reduces risk of major bleeding,
intracranial hemorrhage (ICH) than fibrinolysis
65

PCI in NSTE-ACS
 Whether an early invasive strategy reduces the risk of
CV or total mortality remains to be established For
NSTE-ACS
 Recent practice guidelines recommend early invasive
(within 24 hours) strategy with interventions,
including left heart catheterization, coronary
angiography and revascularization with either PCI or
CABG surgery
 NSTE-ACS with elevated risk for death or MI, including
those with a high risk score or patients with refractory
angina, acute HF, other symptoms of cardiogenic shock, or
arrhythmias
 symptoms refractory to pharmacotherapy and patients with
66