Acute Coronary Syndromes (ACS)

Mohammed El-Sakkar
MSc (Pediatrics), MD, PhD (Pharmacology)
Consultant in Allergy and Immunology
Professor of Pharmacology
ILOs: By the end of this lecture the students must be able to
Describe pathophysiology of Acute coronary syndrome (ACS)
Describe Spectrum of Acute Coronary Syndromes (ACS)
Discuss Desired Outcomes in ACS
Classify TIMI Risk Score (TRS) for UA/NSTEMI
Describe Approach to UA/NSTEMI (NSTE-ACS)
Describe ST-segment elevation MI (STEMI)
Discuss Antiplatelet Agents
Describe Classical blood coagulation pathway and effects of anticoagulant drugs
Discuss Fibrinolytic (thrombolytic) therapy New abbreviations:
Discuss Anti-Ischemic and other Treatment for ACS HIT heparin-induced thrombocytopenia
Describe Risk factors and lifestyle modifications IVB intravenous bolus
Discuss Prognosis of ACS ICH Intracranial haemorrhage
PUD peptic ulcer disease
CPR Cardiopulmonary resuscitation
BK bradykinin
cTnI cardiac Troponin I
DAPT (Dual antiplatelet therapy)
 Acute coronary syndrome (ACS)
Unstably
(A)
(B) protein Unstable atherosclerotic
Platelet (Plt)Ingraft
gstem plaque w/ a larger lipid
adhesion to

É
core, and a thin fibrous cap
collagen and vWF composed of a single layer
in fissured plaque of smooth muscle cells w/
Ò release ADP/ a fissure or rupture.
TXA2.
Thromboxane A2 (TXA2) is a type of
thromboxane that is produced by
activated platelets during hemostasis
overtime whatnappe
and has prothrombotic properties: it
organization
waken
stimulates activation of new platelets
as well as increases platelet
aggregation. ofthrong
(D)

1,1in
s
(C)
Platelet activation Ò
pi
anti
Tibrin
anticoagulant
If endogenous
anticoagulant proteins fail
VC + Platlet to stop this process,
plattet platelet aggregation
T.gg
aggregation. iafgtIut
GP IIb/IIIa receptors
of Plt cross-links
A BAEK
I
continues and thrombin
(IIa) converts fibrinogen
platelets to each 035 sofibrin Ò stabilizes the
to
other via fibrinogen clot Ò occlusive
bridges. thrombus (sx of ACS).
 Spectrum of Acute Coronary Syndromes (ACS)

Dx Unstable
o
NSTE-ACS
Non-ST-segment elevation MI ST-segment elevation MI
O
Angina (UA) (NSTEMI) 70% majority
O OF
(STEMI) 38%
Flow-limition (mismatch O2
supply vs demand) I
Subtotal d/t stable plaque, VC, embolism, arteritis
t inflames
Total (Thrombus)
abstraction
History Ii
Angina new-onset, crescendo or at rest; >10 min Angina at rest
ECG ± ST depression and/or new T-wave inversion ST elevations

o O
Ote
Troponin cTnI (w/in 6 h) - ++ +++
O MIF
Entry criteria § Ischemic pain on exertion and at rest w/in past
24 h. acting
§ ≥2 contiguous leads ≥ 0.1
mV new deviation (≥ 0.2
§ with evidence of CAD (ST segment deviation or mV in leads V2-V3)
Å marker) § or New LBBB
Risk factors for ACS:

Non-modifiable Modifiable
§ Age (median 68 y) § Smoking tobacco,
male
§
§
§
Gender (♂: ♀ 3:2 ratio)
FHx of premature coronary artery dis,
Personal h/o CAD,
§
§
Dyslipidemia,
Renal insufficiency
fifty
§ Malnutrition (x2 ↑risk for all-cause death)

§ DM,
§ HTN,
§ Abdominal obesity,
§ Sedentary lifestyle,
§ Diet low in fruits and vegetables,
§ Psychosocial stressors,
§ Cocaine use can cause STEMI regardless
of risk factors.
§ COVID-19 attattime
E
 Desired Outcomes in ACS

Short-term Long-term
1) Immediate reperfusion i.e., opening occluded coronary artery Ò § Prevent additional CV events e.g.
o prevent infarct expansion (in case of MI) (“time is muscle”) reinfarction, stroke, and HF
§ Improve quality of life.

Ot
o prevent complete occlusion and MI (in UA);
(2) Prevent sudden death and other MI complications;
(3) Relief of ischemic chest discomfort;

o
(4) Prevent coronary artery re-occlusion;
(5) Resolution of ST-segment and T-wave changes.
É Tools:
§ Control of CV risk factors
§ Aspirin (81 mg/day)
adenosine
§ P2Y12 inhibitor
§ β-blockers

cutfibrin § Statins
Tools:
not § ACEI

ID
§ Reperfusion w/ PCI or CABG or fibrinolytics. dualantiplatlet
§ Ô Thrombus expansion using Aspirin + P2Y12 (ADP) receptor Inhibitors +
§ ARAs

Injectable anticoagulants.
§ O2 + SL NTG ± IV Morphine sulfate
 gets
Enoxaparin (SC) Intrinsic pathway Classical blood coagulation
Extrinsic pathway LMWH
Dalteparin (SC) (Surface contact) pathway
(Damaged tissue) Fondaparinux (SC)
HMW Kininogen
Warfarin
Apixaban (PO) + (VKA)
TF NOAC Rivaroxaban (PO) Antithrombin III Prekalikrein, FXIIa
FVII FVIIa +TF Edoxaban (PO) FXIa FXI
Ca++
FIX FIXa FIXa FIX Inactive vit K Vit k reactivation Active vit K
(FVIIIa, PL, Ca++) (FVIIIa, PL, Ca++) (epoxide) cycle (Liver) (Hydroquinone)
FX FXa FX
FXIII
(FVa, PL, Ca++) Descarboxy
Thrombin (IIa) Prothrombin (FII)
(serine protease) prothrombin
Heparin
+

FILET
Antithrombin III ENOX, Delta
angiomascutting
Fibrinogen
(soluble)
Fibrin
monomer
Dabigatran (PO), Bivalirudin (IV),
Argatroban (IV), lepirudin (IV)
Direct thrombin
inhibitors Itffruct
FXIIIa FIFI
Plasminogen (Fibrin-bound)
Ahtisaari
Non–fibrin-specific (Streptokinase)

É
(circulating)

2
Common pathway Fibrin-specific thrombolytic (at low dose)
Endogenous
(alteplase, reteplase, Tenecteplase)
(t-PA and u-PA)
Plasmin
XL-Fibrin FDPs + D-dimer
(cross linked fibrin mesh) tindegra piasmi.g.ge
Plasmin inhibitors (Aminocaproic/Tranexamic)
 Timbolysisin MI
N
TIMI Risk Score (TRS) for UA/NSTEMI

Calculation of Risk Score

Risk Score Death/MI/urgent
Characteristic Points revascularization by 14 d

e
Historical
Age ≥ 65 y
≥ 3 Risk factors for CAD e
1
1
0-1
2
5%
8%
3 13%
(FHx of premature CAD death/events,
4 20%
intef5
HTN, Ó chol, DM, active smoker)
Known CAD (stenosis ≥ 50%) Éoradl 1
6-7
26%
41%
ASA use in past 7 days 1 0 die
Presentation
Severe angina (≥ 2 episodes w/in 24 h) 1 Higher risk Pts (TRS ≥3) Ò Ó benefit from LMWH, GP

d
ST depression ≥ 0.5 mm
(+) cardiac marker (troponin,gregeninkinase
CK-MB)
1
1
IIb/IIIa inhibitors and early angiography

RISK SCORE = Total points

o
0-7

TIMI (Thrombolysis in Myocardial Infarction)

 morphine Approach to UA/NSTEMI (NSTE-ACS)
o Nitroglycerin
I
MONA: O2 (only if O2 saturation <90%), Aspirin (162-325 mg), SL NTG, ± IV NTG, ± IV Morphine sulfate 05
intravenously
Low-risk score (TRS <3) High risk score (TRS ≥3)

É
notentericcouted cannot
the

Iijima
relive
Ischemia-guided (conservative) Strategy topmasmak Early invasive Strategy chest pain
(avoid early use of invasive procedures) Eminem (diagnostic angiography w/in 24 h) is
OO
Dual antiplatelet therapy (DAPT): ASA + P2Y12 inh
presure
Theater egg
1. Clopidogrel 300-600 mg LD, 75 mg MD or Yadenosin DAPT: ASA + P2Y12 inh
2. Ticagrelor 1. Clopidogrel (as in conservative strategy) or
+ Anticoagulant w/ either
I High risk (s/s O 2. Ticagrelor
of ischemia) or
1. IV UFH 60 U/kg IVB (max 4k U) Ò 12 U/kg/h Refractory to Rx ± GPI inaim arise.bg
selected pts ggn.m

As
(max 1K IU) aPTT 50-70 s. for 48 h or
2. SC ENOX or fondaparinux (24-48 h) Eggs
+ Anticoagulant w/ either
1. IV UFH (as in conservative strategy).
benoxaparin Yndairatactivateen orSC ENOX or fondaparinux (24-48 h)
2.
Stressinnit
test (once stabilized and before discharge) or soju
3. IV bivalirudin
Low risk pix
0
Late hospital care/2ry prevention
1. Aspirin (81 mg/day) indefinitely
250100 e 123 Medical Evaluate cath findings to
2. P2Y12 inhibitor for ≥ 12 mons

50
3. β-blockers (w/in 24 h, for ≥3 ys) was
rs
I
management e
determine either

4. High intensity statin as early as possible

Revascularization
5. ACEI 4-6wk (indefinitely in EF <40%, HTN, DM, CKD)I
o
6. ARAs (if EF <40% + either DM or s/s of HF)
 Kimi
symptom
§ Triple-vessel disease,
Revascularization § Severe Lt main stem artery stenosis, or

if
§ Lt main equivalent dis (ie, ⩾70%
stenosis of LAD and proximal LCA)—
PCI decided CABG decided espec, if LV function impaired

DAPT: ASA + P2Y12 inh either

Elective Urgent
1. Ticagrelor (pref than Clopid) 180 mg LD, 90 mg bid MD T

8
2. Clopidogrel (LD 600 mg x1 PO prior Ò MD 75 mg after)
3. Prasugrel LD 60 mg Ò MD 10 mg (w/in 1h of PCI) § Continue ASA, § Continue ASA,
4. Cangrelor (IVB prior Ò IV infusion during PCI)

E
§ Stop Clopidogrel or § Stop Clopidogrel or Ticagrelor

E
to
± GPI in pts receiving UFH (not w/ bivalirudin) and no Ticagrelor 5 d before 24 h before
adequate Tx w/ P2Y12 inh) § Stop Prasugrel 7 d before § Stop Eptifibatide/tirofiban 2-4
+ h before
Anticoagulants (for 48 h or the end of PCI) § Stop abciximab ≥ 12 h before
1. IV UFH (50-100 U/kg IVB Ò boli to aPTT 250-350s if w/out
GPI, or 200-250s if w/ GPI) or + Jpn
2. SC ENOX or fondaparinux (w/ UFH) or
3. IV bivalirudin (stop UFH 30 mins before its administration) § Continue IV UFH,
§ Discontinue:
1. SC ENOX or fondaparinux 12-24 h after CABG.
O
P PCI
2. IV bivalirudin 3 hs before

Medical
P CABG
management
 rows
r/o mimics e.g. acute aortic
ST-segment elevation MI (STEMI)
Ingen
dissection or acute PE

MONA: O2 (only if O2 saturation <90%), Aspirin (162-325 mg), SL NTG, ± IV Morphine sulfate

PCI Capable Facility Non-PCI Capable Facility

§ Immediate transfer to PCI w/in
120 min if cardiogenic shock or

To
Fibrinolysis w/in 30 min of
DAPT : ASA + P2Y12 inh (same dose as in PCI) failed fibrinolysis arrival (w/in 12-24 h of onset
1. Ticagrelor

for
2. Prasugrel e
§ Transfer for PCI w/in 3-24h after
successful lysis in stable Pts
of sx)
+
± GPI in pts receiving UFH and P2Y12 inhibitor
+ DAPT: ASA + Clopidogrel (as
Anticoagulant (during PCI) either 2050 350s in conservative strategy)
1. IV UFH (same dose as in PCI) OR
2. IV bivalirudin +
Anticoagulant either
Late hospital
care/2ry prevention 1. IV UFH (as in conservative
1. Aspirin (81 mg/day) indefinitely strategy).
Primary PCI (FMC, 2. P2Y12 inhibitor for ≥ 12 mons 2. ENOX or fondaparinux: IVB,
first medical contact 3. β-blockers (w/in 24 h, ≥3 ys) then SC (during hospitalization, or
-device w/in 90 min) 4. High intensity statin early until revascularization)
w/in 12h of sx onset 5. ACEI 4-6wk (indefinitely in EF <40%, HTN, DM, CKD)
6. ARAs (EF <40% + DM or HF)
 Aspirin
Recommendations:
§ NSTE-ACS: all Pts :50-70% Ô Death/MI.
§ STEMI: all Pts (23% Ô Death and MI)
§ Long-term post-ACS: 81 mg daily indefinitely

Contraindications:

o e
§ Hypersensitivity (If allergy, use clopi and/or desensitize to ASA).
§ Active bleeding,

Dose and Duration of Therapy:

§ Hospital day 1 Ò 160-325 mg PO once (non-enteric-coated, chewable, avoid enteric
coated) as soon as possible after onset of sx. Even if the Pt takes an aspirin daily.
§ Hospital day 2 Ò 81-162 mg qd orally indefinitely (81 mg preferred).
§ Limit dose to <100 mg if used w/ ticagrelor.

D tyY HIcardiovascular events and bleeding.

Following MI, the use of NSAIDs ass w/ ↑ rates of
N.B. Celecoxib and meloxicam have the lowest rates.
Tangerines
 Longterm
P2Y12 (ADP) receptor Inhibitors (choose one of the following in addition to ASA)

c/w
Clopidogrel (oral) Prasugrel (oral)
o Rapid (~30 min)
Ticagrelor (oral)
§ As prasugrel.
If
Cangrelor (IV)
Used only during PCI
clopidogrel o Greater plt inhib. § Use only w/ ASA
o Less intersubject <100 mg qd (its

E
response variability effects Ô w/ higher
o Higher bleeding doses).
Indications NSTE-ACS: § Only during PCI. § PCI (preferred § IVB prior to PCI,
o Medically treated § Only for Pts w/ than clopidogrel). then IV infusion
o If PCI Ò given hrs before known coronary § Medically treated during PCI or for 2 h,

STEMI: O
o If CABG Ò d/c 5 d before artery anatomy (to
avoid use in Pts
NSTE-ACS Pts

O
§ If CABG Ò d/c 5 d
whichever longer.
§ To maintain plt
o If Lysis Ò Ó in potency, Ô
mortality, no D in major
needing CABG, d/c 7
d prior if used). O before inhibition after
infusion, initiate oral
bleeding or ICH. P2Y12 inhibitor.
Contraindi § Active bleeding § Same § Same + § Same

OD
cations: § Pts w/ h/o TIA or stroke (Ó § Severe hepatic § Don’t give clopi or
risk of bleeding). impairment, prasugrel during

AEs:
I
§ Use PPIs if h/o GI bleeding
§ Avoid LD if Pt ≥ 75 y waging § Ó freq of dyspnea
infusion of cangrelor
§ High frequency of
§ Morphine delay its absorptio § Ventricular pauses bleeding in elderly
decrease movement
i ntestine
 Glycoprotein IIb/IIIa receptor inhibitors (GPI) when top
given
Indications:
§
heparin Knut
gj.j
witnistadeq high
risk
Ftroponin
Ô Death/MI when added to ASA + clopi in Pts undergoing PCI (esp. in Pts who have aDiabet
qq.gg
Ii
large coronary thrombus). yup
§ No clear benefit for starting GPI prior to PCI and Ó risk of bleeding.
§ No indication in lysis.

§ Efficacy monitored by s/s of recurrent ischemia.

Adverse effects:
§ Thrombocytopenia
§ Bleeding (esp at catheter insertion site).
phasedadjustment
Abciximab, Eptifibatide, Tirofiban w/ same efficacy and bleeding risk

STEMI PPC
If
Eptifibatide and tirofiban require dose adjustments in renal insufficiency.

Enoxaparingbivalirudingfond gun
NSTEearly
invasive
strategy enoxapringfondaparinux nobivalirudin
 Injectable Anticoagulants d
NSTEACSischemia
guided
strategy

I
Unfractionated heparin Enoxaparin (ENOX, Fondaparinux Bivalirudin (Direct
LMW heparin) (Indirect FXa inhibit) thrombin inhibitor)
Prop- Monitored by 8 58
§ More predictable § less bleeding risks § Ass w/ Ô bleeding
erties
c/w
§ aPTT
§ Plt count
today antithrombin effect than ENOX
§ Better safety profile. § higher catheter-
c/w UFH ± GPI or
ENOX.

P
UFH § Inability to monitor related thrombosis § If prior UFH given,
anticoagulation. during PCI. \ d/c UFH for 30 min
§ Longer t½ than UFH supplement w/ UFH before initiating
Ò Ó risk of bleeding if PCI. bivalirudin.

I
if switch b/w enox § Use instead of UFH § Use instead of UFH
and UFH if HIT (no cross react if HIT.
§ SC injection, dosing w/ HIT abs)
based upon body wt
Uses NSTE-ACS: Ô Death/MI.
§ During ischemia or early invasive P P Early invasive only
§ During PCI. P P P
STEMI:
§ Ó coronary a. patency if used w/ P P ̶
fibrin-specific fibrinolytic.
§ During PCI ̶ ̶ P
 Unfractionated heparin Enoxaparin (ENOX, Fondaparinux Bivalirudin (Direct
LMW heparin) (Indirect FXa inhibit) thrombin inhibitor)
Contrain § Active bleeding, severe § Same as UFH § Active bleeding, § Active bleeding,
dications bleeding risk § if CABG surgery severe bleeding § Bleeding disorders
§ Recent stroke planned risk. § Severe HTN.
§ History of HIT.m
§ Ô dose in CrCl <30 mL/min
§ Ô dose in
o CrCI 15-30 (once
(Ó risk of bleeding). instead of bid)
o Age >75 ys
§ Avoid if CrCl <15 § Avoid in CrCl <20 § Avoid in CrCl <30
mL/min (UFH prefer) mL/min mL/min

Side Effects of Unfractionated heparin: at

5poor
0
2. Heparin-induced D
1. Hemorrhage (neutralized by protamine sulfate).
thrombocytopenia (HIT): serious IgG-mediated
reaction Ò irreversible plts aggregation (d/c heparin Ò use
fondaparinux or direct thrombin inhib e.g. Biva, Argatroban, lepirudin).
3. Heparin-induced Thrombocytopenia and Thrombosis (HITT): HIT
00
progress to venous/arterial thromboses. \Platelet counts should be
performed frequently.
4. Long term use ass. w/ osteoporosis.
 GFR % of Chronic Kidney Disease Function Estimated GFR by Age Group
Stage Severity % Function Dosing of anticoagulant acc to stages Age Mean Estimated GFR
2
(mL/min/1.73 m )
Stage 1 Normal - Mild 90%-100%
20-29 116
Stage 2 Mild 60% - 89%
30-39 107
Stage 3(a) Mild to Moderate 45% - 59% Adjust dose Rivaroxaban (2/3 dose)
40-49 99
Stage 3(b) Moderate to Severe 30% - 44%
50-59 93
Stage 4 Severe 15% - 29% Avoid: Fondaparinux, Bivalirudin

É
Adjust dose (Ô): 60-69 85

stages to g § Enoxaparin or dalteparin 70+ 75

§ Dabigatran (1/2 dose), Edoxaban (adjust),

Stage 5
t
Kidney Failure
tsp
<15% or
Apixaban (1/2 dose), Rivaroxaban (2/3 dose)

Avoid:
dialysis § Enoxaparin

s X
§ Apixaban, Edoxaban, Rivaroxaban

§ Normal range of Kidney GFR is 100-130 mL/min/1.73m2 in ♂ and 90-120mL/min/1.73m2 in ♀ < age of 40.
§ GFR decreases progressively after age of 40 y.
Creatinine Clearance Calculator
Estimate glomerular filtration rate (GFR)

(https://clincalc.com/Kinetics/CrCl.aspx)

É
 Fibrinolytic (thrombolytic) therapy

§ Indications:
o Acute STEMI (not NSTEMI) w/in 12 h of onset of chest pain (w/in 30 min of Pt’s arrival
at hospital), if no PCI capable facility, and no contraindication.
o
§ Less effective than PCI bec of ↑ microvascular obstruction may be due to hemorrhagic
transformation and vascular injury during ischemia.

Absolute contraindications to Fibrinolysis Relative contraindications

§ Any prior ICH § H/o severe uncontrolled HTN on presentation
§ Intracranial neoplasm, aneurysm, AVM aprignfmnt.my (SBP >180 or DBF >110)
§ Ischemic stroke or closed head trauma w/in 3 § CPR >10 min; trauma or major surgery w/in 3 wk
mo § Recent internal bleed (w/in 2-4 wk); active PUD
wards
§ Active internal bleeding or known bleeding § Non compressible vascular punctures peptic

Oi
diathesis § Prior Streptokinase exposure (if considering SK)
§ Suspected aortic dissection § Pregnancy
§ Current use of anticoagulants
AVM Arteriovenous malformation, CPR Cardiopulmonary resuscitation
§ ICH is a risk ass w/ thrombolytic therapy. It can result in death or disabling stroke, primarily
in elderly and Pts w/ previous stroke w/in 3 mon.

§ Comparison:
Non–fibrin-specific Fibrin-specific
Streptokinase Alteplase Reteplase Tenecteplase
(rt-PA) (rPA) (TNKase)
Fibrin-specificity No (Ó bleeding) High Less fibrin-spec cw More fibrin-specific
(Bleeding, ICH) (Ô bleeding) t-PA (Ô bleeding) cw t-PA (Ô bleeding)
Other properties § Recent/past use or Intermediate t½ longer t½ Long t½

p tr
strept infxn (strept No hypotension No hypotension No hypotension
st

y
Abs Ô activity)
§ Allergic reaction
§ Transient HToN
bradykinin
(plasmin Ò Ó BK)
Dosage single IVI 1.5 MU in
p 30-60 min
y
15 mg IVB Ò IVI
0.75 mg/kg in 30
IVB double dose,
10 U X 2 (30 min
single IVB, 30–50
mg based on
Gratton min Ò IVI 0.5
mg/kg in 60 min
apart)
each over 2 min
weight
 Anti-Ischemic and other Treatment for ACS
Oxygen
Indications:
Only to Pts w/
§ O2 saturation <90%,
§ respiratory distress,
§ high risk features of hypoxemia
N.B. routine use of O2 in cardiac Pts may Ò coronary VC and Ó risk of mortality

Antiplatelet therapy

Indications:
notentericcoated
§ Chewable, non-coated, aspirin 324 mg to all Pts unless contraindicated.
dose162 325 180 mg
loadingmg or Ticagrelor
§ If contraindicated Ò LD Clopidogrel 300-600

FA spirinallergic or Glintolerance
 Nitroglycerin
Indications:
NSTE-ACS (SL, PO, topical or IV): Ô angina sx, no Ô in mortality.
STEMI (SL or IV): may Ô mortality, relief of sx, control BP, Rx of HF.
Long-term post-ACS: if symptomatic Ò sublingual NTG prn for all
Contraindications:
§ HoTN
§ Recent use of PDE inhibitors (Sildenafil/vardenafil w/in 24 h or Tadalafil w/in 48 h).
§ Extreme caution in sx of RV infarcts

Dose and Duration:

0 9
§ Pts w/ ongoing sx Ò 0.4 mg SL every 5 min up to 3 doses or sx relieved.
§ If persistent s/s or HF or HTN Ò 10 µg/min IV infusion titrated to 100 µg/min until
o Relief of sx OR

A
o Limiting AEs: headache, SBP <90 mmHg or >30% below starting mean arterial BP if
hypertensive. Hr
I Ask 05
ggqjg.gg and
qgngfilnggthig
 or il win 8
β-Blockers
Indications:
Ecb sterapamil

0
NSTE-ACS: should be started w/in 24 h after presentation if (ongoing pain, or HTN) + no s/s
of HF Ò PO or IV to Ô progression to Ml
STEMI: ▪ Ô arrhythmic death or reinfarction,
▪ in 30% Ò Ó cardiogenic shock & no D in overall mortality when given early
esp. if s/s of HF present.
Longterm post-ACS: 23% Ô mortality after MI

a
Indications: contra if HR 50 BB
§ HR <50,

NÉE
§ SBP <90,
§ Decompensated HF,
§ Ó risk for or manifest cardiogenic shock,
§ 2°/3° AVB, oral
§ severe bronchospasm
In existing asthma, selection favor a short-acting agent e.g. metoprolol or the ultrashort-acting
agent e.g. esmolol.
 ACE inhibitors/ARBs if LV Fff 408
ACEIs/ARBs limit post-MI remodeling by Ô LV dilatation, hypertrophy, remodeling, and
ultimately LV dysfunction if started w/in 24 h of STEMI in stable Pt and asx LV dysfunction.
Indications:
§ NSTE-MI: should be initiated in EF <40% (and SBP > 100), HTN, DM, CKD.
§ STEMI: Ô mortality. Greatest benefit in anterior Ml, EF <40% or prior Ml
§ Longterm post-ACS: for 4-6 wk or at least until hospital discharge in all STEMI. Lifelong if
HFrEF <40%, HTN, DM, CKD.

Contraindications:
§ HoTN,
§ Bilateral renal artery stenosis,
§ Serum K >5.5 mmol/L,
§ Acute RF.

ARAs appear to be equal to ACEI

 Eplerenone ARA
§ Adjunct in stable Pts w/ HFrEF ≤40% following MI (start Rx w/in 3–14 d of event)

Calcium channel blockers

Indications:
NSTE-ACS: adjuvant to βb and nitrate or if contraindication to βbs b/c of bronchospasm
(NDCCBs preferred during initial presentation if EF > 40%).
STEMI: not recommended deltazamig Vera pam
Longterm post-ACS: not recommended
Contraindications:
§ Pulmonary edema,
§ evidence of LV dysfunction,
§ SBP <100 mm Hg,
§ 1º, 2 or 3º AV block,
§ HR <60 beats/min
 Morphine sulfate
Indications:
§ No mortality benefit.
§ Relieves pain. Ô anxiety, some venodilation Ò Ô preload, modest Ô HR and SBP.
§ Used when
o pain relief not fully achieved by maximally tolerated nitrates or
o in pul edema (judicious use recommended as may adversely affect outcomes).
platted
Contraindications: anti
babsorbtionof clopidogrel
§ HoTN,
§ Respiratory depression, especially
§ Confusion
Dose and Duration:
Slow 5-10 mg IVB during NTG Rx repeated every 5-30 min as needed to relieve sx (at rate
1-2 mg / min) w/ BP monitoring.

Statins
§ ACS: high intensity (atorvastatin, rosuvastatin).
§ Consider moderate intensity statin for Pts >75 y.
Insulin
§ Treat hyperglycemia >180 mg/dL while avoiding hypoglycemia, no clear benefit for
intensive control
§ Avoid TZDs if HF. mfuppfordigisoffee
Risk factors and lifestyle modifications (the same as in ASCVD)

Cardiac manifestations of COVID-19

Acute myocardial injury as a result of ACS, myocarditis, stress-cardiomyopathy, arrhythmias,
cardiogenic shock, and cardiac arrest.
Probable cause:
o Adrenergic drive,
o Systemic inflammatory sequelae,
o Direct infxn of myocardial and endothelial cells.

§ COVID-19 Pts who presented w/ STEMI have higher thrombus burden than those w/
STEMI in absence of COVID-19.
 Pre Po Loading dose 162325
Aspirin Pttakeitwheatherhemap ornot
P Post maintinanadose 81 indefinitely
PCIorno Pa
102412 receptorinhibitor

stem NSTEMI

Pony inPa

if pttake fibrinolytic stops AT

Age relatedbleeding

aic.IE
Clopidogrel
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