Pharmacotherapy of ACS

Pharmacotherapy of ACS
Abera J. (BPharm., MSc in Clinical Pharmacy)

School of Pharmacy, CHMS, HU.
07/08/2022 By; Abera J 1

Introduction
• Acute coronary syndromes
– Include all clinical syndromes resulting from an
imbalance between myocardial oxygen demand and
supply
– Forms of CHD & most common cause of CVD death
worldwide
– Caused by,
• The rupture of an atherosclerotic plaque
• Platelet adherence, activation, and aggregation and
activation of the clotting cascade
07/08/2022 2
Epidemiology
• Annually
– 1 million cases of ACS
– 239,000 deaths due to MI
– Approximately 7 million ED visits
• Represents 3% of all ED visits
• Most frequent reason for patient presentation:
– Chest discomfort
07/08/2022 3
Etiology
 Endothelial dysfunction Contribute for the
 Inflammation formation of atherosclerotic
coronary artery plaques
 The formation of fatty streaks
 The predominant cause (>90%)

– Atheromatous plaque rupture
– Fissuring or erosion of an unstable atherosclerotic
plaque
07/08/2022 4
Risk factors
Age (>55 years for CKD
male and > 65 for Smoking
female) Physical inactivity
Family history Obesity
HTN Stress
Hyperlipidemia Elevated
DM homocysteine level
07/08/2022 5
Pathophysiology
 Plaque rupture and clot formation
↓
 Exposure of the thrombogenic contents (collagen and tissue
factor) of the plaque to blood elements
↓
 Platelet adhesion and activation
 Promote the release of platelet-derived vasoactive
substances including ADP and TXA2
↓
 Vasoconstriction and platelet activation
07/08/2022 6
Pathophysiology…
• Platelet activation  change in the conformation of
glycoprotein (GP) IIb/IIIa surface receptors of platelets
– Cross-links platelets to each other through fibrinogen
bridges
↓
• Activation of the extrinsic coagulation cascade
• Exposure of blood components to the thrombogenic
lipid core and disrupted endothelium, which are rich
in tissue factor
↓
– Production of thrombin (factor IIa) ----- converts
fibrinogen to fibrin (stabilizes the clot and traps RBCs)
07/08/2022 7
Pathophysiology…
 Ventricular remodeling following an acute MI
Characterized by left ventricular dilation and reduced
pumping function of the left ventricle, leading to
cardiac failure
 Major contributors of ventricular remodeling are the
RAAS and the sympathetic nervous system
 HF as a result of ventricular remodeling is one of the
principal causes of mortality and morbidity following
an MI
07/08/2022 8
Complications
– Mortality----- 60%
– Cardiogenic shock-----5% to 6%
– HF, valvular dysfunction,
– Pericarditis
– Stroke secondary to LV thrombus embolization
– Venous thromboembolism
– LV free wall or ventricular septal rupture
– Ventricular and atrial tachyarrhythmias
07/08/2022 9
Classification
• Classified as STE MI or NSTE ACS (NSTE MI and UA)
according to ECG changes
• STE MI (Q-wave or transmural MI)
– Results in an injury that transects the thickness of the
myocardial wall
– Pathologic Q waves are frequently seen on ECG
– Diagnosed when Pt’s present with
• Symptoms of myocardial ischemia
• New STE with release of biomarkers of myocardial
necrosis
– Mainly troponins T or I, but also creatine kinase-
myocardial band (CK-MB)
07/08/2022 10
Classification…
• NSTE MI (non–Q-wave or non-transmural MI)
– MI limited to the subendocardial myocardium
– No pathologic Q wave on ECG
– Ischemia is severe enough to produce myocardial necrosis
resulting in the release of a detectable amount of mainly
troponins T or I, but also CK-MB
• UA
• Symptoms of myocardial ischemia
• Ischemia is not severe enough to produce myocardial
necrosis
• No biomarkers are detected
07/08/2022 11
Clinical Presentation
• Symptoms
– Classic symptom- a new onset or increasing midline
anterior chest discomfort for at least 20 minutes
• The chest discomfort may radiate to the shoulder,
down the left arm, and to the back or to the jaw
– Accompanying symptoms may include;
• Nausea or vomiting, SOB
• Diaphoresis
07/08/2022 12
Clinical Presentation…
• Signs
– No signs are classic for ACS
– Pt’s present with signs of acute HF
• JVD
• S3 sound on auscultation
• Arrhythmias
– Tachycardia, bradycardia, or heart block
07/08/2022 13
Diagnosis
• Laboratory Tests
– Biochemical markers
• Troponin I or T and CK-MB
– Measured at the time of first assessment and
repeated 6 -9 hours later
» If no positive result, 12 to 24 hours later
– Troponin- appear within 6 hours of infarction and
stay elevated for up to 10 days
– CK-MB- appear within 6 hours of infarction and
returns to normal values within 2 days
07/08/2022 14
Diagnosis…
• Laboratory Tests…
– Blood chemistry tests- potassium & magnesium
– SCr- CrCl for dosing adjustments
– Baseline- CBC and coagulation tests (aPTT and
INR)
– Fasting lipid panel
07/08/2022 15
Diagnosis…
• Other diagnostic tests
– The 12-lead ECG
• Key findings that indicate myocardial ischemia or
infarction
– ST Elevation,
– ST segment depression, and
– T-wave inversion
– Appearance of a new left bundle-branch block
accompanied by chest discomfort - highly specific for
acute MI
07/08/2022 16
Treatment
• Short-term goals
– Early restoration of blood flow to the infarct-related artery
– Prevent complete occlusion and MI (in UA)
– Prevention of death and other MI complications
– Prevention of coronary artery re-occlusion
– Relief of ischemic chest discomfort
• Long-term goals
– Control of CV risk factors
– Prevention of additional CV events including re-infarction, stroke,
and HF
07/08/2022 17
Treatment…
General approach to treatment
– Oxygen administration (if SO2 is low, less than 90%)
– Continuous multi-lead ST-segment monitoring for
arrhythmias and ischemia
– Frequent measurement of vital signs
– Bed-rest for 12 hours in hemodynamically stable Pt’s
– Pain relief (morphine)
– Nitroglycerin (SL, IV)
– Aspirin
07/08/2022 18
Non-pharmacologic Therapy
• Primary PCI for STE MI
– Balloon angioplasty or placement of a bare metal or
drug-eluting intracoronary stent in the artery
associated with the infarct
– Early reperfusion - within 90 minutes of first medical
contact for Pt who present within 12 hours of symptom
onset
– Lower mortality rate when compared to fibrinolytics
----- severe bleeding risk
07/08/2022 19
Non-pharmacologic Therapy …
 PCI is preferred during hospitalization for STE MI Pt,
When fibrinolysis is not successful,
In cardiogenic shock,
With life-threatening ventricular arrhythmias, and
With persistent rest ischemia or signs of ischemia
on stress testing following MI
07/08/2022 20
NSTE ACS
– Coronary angiography with revascularization with
either PCI or coronary artery bypass graft (CABG)
surgery
– For Pt’s at an elevated risk for death or MI, including
those with
• Refractory angina
• Acute HF
• Other symptoms of cardiogenic shock, or
• Arrhythmias
07/08/2022 21
 All Pt’s undergoing PCI should receive,
– Low-dose ASA therapy indefinitely or
– Addition of a 12 month P2Y12 inhibitor antiplatelet
(clopidogrel, prasugrel, or ticagrelor) to the ASA by
weighing the risk of bleeding with the benefit
– Use a drug-eluting stent in longer duration of P2Y12
inhibitor therapy
• Drug-eluting stents reduce the rate of smooth muscle
cell growth causing stent restenosis
07/08/2022 22
Pharmacotherapy of STE MI
• For all Pt’s with STE MI in the emergency room
– Intranasal oxygen (if SO2 is low)
– SL nitroglycerin
– ASA
– A P2Y12 inhibitor (clopidogrel, prasugrel, or
ticagrelor)
– Anticoagulation with bivalirudin, UFH, enoxaparin,
or fondaparinux
– A GP IIb/IIIa inhibitor should be administered with
UFH for Pt’s undergoing primary PCI
07/08/2022 23
Pharmacotherapy of STE MI …
– IV β-blockers and IV NTG should be given in
selected Pt’s
– Oral β-blockers should be initiated within the first day
in Pt’s without cardiogenic shock
– Morphine is administered to Pt’s with refractory
angina as an analgesic and a venodilator that lowers
preload
– An ACE inhibitor - within the first 24 hours in Pt’s
with STE MI who have either an anterior wall MI or a
LVEF ≤40%
07/08/2022 24
• Fibrinolytic Therapy
– Indicated in Pt’s with STE MI who,
• Present to the hospital within 12 hours of the onset
of chest discomfort (highest mortality benefit)
• Have at least a 1mm STE in two or more continuous
ECG leads
• Are not able to undergo primary PCI within 120
minutes of medical contact
– If ongoing ischemia- use fibrinolytics between 12 and
24 hours after symptom onset
07/08/2022 25
Pharmacotherapy of STE MI…
Fibrinolytic Therapy…
– In Pt’s who have a contraindication to fibrinolytics and
PCI, or who do not have access to a facility that can
perform PCIs
– Treatment with an anticoagulant for up to 8 days
can be administered (other than UFH)
07/08/2022 26
Contraindications for fibrinolytic therapy
07/08/2022 27
• Fibrinolytic therapy includes
• A fibrin-specific agents: alteplase, reteplase, or
tenecteplase
– Acceptable as first-line agents
• Non fibrin-specific agent: streptokinase
• A “door-to-needle time” of less than 30 minutes is
recommended
• Side effects
• ICH (higher in fibrin-specific agent)
• Major bleeding (higher in non-fibrin specific agent)
07/08/2022 28
• Aspirin
– The preferred antiplatelet agent in the treatment of
all ACSs
– Acts by inhibiting the synthesis of TXA2 through an
irreversible inhibition of platelet COX-1
– In Pt’s receiving fibrinolytics, ASA reduces mortality,
and its effects are additive to fibrinolysis alone
– In Pt’s undergoing PCI, ASA prevents acute
thrombotic occlusion during the procedure and
reduces the risk of stent thrombosis thereafter
07/08/2022 29
• Aspirin
– Initial dose: 162 - 325 mg non-enteric ASA
to achieve a rapid platelet inhibition
– Daily maintenance dose: 75 -162 mg- indefinitely
• Higher maintenance dose (300-325 mg) has a similar CV
risk reduction but higher bleeding risk than low dose (75-
162 mg)
• Side effects: dyspepsia, nausea, GI bleeding
07/08/2022 30
• Platelet P2Y12 Inhibitors
– Clopidogrel, prasugrel, and ticagrelor
– Block a subtype of ADP receptor, the P2Y12
receptor, on platelets, preventing the binding of ADP
to the receptor and subsequent expression of platelet
GP IIb/IIIa receptors, reducing platelet activation and
aggregation
– Clopidogrel and prasugrel----- bind irreversibly
– Ticagrelor - reversible, noncompetitive inhibitor
07/08/2022 31
 Clopidogrel
 For medically managed Pt’s presenting with STE MI
(no PCI or fibrinolysis)

• Initial dose: 300-600 mg oral loading dose
– Loading dose of 600 mg is recommended over
administration of 300 mg for Pt’s undergoing
primary PCI ----b/c of reduction in CV ischemic
events with the 600 mg
• Maintenance dose: 75 mg QD
– Clopidogrel added to ASA-----should be continued for
at least 14 days (and up to 1 year)
07/08/2022 32
• Increased risk of bleeding with prasugrel compared with
clopidogrel in
• Pt’s older than 75 years and those weighing less than 60
kg
• Prasugrel
– Preferred over clopidogrel in Pt’s undergoing primary PCI
for STE MI and with a history of DM
– Contraindicated in prior stroke or TIA
– Hold prasugrel 7 days before CABG while ticagrelor and
clopidegrol should be held 5 days before CABG
07/08/2022 33
• Side effects
– Clopidogrel- N/V and diarrhea (2%-5%),
thrombocytopenic purpura (rare)
– Prasugrel- N/V and diarrhea (2% to 5%)
– Ticagrelor- nausea (4%) , diarrhea (3%), dyspnea
(14%), ventricular pauses and bradyarrhythmias
(rare), increases in SCr and serum uric acid
07/08/2022 34
• Glycoprotein IIb/IIIa Receptor Inhibitors
– Block the final common pathway of platelet aggregation
• Block cross-linking of platelets by fibrinogen bridges
between the GP IIb and IIIa receptors on the platelet
surface
• Abciximab: 0.25 mg/kg bolus then 0.125-10 mcg/kg for
12 hrs after PCI
• Eptifibatide: 180 mcg/kg IV bolus 2 doses 10 min apart
then 2 mcg/kg/min for 18-24 hrs after PCI
• Tirofiban: 25 mcg/kg IV bolus followed by 0.15
mcg/kg/min 18-24 hrs after PCI
07/08/2022 35
• Glycoprotein IIb/IIIa Receptor Inhibitors…
– Beneficial for Pt’s with STE MI undergoing primary
PCI who are treated with UFH
– Not recommended in Pt’s
– Not undergoing PCI,
– Who have received fibrinolytics,
– Receiving bivalirudin--------increased bleeding
risk
07/08/2022 36
• Glycoprotein IIb/IIIa Receptor Inhibitors (3)
– Abciximab
• No dosage adjustment for renal function is
necessary
– Eptifibatide
• Contraindicated in dialysis Pt’s
• Reduce infusion dose if CrCl < 50 mL/min
– Tirofiban
• Reduce infusion dose by half if CrCl < 30 mL/min
07/08/2022 37
• Glycoprotein IIb/IIIa Receptor Inhibitors (4)
– Side effects
• Immune-mediated thrombocytopenia
– Abciximab: 5%
– Eptifibatide or tirofiban: 1%
• Bleeding
– GP IIb/IIIa inhibitors should not be administered to
Pt’s with a prior history of hemorrhagic stroke or
recent ischemic stroke
– The risk of bleeding is increased in Pt’s with CKD
07/08/2022 38
• Anticoagulants
– For Pt’s undergoing primary PCI
• UFH: 50-70 IU/Kg IV bolus if used with GP IIb/IIIa
inhibitor or 70-100 IU/Kg without GP IIb/IIIa
inhibitor
– Subsequent doses based on aPTT goal
• Bivalirudin: 0.75 mg/Kg IV bolus followed by 1.75
mg/Kg/hr
– Discontinue anticoagulation immediately following the
PCI procedures
– Bivalirudin have similar or greater efficacy but better
safety than UFH
07/08/2022 39
• Anticoagulants …
– For Pt’s treated with fibrinolysis
• UFH ……60 IU/Kg IV bolus (max: 4,000 IU) then 12
IU/Kg/hr (max: 1,000 IU/hr)
– aPTT should be measured at 3 hours
– Continue for a minimum of 48 hours
• Enoxaparin
– Age < 75 years……30mg IV bolus, after 15 minutes 1
mg/kg SC every 12 hours (first two doses max: 100 mg
for those weighing > 100 Kg)
– Age > 75 years……0.75 mg/Kg SC every 12 hours (first
two doses max: 75 mg for wt > 75 Kg)
07/08/2022 40
• Anticoagulants…
– For Pt’s treated with fibrinolytics
• Fondaparinux: 2.5 mg IV bolus followed by 2.5 mg
SC QD starting on hospital day 2
• Enoxaparin: reduces the risk of death but increases
bleeding risk
• Enoxaparin or fondaparinux
– For up to 8 days or for the duration of
hospitalization which ever is shorter
07/08/2022 41
• Anticoagulants …
– In Pt’s who do not undergo reperfusion therapy
• UFH……for up to 48 hours
• Enoxaparin or fondaparinux……for the duration of
hospitalization
– Side effects
• Bleeding
• UFH and enoxaparin……heparin-induced
thrombocytopenia
– Alternatives: Bivalirudin, fondaparinux
07/08/2022 42
• β-Blockers
– Block β1- adrenergic receptors located on the
myocardium
• Reduce HR, myocardial contractility and BP
– Decrease myocardial oxygen demand
– Should be administered early and continued
• For at least 3 years in Pt’s with normal LV function
and
• Indefinitely in Pt’s with LV systolic dysfunction and
an LVEF ≤ 40%
07/08/2022 43
• β-Blockers….
– Initiation of β-blockers should be limited to Pt’s with
• HTN
• Ongoing signs of myocardial ischemia
• No signs or symptoms of acute HF
– Carefully assess for signs of hypotension and HF after
initiation
– Contraindication
• SBP < 90 mmHg
• Shock
• Left ventricular failure with CHF
• Severe reactive airway disease
07/08/2022 44
• β-Blockers…
– Metoprolol
• Initial: 5mg IV push over 1-2 min, repeated every 5 min for 3
doses followed in 1-2 hours by 25-50 mg PO every 6 hours
• Maintenance: 50 -100 mg BID
– Propranolol
• Initial: 0.5-1 mg IV dose followed in 1-2 hours by 40-80 mg
PO TID or QID
• Maintenance: 40-80 mg TID or QID
– Atenolol
• Initial: 5 mg IV followed in 5 minutes by a second dose
followed in 1-2 hrs by 50-100 mg PO QD
• Maintenance: 50-100 mg QD
07/08/2022 45
• Side effects
– Hypotension
– Acute HF
– Bradycardia, and
– Heart block
07/08/2022 46
• Statins
– To all Pt’s prior to PCI, high intensity statin should be
administered to reduce peri-procedural MI
• Atorvastatin
– Initial: 80 mg QD
– Maintenance: 10-80 mg QD
• Rosuvastatin
– Initial: 20 mg QD
– Maintenance: 5-40 mg QD
07/08/2022 47
• Statins: Side effects

– GI upset
– Myalgia
– Myopathy
– Persistent elevations in LFTs
– Cognitive impairment
– Increase in blood glucose and HgbA1c
07/08/2022 48
• Nitrates
– Promote the release of nitric oxide from the
endothelium
• Venous and arterial vasodilation
• Venodilation lowers preload
• Arterial vasodilation lower peripheral resistance and
relieves coronary artery vasospasm
– Use of nitrates lowers myocardial oxygen
demand, improve myocardial blood flow and
oxygenation
07/08/2022 49
• Nitrates…
– To relieve myocardial ischemia
• SL NTG 0.4 mg every 5 minutes for up to three
doses
– Initiate IV in all Pt’s with an ACS who have
• Persistent ischemia, HF or uncontrolled high BP in
the absence of contraindications
– Continue IV NTG for 24 hours after ischemia is
relieved
07/08/2022 50
• Nitrates…
– Contraindications
• In Pt’s who have received oral PDE-5 inhibitors
• Sildenafil and vardenafil………within the last 24
hours
• Tadalafil………within the last 48 hours
– Side effects
• Tachycardia, flushing, headache and hypotension
07/08/2022 51
• CCBs
– Used for relief of ischemic symptoms in Pt’s who
have contraindications to β-blockers
• Diltiazem (SR)……120-360 mg PO QD
• Verapamil (SR)……180 -480 mg PO QD
• Amlodipine……5-10 mg PO QD
– Contraindication
• Hypotension (for all)
• HR < 60 beats/min, PR interval > 0.24 sec, 2nd or 3rd
degree heart block (for diltiazem and verapamil)
– Use amlodipine or felodipine
07/08/2022 52
Pharmacotherapy for NSTE ACSs
• Early Pharmacotherapy for NSTE ACSs

– In the absence of contraindications, all patients
with NSTE ACS should be treated in the ED with
• Intranasal oxygen (if oxygen saturation is low)
• SL NTG,
• ASA, and
• Anticoagulant
07/08/2022 53
Pharmacotherapy for NSTE ACSs (2)
• Early Pharmacotherapy for NSTE ACSs (2)
– High-risk patients should proceed to early angiography
and may receive the following in the emergency
• A GP IIb/IIIa inhibitor (with either UFH or
enoxaparin)
• A P2Y12 inhibitor should be administered to all
patients
• IV β-blockers and IV NTG should be given in selected
patients
• Oral β-blockers should be initiated within the first 24
hours in patients without cardiogenic shock
• Morphine is also administered to patients with
refractory angina
– Fibrinolytic therapy is never administered
07/08/2022 54
• Aspirin
– Reduces the risk of death or developing MI by 50%
– The cornerstone of early treatment for all ACS
• Initial -----162 - 325 mg nonenteric ASA to achieve a
rapid platelet inhibition
– Can be chewed in order to achieve high blood
concentrations and platelet inhibition rapidly
• Maintenance ----- 75 -162 mg daily indefinitely
• Fibrinolytic Therapy
– Fibrinolytic therapy is not indicated for NSTE ACS
• Increased mortality
07/08/2022 55
• Anticoagulants
– For patients treated by an early invasive strategy
• UFH, enoxaparin, or bivalirudin should be
administered
– For an initial conservative strategy
• Enoxaparin, UFH, or low-dose fondaparinux
• In patients treated conservatively fondaparinux
has similar efficacy but a lower bleeding risk
than enoxaparin
07/08/2022 56
• Anticoagulants (2)
– Duration of therapy
• UFH ……… at least 48 hours
• Enoxaparin or fondaparinux………until the
patient is discharged from the hospital (or 8
days, whichever is shorter) or until the end of
PCI or angiography procedure
• Bivalirudin ……… up to 72 hours following
PCI
07/08/2022 57
• For a patient to have subsequent intervention (PCI

or CABG)
– Use UFH……Short duration of action
• If CrCl <30 mL/min
– Use UFH over enoxaparin
– Avoid administering enoxaparin to patients on
dialysis
• Fondaparinux is contraindicated in patients with
– CrCl < 30 mL/min and wt < 50 kg (110 lb)
07/08/2022 58
• Monitoring
– UFH……. monitor and adjust the dose to a
target aPTT
– No monitoring of coagulation is recommended
for bivalirudin and fondaparinux
07/08/2022 59
• P2Y12 & GP IIb/IIIa Inhibitors

– For an initial invasive management strategy,
• In addition to ASA, use either clopidogrel or
ticagrelor, or
• Double-bolus dose eptifibatide plus an
eptifibatide infusion or high-dose tirofiban bolus
plus infusion administered at the time of PCI
– Dual oral antiplatelet therapy is continued for at
least 12 months
07/08/2022 60
• P2Y12 Inhibitors
– For patients receiving an initial conservative
treatment
• Administer either clopidogrel or ticagrelor in
addition to ASA early
– Dual antiplatelet therapy is continued for at least
12 months
– If patient continue to experience recurrent
ischemia
• a GP IIb/IIIa inhibitor may be added to ASA
and clopidogrel prior to the angiogram
07/08/2022 61
• Nitrates
– SL NTG followed by IV NTG should be
administered to NSTE ACS patients with
• Ongoing ischemia,
• HF, or
• Uncontrolled high BP
– Dosing same as STEMI
– IV NTG is typically continued for approximately
24 hours following ischemia relief
07/08/2022 62
• β-Blockers
– Oral β-blockers should be initiated within 24
hours of hospital admission to all patients in the
absence of contraindications
– Duration of therapy
• Indefinitely in patients with LVEF less than or
equal to 40%
• For at least 3 years in patients with normal LV
function
07/08/2022 63
• Calcium Channel Blockers

– Second-line treatment for patients with
contraindications to β-blockers and continued
ischemia despite β-blocker and nitrate therapy
– Diltiazem or verapamil preferred unless the
patient has LV systolic dysfunction, bradycardia,
or heart block
– If contraindication for nondihydropyridine CCBs
• Use amlodipine or felodipine
• Nifedipine is contraindicated……reflex tachycardia
07/08/2022 64
07/08/2022 65
Secondary prevention following MI
• The long-term goals following MI are to

– Control modifiable CHD risk factors
– Prevent the development of systolic HF
– Prevent recurrent MI and stroke
– Prevent death, including sudden cardiac death;
and
– Prevent stent thrombosis following PCI
07/08/2022 66
Secondary prevention following MI (2)
• Pharmacotherapy should be initiated prior to hospital

discharge for secondary prevention
• In the absence of contraindications, patients should receive
indefinite treatment with
– ASA
– An ACEI, and
– A “high-intensity” statin
• A β- blocker should be continued
– For at least 3 years in patients without HF
– Indefinitely in patients with LV systolic dysfunction or HF
symptoms
07/08/2022 67
• A P2Y12 inhibitor should be continued for at

least 12 months for patients undergoing PCI
and for patients with NSTE ACS receiving a
medical management
• Treat and control modifiable risk factors
such as HTN, dyslipidemia, obesity, smoking,
and DM
07/08/2022 68
• ACE Inhibitors and ARBs

– ACE inhibitors should be initiated in all patients
following MI to
• Reduce mortality
• Decrease re-infarction, and
• Prevent the development of HF
– Prevent cardiac remodeling
– Cornerstone of therapy in patients with left
ventricular dysfunction (low LVEF) or HF
symptoms
07/08/2022 69
• ACE Inhibitors and ARBs (2)

– Initiate PO ACEIs early (within 24 hours) of
symptom onset
– Administration of ACE inhibitors should be
continued indefinitely
– ARBs are effective alternatives if the patient is
intolerant to ACEIs
– Candesartan, valsartan, and losartan
07/08/2022 70
• Mineralocorticoid Receptor Antagonists

– In patients with LVEF of ≤ 40%, HF symptoms or
DM, initiate eplerenone or spironolactone within
the first 7 days following MI
– Aldosterone promotes
• Vascular and myocardial fibrosis
• Endothelial dysfunction
• Hypertension
• Left ventricular hypertrophy
• Sodium retention
• Potassium and magnesium loss, and
• Arrhythmias
07/08/2022 71
• Mineralocorticoid receptor antagonists (2)

– Contraindicated in patients with
• SCr greater than 2.5 mg/dL (221 μmol/L),
• CrCl less than 30 mL/min, or
• Serum potassium concentration of greater
than 5 mEq/L (5 mmol/L)
07/08/2022 72
• Lipid-lowering agents
– Statins should be initiated as early as possible in
ACS
– Higher-dose statin therapy reduces CAD risk
• Atorvastatin 40 to 80 mg daily
• Rosuvastatin 10 to 20 mg daily
07/08/2022 73
Modifiable risk factors
• Secondary prevention of CHD events includes
• Smoking cessation,
• Managing HTN,
• Treatment of dyslipidemia,
• Weight loss,
• Exercise, and
• Tight glucose control for patients with DM
07/08/2022 74
Outcome evaluation
• Monitor patients for
– Relief of ischemic discomfort,
– Return of ECG changes to baseline, and
– Absence or resolution of HF signs and symptoms
• Monitor for hypotension and bleeding
• Counseling on medication adherence (secondary
prevention)
07/08/2022 75
Outcome evaluation (2)
07/08/2022 76
•
07/08/2022 77
07/08/2022 78
07/08/2022 79

Pharmacotherapy of ACS

Uploaded by

Document Information

Original Description:

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Pharmacotherapy of ACS

Uploaded by

Copyright:

Available Formats

Pharmacotherapy of ACS

Abera J. (BPharm., MSc in Clinical Pharmacy)

07/08/2022 By; Abera J 1

 The predominant cause (>90%)

Contraindications for fibrinolytic therapy

(no PCI or fibrinolysis)

• Statins: Side effects

• Early Pharmacotherapy for NSTE ACSs

• For a patient to have subsequent intervention (PCI

• P2Y12 & GP IIb/IIIa Inhibitors

• Calcium Channel Blockers

• The long-term goals following MI are to

• Pharmacotherapy should be initiated prior to hospital

• A P2Y12 inhibitor should be continued for at

• ACE Inhibitors and ARBs

• ACE Inhibitors and ARBs (2)

• Mineralocorticoid Receptor Antagonists

• Mineralocorticoid receptor antagonists (2)

You might also like