ACS.ppt

Acute coronary syndromes
Presenter: Mohamed Ali (PGY1)
Moderator: Dr. Zemir Abdi (internist at
Haramaya university)

Classification of ACS
• Patients with ACS are classified into 2
groups:
STEMI
NSTE-ACS
NSTE-ACS include both NSTEMI (have evidence
of myocardial necrosis), and UA ( who don’t have
evidence of myocardial necrosis)
Incidence of NSTEMI>UA due to increased burden
of DM and CKD in an aging population.
UA is falling due to the wider use of highly
sensitive troponin assays.

• Incidence:
One of the most common diagnoses in
hospitalized patients in industrialized
countries
 Age
Incidence increases with advancing age.
Sex
More common in men

• Risk factors:
Common
Age
– Men ≥50 years
– Women ≥60 years
– Incidence increases with age in both sexes.
Cigarette smoking
Hypertension
– Blood pressure ≥140/90 mmHg or using antihypertensive
medication
Low high-density lipoprotein cholesterol level
– <40 mg/dL

High low-density lipoprotein cholesterol level
– >130 mg/dL
Diabetes mellitus
Metabolic syndrome
Family history of premature coronary heart disease
(CHD)
– CHD in male first-degree relative <55 years
– CHD in female first-degree relative <65 years

Pathophysiology • STEMI usually occurs
when coronary blood
flow ceases or
decreases abruptly,
after thrombotic
occlusion of a
coronary artery
previously affected by
atherosclerosis.
• In most cases, infarction
occurs when an
atherosclerotic plaque
ruptures or fissures, and
when conditions (local
or systemic) favor
thrombogenesis.

presentation
• Chest pain
 Character
• Associated symptoms
 Weakness
 Nausea/vomiting
 Sweating
 Apprehension, anxiety, sense
of impending doom
• Other presentations, with or
without pain
 Sudden-onset breathlessness
 Sudden loss of
consciousness
 Confusional state
 Sensation of profound
weakness
 Arrhythmia
 Evidence of peripheral
embolism
 Unexplained decrease in
arterial pressure

STEMI
Clinical finding
EKG
Serum markers
Risk assessment
Non-cardiac
chest pain
Stable
angina
UA NSTEMI
Negative Positive
ST-T wave
changes
ST
elevation
Low
probability
Medium-high
risk
Thrombolysis
Primary PCI
Aspirin + GP IIb/IIIa inhibitor
clopidogrel + heparin/
LMWH + anti-ischemic Rx
Early invasive Rx
Discharge
Negative
Diagnostic
rule out MI/ACS
pathway
STEMI
Negative
Atypical
pain
Low
risk
Aspirin, heparin/low-molecular-
weight heparin (LMWH) +
clopidogrel
Anti-ischemic Rx
Early conservative therapy
Ongoing
pain
DM=diabetes mellitus.
Cannon, Braunwald. Heart Disease. 2001.
Rest pain, Post-MI,
DM, Prior Aspirin
Exertional
pain
The Spectrum of ACS

• Physical examination
 Pallor
 Diaphoresis
 Cool extremities
 Pulse rate and blood pressure
Many patients have normal pulse rate and blood
pressure within the first hour of STEMI.
Patients with large infarctions have hypotension
(systolic blood pressure <100 mmHg and/or sinus
tachycardia >100/min)
Anterior infarction: About one-fourth of patients have
manifestations of sympathetic nervous system
hyperactivity (tachycardia and/or hypertension).
 Inferior infarction: Up to half of patients show evidence
of parasympathetic hyperactivity (bradycardia and/or
hypotension).

• Apical impulse may be difficult to palpate.
• Anterior wall infarction: an abnormal systolic
pulsation caused by dyskinetic bulging of
infarcted myocardium may develop in the
periapical area within the first days of the illness
and then may resolve.
• RV infarction: JVD is common.
• Signs of ventricular dysfunction
Third and fourth heart sounds
Decreased intensity of the first heart sound
Paradoxical splitting of the second heart sound

• Transient midsystolic or late systolic apical systolic
murmur due to dysfunction of the mitral valve
apparatus may be present.
• Pericardial friction rub
• Carotid pulse is often decreased in volume,
reflecting reduced stroke volume.
• Temperature elevations up to 38 °C may be
observed during the first week after STEMI.
• Arterial pressure is variable.
In most transmural infarctions, systolic pressure decreases
by approximately 10–15 mmHg from the preinfarction
state.
• New, loud (≥Gr 3/6) precordial systolic murmur in
ruptured ventricular septum and mitral regurgitation

• ECG findings :
hyperacute T waves are often the first sign of
MI but often only persists for a few minutes
ST elevation may then develop
the T waves typically become inverted within
the first 24 hours. The inversion of the T
waves can last for days to months
pathological Q waves develop after several
hours to days. This change usually persists
indefinitely

• Laboratory tests:
Serum cardiac biomarkers
Myoglobin
Nonspecific reaction to myocardial injury
Leukocyte count
Erythrocyte sedimentation rate

• Cardiac biomarkers:
 Assess the magnitude of STEMI and should be
measured at presentation, 6–9 hours later, and then
at 12–24 hours if diagnosis remains uncertain
 Cardiac-specific troponin T and I
 Highly specific for myocardial injury
 Preferred biochemical markers for diagnosis of acute MI
 Levels of both markers remain elevated for 7–10 days after
STEMI.

• Level of MB isoenzyme of creatine kinase
(CK)
 Increases within 4-8 hours
 Peaks at 24 hours without reperfusion
 Returns to normal by 48–72 hours
Peaks earlier (about 8 hours) and returns to
normal earlier (about 48 hours) after acute
reperfusion therapy
Considerably more specific than CK;
however, cardiac surgery, myocarditis, and
electrical cardioversion often result in
elevated serum levels of MB isoenzyme

• Ratio of CK-MB mass to CK activity ≥2.5
suggests acute MI.
 Less useful when levels of total CK are high owing to
skeletal muscle injury or when the total CK level is
within the normal range but the CK-MB level is
elevated
• Myoglobin
 One of the first serum cardiac markers that increases
above the normal range
 Lacks cardiac specificity
 Blood levels return to the normal range within 24
hours of the onset of MI.

• Leukocyte count
 Nonspecific polymorphonuclear leukocytosis appears
within a few hours after the onset of pain and persists
for 3–7 days.
 Leukocyte count often reaches 12,000–15,000/μL.
• Erythrocyte sedimentation rate
 Increases more slowly than leukocyte count, peaking
during the first week and sometimes remaining
elevated for 1 or 2 weeks

• Imaging:
2-dimensional echocardiography
 Abnormalities of wall motion are almost universally
present.
 Echocardiography cannot distinguish acute STEMI
from an old myocardial scar or from acute severe
ischemia, but ease and safety make it useful as a
screening tool to aid in management decisions.
 Estimation of left ventricular (LV) function is useful
prognostically.
 May identify the presence of right ventricular (RV)
infarction, ventricular aneurysm, pericardial effusion,
and LV thrombus

Doppler echocardiography
Useful in detection and quantitation of a ventricular
septal defect and mitral regurgitation
Myocardial perfusion imaging (201thallium or
99mtechnetium sestamibi)
Sensitive for regions of decreased perfusion, but not
specific for acute MI
Cardiac magnetic resonance imaging
Demonstrates hyperenhancement with myocardial
necrosis

• ECG
Typical STEMI: Q-wave MI develops
Initial ST elevation
Followed by T-wave inversion
Followed by Q-wave development over several
hours
STEMI leading to non–Q-wave MI
Small proportion of STEMI patients
Initial ST elevation
No development of Q waves

If no ST-segment elevation is seen
 Initially considered to be experiencing either
unstable angina or NSTEMI
 NSTEMI is diagnosed when cardiac biomarkers
are elevated.
 A minority of patients may develop a Q-wave
MI.

• Initial goals of therapy are to:
Quickly identify via 12-lead ECG whether
patient has ST elevation and therefore is a
candidate for immediate reperfusion therapy
Relieve pain
Prevent/treat arrhythmias and mechanical
complications

• Pre-hospital care
Recognition of symptoms by the patient and prompt
seeking of medical attention
Rapid deployment of an emergency medical team
capable of performing resuscitative maneuvers,
including defibrillation
Expeditious transportation of the patient to an
appropriately staffed hospital facility

• Management in the emergency department
o Anti-ischemic therapy
Aspirin
Supplemental oxygen
Control of pain
Nitroglycerin
Morphine
Beta blockers
o Reperfusion therapy (comes first in STEMI)
Expeditious implementation of reperfusion therapy
Transfer to catheterization laboratory for primary PCI or
Immediate fibrinolysis in the emergency department
o Anti-coagulation therapy

• Initial therapy
Aspirin
 Administer aspirin immediately, unless the patient
is aspirin intolerant.
Dosage: 81-162 mg chewed at presentation, then
162–325 mg PO qd

SGLT2 inhibitors and MI?
Sodium
Glucose
Cotransporte
r-2 Inhibition
for Acute
Myocardial
Infarction
Jacob A.
Udell and
others
Reduction in the incidence of myocardial infarction with sodium–glucose
linked cotransporter-2 inhibitors: evident and plausible
Richard E. Gilbert & Kim A. Connelly

• Reperfusion: general considerations
 PCI or intravenous fibrinolytic agent
 Reduces infarct size, LV dysfunction, and
mortality
 Identify candidates for reperfusion.
First, use 12-lead ECG to identify STEMI.
ST-segment elevation of ≥2 mm in 2 contiguous
precordial leads and 1 mm in 2 limb leads
 In the absence of ST-segment elevation,
fibrinolysis is not helpful and may be harmful.

PCI vs CABG?
CABG versus PCI — End of the Debate?
Frederick G.P. Welt, M.D.

• Primary PCI (angioplasty or stenting)
Effective in restoring perfusion in STEMI when carried
out on an emergency basis in the first few hours of
STEMI
More effective than fibrinolysis in opening occluded
coronary arteries
Better short-term and long-term clinical outcomes
compared to fibrinolysis when performed:
 By experienced operators (≥75 PCI cases per year)
 In dedicated medical centers (≥36 primary PCI cases per
year)

• Compared with fibrinolysis, primary PCI is
generally preferred when:
 Diagnosis is in doubt
 Cardiogenic shock is present
 Bleeding risk is increased
 Symptoms have been present for >2–3 hours (when the clot is
more mature and less easily lysed by fibrinolytic drugs)
• GP inhibitors and clopidogrel appear useful for
preventing thrombotic complications in patients
undergoing PCI.

• Fibrinolysis
 If PCI is not available or if logistics would delay PCI > 1
hours longer, fibrinolysis could be initiated.
 Preferable if symptoms to needle time <2–3 hours, but
can be useful up to 12 hours if chest pain is persistent or
ST remains elevated in leads that have not developed
new Q waves
 Door-to-needle time should be <30 minutes for
maximum benefit.

• Absolute contraindications:
History of cerebrovascular hemorrhage at any time
Non-hemorrhagic stroke or other cerebrovascular
event within the past year
Marked hypertension (a reliably determined systolic
arterial pressure > 180 mmHg and/or diastolic
pressure >110 mmHg) at any time during the acute
presentation
Suspicion of aortic dissection
Active internal bleeding (excluding menses)

• Relative contraindications
Current use of anticoagulants (international
normalized ratio ≥ 2)
Recent (<2 weeks) invasive or surgical procedure or
prolonged (>10 minutes) cardiopulmonary
resuscitation
Known bleeding diathesis
Pregnancy
Hemorrhagic ophthalmic condition (e.g., hemorrhagic
diabetic retinopathy)
Active peptic ulcer disease
History of severe hypertension that is currently
adequately controlled

• Complications
Hemorrhage/bleeding
Hemorrhagic stroke in 0.5–0.9% of patients; rate
increases with advancing age
Reperfusion arrhythmias
Streptokinase
Allergic reactions (2% of patients)
 Minor degree of hypotension in 4–10% of patients

• Agents of reperfusion approved by the U.S. FDA
Direct plasminogen activators
Tenecteplase
Single weight-based intravenous bolus of 0.53 mg/kg
over 10 seconds
Reteplase
Double-bolus regimen consisting of a 10-million U bolus
given over 2– 3 min, followed by a second 10-million U
bolus 30 minutes later
 Tissue plasminogen activator
 15-mg bolus
Followed by 50 mg IV over the first 30 minutes
Followed by 35 mg over the next 60 minutes

Indirect plasminogen activators
Streptokinase
 1.5 million U IV over 1 hour

• Antiplatelet and antithrombotic drugs
Unfractionated heparin
60 U/kg (maximum, 4,000 U), then 12 (U/kg) per
hour (maximum, 1,000 U/h)
Maintain activated partial thromboplastin time at
1.5–2.0 times control values (~50– 70 seconds).
Should be initiated with fibrinolytic agents other
than streptokinase
Elective use with streptokinase

• Anticoagulation/antiplatelet agents
Continue aspirin, 75–162 mg/d.
Clopidogrel: 300-mg loading dose followed by
75 mg/d in aspirin-intolerant patients
Continue clopidogrel maintenance for at least
6 months in patients who have undergone
PCI with drug-eluting stents and at least 1
month in patients with bare metal stents.

• Diet
Nothing by mouth or clear liquids for first 4–12 hours
Soft diet
• Stool softeners
Docusate sodium, 100–200 mg/d
• Strict control of blood glucose in diabetic patients.
• Serum magnesium level repleted if necessary to reduce
risk of arrhythmias
• Calcium antagonists are not recommended.

• Monitoring
 Continuous ECG monitoring
 Continuous hemodynamic monitoring in selected patients
 Uncomplicated STEMI
Usual duration of hospitalization is 4–5 days.
On return home from hospital
– First 1–2 weeks
» Increase activity indoors and outdoors.
– After 2 weeks
» Coordinate level of activity with patient on
the basis of exercise tolerance.
» May resume normal sexual activity
– Most patients can return to work within 2–4 weeks.

• Complications
Cardiac arrest
This most commonly occurs due to patients
developing ventricular fibrillation and is the most
common cause of death following a MI.
Patients are managed as per the ALS protocol with
defibrillation.

Chronic heart failure
 As described above, if the patient survives the acute
phase their ventricular myocardium may be
dysfunctional resulting in chronic heart failure.
 Loop diuretics such as furosemide will decrease fluid
overload.
 Both ACE-inhibitors and beta-blockers have been
shown to improve the long-term prognosis of patients
with chronic heart failure.

Tachyarrhythmia
 Ventricular fibrillation, as mentioned above, is the
most common cause of death following a MI. Other
common arrhythmias including ventricular
tachycardia.
Brady arrhythmias
 Atrioventricular block is more common following
inferior myocardial infarctions.

Pericarditis
Pericarditis in the first 48 hours following a transmural MI is
common (c. 10% of patients).
Dressler's syndrome tends to occur around 2-6 weeks
following a MI.
Left ventricular aneurysm
Left ventricular free wall rupture
This is seen in around 3% of MIs and occurs around 1-2
weeks afterwards.
Ventricular septal defect
Rupture of the interventricular septum usually occurs in the
first week and is seen in around 1-2% of patients.
Acute mitral regurgitation

• Prognosis
The 2006 Global Registry of Acute Coronary
Events (GRACE) study has been used to
derive regression models to predict death in
hospital and death after discharge in patients
with acute coronary syndrome

• Poor prognostic factors
age
– development (or history) of heart failure
– peripheral vascular disease
– reduced systolic blood pressure
– Killip class*
– initial serum creatinine concentration
– elevated initial cardiac markers
– cardiac arrest on admission
– ST segment deviation

Pathophysiology of NSTE-ACS
• NSTE-ACS occurs as a result of
imbalance btw oxygen supply and
demand, due to one of or more of 4
processes:
1) Disruption of an unstable coronary plaque
2) Coronial arterial vasoconstriction
3) Gradual intraluminal narrowing
4) Increased myocardial oxygen demand

• Among patients with NSTE-ACS studied at
angiography, ~10% have stenosis of the left
main coronary artery, 35% have three-vessel
coronary artery disease, 20% have two-vessel
disease, 20% have single vessel disease, and
15% have no apparent critical epicardial
coronary artery stenosis; some of the latter may
have obstruction of the coronary microcirculation
and/or spasm of the epicardial vessels.

Clinical presentation
• Diagnosis of NSTE-ACS is based on clinical
presentation.

• History:
Chest pain* with at least 1 of 3 features:
Occurrence at rest/minimal exertion, lasting >10
min
Of relatively recent onset
Crescendo pattern
Dx is made of NSTEMI if a patient with any of
these features(without ST segment elevation
on ECG) develops evidence of myocardial
necrosis, reflected by biomarkers.

Anginal equivalents (dyspnea, epigastric
discomfort, nausea or weakness), may occur
instead of chestpain, and are more common
in females,elderly, and DM patients.
• Physical examination:
Unremarkable
If large area of infarction, physical findings
may include (diaphoresis, pale/cool skin,
sinus tachy, a 3rd and/or 4th heart sound,
basilar crackles and sometimes hypotension)

• EKG:
New ST-segment depression occurs in about
one-third of patients with NSTE-ACS.
Transient but persists for several days.
T-wave changes are more common, but less
specific, unless new and deep T-wave
inversions exist (≥0.3 mV).

• Biomarkers:
Patients with NSTEMI have elevated biomarkers of
necrosis, such as cardiac troponin (cTn) I or T (cTnI
or cTnT). cTns are sensitive, relatively specific, and
the preferred markers of myocardial necrosis.
Elevated levels of cTn with a dynamic early change
distinguish patients with NSTEMI from those with UA.
 peaking at 12–24 h after onset of symptoms and
gradually decreasing thereafter.

Imaging
• Coronary computed tomographic
angiography (CCTA) may be useful in
improving the accuracy and speed of the
diagnostic evaluation.

Risk stratification (TIMI/GRACE/HEART)

TIMI, thrombosis in myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation
myocardial infarction; CAD, coronary artery disease.
Antman EM, et al. JAMA. 2000;284:835-842.
TIMI Risk Score for UA/NSTEMI:
7 Independent Predictors
– Aged ≥65 years
– ≥3 CAD risk factors
– Prior CAD (stenosis >50%)
– Aspirin in last 7 days
– >2 anginal events in
≤24 hours
– ST deviation
– Elevated cardiac markers
(CK-MB or troponin)

• Early risk assessment is useful in
identifying patients who would derive the
greatest benefit from an early invasive
strategy

Treatment of NSTE-ACS
• Medical treatment
Initial treatment
Long term management
• Invasive strategy
• Conservative strategy

Acute Management of UA/NSTEMI
• Anti-Ischemic Therapy
Oxygen, bed rest, ECG monitoring
Nitroglycerin
-Blockers
ACE inhibitors
• Antithrombotic Therapy
 Antiplatelet therapy
 Anticoagulant therapy

TIMI, Thrombosis in Myocardial Infarction; ESSENCE, Efficacy and Safety of Subcutaneous Enozapam in
Non–Q-Wave Coronary Events; UHF, unfractionated heparin; ENOX, enoxaparin; MI, myocardial infarction;
OR, odds ratio.
Antman EM, et al. Circulation. 1999;100:1602-1608. (with permission)
TIMI IIB/ESSENCE Metanalysis:
Enoxaparin vs Unfractionated Heparin
8.6 7.1 0.82 (0.69-0.97) 18 .02
6.5 5.2 0.79 (0.65-0.96) 21 .02
5.3 4.1 0.77(0.62-0.95) 23 .02
1.8 1.4 0.80 (0.55-1.16) 20 .24
0.5 1 2
Day
2
8
14
43
UFH
(%)
ENOX
(%)
OR
(95 CI)
Favors
ENOX
Favors
UFH
P
OR
Death or MI %

• If initial conservative(non-invasive)
strategy is selected:
Begin DAPT with aspirin plus clopidogrel or
ticagrelor (a loading dose followed by
maintenance dose) as soon as possible after
admission and continue for up to 12 months.

0.00
0.02
0.04
0.06
0.08
0.10
0.12
0.14
Cumulative
Hazard
Rate
Clopidogrel
+ Aspirin*
3 6 9
Placebo
+ Aspirin*
Months of Follow-Up
P<0.001
N=12,562
0 12
*Other standard therapies were used as appropriate.
CV=cardiovascular.
CURE Trial Investigators. N Engl J Med. 2001;345:494-502.
20%
Relative-risk
Reduction
CURE: Primary Endpoint:
MI/Stroke/CV Death

• If an initial invasive strategy is selected in
addition to aspirin, start DAPT any of the
following:
Before(upstream of) diagnostic angiography:
Consider GB2B3A inhibitor(tirofiban or eptifibatide)
in addition to aspirin and ticagrelor or clopidogrel in
high risk pts (elevated troponins,DM, or significant
ST segment depression NOT at a high risk of
bleeding)
Do not use upstream GB2B3A inhibitors if at high
risk of bleeding (or a low risk for inschemic events,
such as thrombolysis in MI, TIMI score) and
already receiving aspirin and a P2Y12 receptor
inhibitor.

• At the time of PCI:
• Give 1 of the following:
Prasugrel 60mg then 10 mg PO/OD(but consider
5MG OD if <60kg) is preferred over clopidogrel in
pts NOT at high risk for bleeding.
Clopidogrel loading dose PO 300-600mg followed
by maintenance dose of 75mg/day if not started
before.
Ticagrelor loading dose 180mg PO followed by
maintenance dose 90mg PO BID
IV GB2A3B
IV cangrelor 30mcg/kg bolus dose before PCI
followed by infusion of 4mcg/kg/min for duration of
procedure of ≥2hrs, whichever is longer.

• Give/continue anticoagulant therapy at the
time of PCI with 1 of the following:
IV unfractionated heparin
Bivalirudin if the pt was not previously was not
previously treated with UFH
Enoxaparin and give and additional dose(0.3
mg/kg IV) in pts given <2 doses of 1mg/kg SC or
given the last dose 8-12 hrs before PCI
Fondaparinux, and give UFH 85 units/kg
immediately prior to PCI, at the time of PCI, or 60
units/kg IV if GB2B3A inhibitor was used, to reduce
the risk of catheter thrombosis.

• Don’t give fondaparinux as the sole
anticoagulant in pts having PCI due to high risk
of catheter thrombosis.
• For pts having PCI with stenting and who aren’t
already of DAPT, give loading dose of oral
P2Y12 inhibitor with 1 of the following:
Ticagrelor 180mg
Clopidogrel 600mg
Prasugrel 60mg
• Don’t give prasugrel to pts with prior history of
stroke or TIA.

• If the decision is to proceed with CABG
after angiography
Continue aspirin 81-325mg/day
If taking P2Y12 receptor inhibitor, discontinue
drug to allow for dissipation of antiplatelet
effect, unless need for revascularization
and/or net benefit of P2Y12 receptor inhibitor
outweighs potential risk of excessive
bleeding.
Stop clopidogrel/ticagrelor ≥5 days before elective
CABG AND ≥ 24hrs before urgent CABG.
Stop prasugrel ≥ 7days before elective CABG

Stop IV GB2B3A inhibitor
Eptifibatide or tirofiban ≥2-4 hrs before CABG
Abciximab ≥12 hrs before CABG
Manage anticoagulant therapy as follows:
Continue UFH
D/C other anticoagulants before CABG(enoxaparin
12-24 hrs prior, fondaparinux 24 hrs prior,
bivalirudin 3hrs prior) and dose UFH per
institutional practice.

• If medical therapy is selected as strategy after
angiography:
• If coronary artery disease found on angiography
Continue aspirin indefinitely
Give loading dose of clopidogrel or ticagrelor if not
started before diagnostic angiography
Stop iv GB2B3A inhibitor if started previously
• If anticoagulant therapy given before diagnostic
angiography
Continue IV UFH for at least 48hrs or until
discharge
Continue enoxaparin/fondaparinux for the duration
of hospitalization (up to 8 days)
Either D/C bivaluridin or continue at 0.25mg/kg.hr
up to 72hrs at physicians discretion.

• DAPT duration with aspirin and P2Y12
inhibitor
Give at least for 12 months
Consider>12 months in pts who have tolerated
DAPT without bleeding complication and/or who
are not at high risk of bleeding
Consider D/C of P2Y12 inhibitor therapy after 6
months in pts who develop either high risk of
bleeding or who have significant overt bleeding.
Continue P2Y12 inhibitor therapy for minimum of
14 days and ideally for at least 12 months in pts
treated with fibrinolytic therapy
Consider use of risk score (such as DAPT or
PRECISE-DAPT) to evaluate risk and benefits of
different DAPT durations (such as more than >1yr)

• Long-term management
• Modify risk factors
There is evidence of benefit with long-term therapy
with five classes of drugs that are directed at
different components of the atherothrombotic
process.
BB
LLD (statins at high dose, e.g., atorvastatin 80 mg/d, with
ezetimibe if needed to achieve an LDL-C below 70
mg/dL),
ACE inhibitors or ARBs are recommended.

• The recommended antiplatelet regimen consists
of the combination of low-dose (75–100 mg/d)
aspirin and a P2Y12 inhibitor (clopidogrel,
prasugrel, or ticagrelor) for 1 year, with aspirin
continued thereafter.
• In selected patients at high ischemic risk (e.g.,
those with prior MI, DM, vein graft stent, CHF)
who are also at low risk of bleeding, continuation
of DAPT out to 3 years has been shown to be
beneficial.

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