Acute Coronary Syndrome

By
Ph./ Khlood Mohamed Kettana
Clinical Pharmacy Teaching Assistant
Acute Coronary Syndrome
Acute Coronary Syndrome
• Acute coronary syndrome (ACS) is an umbrella term that includes
patients who present with either unstable angina (UA) or acute
myocardial infarction (AMI) which is further differentiated into ST
segment elevation myocardial infarction (STEMI) or non–ST segment
myocardial infarction (NSTEMI).
• The terminology, non–ST segment elevation-ACS (NSTE-ACS)
includes both UA and NSTEMI.
• These two conditions are determined based upon the presence
(NSTEMI) or absence (UA) of biomarkers associated with necrosis.
Acute Coronary Syndrome

STEMI NSTEMI or UA
Clinical presentation
• The pain is typically midline anterior chest discomfort that can radiate
to the left arm, back, shoulder, or jaw.
• May be associated with diaphoresis, dyspnea, nausea, and vomiting
as well as unexplained syncope.
• Increasing the frequency of exertional angina or chest pain at rest,
new-onset severe chest discomfort, or increasing angina with a
duration exceeding 20 minutes.

• Not relived by rest or NTG.

Clinical presentation
• Some patients, most commonly elderly, women and patients with
diabetes, may present with atypical symptoms including indigestion,
gastric fullness, and shortness of breath or anxiety , and less likely to
present with classic symptoms.
Laboratory changes
• When a cardiac cell is injured, proteins are released into the
circulation. The measurement of these sensitive and specific proteins
(troponins T or I and creatine kinase) is routine in establishing the
diagnosis of AMI.
• Cardiac biomarkers are not typically elevated in patients with UA.
• A cardiac injury profile will be measured at presentation and every 3 to
6 hours for the first 12 to 24 hours and periodically thereafter.
• several conditions other than AMI are associated with elevated
troponin so it is important to assess other diagnostic criteria such as
ECG changes, chest pain, presence of atherosclerotic risk factors, and
echocardiographic findings.
Goals of therapy
• Early restoration of blood flow to the infarct-related artery to prevent
infarct expansion (in the case of MI) or prevent complete occlusion
and MI (in UA).
• Prevention of death and other MI complications.
• Prevention of coronary artery reocclusion.
• Relief of ischemic chest discomfort.
• Resolution of ST-segment and T-wave changes on the ECG.
Management of STEMI
Management of STEMI
• Fibrinolytic therapy is indicated in patients with STEMI who present to
the hospital within 12 hours of symptom onset and are unable to
undergo primary PCI within 120 minutes from first medical contact.
• The benefit derived from fibrinolytic therapy is directly related to the
time from the onset of chest pain to the time of administration.
• The guidelines recommend a “door-to-needle time” of 30 minutes.
• Once stabilized, the patient should be transferred to a facility capable
of PCI in case reperfusion fails or reocclusion occurs.
Management of STEMI
Contraindications of fibrinolytics
Treatment of NSTE-ACS
Risk Stratification Tools for Acute Coronary
Syndrome
Treatment of NSTE-ACS
• In patients with NSTE-ACS, fibrinolytic agents are not
recommended.
• Thrombi in this population are primarily platelet-rich rather than fibrin-
rich, and less responsive to fibrinolytic therapy.
• Data from clinical trials suggest that use of fibrinolytics was not
associated with any improvement and was associated with an increased
incidence in fatal and nonfatal MI.
Early pharmacological therapy for ACS
(in the first 24 hrs.)
• Intranasal oxygen (if oxygen saturation is below 90%).
• Nitrates.
• Morphine to patients with refractory angina.
• DAPT: ASA, a p2y12 inhibitor (agent dependent on reperfusion
strategy).
• Anticoagulant (agent dependent on reperfusion strategy).
• IV β -blocker. (Unless contraindicated)
• ACE inhibitor.
• High-intensity statin therapy.
• Stool softener.
Long-Term Therapy (Discharge medications)

• Antiplatelet.
• High intensity statins.
• ACEIs/ARBs.
• Oral β-blocker. (prevent ventricular remodeling)
• Aldosterone receptor blockers in select patients.
• Vaccinations. (influenza)
• Control of modifiable risk factors.
Oxygen
• Many patients are modestly hypoxemic during the initial hours of an
AMI.
• Supplemental oxygen should be administered to patients with ACS
with an arterial saturation less than 90%, respiratory distress, or other
high-risk features for hypoxemia.
• Patients with severe hypoxemia or pulmonary edema may require
intubation and mechanical ventilation.
Nitrates
• NTG spray or sublingual tablet every 5 minutes for up to 3 doses.
• NTG IV; titrate to chest pain relief for persistent chest pain.
• IV NTG is typically continued until revascularization is performed or
for approximately 24 hours following ischemia relief.
Morphine
• Morphine sulfate (2 to 4 mg IV with increments of 2 to 8 mg IV
repeated at 5-to-15-minute intervals.)
• If pain is not relieved despite maximally tolerated NTG (analgesic).
• Venodilator that lowers preload.
• Reduce stress and anxiety (euphoria).
• CI in respiratory depression.
Dual anti-platelet therapy (DAPT)
• Aspirin:
o LD: 325 mg orally once on hospital day 1, (chewed).
o MD: 81 mg orally once continued indefinitely in all patients.
• P2Y12 receptor antagonist (ADP antagonists):
o Clopidogrel/ Prasugrel/ Ticagrelor.
o Continue for at least 12 months in patients with ACS (added to
aspirin).
Anticoagulants
• UFH ,Enoxaparin, Fondaparinux, & Bivalirudin.
• All patients should receive an anticoagulant in addition to DAPT
regardless of ACS type.
• Should be maintained for a minimum of 48 hours (for UFH) and
preferably for the duration of the hospitalization after fibrinolysis or
until reperfusion is performed to support patency and prevent
reocclusion of the affected artery.
Statins
• High-intensity statin therapy (atorvastatin 40–80 mg/day, rosuvastatin
20–40 mg/day)
• Should be initiated regardless LDL cholesterol level.
• Continued in all patients without CI.

• Pleiotropic effects: plaque stabilization, anti-inflammation,

antithrombogenicity, enhancement of arterial compliance, and
modulation of endothelial function.
ACEIs/ARBs
• Intravenous ACE inhibitors should be avoided because they cause
excessive hypotension and do not improve survival.
• Oral ACE inhibitors should be started within 24 hours of diagnosis,
after BP and renal function have stabilized and continued indefinitely
for all patients with LVEF ≤40% and in those with HTN, DM, or stable
chronic kidney disease unless CI.
• Initial doses should be low and then titrated as quickly as possible.
• ARBs are recommended in patients with ACS who cannot tolerate
ACEIs.
Aldosterone Antagonist
• Indicated in patients after MI already receiving ACE inhibitor and β-
blocker and who have LVEF ≤40% and either symptomatic HF or DM,
unless CI.
Stool Softeners
• It is common to administer agents such as docusate to prevent
constipation in AMI patients because straining causes undesirable
stress on the cardiovascular system.
Calcium channel blockers
• CCBs are recommended for ischemic symptoms when β-blockers are
not successful, are contraindicated, or cause unacceptable side
effects.
Case Study
• P.H., a 68-year-old, 80-kg man, is being admitted to the ED after
experiencing an episode of sustained chest pain during rest. After
waiting 1 hour, he called 911 and was transported to the ED.
• Physical examination reveals a diaphoretic man who appears ashen.
Heart rate and rhythm are regular. Vital signs include BP 180/110 mm
Hg, heart rate 105 beats/minute, and respiratory rate 32
breaths/minute. P.H.’s chest pain radiates to his left arm and jaw, and
he describes the pain as “crushing” and “like an elephant sitting on my
chest.”
Case Study
• He rates it as a “10/10” in intensity. Thus far, his pain has not
responded to five sublingual (SL) nitroglycerin (NTG) tablets at home
and three more in the ambulance. His ECG reveals a 3-mm ST
segment elevation. Based on his history and physical examination, P.H.
is diagnosed with an anterior myocardial infarction.

• Laboratory values include the following:

Sodium (Na) 141 mEq/L, Potassium (K) 3.9 mEq/L, Blood urea nitrogen
(BUN), 19 mg/dL, Serum creatinine (SCr), 1.2 mg/dL, Glucose, 149
mg/dL, CK, 1200 U/L, with a 12% CK-MB fraction (normal, 0%–5%),
Troponin I, 60 ng/mL (normal, <2), Cholesterol, 259 mg/dL,
Triglycerides, 300 mg/dL
Case Study
• P.H. has a prior history of coronary artery disease (CAD). A
previous cardiac catheterization 2 years ago revealed lesions in
his middle left anterior descending coronary artery (75%
stenosis) and proximal left circumflex artery (30% stenosis). His
echocardiogram at the time showed an EF of 58%.

• He also has a history of recurrent bouts of bronchitis, diabetes

mellitus treated with insulin for 18 years with a hemoglobin A1C
of 7.4%, and stage 1 hypertension with blood pressures usually
140/85 mm Hg.
Case Study
• His father died of an MI at age 70. His mother and siblings are all alive
and well. P.H. has smoked one pack of cigarettes a day for 30 years,
and he drinks approximately one six-pack of beer a week. He has no
history of IV drug use.

• On admission, P.H.’s medications include insulin glargine 40 units

daily; albuterol inhaler, as needed (PRN); hydrochlorothiazide, 25 mg
daily; NTG patch, 0.2 mg/hour; and NTG SL, 0.4 mg PRN for chest
pain.
Case Study
What signs and symptoms does P.H. have that are consistent
with the diagnosis of AMI?

• Symptoms: His pain as a pressure sensation, “10/10” in

intensity, > 30 mins.

• P.H. is diaphoretic, a common finding.

• Signs: The ECG (ST segment elevation), and the laboratory

findings ( increased troponin & CK- MB).
Case Study
What are the risk factors for coronary artery disease in P.H.?

• Non Modifiable: age, male, family history

• Modifiable: Diabetes, hypertension, smoking and hyperlipidemia in

P.H. are all risk factors for coronary disease.
Case Study
QUESTION 3: What laboratory abnormalities can you expect to see in
P.H.?

• Both his CK-MB and troponin are elevated, consistent with myocardial
necrosis.

• Hyperglycemia, elevated blood pressure may develop because of

either poor control or a stress response.
Case Study
QUESTION 4: What are the immediate and long-term therapeutic
objectives in treating P.H.?

• The immediate therapeutic objectives:

restore blood flow to the infarct-related artery, arrest infarct expansion,
alleviate his symptoms, and prevent death.

• The long-term therapeutic objectives:

prevent or minimize recurrent ischemic symptoms, reinfarction, HF,
minimize complications, and sudden cardiac death.
Case Study
If the hospital has PCI facility, what will be the best option?
• PCI
• Thrombolytics

What is the target time for PCI from presentation?

• 30 mins
• 60 mins
• 90 mins
• 120 mins
Case Study
He underwent percutaneous transluminal coronary angioplasty and
drug-eluting stent (DES) placement, Which duration best represents the
minimum time DAPT should be continued?
• At least 1 month.
• At least 3 months.
• At least 6 months.
• At least 12 months.
Case Study
Do anticoagulants have a role?

All ACS patients (regardless of treatment strategy) :

2 antiplatelet agents + 1 anticoagulant
Case Study
Statins will be used, which therapy is best?
• High intensity
• Moderate intensity
• Low intensity

atorvastatin 40–80 mg/day, rosuvastatin 20–40 mg/day

Continued for ( 3 years/ 12 months / lifelong)