Transcript ST elevation

ST-elevation myocardial
infarction
Done by :
Raghad Harb
Salam Ashour
Sara Al-Oran
 ST elevations refers to a finding on
an electrocardiogram, where in the trace in the ST
segment is abnormally high above the isoelectric line.
 The ST segment corresponds to a period of
ventricle systolic depolarization, when the cardiac
muscle is contracted.
 When the cardiac muscle is damaged or undergoes a
pathological process Usually, this leads to early
repolarization, or premature ending of the systole.
Aspirin
 Class 1 recommendation FOR ALL PATIENTS
 has established benefit in a variety of cardiovascular disorders
including primary and secondary prevention of coronary heart
disease, transient ischemic attack and stroke, and in the acute
therapy of patients with an ST elevation myocardial infarction
(STEMI).
 The loading dose should be given as soon as possible to any
patient with a STEMI, irrespective of treatment strategy. The
loading dose is 162 to 325 mg of uncoated aspirin
 There is no evidence that higher doses are more effective,
recommend this lower dose (75 to 162 mg/day) of aspirin in
which there was no significant difference in cardiovascular
outcomes, but lower risk of gastrointestinal bleeding, with lowdose (75 to 100 mg daily) aspirin (compared with higher dose of
300 to 325 mg daily).
Thienopyridines
 Although aspirin is effective in the setting of ACS, it is a relatively
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weak platelet inhibitor that blocks platelet aggregation through
only one pathway.
The thienopyridines, ticlopidine, clopidogrel, and prasugrel, are
antiplatelet agents that mediate their antiplatelet effects
through a blockade of ADP P2Y12 receptors on platelets.
Because ticlopidine is associated with the occurrence of
neutropenia that requires frequent monitoring of the complete
blood count (CBC) during the first 3 months of use,
either clopidogrel or prasugrel are the preferred thienopyridines
for ACS and PCI patients.
Clopidogrel is currently recommended by the AHA/ACC
guidelines as an alternative to aspirin for patients who have an
allergy to aspirin.
For STE MI, either clopidogrel or prasugrel, in addition to aspirin
325 mg, should be administered to patients undergoing primary
PCI.
Glycoprotein IIb/IIIa Receptor Inhibitors
 GP IIb/IIIa receptor inhibitors block the final common pathway
of platelet aggregation, namely, cross-linking of platelets by
fibrinogen bridges between the GP IIb and IIIa receptors on the
platelet surface.
 most commonly eptifibatide or abciximab, should be added to
UFH (in addition to clopidogrel or prasugrel and aspirin)
 reduce the likelihood of reinfarction for patients who have not
received fibrinolytics.
 GP IIb/IIIa inhibitors should not be administered for medical
management of the patient with STE MI who will not be
undergoing PCI.
 Abciximab, in combination with aspirin, a thienopyridine, and
UFH (administered as an infusion for the duration of the
procedure) reduced amortality and reinfarction without
increasing the risk of major bleeding in a meta-analysis of
primary PCI clinical trials.
Anticoagulants
 Options for anticoagulant therapy For patients
undergoing primary PCI
 either UFH(Unfractionated heparin) or
bivalirudin is preferred whereas for fibrinolysis,
enoxaparin is preferred.
 Unfractionated heparin has been the traditional
anticoagulant administered to patients with STE
MI to prevent reocclusion of an infarct artery for
more than 40 years
 Limitations of UFH anticoagulation therapy is the
risk of heparin-induced thrombocytopenia.
 Bivalirudin is a direct thrombin inhibitor that has
been associated with similar outcomes and
reduced bleeding rates in primary PCI compared
with UFH.
Beta-blockers
 For patients with acute myocardial infarction (MI), beta blocker
therapy reduces infarct size and early mortality when started
early and lowers the risk of death when continued long term.
 The evidence supporting the benefit of beta blockers has been
obtained primarily from randomized trials that included
predominantly patients with ST-elevation MI (STEMI).
 Randomized trials performed before the use of reperfusion
therapy with either fibrinolysis or PCI consistently showed a
reduction in cardiovascular mortality of 10 to 25 percent in
patients treated with propranolol, metoprolol, or atenolol
 We start with a beta-1-selective agent in most patients. Usual
initial doses are metoprolol tartrate (immediate release
preparation) 50 to 100 mg twice daily or metoprolol succinate
(extended release preparation) 50 or 100 mg daily or atenolol 50
to 100 mg divided twice daily
Nitrate
 Sublingual, intravenous, and oral nitrate preparations are used in the
management of acute coronary syndromes.
 Most of the published data come from patients with myocardial
infarction (MI), but the conclusions would apply to patients with
unstable angina
 Nitrates can be useful during the first 24 to 48 hours in patients with
recurrent ischemia, hypertension, or heart failure.
 nitrates should be avoided in patients with a right ventricular MI in
whom the reduction in preload can lower the cardiac output
 Nitrates used for this purpose include ISOSORBIDE DINITRATE ,
ISOSORBIDE MONONITRATE or NITROGLYCERINE
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Calcium channel blockers
 Administration of calcium channel blockers in the
setting of STE MI is reserved for patients who have
contraindications to -blockers and is used for relief of
ischemic symptoms.
 No calcium channel blocker has been shown to reduce
mortality in acute STEMI, and in certain patients they
may be harmful, such as those with evidence of HF,
left ventricular dysfunction, or atrioventricular block
 When a calcium channel blocker is used for the
indications above, only diltiazem and verapamil are
recommended in patients with STEMI. Immediate
release nifedipine is contraindicated because of the
reflex sympathetic activation, tachycardia, and
hypotension associated with its use.
 The second generation dihydropyridine calcium
channel blockers, amlodipine and felodipine, appear
to be safe in other forms of cardiovascular disease.
Extrapolation from the results of these trials does not
necessarily confirm that amlodipine or felodipine are
safe in patients with an acute STEMI. Nonetheless,
these agents, especially amlodipine, are often used
when hypertension is not adequately controlled by
other therapy of proven benefit
Morphine sulphate
 STEMI class I recommendation for patients whose
symptoms are not relieved after three serial SL
nitroglycerin tablets or whose symptoms recur
with adequate anti- ischemic therapy
Statins
 Intensive statin therapy should be initiated as early as
possible in all patients with STEMI
 Initial intensive statin therapy, rather than gradual
dose titration is recommended
ACE inhibitors
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class I recommendation for patients with heart failure,
left ventricular dysfunction and EF 40%, type 2 diabetes
mellitus or chronic kidney disease in the absence of
contraindications
 management of STEMI gave a strong recommendation for
chronic therapy with an ACE inhibitor (unless
contraindicated) for patients with STEMI with anterior
location, heart failure (HF), or left ventricular ejection
fraction less than or equal to 40 percent.
 An ARB was recommended for those who are intolerant of
ACE inhibitors
 An ARB should not be given in addition to an ACE
inhibitor in the immediate post-MI setting
Patient Presentation
Chief Complaint
"This is the worst pain I have ever felt in my life."
HPI
Gary Roberts is a 68-year-old man admitted to the ED complaining
of chest pressure/pain lasting 20–30 minutes occurring at rest.
He describes the pain as substernal, crushing, and pressurelike
that radiates to his jaw and is accompanied by nausea and
diaphoresis. The pain first started approximately 6 hours ago
after he ate breakfast and was unrelieved by antacids or SL NTG x
3. He also states he has been experiencing intermittent chest
pain over the past 3–4 weeks with minimal exertion.
• PMH
 HTN
 Type 2 DM
 Dyslipidemia
 CAD with PCI(percutaneous coronary
intervention) with a bare metal stent 10 years ago
 Father died from heart failure at age 75 and mother
is alive at age 88 with HTN and type 2 DM.
SH
 (+) Tobacco x 20 years but quit when he received
his BMS 10 years ago; drinks beer usually on
weekends; denies illicit drug use.
Meds
 Aspirin 81 mg po daily
 Metoprolol tartrate 25 mg po BID
 Simvastatin 40 mg po QHS
 Metformin 500 mg po BID
 SL NTG PRN CP
 All
 NKDA
 ROS
 Positive for some baseline CP(chest pain) on exertion for the past
3–4 weeks, now with CP at rest
Physical Examination
Gen
 WDWN man, A & O x 3, still with ongoing chest pain, somewhat
anxious
VS
 BP 145/92, P 89, RR 18, T 37.1°C; Wt 95 kg, Ht 5'10″
 HEENT
 PERRLA, EOMI, fundi benign; TMs intact
 Neck
 No bruits; mild JVD; no thyromegaly
 Lungs
 Few dependent inspiratory crackles; bibasilar rales; no wheezes
 Cv
 Normal S1 and S2, no MRG
( MRG: murmurs ,rubs , gallops )
 Abd
 Soft, nontender; liver span 10–12 cm; no bruits
 Normal liver span (6-12cm)
 Genit/Rect
 Deferred
 MS/Ext
 Normal ROM; muscle strength on right 5/5 UE/LE; on
left 4/5 UE/LE; pulses 2+; no femoral bruits or
peripheral edema
 UE: upper extremity
 LU: lower extremity
 Neuro
 CNs II–XII intact; DTRs decreased on left; negative
Babinski's sign
 DRTs: deep tendon reflex
Parameter
Patient’s
result
Normal
range
State of the
patient
Na
134 mEq/L
135_152
mEq/L
Normal
Ca
9.8 mg/dL
8.6_10.8
mg/dL
Normal
K
4.4 mEq/L
3.5_5.3
mEq/L
Normal
Mg
2.0 mg/Dl
1.6_2.5
mg/dL
Normal
Cl
102 mEq/L
98_110
mEq/L
Normal
Hgb
14.0 g/dL
13.8_17.2 g/dL
Normal
HbA1c
7.6 %
<7% for
dibetics
High
Parameter
Patient’s
result
Normal
range
State of the
patient
Hct
44%
37_52 %
Normal
WBC
5*10^3/mm^
3
4_11*10^3/m
m^3
Normal
Glucose
140 mg/dL
70_130
mg/dL
High
PO4
2.4 mg/dL
2.5_4.2
mg/dL
Slightly low
CO2
23 mEq/L
23_30 mEq/L
Normal
AST
22 U/L
<33 U/L
Normal
ALT
30 U/L
<35 U/L
Normal
Parameter
Patient’s
result
Normal
range
State of the
pateint
Alk.phos
75 U/L
30-115 U/L
Normal
Platelet
268*10^3/m
m^3
140_440*10^3 Normal
/mm^3
Total
cholesterol
159 mg/dL
<200 mg/dL
Normal
Triglyceride
92 mg/dL
<150 mg/dL
Normal
LDL
105 mg/dL
80_130
mg/dL
Normal
HDL
36 mg/dL
40_80 mg/dL Low
BUN
15 mg/dL
6_20 mg/dL
Normal
Parameter
Patient’s
result
Normal
range
State of the
patient
PT
12.5 sec
12_13 sec
Normal
aPTT
32.4 sec
30_50 sec
Normal
SCr
1.0 mg/dL
0.6_1.2
mg/dL
Normal
Tropnin I
8.6 ng/dL
<1 ng/dL
High
INR
1.0
0.9_1.1
Normal
 ECG
 2- to 3-mm ST-segment elevation in leads II, III, and
aVF
 ECG taken on arrival in the emergency department
showing ST-segment elevation (arrows) in leads II,
III, and aVF, consistent with acute inferior
myocardial infarction. Right bundle branch block is
also present in leads V1–V3.
 aVF : the positive electrode on the left leg
 Lead : voltage difference between two electrodes of
the ECG
 Lead II : voltage difference between the right arm
and left leg
 Lead III : voltage difference between the left leg and
the left arm
 Electrodes label :
 V1 : in the 4th intercostal space , between 4th and 5th
ribs to the right of the sternum
 V3 : between V2 and V4
 V2 : in the 4th intercostal space , between 4th and 5th
ribs to left of the sternum
 V4 : 5th intercostal space between the 5th and 6th ribs
Assessment
Acute inferior STEMI
Questions
Problem Identification
1.a. Which findings in this patient’s case
history are consistent with acute STEMI?
•
•
•
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Substernal , crushing , pressurelike chest pain that
radiate to his jaw and lasts 20-30 minutes ,and the SB
NTG provide no relief
Nausea and diaphoresis occur during acute MI .
ECG showing ST-segment elevation (2 – 3 mm ) in
leads II, III, and aVF is consistent with inferior MI.
Serum biomarkers are elevated b/c 6h on the onset of
pain. Troponin needs 3-6h to rise and peak in 120-24 h
and needs 7-14 days to return normal
1.b. What risk factors for the
development of CAD are present in
this patient?
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HTN
Type 2 diabetes mellitus
Dyslipidemia
CAD (coronary artery disease ) with PCI
(percutaneous coronary investigation ) with a bare
metal stent
 Obesity
 Male≥45 years
Desired Outcome
2.a. What is the immediate goal of
therapy in this patient?
Rapid evaluation of eligibility for reperfusion therapy is
indicated in all patients with STEMI. Prompt restoration
of blood flow in the occluded infarct-related artery
(IRA)is the main determinant of both short- and longterm outcomes, including mortality. Reperfusion can be
accomplished by pharmacologic therapy
with thrombolytic drugs or by mechanical
intervention with PCI.
2.b. How can this goal be achieved using
pharmacotherapy?
Drugs that increase oxygen supply:
 Thrombolytics (e.g., alteplase, reteplase, and tenecteplase) .
 Unless contraindicated (i.e., history of hemorrhagic stroke, other
strokes or cerebrovascular events within 1 year, known intracranial
neoplasm, active internal bleeding, suspected aortic dissection),
thrombolytics should be given to patients who present with an acute
STEMI within 12 hours of the onset of chest pain and have ST-segment
elevation in two contiguous leads on ECG or a new left bundle branch
block (LBBB). Current guidelines recommend that thrombolytic
therapy be initiated within 30 minutes of the patient’s arrival at the
hospital.
 Reteplase requires two IV boluses given 30 minutes apart, whereas
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tenecteplase can be administered as a single IV bolus with the dose
adjusted based on the patient’s weight.(and b/c they are given as IV
bolus they are prefered over altaplase that’s given as infusion)
Patients receiving thrombolytic therapy should also receive
concomitant anticoagulant therapy with unfractionated heparin
(UFH), enoxaparin, or fondaparinux.
The dose for UFH is an initial IV bolus of 60 Units/kg (maximum
4,000 Units) followed by a maintenance IV infusion of 12 Units/kg/h
(maximum 1,000 Units/h).
The dosing for enoxaparin is dependent on renal function and age.
For patients less than 75 years of age, an initial 30-mg IV bolus is given.
Fifteen -minutes later, a subcutaneous injection of 1 mg/kg every 12
hours is started. If the patient is ⩾75 years, the initial IV bolus is
eliminated and the maintenance dose is reduced to 0.75 mg/kg every 12
hours. Regardless of age, if the creatinine clearance is <30 mL/min, the
subcutaneous dose is 1 mg/kg every 24 hours.
If fondaparinux is the anticoagulant agent used, an initial 2.5-mg IV
dose followed by subcutaneous injections of 2.5 mg once daily is
recommended as long as the serum creatinine is >3.0 mg/dL.
Therapeutic Alternatives
3.a. What nonpharmacologic therapeutic alternative
can also achieve the immediate goal in this patient?
 Primary PCI is a nonpharmacologic alternative
to thrombolytic therapy in patients with STEMI and can be
used in patients who have contraindications to
thrombolytics. It typically involves coronary angiography to
identify the infarct-related artery followed by balloon
angioplasty of the vessel to compress the atherosclerotic
plaque and dilate the stenotic coronary artery to restore
blood flow. The angioplasty is commonly accompanied by
placement of a stent in the vessel to help maintain patency.
Most stents placed today are drug-eluting stent(DES),
which significantly reduce the risk of restenosis compared
with base metal stent(BMS)
Recent evidence indicates
that, compared with
thrombolytic therapy,
primary PCI is associated
with reduced morbidity and
mortality. Primary PCI is not
without limitations ; There is
a risk of major bleeding and
vascular complications,
usually at the femoral artery
access site. Acute renal failure
can occur in 0.5-13% of
patients due to the contrast
media used during the
procedure. In addition, many
institutions do not have the
necessary facilities or
expertise to perform primary
PCI.
3.b. What is the role of adjunctive anticoagulant therapy
during PCI, and how should these therapies be monitored?
 This patient is at high risk of acute vessel closure after stent implantation
because of his diagnosis of acute MI. Additionally, placement of a coronary
stent damages the endothelium that activates the coagulation cascade, and
generation of thrombin converts fibrinogen to fibrin that can ultimately
lead to thrombus formation without appropriate anticoagulation.
 UFH should be given concomitantly during the stent implantation. UFH is
easily monitored but has no activity against clot-bound thrombin and is
associated with heparin-induced thrombocytopenia (HIT). We must
monitor the clotting time.
 Enoxaparin , a low-molecular-weight heparin, has a more predictable
antithrombin effect compared to UFH as well as better safety profile but its
use is limited primarily by an inability to monitor levels of anticoagulation.
Additionally, dosing with enoxaparin can be confusing. If the last
subcutaneous dose was administered ⩽8 hours before PCI, no additional
enoxaparin is needed during the procedure. If the last dose was >8 hours,
an IV dose of 0.3 mg/kg should be given during PCI.
 Bivalirudin, a direct thrombin inhibitor not associated with
development of HIT(heparin-induced thrombocytopenia ), is
associated with less bleeding than UFH or enoxaparin, but whether it is
more efficacious is controversial. Concomitant use of preprocedure
thieno pryidine play significant role in reducing morbidity and
mortality with Bivarudin
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Fondaparinux, an indirect factor Xa inhibitor, is associated with less
bleeding risks than enoxaparin but has been associated with catheterrelated thrombosis during PCI and therefore requires the addition of
UFH during PCI.
 Regardless of which anticoagulant therapy is administered during PCI,
all patients should have a CBC ( complete blood count ) determined
before and after PCI and be adequately monitored for signs and
symptoms of bleeding. Additionally, patients receiving enoxaparin or
fondaparinux should have a serum creatinine determined
and creatinine clearance calculated to help guide dosing and to reduce
the risk of serious adverse bleeding events.
3.c. What is the role of adjunctive antiplatelet
therapy before, during, and after PCI, and how
should these therapies be monitored?
In addition to activation of thrombus formation, fibrin also
increases platelet aggregation.
• Aspirin. The rapid onset of antiplatelet activity of aspirin has
been shown to reduce mortality if given during acute MI. Unless
contraindicated, the first dose of aspirin (81-325 mg), non-entericcoated) should be chewed and swallowed as soon as possible after
the onset of symptoms or immediately after presentation to the
emergency department (ED). Even if the patient takes an aspirin
daily, an additional tablet should be given in the ED. Therapy can
then be continued at 81 mg per day . However, in this patient who
received a sirolimus-eluting stent, the recommended daily aspirin
dose is 325 mg for at least 3 months.
• Thienopyridines:

Clopidogrel. Is a prodrug activated by CYP2c19 so it has
interaction with drugs inhibiting this enzyme (omeprazole)
Clopidogrel inhibits the platelet adenosine diphosphate
(ADP) receptor subtype P2Y12, providing additional
antiplatelet activity. Because of the slow onset of
antiplatelet activity with the usual maintenance dose of 75
mg daily, patients undergoing PCI usually receive a loading
dose before the procedure. Current literature suggests
giving a 600-mg clopidogrel-loading dose as early as
possible before or at the time of primary PCI. After PCI,
clopidogrel is continued at a maintenance dose of 75 mg per
day for at least 12 months regardless of the type of stent
used. If a patient is at risk for bleeding, earlier
discontinuation of thienopyridine therapy can be
considered. The longer duration of clopidogrel therapy is
important for prevention of late stent thrombosis in
patients receiving drug-eluting stent.

Prasugrel.
Prasugrel also inhibits the P2Y12 receptor. Similar to clopidogrel,
prasugrel is a prodrug that requires bioactivation by hepatic
cytochrome P450 enzymes to an active metabolite. However,
formation of the prasugrel active metabolite is significantly more
efficient than that of clopidogrel resulting in a greater inhibition of
platelet activity with less intersubject variability in response.
Prasugrel is approved for use in the treatment of ACS (acute coronary
syndrome) in patients managed with PCI. It is administered as a 60mg loading dose followed by a maintenance dose of 10 mg once daily.
The recommended duration of therapy after PCI is the same as for
clopidogrel . prasugrel is associated with an increased risk of
bleeding compared to clopidogrel.
Prasugrel is contraindicated in patients with active bleeding or a
history of TIA (Transient ischemic attack) or stroke.
Because of the increased risk of bleeding, prasugrel is generally not
recommended in patients ⩾75 years of age or in patients whose body
weight is <60 kg.
 Ticagrelor
Not thienopyridine but a new drug from
cyclopentyltriazolopyrimidine. It reversibly inhibit
P2Y12 receptor. Indicated for ACS with or without PCI
as 180mg loading dose followed by 90mg twice daily.
Not a prodrug so it’s faster . Contraindicated in severe
hepatic impairment, history of intracranial
hemorrhage, active bleeding. Not used with aspirine
>100mg daily b/c its effects may be attenuated with
higher doses
• GPIs.
(Glycoprotein IIb/IIIa inhibitors)
The GPIs block the final pathway of platelet aggregation . Current evidence
suggests the addition of GPIs during primary PCI might provide more benefit in
patients who have a large thrombus in their coronary artery or in patients who did
not receive adequate thienopyridine loading prior to PCI.
Abciximab (ReoPro) has been evaluated in patients undergoing stent
implantation in association with primary PCI and found to reduce mortality,
target vessel revascularization, and major adverse cardiac events at 6 months
after STEMI. It should be initiated at the beginning of the procedure as an IV
bolus (0.25 mg/kg) and continued as an infusion (0.125 mcg/kg/min) for 12
hours.
 eptifibatide (Integrilin) and tirofiban (Aggrastat). Studies comparing
these agents with abciximab in STEMI patients undergoing primary PCI found
no statistically significant difference in cardiovascular outcomes or major
bleeding. Based on these studies, the 2009 guidelines for PCI and STEMI state
that all three GPIs have similar efficacy in the setting of primary
PCI. Eptifibatide is administered as two boluses of 180 mcg/kg given 10 minutes
apart followed by an infusion of 2 mcg/kg/min for 18-24 hours. Tirofiban is
dosed as a 25 mcg/kg bolus over 3 minutes followed by an infusion of 0.15
mcg/kg/min for 24-48 hours.

 The efficacy of GPIs can be monitored by signs and
symptoms of recurrent ischemia.
 Adverse effects are thrombocytopenia and bleeding,
primarily at the groin site where the catheter was
inserted for the PCI. Platelet counts, hematocrit, and
hemoglobin should be monitored. The effects of
abciximab, but not eptifibatide or tirofiban, on platelet
function can be reversed with platelet transfusion. Both
eptifibatide and tirofiban require dose adjustments in
patients with renal insufficiency. It is important to
assess the patient’s creatinine clearance prior to
administration of either of these two GPIs to avoid
excessive dosing and subsequent increased risk of
bleeding.
Optimal Plan
4.a. What are other important goals of therapy in
this patient?
 To minimize infarct size and salvage viable
myocardium, because the size of the infarction is the
main determinant of prognosis. Therapies to achieve
these goals are directed toward decreasing
myocardial oxygen demand and increasing myocardial
oxygen supply.
 To relieve patient symptoms (e.g., chest pain).
 To prevent or minimize long-term complications such
as reinfarction and remodeling.
 To decrease mortality
4.b. Based on the history and presentation, what initial drug
therapy is indicated in this patient?
Drugs that decrease oxygen demand:
• Analgesics. Pain and anxiety may increase heart rate and blood
pressure, resulting in increased oxygen demand. Morphine is also
an arterial and venous vasodilator, resulting in decreases
in afterload and preload, respectively. Morphine given IV is the
drug of choice in most patients and should be administered in
doses of 2-4 mg every 5 minutes as needed for pain.
• NTG decreases oxygen demand by reducing preload (may also
reduce afterload at higher doses). Venodilation results in less
infarct expansion. NTG also increases myocardial oxygen supply by
coronary vasodilation. Nitrates administered acutely during an MI
can reduce infarct size but do not have any beneficial effect on
mortality. NTG is usually given as a continuous IV infusion (50
mg/250 mL) in acute MI beginning at 5-10 mcg/min and titrated
upward based on chest pain, blood pressure, and heart rate. The
goal is to relieve chest pain .
.β-blockers .
- decrease oxygen demand by slowing heart rate and
decreasing blood pressure and myocardial contractility. They
are particularly useful in patients with tachycardia
and hypertension.and also they increase coronary perfusion
by reducing HR. β-blockers should be started promptly
(within 12 hours of onset of symptoms) if
no contraindications exist.
-Metoprolol is initially administered orally at 25-50 mg
every 6 hours for 48 hours, and then 100 mg po every 12
hours, titrated to heart rate and blood pressure. Other βblockers are also effective, including both nonselective and
cardioselective drugs.
-Agents with intrinsic sympathomimetic activity (ISA),
such as pindolol and acebutolol, should be avoided.
 Additional drug therapy:
• Angiotensin-converting enzyme (ACE) inhibitors limit post-MI
remodeling by decreasing LV dilatation, hypertrophy, remodeling, and
ultimately LV dysfunction if started within 24 hours of a STEMI. Early
administration (within the first 24 hours) of an oral ACE inhibitor is
recommended in all patients with a STEMI, unless specific
contraindications exist . Recent guideline revisions suggest ACE
inhibitors should be started and continued indefinitely in all patients
with STEMI with pulmonary congestion or LVEF ⩽40%. (this patient is
35% so need life long ACE inhibitors)
-Lisinopril is a reasonable option, as it can be administered once daily
(5 mg po initially, and then titrated to 10-20 mg po once daily), as
are enalapril , ramipril , trandolapril , etc.
.Angiotensin receptor blockers (ARBs) are alternatives in patients
unable to tolerate ACE inhibitors (usually due to cough). They have not
been as thoroughly investigated in patients with STEMI as ACE
inhibitors. The only two ARBs with established efficacy in this setting are
candesartan and valsartan .
• HMG-CoA reductase inhibitors (“statins”) should be initiated before
discharge and preferably within 24-96 hours of an acute coronary event.
The aim is to reach a goal LDL of <100 mg/dL, with further reduction to
<70 mg/dL considered reasonable. Any statin is acceptable to use in this
setting as long as the goal LDL can be attained. Intensive statin therapy
with higher doses, such as atorvastatin 80 mg per day, has been proven
to provide greater protection against death or major cardiovascular events
than a moderate LDL-lowering regimen using pravastatin 40 mg in
patients experiencing an acute coronary event. Patients hospitalized for
treatment of CHD who have statin therapy initiated before hospital
discharge are significantly more likely to still be taking the medication at
6 months after discharge. A fasting lipid profile should be evaluated in all
STEMI patients ideally within 24 hours of hospitalization but at least
prior to discharge.
 • Aldosterone
antagonists(spironolactone or eplerenone) are
recommended in post-MI patients with an LVEF ⩽40% and
either diabetes or heart failure. Because these agents are
associated with hyperkalemia(by preventing Na
reabsorbtion and K excretion), they should only be used in
patients without significant renal dysfunction (serum
creatinine <2.5 mg/dL in men or <2.0 mg/dL in women)
and without elevated serum potassium (i.e., pretreatment
potassium should be <5.0 mEq/L before initiating these
agents).
 the potassium-sparing effects can have significant
consequences. In the heart, aldosterone antagonists inhibit
cardiac extracellular matrix and collagen deposition,
thereby attenuating cardiac fibrosis and ventricular
remodeling. Use of these agents is associated with
decreased overall mortality and a reduction in
hospitalizations. Typical daily spironolactone and
eplerenone doses are 12.5-50 and 25-50 mg, respectively
Outcome Evaluation
 5. How should the recommended therapy be monitored
for efficacy and adverse effects?
 • For analgesics, pain relief is the desired therapeutic endpoint.
Continue therapy until pain relief is achieved or systolic blood pressure
is <100 mm Hg. Adverse effects include hypotension, respiratory
depression, and bradycardia.
 • NTG’s efficacy is assessed by relief of chest pain and by effects on
heart rate and blood pressure. Titration endpoints include
resolution/reduction in pain while maintaining an adequate blood
pressure (i.e., systolic blood pressure >90 mm Hg) and heart rate (<110
beats/min). Adverse effects include hypotension, bradycardia,
tachycardia, and headache.
 • Efficacy parameters for β-blockers include heart rate and blood
pressure reduction and resolution of chest pain. Adverse effects include
bradycardia, atrioventricular (AV) block, hypotension, and heart
failure.
 • Efficacy of ACE inhibitors is judged by prevention of LV dysfunction
and remodeling and reductions in mortality, heart failure progression,
and clinical signs/symptoms of heart failure. Adverse effects include
hypotension, angioedema , hyperkalemia, renal dysfunction, and
cough.
 • Efficacy of statins is determined by their ability to attain the goal
LDL. The most common adverse effects of statins are myopathy and
myalgias. Less commonly, elevations of liver enzymes
or rhabdomyolysis can occur.
 • The primary efficacy endpoints for aldosterone antagonists are
reductions in remodeling, heart failure progression, hospitalizations,
clinical signs/symptoms of heart failure, and mortality. Adverse effects
include hyperkalemia, gynecomastia (spironolactone only), and
worsening renal function.
 Patient Education
 6.a. Based on his hospital course, what discharge
medications would be most appropriate for this
patient?
 • Antiplatelet therapy :
 Aspirin reduces risk of vascular death, nonfatal reinfarction, nonfatal
stroke, the combined endpoint of nonfatal MI, sudden death, and
overall mortality. Typical doses range from 81 to 325 mg po daily.
(higher doses means higher risk of bleeding)
 In patient who received a drug-eluting stent, aspirin in combination
with clopidogrel or prasugrel or ticagrelor is the agent of choice to
prevent stent thrombosis. Aspirin is administered indefinitely.
Clopidogrel or prasugrel should be given for at least 12 months
according to current guidelines. Earlier discontinuation of clopidogrel
or prasugrel can be considered if the risk of bleeding is considered to
be greater than the anticipated benefit of continued therapy.
 • β-blockers reduce post-MI mortality.
 Metoprolol, propranolol, atenolol, and timololare FDA-approved
for this indication and are reasonable choices; other β-blockers without
ISA could also be used. Drugs with ISA do not decrease post-MI
mortality and should be avoided. If LVEF <40% then only use
(metoprolol succinate, carvidolol or bisoprolol) to reduce mortality b/c
LV dysfunction
 • ACE inhibitors
 reduce mortality when initiated within 24 hours of the onset of chest
pain. Examples of recommended doses include captopril 50 mg bid
to tid or lisinopril 10-20 mg once daily.
 ACE inhibitors reduce mortality, slow the progression of heart failure,
and decrease reinfarction rates in these patients. Therefore, ACE
inhibitors should be considered in all post-MI patients in conjunction
with other secondary prevention treatments (e.g., statins and βblockers) regardless of EF . So in high risk STEMI patient / LV systolic
dysfunction / DM / EF≤40% need life long treatment with ACE
inhibitors
 • Lipid-lowering therapy with a statin is indicated in this
patient whose LDLcholesterol is 105 mg/dL. In this patient
with increased LDL cholesterol, current guidelines indicate
a statin should be given, with the goal of achieving an LDL
⩽100 mg/dL. However, this patient with STEMI is at a very
high risk for a recurrent event, and further reduction of
LDL to ⩽70 mg/dL should be considered. any statin that
will achieve the goal LDL would be a reasonable choice but
the clinical studies suuports the use of atorvastatin and
simvastatin
 • SL NTG should be prescribed for the patient to take as
needed for treatment of acute ischemic episodes.
 • Aldosterone antagonists
 (spironolactone or eplerenone) reduce mortality and
hospitalizations in patients with moderately severe or
severe heart failure symptoms and in those with LV systolic
dysfunction after MI . Clinical trial results indicate either
agent would be effective .start with spironolactone b/c it’s
cheaper but If patients experience gynecomastia with
spironolactone, switching to eplerenone, which is not
associated with this adverse effect, is a reasonable
alternative.
 • Continued treatment of the patient’s diabetes
with metformin is indicated. But since A1C =7.6% and it
should be ≤7% so we increase the dse to 1g BID .
 • Continued treatment for the patient’s hypertension is also
indicated to minimize the risk of both recurrent MI and
progression of LV systolic dysfunction. In most patients,
this can be accomplished with the use of ACE inhibitors or
ARBs, β-blockers, and diuretics. Current guidelines
recommend a goal blood pressure of <120/80 mm Hg in
patients with LV dysfunction. In post-MI patients without
LV dysfunction, the goal blood pressure is <130/80 mm Hg.
 6.b. What education should you provide to this
patient?
 Risk factor modification:
 Weight loss (we must calculate the BMI for him)
 diet modification
 Exercise program
 Drug therapy:
 • Aspirin: Take this once daily with food as prescribed .And consult the

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physician for OTC medications b/c it can contain levels of aspirine . Be
aware of signs and symptoms of bleeding, including easy bruising;
nosebleeds; bleeding gums; pink, red, or brown urine; red or black
tarry stools; vomiting of blood; coughing up blood; and severe
headache.
• Clopidogrel/prasugrel/ticagrelor: Take this once daily as
prescribed for at least 12 months . It may take you longer than usual to
stop bleeding while taking this medication. Inform your physicians or
dentists that you are taking this medication before undergoing any
surgery or other invasive procedures. Be aware of signs and symptoms
of bleeding, as with aspirin.
In addition, skin rash may develop in some patients taking clopidogrel
.
Do not take other aspirin-containing products or other nonsteroidal
anti-inflammatory medications
(naproxen/ibuprofen/ketoprofen)without consulting your physician or
pharmacist.
Do not stop taking this medication without discussing it with your
cardiologist, even if you have been told by another health care provider
to discontinue clopidogrel or prasugrel.
 • β-blocker (e.g., metoprolol succinate): Take this medication
as directed. Do not suddenly stop taking it. If you miss a dose,
take it as soon as possible. If you do not remember to take the
missed dose and your next regularly scheduled dose is less than 4
hours away, skip the missed dose and take only the next
scheduled dose. This medication may cause dizziness,
lightheadedness, fatigue, cold hands or feet, slow heartbeat,
confusion, and nightmares. It may also cause drowsiness. Use
caution when driving or performing other tasks requiring
alertness until you become familiar with the medication’s effects.
Notify your physician immediately if you experience shortness of
breath (either on exertion or when lying down), feet/ankle
swelling, or chest pain.
 • ACE inhibitor (e.g., lisinopril): Take this medication as
directed. Notify your physician immediately if you notice trouble
breathing or swelling of any part of the head or neck. You
may develop a rash or a dry, persistent cough while taking this
medicine. Contact your physician if these are severe or
troublesome. These side effects will go away when you stop the
medicine.
 • Statin (e.g., simvastatin): Take this every night at
bedtime. Notify your physician immediately if you notice
any muscle weakness or aches.
 • SL NTG: Take only as needed for chest pain. Do not
swallow the tablets. Place one tablet under the tongue at
the first sign of chest pain. If the pain is not relieved in 5
minutes, call 911 immediately to access emergency medical
services (EMS).
 Do not attempt to drive to the hospital or to your
physician’s office. Sit down before taking this medication.
This medication may cause a tingling sensation under the
tongue, headache, dizziness, lightheadedness, and
flushing.
 Store these tablets in their original brown glass container,
and keep the container closed tightly after each use.
 Metformin: Take this medication twice a day with meals.
Gastrointestinal side effects may occur with the increased dose. Notify
your physician if severe diarrhea or vomiting occurs. This medication
can cause a rare but serious side effect called lactic acidosis. Notify your
physician if you experience unusual tiredness, weakness, muscle pain,
trouble breathing, fever, or nausea.
 • Spironolactone: Take this medication once a day with or without
food. Do not use salt substitutes containing potassium while taking
this medication. Do not take nonsteroidal anti-inflammatory
medications such as ibuprofen (Advil, Motrin IB, Nuprin) and
naproxen (Aleve) without consulting your physician or pharmacist.
 Tell your physician if you have ever had high blood levels of potassium
or kidney disease. Notify your physician if you experience headache,
dizziness, diarrhea, excessive tiredness, and breast enlargement or
tenderness .
 Follow-Up Questions
 1. What is the cause of this patient’s myopathy, and how should
his regimen be modified taking into consideration his adverse
effects and his goal LDL?
 • Mr Roberts likely developed myopathy due to the high dose
of simvastatin that he was taking. A recent FDA safety review of
simvastatin states that there is an increased risk of muscle injury in
patients taking the highest approved dose of 80 mg.
 Muscle injury is a side effect of all statins but the higher the dose of
statin, the higher the risk for developing this adverse drug event.
 This patient’s LDL is currently at 78 mg/dL on simvastatin 80 mg
daily. If his goal LDL needs to be <70 mg/dL, then one therapeutic
alternative is to change him to a lower dose of a more potent
hydrophilic statin such as rosuvastatin. Switching to rosuvastatin
10-20 mg daily may provide the needed reduction without causing
the side effects of myopathy.
The End ^_^
Many
Thanks