ACUTE CORONARY

SYNDROMES
Acute Coronary
Syndromes
 Unstable angina (UA) and non-ST segment
elevation myocardial infarction (NSTEMI)
form the group of acute coronary syndromes
(ACS) usually caused by atherosclerotic disease.
 common pathophysiology and may be
undistinguishable at initial presentation;
 the approach to risk stratification and treatment are
the same and are differentiated only by the
presence or absence of elevated cardiac
biomarkers.
Atherosclerosis

1
Vulnerable Plaque
 Acute Coronary Syndrome

No ST Elevation ST Elevation
NSTEMI

Myocardial Infarction
Uns Angina NQMI Qw MI
Pathophysiology
 NSTE-ACS is usually caused by an
unstable atherosclerotic plaque
rupture with sub-sequent platelet- rich
thrombus overlying the culprit lesion
causing severe narrowing.
 This abrupt decrease in blood supply often
results in chest pain and ECG changes
indicative of ischemia, and, if prolonged,
results in myocardial necrosis and enzyme
elevation
Definition of Unstable Angina
 UA is defined, and differs from stable angina, by
the duration and intensity of angina as graded by
the Canadian Cardiovascular Society (CCS)
classification
 There are 3 possible presentations of UA:
1. Rest angina (lasting > 20 min)
2. New- onset angina (at least CCS III intensity)
3. Accelerated angina (angina with activity that is
occurring earlier, more intense CCS class or with
increased duration. Patients initially diagnosed
with UA may later be diagnosed with a NSTEMI if
initial or serial cardiac biomarkers become
elevated.
Clinical Assessment
 When symptoms raise suspicion for ACS, the
goal of the medical evaluation is to answer
2 questions:

 What is the likelihood (high, intermediate,

low) that the patients’s presentation is
consistent with coronary ischemia?

 If so, what is their risk?

History
 Factors derived from the clinical history which
increase the likelihood that the presenting
symptoms are secondary to acute myocardial
ischemia include the presence of chest or left
arm pain, older age and male sex
 The pain radiating to a shoulder or arm, chest pain
that is worse with exertion associated with
diaphoresis, nausea or vomiting and chest pain that
is worse or similar to symptoms of a prior MI.
 Women with ACS tend to present with
atypical symptoms
Physical exam
 prompt review of vital signs can show signs of
possible cardiogenic shock: systolic hypotension
(systolic BP<100mmHg), tachycardia (HR> 100)
and tachypnea.
 The presence of a new mitral regurgitation
murmur or increased intensity of a preexisting
murmur indicates ischemic dysfunction of a
papilary muscle or mitral apparatus.
 A third or fourth heart sound suggests a
significant amount of ischemia
 The presence and extent of pulmonary rales in
acute myocardial ischemia impacts prognosis
Killip Classification

Class Exam findings

I No signs of heart failure
II S3
Elevated JVP
Rales < ½ of posterior lung fields
III Overt pulmonary edema
IV Cardiogenic shock
Electrocardiogram
 First ECG within 10 min after FMC(first
medical contact),
 Additional 12 lead ECG in case of recurrent
symptoms or dgn uncertainity
 Additional ECG leads (right leads, posterior
leads) if standard leads are inconclusive
 Electrocardiogram
 Up to 4% of pts with NSTE-ACS have a completely
normal ECG.
 More commonly, nonspecific ST-segment
depression (<0.05 mV) or T wave inversion
(<0.2 mV) are present and provide no significant
prognostic information.
 Transient ST-segment changes of>0,05 mV that
develop during a symptomatic episode and resolve
with symptom resolution are strongly suggestive of
severe CAD.
 Symmetric T wave inversion of > 0,2 mV across
precordial leads suggests acute ischemia of LAD
artery.
LAB TESTS CARDIAC
BIOMARKERS
LAB TESTS CARDIAC
BIOMARKERS
 Troponins (cTnI and T) are considered the
best and preffered- greater sensitivity and
specificity for measuring injury to the heart
muscle
 A rise of Tn occurs in 2-3 h after injury and
peaks within 1-2 days
 High sensitivity Tn assays is the latest
generation of the cardiac enzyme testing
that allows for detection of very low levels
of troponin
Laboratory testing
 Creatinkinase muscle and brain subunits
(CK-MB) is the best alternative if troponin
are not available (not so specific)
 CKMB and troponin T or I should be
assessed at least twice 6 to 12 hours
apart( because level of cardiac biomarkers
rise over time).
 Check for anemia and renal failure, lipid
prifile, glucose level
 Worse outcome when BNP and CRP positive
Principles of Management
 The immediate or early invasive strategy –
recommended for pts at very high or high risk:
coronary angiography within 2 h or 24 h with
angiographicaly directed revascularization.

 Low risk pts. may be assigned to the early

conservative strategy (noninvasive evaluation
after a a period of observation).
 Figure 9 Selection of
non-ST-segment
elevation acute
coronary syndrome
treatment strategy and
timing according to
initial
risk stratification

©E SC
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without
www.escardio.org/guidelines
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa575)
Grace risk score
Initial Medical Therapy
 Adm. of antithrombotic (antiplatelet and
anticoagulant) agents
 Relief of ischemic pain and ST deviation
 Correction of hemodynamic abnormalities
 Determination of the timing of angiography
Antiplatelet therapy
 Aspirin is recommended for all patients
without contraindications at an initial oral LD
of 150-300 mg (or 75-250 mg i.v.), and at a
MD of 75-100 mg o.d. for long-term
treatment.
 The first dose should be chewed, as there is
measurable platelet inhibition within 60 min.
Aspirin reduces the risk of death by about
1/6 and the risk of nonfatal myocardial
infarction by about one-third in pts. with
ACS
Antiplatelet therapy
 A P2Y12 receptor inhibitor is recommended
in addition to aspirin, and maintained over
12 months unless there are
contraindications or an excessive risk of
bleeding
 Options are:
Antiplatelet therapy

Prasugrel in P2Y12 receptor inhibitor-in

patients proceeding to interventional treat.
 Ticagrelor irrespective of the planned
treatment strategy (invasive or
conservative) (180 mg LD, 90 mg b.i.d.)
 Clopidogrel (300-600 mg LD, 75 mg daily
dose), only when prasugrel or ticagrelor are
not available, not tolerated, or are
contraindicated.
Antiplatelet therapy

 GP IIb/IIIa antagonists i.v.should be

considered for bail-out if there is
complication at PCI
Anticoagulant treatment
 Parenteral anticoagulation is recommended for all
patients, in addition to antiplatelet treatment, at
the time of diagnosis and, especially, during
revascularization procedures according to both
ischaemic and bleeding risks.
 UFH
 Or LMWH (fondaparinux, enoxaparin)
 Discontinuation of parenteral anticoagulation
should be considered immediately after an invasive
procedure.
Anticoagulant
Administration
 UFH- unless the patient is actively bleeding or has a
history of heparin- associated thrombocytopenia
(HIT).
 Advantages of LMWH, ease of adm., no need for
frequent monitoring of APTT, lower incidence of
HIT.
 LMWH is CI in pts with severe renal failure
Thrombolytics

 Thrombolytic therapy has no

docummented benefit in NSTE-ACS.
 Relief of Ischemic Pain

 i.v. beta- blockers, followed by upwards titration of

oral therapy. B- blockers relieve ischemia by
decreasing contractility, heart rate and ventricular wall
tension (preload). Cardioselective agents (atenolol,
metoprolol) are preferred.
 B-blockers not recommended in the setting of high-
degree AV block, cardiogenic shock and severe
reactive airway disease.
 Nitrates adm. sublingually and if pain still present,
i.v. (provided systolic BP>90mmHg).
 Narcotics (e.g., morphine sulfate) should be adm.
only if the pain persists despite previously mentioned
drugs.
 Statins are recommended in all ACS.
 Goals: reduce LDL cholest by > 50% from
baseline and to achieve LDL cst of 55 mg/dl.
 ACE inhibitors in patients with HF,
diabetes, HT.
Acute Myocardial
Infarction
 Acute myocardial infarction

 death or necrosis of myocardial cells.

 occurs when myocardial ischemia exceeds a
critical threshold and overwhelms myocardial
cellular repair mechanisms that are designed
to maintain normal operating function and
haemostasis.
 Ischemia at this critical threshold level for an
extended time period results in irreversible
myocardial cell damage or death.
 Critical myocardial ischemia - a result of
increased myocardial metabolic demand and/or
decreased delivery of oxygen and nutrients to the
myocardium via the coronary circulation.
 An interruption in the supply of myocardial oxygen
and nutrients occurs when a thrombus is
superimposed on an ulcerated or unstable
atherosclerotic plaque and results in coronary
occlusion.
 Conditions associated with increased myocardial
metabolic demand include extremes of physical
exertion, severe hypertension (including forms of
hypertrophic obstructive cardiomyopathy), and
severe aortic valve stenosis.
 Myocardial infarction -transmural
-nontransmural.
 A transmural MI = ischemic necrosis of the full
thickness of the affected muscle segment(s),
extending from the endocardium through the
myocardium to the epicardium.
 A nontransmural MI = an area of ischemic
necrosis that does not extend through the full
thickness of myocardial wall segment(s); the area
of ischemic necrosis is limited to either the
endocardium or the endocardium and myocardium.
 An older sub classification of MI- presence or
absence of Q waves on an electrocardiogram
(ECG).
 Prevalence

 Myocardial infarction = the leading cause of death in

the United States (US) as well as in most industrialized
nations throughout the world.
 The survival rate for US patients hospitalized with MI is
approximately 90% to 95%.
 In general, MI can occur at any age, but its incidence
rises with age. Approximately 50% of all MI's in the US
occur in people younger than 65 years of age. However,
in the future, as demographics shift and the mean age
of the population increases, a larger percentage of
patients presenting with MI will be older than 65 years.
Mechanism of occlusion

 Most MIs are caused by a disruption in the

vascular endothelium associated with an
unstable atherosclerotic plaque that
stimulates the formation of an intracoronary
thrombus, which results in coronary artery
blood flow occlusion.
 If such an occlusion persists long enough
(20 to 40 min), irreversible myocardial cell
damage and cell death will occur.
The severity of an MI is dependent on three
factors:
1. the level of the occlusion in the coronary artery
2. the length of time of the occlusion
3. the presence or absence of collateral
circulation.
 the more proximal the coronary occlusion, the
more extensive is the amount of myocardium at risk
of necrosis.
 The larger the MI, the greater is the chance of
death due to a mechanical complication or pump
failure.
 The longer the time period of vessel occlusion, the
greater the chances of irreversible myocardial
damage distal to the occlusion.
 Generally, after a 6- to 8-hour period of
coronary occlusion, most of the distal
myocardium has died.
 The extent of myocardial cell death defines
the magnitude of the MI.
 If blood flow can be restored to at-risk
myocardium, more heart muscle can be
saved from irreversible damage or death.
Signs and Symptoms of a Myocardial
Infarction

 Chest pain described as a pressure sensation,

fullness, or squeezing in the midportion of the
thorax
 Radiation of chest pain into the jaw/teeth,
shoulder, arm, and/or back
 Associated dyspnoea or shortness of breath
 Associated epigastric discomfort with or without
nausea and vomiting
 Associated diaphoresis or sweating
 Syncope or near-syncope without other cause
 Signs and Symptoms of a
Myocardial Infarction

 A MI may occur at any time of the day, but

most appear to be clustered around the
early hours of the morning and/or are
associated with demanding physical
activity.
 Approximately 50% of patients have some
warning symptoms (angina pectoris or an
anginal equivalent) prior to the infarct.
Diagnosis

-typical patient: has a number of

atherosclerotic risk factors+ symptoms
consistent with a lack of blood flow to
the heart
- If there is a suspicion of acute MI:
ECG, blood testing, echocardiography
Diagnosis

 1. History
 2. ECG
 3. Enzymes
 The diagnosis of myocardial infarction
requires two out of three components
Electrocardiography
 Blood tests
 Blood sampling for serum markers is routinely
carried out in the acute phase. This is indicated,
but should not delay the reperfusion
strategy/treatment
 To detect evidence of myocardial cell death:
Analysis Normal range
CPK 30- 200/L
CK-MB fraction 0.0- 8.8 ng/ml
Troponin I 0.0- 0.4 ng/ml
Troponin T 0.0- 0.1ng/ml
Echocardiography
 Detect wall motion abnormalities
 To detect which portion of the heart
affected by MI
 Evaluate LVEF
 Detect mechanical complications

 But wall motion abnormalities may be due

to a previous (old) MI
 Complications of Acute
Myocardial Infarction
Supraventricular Arrhythmias after AMI
Sinus bradicardia: the most common arrhythmia
occuring during the early hours after MI; may occur
in up to 40% of inferior and posterior
infarctions.
 Bradicardia may be related to autonomic imbalance
or to atrial or sinus node ischemia.
 Atropine i.v. successful; temporary pacing rarely
required
 Complications of Acute
Myocardial Infarction
Sinus Tachycardia- may occur in up to one- third of
pts. in peri- infarct period, especially in anterior MI,
as a need of augmentation of cardiac output by an
increase of heart rate.
 Other causes: sympathetic stimulation, anemia,
hypo or hypervolemia, hypoxia, pericarditis,
inotropic drugs, pain, fear.
 Treatment:- oxygenation, correction of anemia
and electrolyte and acid- base abnormalities, pain
control, anxiolythic agents.
- β-blockers for pts. without evidence of
LV dysfunction or hypovolemia.
 Complications of Acute
Myocardial Infarction
Premature atrial contractions- may be present in
up to one- half of pts. with MI. Their occurrence
may be due to atrial or sinus node ischemia, atrial
infarction, pericarditis, anxiety or pain. Premature
atrial contactions have no prognostic
significance after MI.
.
 Complications of Acute
Myocardial Infarction
Atrial Fibrillation- occurs in 10-20% of pts, usually transient.
It usually occurs in older pts., those with history of
hypertension, larger LA, mitral regurgitation.
 New atrial fibrillation in the peri- infarct period is asssociated
with a higher infarct mortality
 Complications of Acute Myocardial
Infarction

Ventricular Arrhythmias after AMI

Ventricular Fibrillation- the incidence of VF in MI is
about 5% in pts in whom a documented rhythm is
obtained and occurs without antecedent-warning
arrhythmias in over half.
 Factors associated with an increased incidence of VF:
current smoking, left BBB, hypokalemia.
 Pts. with anterior MI and VF have a worse long- time
prognosis than those with VF associated with inferior MI.
 VF may occur with reperfusion after thrombolytic
therapy.
 Treatment: prompt defibrillation, chronic β-blocker
therapy.
Ventricular tachycardia
 Occurs in 10% to 40% of cases of MI.
 Early VT (during the first 24 h) is usually
transient and benign.
 Late- occuring VT is associated with transmural
infarction, LV dysfunction, hemodynamic
deterioration and a markedly higher mortality,
both in hospital and long term.
 Treatment of sustained VT: cardioversion. If the
rate is slow and hemodynamically tolerated,
cardioversion might be attempted with drugs. Rapid
VT (> 150/min) or VT associated with
hemodynamic deterioration should be treated with
prompt DC cardioversion.
 Accelerated Idioventricular
Rhythm
 AIVR is an ectopic ventricular rhythm consisting of
three or more consecutive ventricular beats
with a rate faster than the normal ventricular
escape rate of 30 to 40 beats /min, but
slower than VT. Onset and offset usually are
gradual.
 AIVR has been reported in 10% to 40% of cases of
MI, especially with early reperfusion.
 The presence of AIVR during the peri-infarct
period is not correlated with increased
mortality or incidence of VF.
 Premature Ventricular
Complexes
 PVC occur frequently during MI.
 Their significance in predicting VT and VF is
unclear. Treatment of PVCs in peri-infarct period
has not ben shown to decrease the incidence of
malignant arrhythmias or to improve mortality;
pooled results of randomised trials in which PVCs
were treated prophylacticaly in the peri-infarct
period with lidocaine demonstrated an increased
mortality.
 Best option for treatment: β-blockers.
Premature Ventricular
complexes
Conduction Disturbances after AMI

 Conduction abnormalities after AMI

result from autonomic disturbances or
interruption of the blood supply to the
conduction system.
 First -Degree Block: occurs in 5% to
10% of pts with AMI; it might be
associated with drugs that prolong
atrioventricular conduction.
 Conduction Disturbances after
AMI
 Second Degree, Mobitz Type I Block
(Wenckebach)- seen in up to 10% of cases of
AMI, typically inferior infarcts, and is due to
increased vagal tone or ischemia. Usually responds
to atropine; resolution usually occurs after 48 to 72
hours.
 Late occuring Wenkebach is less sensitive to
atropine and may be due to recurrent ischemia.
 Wenkebach rhythm in the peri- infarct period
has no impact on long- term prognosis.
 Conduction Disturbances after
AMI
 Second-Degree, Mobitz type II Block- occurs
in 1% of cases of MI, more common after
anterior MI. There is a high risk of progression to
higher degrees of block, including sudden complete
heart block with ventricular asystole.
 Patients should have a temporary pacing wire
placed prophylacticaly.
 Long term prognosis is related primarily to the size
of the infarct rather than to the conduction
abnormality.
 Conduction Disturbances after
AMI
 Third- Degree (Complete) Block- may occur
with either an anterior or inferior MI.
 With inferior infarcts, the conduction defect is
likely to be transient, with escape rhythms
exceeding 40/min;
 with anterior MI, the conduction defect is
infranodal, usually less than 40/min, with a wide
QRS complex.
 Temporary pacing may be required for pts with
inferior MI if the patient is hemodynamicaly
unstable.
 Temporary pacing should always be used in pts
with anterior infarcts if progressive or complete
heart block is present.
Bundle Branch Block
 New BBB has been reported in about 15%
cases of MI and is associated with an
increased risk of complete heart block,
congestive heart failure, cardiogenic shock,
ventricular arrhythmias and sudden death.
 Thrombolythic therapy and catheter-based
early reperfusion appear to decrease the
incidence of BBB in the peri-infarct period.
 Cardiogenic shock

 Cardiogenic shock is persistent hypotension,

conventionally defined as a systolic
pressure<80mm Hg for more than 30 min in
the absence of hypovolemia.

 Hypovolemia results in hypotension due to

inadequate LV end-diastolic filling pressure
(LVEDP) typically measured clinically by its
surrogate- a pulmonary capillary wedge
pressure (PCWP)<18 mmHg.
 Cardiogenic shock
 Hypotension due to hypovolemia responds to
fluid replacement while cardiogenic shock is
associated with an elevated LVEDP and PCWP
and is refractory to fluid challenge.

 Cardiogenic shock is frequently associated

with oliguria or anuria, metabolic acidosis,
peripheral hypoperfusion and cerebral
hypoxia.
 Cardiogenic Shock

The most common causes of cardiogenic shock

include:

1) Large LV infarct (usually > 40% of LV)

2) Right ventricular infarct in 10% of shock
pts.
3) Mechanical complications of AMI
(ventricular septal defect, acute mitral
regurgitation, tamponade), in 10% of shock
pts.
 Cardiogenic shock
The incidence of cardiogenic shock is about 8%
of all pts with AMI, and mortality is about 80%
with conservative management.
Thrombolytics are generally ineffective once
hypotension has become established.
Primary percutaneous coronary
intervention (PCI) is generally the
treatment of choice for cardiogenic shock
with inotropic support from an intra-
aortic balloon pump and/or positive
inotropic drugs.
 Pericardial Effusion and
Pericarditis
 Early pericarditis and pericardial effusion occur in about 10%
of pts with AMI and result from localized area of
pericardial inflammation usually over the site of a
transmural infarct.
 Pericarditis may be associated with non-ischemic type
chest pain and a pericardial rub and is more common in
pts with anterior infarcts, transmural infarcts, and heart
failure.
 Treatment is with aspirin 650 mg every 4 to 6 hours.
 Steroids and NSAID’s are generally contraindicated
due to their effect on fluid retention and the risk of
precipitation of heart failure, and their adverse effect
on myocardial wound healing and possible association
with myocardial rupture.
 Postinfarction Syndrome
(Dressler’s syndrome)
 Dressler’s syndrome (~35% of pts) consists of pleuro-
pericardial chest pain often associated in the early stages with
an auscultatory friction rub, fever, arthralgia, leukocytosis and
pulmonary infiltrates.
 It typically occurs several weeks after infarction and
may be recurrent.
 Histologically it is characterized by a localized fibrinous
pericarditis and neutrophil infiltration and has been
associated with the presence of antibodies to cardiac
tissue.
 Treatment is with aspirin 650 mg every 4 to 6 hours or as an
alternative NSAID’s, provided ventricular and renal function
are well preserved. Steroids should be avoided.
 Left Ventricular Mural
Thrombus
 Mural thrombus formation on the endocardial
surface of the LV is common (~50%) in pts with
large anterior wall myocardial infarctions.
 LV thrombi are associated with reduced global LV
function and diminish patient survival.
 Peripheral embolization may occur in ~10% of pts.,
while chronic anticogulation reduces the incidence
of LV thrombi and embolization.
Therapy

Goals of therapy:
 urgent restoration of normal coronary blood
flow
 maximum salvage of functional myocardium

Primary obstacles:
 patient’s failure to quickly recognize MI
symptoms
 the delay in seeking medical attention
 Treatment Delayed is Treatment Denied

Symptom Call to PreHospital ED Cath Lab

Recognition Medical System

Increasing Loss of Myocytes

Delay in Initiation of Reperfusion Therapy

Reperfusion Strategy for STEMI
Two important principles guide our approach to
myocardial reperfusion:
1. “Time is heart muscle”- early reperfusion of
the infarct related artery as quickly as possible
within the first 12 hours of artery occlusion limits
infarct size, increases myocardial salvage,
preserves LV function and improves patient
survival.
2. “Open artery hypothesis”- late mechanical
opening of the infarct related artery at 12 to 48
hours following artery occlusion may reduce
infarct size by salvaging stunned and hibernating
myocardium supplied by collaterals vessels and
improves LV remodeling.
Reperfusion Strategy for STEMI

Based on current trial data and guidelines, there are

2 proven reperfusion strategies for pts. with
STEMI- namely:
A. full- dose fibrinolysis or,
B. primary percutaneous coronary
intervention (PCI).
Advances in STEMI treatment over the past 2 decades
have lowered 30- day mortality to 6% or less
among those treated with fibrinolysis and to 4% or
less with primary PCI.
 Reperfusion Strategy for STEMI
Interpretation of the 12 lead ECG makes the diagnosis of
STEMI and a tracing should be obtained immediately
in all pts. presenting with chest discomfort.

Definition of STEMI:
1. ECG demonstrates ST- segm. elevation greater
than 0.1 mV in at least 2 contiguous precordial
leads or at least 2 adjacent limb leads.
2. ECG demonstrates new or presumed new LBBB.
3. If the initial ECG is not diagnostic but clinical
suspicion is high for STEMI, obtain serial ECG at
5 to 10 minute interval.
 Figure 3 Maximum target times according to reperfusion strategy
selection in patients presenting via EMS or in a ...

Eur Heart J, Volume 39, Issue 2, 07 January 2018, Pages 119–177, https://doi.org/10.1093/eurheartj/ehx393
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 Percutaneous coronary
interventions PCI

= preffered therapy to fibrinolysis if performed by a

experienced personnel
 PCI can successfully restore coronary blood flow in
90-95% of MI pts.
 PCI has advantage over fibrinolysis in terms of
short-term mortality, bleeding rates,
reinfarction rates, for pts. in cardiogenic
shock, pts. with CI to fibrinolysis.
 The use of stents with PCI for MI is superior to the
use of PCI without stents, primarily because
stenting reduces the need for subsequent
target-vessel revascularization.
3
 Fibrinolytics:
Indications: pts. with MI and ST segment elevation
greater than 0.1 mV in 2 contiguous EKG leads, or
new onset of bundle branch block, who present less
than 12 h but no more than 24 h after symptom
onset.
 They have been shown to restore coronary blood
flow in 50% to 80% of MI pts.
 The most critical variable in achieving successful
fibrinolysis is time from symptom onset to drug
administration. A fibrinolytic is most effective
when the “door- to-needle” time is 30 minutes
or less.
Absolute Contraindication
for Thrombolysis in STEMI
1) Any prior intracranial hemorrhage
2) Known structural cerebral vascular lesion
(e.g., arteriovenous malformation)
3) Known malignant intracranial neoplasm
(primary or metastatic)
4) Ischemic stroke within 3 months except
acute ischemic stroke within 3 hours
5) Suspected aortic dissection
6) Active bleeding or bleeding diathesis
7) Significant closed-head or facial trauma
within 3 months
 Antiplatelet agents

 Aspirin –at least 160 mg and up to 325 mg should be adm.

immediately.
 Aspirin interferes with function of cyclo- oxygenase and
inhibits the formation of thromboxane A2. Within minutes,
aspirin prevents additional platelet activation and interferes
with platelet adhesion and cohesion.
 Aspirin alone has one of the greatest impacts on the reduction
of MI mortality. Long- term benefit is sustained even at 75
mg/day.
Antiplatelet agents
 In addition to Aspirin, a potent P2Y12
inhibitor (Prasugrel or Ticagrelor) or
Clopidogrel if these are not available or are
contraindicated is recommended before PCI
and maintained for 12 months unless there
are contraindications as an excessive risk of
bleeding.
 GPIIb IIIa inhibitors i.v only for
complications during PCI.
 ANTICOAGULANT
THERAPY
 Anticoagulation is recommended for all
patients in addition to antiplatelet
therapy during primary PCI or after
fibrinolysis
 UFH
 LMWH-Enoxaparine
 Heparin

 Unfractionated Heparin: -recommended in patients with a

MI who undergo percutanous revascularization or
fibrinolytic therapy .
-in patients with a MI at increased
risk for systemic emboli (prior embolic event, large or anterior
wall myocardial infarction, known LV thrombus or atrial
fibrillation).
 The desired clinical effect of heparin is the inhibition of
additional formation and propagation of thrombi. It is
beneficial until the inciting thrombotic cause (ruptured plaque)
has completely resolved.
 Effective when adm. i.v minimum 48 h or longer, depending on
the individual clinical scenario.
 Heparin
Low- molecular- weight Heparin
(LMWH)
 Fixed doses that are easy to administer,
laboratory testing to measure their
therapeutic effect not necessary.
Supplemental Oxygen
 For pts. with pulmonary edema or less than
90% blood oxygen saturation
 Rationale: erythrocytes will be saturated to
maximum carrying capacity.
 Recommended duration of O2 adm.: 2 to 6
hours or longer if congestive heart failure or
oxygen saturation is less than 90%
 Nitrates
 I.V. nitrates should be adm. to patients with MI
and congestive heart failure, persistent
ischemia, hypertension, or large anterior wall
MI.
 Primary benefit derived from its vasodilator effect;
metabolized to nitric oxide in the vascular
endothelium.
 NO relaxes vascular smooth muscle and dilates the
blood vessel lumen. Vasodilatation reduces preload
and afterload.
 When adm. sublingually or iv, Ntg. has a rapid
onset of action.
 Used for up to 48 h in MI.
 Side- effects: low BP, headache, tachyphylaxis.
 Beta-blockers
 Recommended within 12 h of MI symptoms and
continued indefinitely.
 BB decreases the rate and force of myocardial
contraction and decreases overall myocardial oxygen
demand- minimizes myocardial injury and death.
 Adverse effects: heart failure, bradycardia,
bronchospasm.
 During the acute phase of MI, BB therapy may be
initiated i.v.
Selective BB:
Metoprolol – 25-200 mg every 12 h; Atenolol 25-
100 mg every 24 h; Betaxolol 5-20 mg every 24 h,
Bisoprolol 5-20 mg every 24 h
Angiotensin Converting Enzyme
Inhibitors (ACEI)

 Recommended in MI pts within the first 24 h of

symptom onset, if no CI.
 CI: hypotension, declining renal function with ACEI
use.
 Use of ACEI especially after MI recommended for pts
with congestive heart failure, LV dysfunction
(EF<40%), hypertension or diabetes.
 ACEI decrease myocardial afterload through
vasodilatation.
 Start with a low dose, short acting agent and titrate
the dose upward towards a stable maintenance dose
at 24-48 h after symptom onset.
 Surgical Revascularization
 Urgent coronary artery bypass graft surgery is warranted in the
setting of failed PCI in pts. with hemodynamic instability
and coronary anatomy amenable to surgical grafting.
 Also indicated in case of mechanical complications:
ventricular septal defect, free wall rupture, acute mitral
regurgitation.
 Emergency CABG can limit myocardial injury if performed within
2-3 h after symptom onset (but higher risk of bleeding and MI
extension) than with elective CABG.
 Risk of operative mortality increased in pts. in cardiogenic shock,
multi-vessel disease, advanced age.
 Elective CABG improves survival in post-MI pts. who have
left main artery disease, 3-vessel disease, or 2-vessel disease
that is not amenable to PCI.
 Outcomes
 Cardiac Stress Testing: established value in risk stratification
and assessment of functional capacity; not recommended within
several days post-MI.
 Only sub- maximal stress tests should be performed in stable
pts. 4 to 7 days after MI; symptom- limited stress tests are
recommended 14 to 21 days after MI.
 An inability to exercise and exercise-induced ST-
segment depression are associated with higher cardiac
morbidity and mortality.
 Exercise testing identifies pts. with residual ischemia for
additional efforts at revascularization.
 Exercise testing provides prognostic information and acts
as a guide for post-MI exercise prescription and cardiac
rehabilitation.
Lipid Management

 Start intense statin therapy as early as

possible and maintain it long term:
LDL goal< 55 mg/dl or at least
reduction with 50%.
 Recent data indicate that all MI
pts should be on statin therapy,
regardless of lipid levels or diet.
Management of
hyperglicaemia
 Measure glycaemic levels at initial
evaluation in every patient, and
perform monitoring in patients with
high levels or with known diabetes
 Glucose lowering therapy (insulin)in
pts with glycaemia>180 mg/dl, but
hipoglycaemia should be avoided
 Long-term Medications

 Most oral medications instituted in the hospital at

the time of MI will be continued long-term.
 Therapy with aspirin and beta-blockade is
continues indefinitely in all pts.
 Dual antiplatelet therapy in the form of
aspirin plus ticagrelor or prasugrel (or
clopidogrel if ticagrelor or prasugrel are
contraindicated or unavailable) is
recommended 12 months after PCI.
Long-term Medications

 ACEI is continued indefinitely in

pts. with congestive heart failure, LV
dysfunction (EF<40%), hypertension
or diabetes.
 A lipid-lowering agent, specifically a
statin, in addition to dietary
modification is continued
indefinitely.
 Implantable Cardiac
Defibrillators
 Results of the multi-center automatic defibrillator
implantation trial MADIT II have expended the
indications for automatic implantable cardiac
defibrillators (AICD) in pts. post-MI. The trial
demonstrated a 31% relative risk reduction in
all-cause mortality with the prophylactic use
of an AICD in pts. post MI with LVEF< 30%.
 The implication of the results of this trial is likely to
be tempered initially by the cost for therapy on a
local, regional and national level.
Implantable Cardiac
Defibrillators
 In the absence of a reversible cause, late
(>48 hours) in-hospital sustained VT/VF is
an indication for ICD therapy for secondary
prevention of SCD.
 For other at-risk patients, particularly those
with significantly reduced left ventricular
ejection fraction (LVEF), candidacy for ICD
therapy for primary prevention of SCD
should be reassessed at ≥40 days after
discharge
 Lifestyle Risk Factor Management

 Patients with AMI who smoke must be counseled

to immediately stop smoking
 All AMI pts should receive rehabilitation and
exercise counseling
 Pts who are obese end overweight should receive
intense lifestyle modification instructions. The
morbidly obese may be candidates for surgical
therapies for obesity management.
 DIET

 Diet similar to the mediteraneean diet:

max 10% energy intake from
saturated fat; 30-45 g fiber/day, >
200 g fruits and 200 g
vegetables/day, fish 1-2 times/week;
30 g unsalted nuts daily
 Limited alcohol intake (max 2 glasses
(20g) daily for men and 1 for women)
 Cardiac Rehabilitation

 Participation in cardiac rehabilitation

programs post-MI is associated with a
decrease in subsequent cardiac morbidity
and mortality.

 Other benefits include improvement in

quality of life, functional capacity and
social support.