Clinical diagnosis of MI requires a syndrome indicative of myocardial ischemia with some combination of myocardial necrosis detected by biochemical, ECG, or imaging modalities

1. STEMI
DR SHADAB

2. • Clinical diagnosis of MI requires a syndrome indicative of myocardial
ischemia with some combination of myocardial necrosis detected by
biochemical, ECG, or imaging modalities.

3. THIRD UNIVERSAL DEFINITION OF MI
CRITERIA FOR ACUTE MI
The term acute MI should be used when there is evidence of myocardial necrosis in a
clinical setting with acute myocardial ischemia. Under these conditions, any of the
following criteria meets the diagnosis for MI:
• Detection of a rise &/or fall in cadiac biomarker values (preferably cTn), with at least one
value above the 99th percentile URL and with at least one of the following:
• Symptoms of ischemia
• New or presumed new significant ST-T changes or new LBBB
• Development of pathologic Q waves on the ECG
• Imaging evidence of new loss of viable myocardium or new RWMA
• Identification of an intracoronary thrombus by angiography or autopsy
• Cardiac death with symptoms suggestive of myocardial ischemia and presumed new
ischemic changes on the ECG or new LBBB, buy death occurred before cardiac
biomarkers were determined or before cardiac biomarkers values would be increased.

4. CONT…
• PCI related MI is arbitrarily defined by elevation of cTn values
(to>5x99th percentile URL) in patients with normal baseline values
(≤99th percentile URL) or a rise in cTn values >20% if the baseline
values are elevated and are stable or falling. In addition, either
• Symptoms suggestive of myocardial ischemia,
• New ischemic changes on the ECG
• Abgiographic findings consistent with a procedural complication, or
• Imaging demonstration of new loss of viable myocardium or new RWMA is
required.

5. CONT…
• Stent thrombosis associated with MI when detected by coronary
angiography or autopsy in the setting of myocardial ischemia and with
a rise and/or fall in cardiac biomarker values and at least one value
higher than the 99th percentile URL
• CABG related MI is arbitrarily defined by elevation of cardiac
biomarker value (to>10x99th percentile URL) in patients with normal
baseline cTn values (≤99th percentile URL). In addition, either
• New pathologic Q waves or new LBBB
• Angiographically documented new graft or new native coronary occlusion, or
• Imaging evidence of new loss of viable myocardium or new RWMA is
required

6. CRITERIA FOR PREVIOUS MI
Any of the following criteria meets the diagnosis for prior MI:
• Pathologic Q waves with or without symptoms in the absence of
nonischemic causes.
• Imaging evidence of a regional loss of viable myocardium that is
thinned and fails to contract in the absence of a nonischemia cause.
• Pathologic findings of previous MI

7. THIRD UNIVERSAL MI CLSSIFICATION OF TYPE
Type 1: spontaneous MI
• Spontaneous MI related to atherosclerotic plaque rupture, ulceration,
fissuring, erosion, or dissection with resulting intraluminal thrombus
in one or more of the coronary arteries that leads to decreased
myocardial blood flow or distal platelet emboli with ensuing myocyte
necrosis.
• The patient may have underlying severe CAD buy on occasion
nonobstructive or no CAD

8. CONT…
Type 2: MI secondary to ischemic imbalance
In cases of myocardial injury with necrosis in which a condition other
than CAD contributes to an imbalance between myocardial O2 supply
&/or demand (eg., coronary endothelial dysfunction, coronary artery
spasm, coronary embolism, tachy/bradyarrhythmias, anemia, respiratory
failure, hypotension, hypertension±LVH)

9. CONT…
Type 3: MI resulting in death when biomarker values are unavailable
Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ischemic changes on the ECG or new LBBB, but death
occurring before samples could be obtained, before cardiac biomarkers
could rise, or in rare cases, when cardiac biomarkers were not collected.

10. CONT…
• Type 4a: MI related to PCI
• MI associated with PCI is arbitrarily defined by elevation of cTn values to
>5x99th percentile URL in patients with normal baseline values (≤99th percentile
URL) or a rise in cTn values > 20% if baseline values are elevated and are stable
or falling. In addition, either
• Symptom suggestive of myocardial ischemia,
• New ischemic changes on ECG or new LBBB
• Angiographic loss of patency of a major coronary artery or a side branch or persistent slow
flow or no flow or embolization, or
• Imaging demonstration of new loss of viable myocardium or new RWMA is required.
• Type 4b: MI related to stent thrombosis
MI associated with stent thrombosis is detected by coronary angiography or autopsy
in the setting of myocardial ischemia and with a rise and/or fall in cardiac
biomarkers values with at least one value above the 99th percentile URL

11. CONT…
Type 5: MI related to CABG
• MI related to CABG is arbitrarily defined by elevation of cardiac
biomarker values to 10x99th percentile URL in patients with normal
baseline cTn values (<99th percentile URL). In addition, either
• New pathologic Q wave or new LBBB
• Angiographically documented new graft or native coronary artery occlusion,
or
• Imaging evidence of new loss of viable myocardium or new RWMA is
required.

12. CHANGING PATTERN IN INCIDENCE
• The rate of MI rises sharply in both men and women with increasing age.
• Racial differences exist, with MI occurring more frequently in black men &
women compared to white, regardless of age.
• The overall number of deaths from STEMI has declined steadily over the
past 30 years, but it has stabilized over the past decade.
• According to estimate from AHA, the short-term mortality rate of patients
with STEMI ranges from 5-6% during the initial hospitalization & from 7-
18% at 1 year
• The highest risk of ischemic complications following MI occurs within 180
days, after which the risk becomes fairly linear (this pattern is most evident
in patients > 80 years)

13. POTENTIAL OUTCOME OF ISCHEMIA

14. RV INFARCTION
• Approx. 30-50% of patients with IWMI have some involvement of the
RV, bus isolated infarction of the RV is seen in just 3-5% of MI
• The classic presentation of an RV infarct is hypotension , clear lung
fields, & elevated JVP.
• Acute management of RV infarction complicated by cardiogenic shock
includes judicious volume replacement, early revascularization,
maintenance of AV synchrony, & in refractory cases, mechanical
circulatory support.
• In contrast to LV, the RV can sustain long periods of ischemia but still
demonstrate excellent recovery of contractile function after
reperfusion.

15. ATRIAL INFARCTION
• Atrial infarction occurs in up to 10% of patients with STEMI if PR-
segment displacement is used as the criteria.
• It often occurs in conjugation with ventricular infarction & causes
rupture of the atrial wall
• Isolated atrial infarction is observed in <5% of patients with STEMI.
• More common on RA than LA & occur more frequently in the atrial
appendages than in the lateral or posterior wall & can result in
thrombus formation.
• Atrial arrhythmias frequently accompany.

16. NON-ATHEROSCLEROTIC CAUSES OF ACUTE MI
• Embolization-infective endocarditis, nonbacterial thrombotic endocarditis,
mural thrombi, prosthetic valves, neoplasms, air embolism, calcium
• In-situ thrombosis-chest wall trauma, hypercoagulable states.
• Spontaneous coronary artery dissection-account for 10-30% of MIs in
younger women (<50 years age)
• Conservative management with oral & IV antithrombotic therapy alone is recommend
if coronary flow is preserved
• Revascularization with PCI or CABG should be considered for occlusive lesions
• Rare causes-syphilitic aortitis, Takayasu arteritis, necrotizing arteritis,
polyarteritis nodosa, Kawasaki disease, SLE & giant cell arteritis,
mediastinal radiation, amyloidosis, Hurler syndrome, pseudoxanthoma
elasticum, & homocystinuria, cocaine abuse

17. MI WITH NONOBSTRUCTIVE CORONARY ARTERIES (MINOCA)
• Coronary artery spasm, plaque erosion or rupture, and coronary
dissection are common etiologies
• Patients tends to be young & more often females
• 1/3rd of patients present with STEMI
• Approx. half of patients have normal coronaries whereas other half has
some nonobstructive disease
• Long term prognosis is better

18. STRESS (TAKOTSUBO) CARDIOMYOPATHY
• Typically involves transient wall motion abnormalities involving the LV
apex and midventricle.
• Occurs in the absence of obstructive epicardial CAD & can mimic STEMI
• More tha half of patients with takotsubo CMP have an active of history of a
neurologic or psychiatric disorder, linking neurologic-mediated
vasoconstriction
• Different patters of ST elevations across the different coronary territories
could distinguish stress cardiomyopathy from ACS with excellent
specificity
• Most patients experiences rapid recovery of ventricular function, although
>20% patients do suffer in-hospital complications, such as, HF, arrhythmias,
& death

19. PATHOPHYSIOLOGY OF LV FUNCTION
Systolic Function
• Following interruption of antegrade flow in an epicardial coronary artery, the zone of
myocardium supplied by that vessel immediately loses its ability to shorten & perform
contractile work
• Four abnormal contraction pattern develop in sequence:
• Dyssynchrony (dissociation of time course of contraction of adjacent segment)
• hypokinesis( (reduction of extent of shortening)
• Akinesis (cessation of shortening)
• Dyskinesis (paradoxical expansion & systolic bulging
• The hyperkinesis of noninfarcted zone (acute compensatory mechanism) subsides within
2 weeks of infarction
• Ischemia at a distance patients with STEMI may also have reduced myocardial
contractile function in noninfarct zones, results from previous obstruction of the coronary
artery supplying the nonifarcted region of the ventricle and loss of collaterals from the
freshly occluded infarct-related vessel

20. • When the abnormally contracting segment exceeds 15% of the
myocardium, the EF may decline, and LVEDP and volume may
increase.
• Clinical heart failure accompanies areas of abnormal contraction
exceeding 25%, and
• Loss of >40% of LV myocardium usually leads to cardiogenic shock

21. SILENT MI WITH ATYPICAL FEATURES
• Nonfatal STEMI can be unrecognized by the patient.
• Approx. half of unrecognized STEMI are truly silent, with patient unable to recall any symptoms
• The other half portion of patients can recall an event characterized by symptoms compatible with
acute MI
• Atypical features include:
• HF (i.e., dyspnea without pain beginning de novo or worsening of established failure)
• Classic angina pectoris without a particularly severe or prolonged episode
• Atypical location of pain
• CNS manifestations resembling those of stroke secondary to a sharp reduction in cardiac output in patients
with cerebral arteriosclerosis
• Apprehension & nervousness
• Sudden mania or psychosis
• Syncope
• Overwhelming weakness
• Acute indigestion &
• Peripheral embolization

22. PHYSICAL EXAMINATION
GENERAL APPEARANCE
• Patients suffering from STEMI may appear anxious and in considerable
distress or may lie, sit, or stand still
• They often massage or clutch their chests and frequently describe their pain
with a clenched fist held against the sternum (Levine sign)
• In patients with LV failure, cold perspiration and skin pallor may be
evident and they typically sit or propped up in bed and gasp for breath.
• Cough producing frothy, pink, or blood streaked sputum may occur if
pulmonary edema is present
• In patients in cardiogenic shock, their skin is cool and clammy and there is
marked facial pallor with severe cyanosis of the lips and nail beds

23. HEART RATE
• Bradycardia or a rapid regular of irregular tachycardia
• PVCs are common
*Tachycardia at presentation is associated with a higher risk for fatal complication of MI
BLOOD PRESSURE
• Most uncomplicated STEMI are normotensive
• Reduced stroke volume and tachycardia can cause decline in systolic BP and pulse
pressure and elevation of diastolic BP
• Hypertensive response occasionally seen (in previously normotensive patients)
• Cardiogenis shock (defined as SBP<90 mm Hg and evidence of end-organ
hypoperfusion)
• Hypotension alone does not necessarily signify cardiogenic shock

24. TEMPERATURE & RESPIRATION
• Fever develops in most patients with extensive STEMI within 24-48
hours (a nonspecific response to tissue necrosis) & may reach 101˚F to
102˚F
• Usually resolves by 4th or 5th day after MI
• Respiratory rate may rise slightly (anxiety or pain) in patients without
heart failure
• In patients with LV failure, respiratory rate correlates with severity of the
failure

25. JVP
• Usually normal in STEMI involving the LV
• a-wave may be prominent in patients with pulmonary hypertension secondary to LV
failure
• RV infarction often results in marked jugular venous distention
• Tall c-v wave of TR
CAROTID PULSE
• Provides a clue to LV stroke volume
• A small pulse suggests reduced stroke volume
• A sharp, brief upstroke often occurs in MR or a VSR with L→R shunt
• Pulsus alternans reflects severe LV dysfunction

26. THE CHEST
• Diffuse wheezing can occur in patients with severe LV failure.
• Cough with hemoptysis, suggesting pulmonary embolism with infarction,
can also occur
• Killip classification, a prognostic classification, proposed by Thomas Killip
in 1967
• Class I-Patients are free of rales and S₃
• Class II-Patients have rales, but only to a mild to moderate degree (<50% of lung
fields), and may or may not have an S₃
• Class III-Patients have rales in >50% of each lung field and frequently have
pulmonary edema
• Class IV-Patients have cardiogenic shock

27. CARDIAC EXAMINATION
PALPATION
• May yield normal results
• A presystolic pulsation synchronous with S₄ (reflecting vigorous LA contraction
filling a ventricle with reduced compliance)
• A diffuse or dyskinetic LV impulse, or an outward movement of the LV palpable
in early diastole, coincident with an S₃ (in patients with LV systolic dysfunction)

28. AUSCULTATION
HEART SOUNDS
• S₁ is usually muffled immediately after an infarct
• A soft S₁ may also reflect prolongation of PR interval
• Paradoxical splitting of S₂ in patients with marked ventricular dysfunction
&/or LBBB
• S₄ is almost universally present in patients in sinus rhythm with STEMI
• S₃ usually reflects severe LV dysfunction with elevated ventricular filling
pressure
• It reflects rapid deceleration of transmitral blood flow during protodiastolic filling of
LV
• Detected best at the apex in left lateral recumbent position
• It may also result from MR or VSR

29. MURMURS
• Typically systolic murmurs, transient or persistent, generally result
from MR secondary to dysfunction of papillary muscle or LV dilation
• VSR produces murmur & thrill, usually most prominent along the left
sternal border and may be audible at the right sternal border as well
• Systolic murmur of TR (from RV failure caused by pulmonary
hypertension, RV infarction, or infarction of an RV papillary muscle)
is also heard along the left sternal border
• Characteristically intensified by inspiration
• A prominent c-v wave in JVP and
• An RV S₄

30. FRICTION RUB
• Can be heard within 24 hours or as late as 2 weeks after MI (most
frequent on 2nd or 3rd day)
• Delayed onset and associated discomfort of pericarditis (as late as 3
months) characterizes the rare post-MI (Dressler) syndrome
• Most readily audible along the left sternal border or just inside the
apical impulse

31. ECG MANIFESTATIONS OF MI
ECG MANIFESTATIONS OF ACUTE MYOCARDIAL ISCHEMIA (IN ABSENCE OF LBBB)
• ST Elevation: New ST elevation at the J point in two contiguous leads with
the following cut points:-
• ≥0.1 mV in all leads (except V₂-V₃)
• In leads V₂-V₃ the following cut points apply:
• ≥0.2 mV in men ≥40 years
• ≥0.25 mV in men <40 years
• ≥0.15 mV in women
• ST Depression & T wave changes:
• New horizontal or downsloping ST depression ≥0.05 mV in two contiguous leads
• T-wave inversion ≥0.1 mV in two contiguous leads with a prominent R wave or R/S
ratio >1

32. ECG MANIFESTATION OF ISCHEMIA IN THE SETTING OF LBBB
• ST-segment elvation ≥1 mm and concordant with the QRS complex-5
points
• ST-segment depression ≥1 mm in lead V₁, V₂ or V₃-3 points
• ST-segment elevation ≥5 mm and discordant with the QRS complex-2
points
*A score of ≥3 had a specificity of 98% for acute MI

33. ECG CHANGES ASSOCIATED WITH PREVIOUS MI (IN ABSENCE OF LVH OR LBBB)
• Any Q wave in leads V₂-V₃ ≥0.02 sec or a QS complex in leads V₂
and V₃
• Q wave ≥0.03 sec and ≥0.1 mV deep or QS complex in lead I, II, aVL,
aVF, or V₄-V₆ in any 2 leads of a contiguous lead grouping (I, aVL;
V₁-V₆; II, III, aVF)
• R wave ≥0.04 sec in V₁-V₂ and R/S≥1 with a concordant positive T
wave in absence of a conductions defect

34. Q WAVE AND NON-Q WAVE INFARCTION
• The presence or absence of Q waves on the surface ECG does not
reliably distinguish between transmural and
nontransmural(subendocardial) MI
• Q wave on ECG not synonymous with irreversible myocardial damage
• Q waves are associated with worse outcomes
• The absence of Q waves may simply reflect the insensitivity of the
ECG, especially in zone of the LV supplied by the LCx

35. ISCHEMIAAT A DISTANCE
• New Q waves and ST segment elevation diagnostic of STEMI in one
territory often have ST segment depression in other territories, which
result either from ischemia in a territory other than the area of
infarction (termed ischemia at a distance) or from reciprocal electrical
phenomena.
• ST segment depression in the anterior leads in the setting of acute
inferior STEMI may be caused by- concurrent anterior ischemia,
inferolateral wall infarction, or true reciprocal changes.

36. IMAGING
• Most STEMI do not require imaging for diagnosis unless the ECG is
nondiagnostic or the clinical scenario is questionable
• Imaging is key to determine-
• The extent of the infarct
• The presence of mechanical complications, and
• The overall function of the RV and LV

37. CHEST X-RAY
• Chest imaging should not delay primary reperfusion strategies, unless
there is a reason to evaluate a particular suspected pulmonary
pathology.
• Up to 12 hours can elapse before pulmonary edema accumulates after
ventricular filling pressure has increased.
• Up to 2 days is required for pulmonary edema to resolve and x-ray
signs of pulmonary congestion to clear after ventricular filling
pressure have returned toward normal.

38. ECHOCARDIOGRAPHY
• Typical chest pain with a nondiagnostic ECG, RWMA on echo
supports the diagnosis of myocardial ischemia.
• LV function estimation is useful in establishing the prognosis after MI
• Early use of echo can aid in early detection of-
• Potentially viable but stunned myocardium (contractile reserve)
• Residual provocable ischemia
• Patients at risk for HF after MI and
• Mechanical complications of MI (such as acute MR or TR or VSR)

39. ESTIMATION OF INFARCT SIZE
ECG
• The sum of ST elevations measured from multiple precordial leads correlates with the extent of
myocardial injury in patients with anterior MI.
CARDIAC MARKERS
• Serial measurements of proteins released by necrotic myocardium can help to determine MI size.
• Clinically, the peak CK, CKMB, or troponin level provides an approximate estimate of infarct size.
• Cardiac specific troponin level several days after SYEMI (even in cases of successful reperfusion),
may provide a reliable estimate of infarct size
ECHOCARDIOGRAPHY
• The most frequently used modality for assessing infarct size and LV function
OTHER TECHNIQUES
• Contrast enhanced CMR
• Nuclear imaging

40. STEMI MANAGEMENT GOAL

41. MANAGEMENT IN EMERGENCY DEPARTMENT
• A history of ischemic type discomfort
and the initial 12 lead ECG are the
primary tools & should be obtained
promptly (≤10 min. after hospital
arrival)
• Prehospital ECG also facilitate early
triage of patients with STEMI
• All patients should have bedside
monitoring of the ECG and IV access
(because lethal arrhythmias can occur
suddenly)
• In non-PCI capable hospitals, the
initial assessment should include
evaluation of the contraindications of
fibrinolysis

42. GENERAL TREATMENT MEASURES
ASPIRIN
• 162-325 mg should be administered at
the first opportunity after initial
medical contact
• Patient should chew a non-enteric-
coated tablet to promote buccal
absorption bypassing the gastric
mucosa
CONTROL OF PAIN
Typically achieved with a combination
of analgesics (eg., morphine, meperidine
and pentazocine), oxygen (in the setting
of hypoxia), nitrates, and beta-
blockers(in selected patients)
Morphine: 4-8 mg IV initially followed
by 2-8 mg repeated at interval of 5-15
min. until the pain is relieved or side
effect emerge (hypotension, depression
of respiration, or vomiting)
Nitrate:once hypotension is excluded,
an SL nitroglycerine tablet should be
administered & observed for
improvrment in symptoms or change in
hemodynamics.
• If an initial dose is well tolerated and
appears to be beneficial, further nitrates
should be administered
• In patients of a prolonged period of chest
pain, IV nitroglycerine may help

43. CONT…
Beta blockers
• First exclude patients with HF,
hypotension(SBP<90 mm Hg), bradycardia(HR<60
bpm), or significant AV block
• Administer metoprolol in three 5-mg IV boluses.
• Observe the patient for 2-5 min after each bolus,
and if HR falls below 60bpm, or SBP<100 mm Hg,
do not administer any further drug
• If hemodynamic stability continues 15 min after the
last IV dose, begin oral metoprolol tartrate 25-50
mg every 6 hours for 2-3 days and then switch to
100 mg twice daily(if tolerated)
• Infusion of an extremely short acting beta blocker
(such as esmolo) 50-250 μg/kg/min, may be useful
in patients with relative contraindications to the
beta blocker
Oxygen
• Augmentation of the FiO₂ does not elevate O₂
delivery significantly in patients who are not
hypoxemic
• Furthermore, it may increase systemic vascular
resistance and arterial pressure, promote coronary
vasoconstriction, and result in greater oxidative
stress
• O₂ therapy can be omitted if the oximetric findings
are normal
• Patients with STEMI and arterial hypoxemia (eg.,
SaO₂<90%) should receive O₂
• Patients with severe pulmonary edema,
endotracheal intubation and mechanical ventilation
may be necessary

44. CONT…
OXYGEN
• Augmentation of the FiO₂ does not elevate O₂ delivery significantly in
patients who are not hypoxemic
• Furthermore, it may increase systemic vascular resistance and arterial
pressure, promote coronary vasoconstriction, and result in greater oxidative
stress
• O₂ therapy can be omitted if the oximetric findings are normal
• Patients with STEMI and arterial hypoxemia (eg., SaO₂<90%) should
receive O₂
• Patients with severe pulmonary edema, endotracheal intubation and
mechanical ventilation may be necessary

45. MEASURES FOR LIMITATION OF INFARCT SIZE
Approaches:
1. Early reperfusion
2. Reduction of myocardial energy demands
3. Manipulation of energy production sources in the myocardium, and
4. Prevention of reperfusion injury
Ischemic preconditioning: Brief episodes of ischemia in one coronary vascular bed may precondition
myocardium in a remote zone and thereby attenuate the size of infarction in the latter when sustained
coronary occlusion occurs.
• Myocardial O₂ consumption should be minimized by maintaining the patient at rest both physically
and emotionally (by using mild sedation & a quiet atmosphere)
• Severe anemia (Hb<7 g/dl) can be corrected by PRBC, accompanied by a diuretic(if any evidence
of LV failure)
• Associated infections and accompanying tachycardia, fever, and elevated myocardial O₂ needs,
require management.

46. REPERFUSION INJURY
Types of reperfusion injury
• Lethal reperfusion injury- reperfusion induced death of cells that were still
viable at restoration of coronary blood flow
• Vascular reperfusion injury- progressive damage to the microvasculature such
that there is an expanding area of no-reflow and loss of coronary vasodilatory
reserve
• Stunned myocardium- salvaged myocytes display a prolonged period of
contractile dysfunction after restoration of blood flow because of abnormality
in intracellular metabolism, leading to reduced energy production, and
• Reperfusion arrhythmias- bursts of VT/VF that occur within seconds of
reperfusion

47. REPERFUSION ARRHYTHMIAS
• Transient sinus bradycardia (in patients of IWMI) often accompanied
by some degree of hypotension-Bezold-Jarisch reflex
• PVCs, accelerated idioventricular rhythm, and NSVT also usually
follow successful reperfusion
• This brief electrical storm generally does not warrant prophylactic
antiarrhythmic therapy, except in rare case of symptomatic or
hemodynamically significant reperfusion arrhythmias.

48. ASSESSMENT OF REPERFUSION
• TIMI Flow grade
• TIMI Frame count 21
• Coronary blood flow(ml/cm) = X 1.7
(Observed TIMI Frame count)
• ECG (ST segment resolution)
• Echocardiography
• Myocardial contrast-enhanced echo (correlates with RWMA)
• Dobutamine stress echo (lack of myocardial viability)
• Contrast enhanced CMR (identify regions of microvascular obstruction)
• TIMI myocardial perfusion (TMP) grade

49. COMPARISON OF FIBRINOLYTIC AGENTS

50. COMPLICATIONS OF FIBRINOLYTIC THERAPY
• Bleeding complications (most common)
• Intracranial hemorrhage (most serious, <1%)
• Antibody-mediated resistance to streptokinase ( and anistreplase)
• Patients should not receive streptokinase for STEMI if they have been treated
with a streptokinase product within 6 months
• Hypersensitivity reaction
• Streptokinase is highly antigenic & is absolutely contraindicated within 6
months of previous exposure

51. RECOMMENDATIONS FOR FIBRINOLYTIC THERAPY
• When a patient arrives at a PCI capable facility, primary PCI is the preferred mode
of reperfusion therapy
• If the delay from first medical contact to performing primary PCI is anticipated to
exceed 120 min, administration of a fibrinolytic is indicated within 12 hours of
onset & in the absence of contraindications.
• The choice of fibrinolytics is generally driven by ease of dosing, cost, and other
institutional preference
• In patients whose risk for death is low (eg., young patient with small IWMI) and whose risk
for intracranial hemorrhage is increased (eg., acute hypertension), administration of
streptokinase is reasonable
• It is still reasonable to consider fibrinolytic therapy for appropriately selected
patients with clinical & ECG evidence of ongoing ischemia within 12-24 hours
• Elderly patients treated with fibrinolytic agents >12 hours after symptoms onset
have an increased risk for cardiac rupture, so restricting late administration of a
fibrinolytic to patients younger than 65 years with ongoing ischemia is preferable

52. CATHETER BASED REPERFUSION STRATEGIES
APPROACHES:
• Direct or primary PCI
• Rescue PCI
• Routine delayed angiography and PCI after successful fibrinolytic therapy
• Elective PCI (when spontaneous or exercise provoked ischemia occurs)

53. SURGICAL REPERFUSION
• Patients with STEMI are currently referred for CABG for
• Persistent or recurrent ischemia despite fibrinolysis or primary PCI
• Residual coronary disease not amenable to PCI,
• High risk coronary anatomy (eg., LMCA stenosis) discovered at initial
catheterization, or
• A complication of STEMI such as VSR or severe MR

54. PATIENTS NOT ELLEGIBLE FOR REPERFUSION
THERAPY ?

55. • In the setting of absolute contraindications to fibrinolysis and lack of
access to PCI facilities, antithrombotic therapy should be initiated.

56. THANK YOU