This document discusses the definitions, types, diagnosis, and clinical features of acute myocardial infarction. It defines the types of MI based on etiology (Types 1-5) and provides criteria for diagnosing acute MI, including elevated cardiac troponin levels and clinical evidence of ischemia. The document also discusses evaluating patients for signs of ischemia, infarction or injury on electrocardiogram and assessing cardiac biomarkers, vital signs, symptoms and physical exam findings to diagnose acute coronary syndrome and myocardial infarction.

1. DR JITENDRA SINGH
DM CARDIOLOGY RESIDENT

2. The term acute myocardial infarction should be used when there is acute
myocardial injury with clinical evidence of acute myocardial ischemia and with
detection of a rise and/or fall of cTn values with at least one value above the 99th
percentile URL and at least one of the following:
 Symptoms of myocardial Ischemia
 New Ischemic ECG changes
 Development of pathologicQ waves
 Imaging evidence of new loss of visible myocardium or new regional wall motion
abnormality in a pattern consistent with an ischemic etiology
 Identification of a coronary thrombus by angiography or autopsy.

3. TYPE OF ACUTE MYOCARDIAL INFARCTION:
Type 1 MI: Postmortem demonstration of acute atherothrombosis in the artery
supplying the infarcted myocardium.
Type 2 MI:Evidence of an imbalance between myocardial oxygen supply and
demand unrelated to acute atherothrombosis.
Type 3 MI:Cardiac death in patients with symptoms suggestive of myocardial
ischemia and presumed new ischemic ECG changes before cTn values become
available or abnormal.
Type 4 MI: Percutaneous coronary intervention (PCI)-related MI.
Type 4a- Coronary procedure related MI ≤48 hr after the index
procedure is arbitrarily defined by an elevation of cTn values>5times.
Type 4b- stent thrombosis.
Type 4c- Instent restenosis.
Type 5 MI: Coronary artery bypass grafting (CABG) related MI. An elevation of
cTn values >10 times of the 99th percentile URL in patients with normal
baseline values.

4. Patients with elevated preprocedural cTn values, in whom the preprocedural cTn
level is stable (≤20% variation) or falling, must meet the criteria for a >5-or>10-fold
increase and manifest a change from the base line value of >20%. In addition with
at least one of the following :
 New Ischemic ECG changes
 Development of new Pathological Q waves
 Imaging evidences of loss of visible myocardium that is presumed to be new and
in a pattern consistent with an ischemic etiology.
 Angiographic findings consistent with a procedural flow-limiting complication
such as coronary dissection, occlusion of a major epicardial artery or graft, side-
branch occlusion- thrombus, disruption of collateral flow,or distal embolization.

5. CRITERIA FOR PRIOR OR SILENT/UNRECOGNIZED MYOCARDIAL INFARCTION:
Any one of the following criteria meets the diagnosis for prior or silent/
unrecognized MI:
 Abnormal Q wave’s with or without symptom’s in the absence of non
Ischemic causes.
 Imaging evidence of loss viable myocardium in a pattern consistent with
ischemic etiology.
 Pathoanatomical findings of a prior MI.

6. MYOCARDIAL INJURY: indicated by elevated cardiac troponin values with atleast
one value above the 99th percentile URL.
Acute  Rise or Fall of cTn values
ChronicElevated above URL but No rise or fall.
ACUTE MYOCARDIAL INFARCTION:
Myocardial Ischemia + Acute Myocardial Injury
At least one of the following:
 Symptoms of Ischemia
 ECG s/o New Ischemic changes
 Pathological Q waves
 Imaging evidence of-
-New loss of viable myocardium
-New regional wall motion abnormality
 Identification of an intracoronary thrombus
by angiography
Rise or fall of cTn with atleast one value
above 99th percentile

7. ACUTE CORONARY SYNDROME (ACS) INCLUDES:
 ST-elevation myocardial infarction (STEMI)
 Non-ST-Elevation myocardial infarction (NSTEMI)
 Unstable angina (UA)

8. DIAGNOSIS OF ACS
CLINICAL HISTORY:
CARDIAC Angina
Rest or
unstable
angina
Acute MI
Pericarditis
Retrosternal chest pressure, burning, or
heaviness; radiating occasionally to the neck,
jaw, epigastrium, shoulders, left arm
Same as angina, but may be more severe
Same as angina, but may be more severe
Sharp, pleuritic pain aggravated by changes in
position; highly variable duration
Precipitated by exercise, cold
weather, or emotional stress;
duration of 2–10 min
Typically <20 min; lower tolerance for
exertion; crescendo pattern
Sudden onset, usually lasting ≥30
min; often associated with shortness
of breath, weakness, nausea,
vomiting
Pericardial friction rub
VASCULAR Aortic
dissection
Excruciating, ripping pain of sudden onset in the
anterior aspect of the chest, often radiating to
the back
Marked severity of unrelenting pain;
usually occurs in the setting of
hypertension or underlying
connective tissue disorder such as
Marfan syndrome

9. Pulmonary
embolism
Sudden onset of dyspnea and pain, usually pleuritic
with pulmonary infarction
Dyspnea, tachypnea, tachycardia,
signs of right-sided heart failure
Pulmonary
hypertension
Substernal chest pressure, exacerbated by exertion Pain associated with dyspnea and
signs of pulmonary hypertension
OTHER FEATURES:
Nausea and vomiting (more frequently in patients with inferior STEMI
than with anterior STEMI )
Feelings of profound weakness
Dizziness,
Palpitations,
Cold perspiration, and a
Sense of impending doom

10. GENERAL EXAMINATION:
Appear anxious and in considerable distress
Clutch their chests and frequently describe their pain with a
clenched fist held against the sternum (Levine sign).
Cold perspiration, and skin pallor (In patients with LV failure and
sympathetic stimulation)
feeling of suffocation
Cough producing frothy, pink, or blood-streaked sputum (In
pulmonary edema )
skin is cool and clammy, with a bluish or mottled color over the
extremities, and marked facial pallor with severe cyanosis of the
lips and nailbeds( Cardiogenic shock)

11. HEART RATE : Tachycardia at presentation associates with a higher risk for
fatal complications of MI.
CAROTID PULSE:A small pulse suggests reduced stroke volume.
A sharp, brief upstroke -In patients with mitral regurgitation
or a
ruptured ventricular septum with a left-to-right shunt.
Pulsus alternans reflects severe LV dysfunction.
THE CHEST : Moist rales OR Diffuse wheezing In pulmonary edema due to
LV
Failure.
Cough with hemoptysis- pulmonary embolism with infarction.

12. KILLIP CLASSIFICATION:The Killip classification still remains useful for
prognostication.

13. CARDIAC EXAMINATION:
PALPATION : A presystolic pulsation synchronous with an audible fourth
heart sound (S4) a finding reflecting vigorous left atrial contraction filling a
ventricle with reduced compliance.
Diffuse or dyskinetic LV impulse, or an outward movement of the left
ventricle palpable in early diastole coincident with an S3LV systolic
dysfunction.
AUSCULTATION :
S1 Soft prolongation of the PR interval.
S2 Paradoxical splitting LBBB or marked ventricular
dysfunction
S4 usually present in all case of sinus rhythm with STEMI
S3 In STEMI  severe LV dysfunction with elevated
ventricular
filling pressure.
S3 is detected best
at the apex with the
patient in the left
lateral recumbent
position
MURMURS: Transient or persistent systolic murmurs due to
mitral regurgitation secondary to dysfunction of the mitral valve
apparatus.

14. Apical holosystolic murmur with thrill Rupture of a head of a papillary muscle.
Holosystolic murmur with thrill at left sternal border Rupture of the
interventricular
septum
Systolic murmur of TR at left sternal border  RV Failure due to RV Infarction
or PH. Prominent c-v wave in JVP
RV S4
FRICTION RUBS: occur most frequently on the second or third day.
Heard within 24 hours or as late as 2 weeks after onset of
infarction.
Have a pericardial effusion ((Dressler syndrome)
Audible along the left sternal border or just inside the apical
impulse.

15. EXTREMITIES:
Systemic atherosclerosis
History of intermittent claudication
Cyanosis of the nailbeds  Severe LV failure and cardiogenic shock.
NEUROPSYCHIATRIC FINDINGS: Intense Anxiety, Denial, And
Depression.
Altered mental status In STEMI Greatly reduced cardiac output and
cerebral
hypoperfusion
Cerebral embolism secondary to mural thrombus.

16. LABORATORY FINDINGS : CARDIAC BIOMARKER
Elevations in cTnI may
persist for 7 to 10 days after
MI.
Elevations in cTnT may
persist for up to 10 to 14
days.
The prolonged time course
of the elevation in cTnT and
cTnI is advantageous for the
late diagnosis of MI.
Patients with STEMI who
undergo successful
recanalization of the infarct-
related artery have a rapid
release of cardiac troponins,
which can indicate
reperfusion.

17. Detecting reinfarctions should be
based on the clinical scenario,
ECG, and at least two serial tests.
Measuring concurrent CKMB
may help identify early
reinfarction because CKMB
levels decline much faster than
cTn.
Natriuretic peptides are released early after STEMI, with a peak at approximately
16 hours.

18. The rise in B type natriuretic peptide (BNP) and N-terminal pro-B-type
natriuretic peptide (NT-proBNP) after STEMI correlates with infarct size and
regional wall motion abnormalities.
SERUM LIPIDS :
 Fall in HDL cholesterol after STEMI is greater than the fall in total
cholesterol
 All patients with STEMI should receive high-intensity statin therapy.
 Increased triglycerides may offer additional risk stratification beyond
LDL and
HDL cholesterol levels
HEMATOLOGIC FINDINGS :
 Elevation of WBC within 2 hours after the onset of chest pain,
Peak 2 to 4 days after infarction
Returns to normal in 1 week
(peak WBC ranges between 12 and 15 × 103/mL )
 High WBC at initial evaluation in patients with an ACS  An increased
risk for adverse clinical outcomes.
 Cardiovascular mortality increases as the initial Hb falls below 14 to
15 g/dL; And rises in Hb level above 17 g/dL.

19. ELECTROCARDIOGRAM:
2018 ESC/ACC/AHA/WORLD HEALTH FEDERATION UNIVERSAL DEFINATION OF MI:
STEMI: New ST segment elevation at the J point in two contiguous leads with cut
points
 >1mm in all leads except V2-V3
 In leads V2-V3 the following cut points apply:-
>2mm in Men >40 years
>2.5 mm in Men <40 years
>1.5 mm in women
NSTEMI/UNSTABLE ANGINA:
 New horizontal or downsloping ST depression >0.5mm in two contiguous
leads.
 T wave inversion >1mm in two contiguous leads with prominent R wave or
R/S ratio >1

20. ELECTROCARDIOGRAPHIC MANIFESTATIONS OF ISCHEMIA IN THE SETTING OF LBBB:
ST segment elevation >1 mm and concordant with the QRS complex 5 points
ST segment Depression >1mm in leads V1,V2,or V3 3 points
ST segment elevation >5mm and discordant with the QRS complex 2 points
A SCORE >3 HAD A SP OF 98% FOR ACUTE MI

21. MODIFIED SGARBOSSA CRITERIA:
1. Unchanged
2. Unchanged
3. Abnormal Excessive Discordance-
>1 Lead With >1mm ST Segment Elevation And Proportionally Excessive
Discordan ST Elevation As Defined By STE >25% Of The Depth Of The
Preceding S Wave
ECG CHANGES ASSOCIATED WITH PREVIOUS MI(IN THE ABSENCE OF LVH AND LBBB):
 Any Q wave in leads V2-V3 >0.5mm or QS complex in leads V2-V3
 Q wave >0.03sec and >1mm deep or QS complex in leads I II aVL aVF or V4-V6.
 R wave >0.04sec in V1-V2 and R/S >1 with a concordant positive T wave in absence
of a conductions defect.

22. STEMI EQUIVALENTS:
 ISOLATED PWMI
 WELLENS T WAVES.
 DE WINTERS SIGN.
 ST ELEVATION IN LEAD AVR.
 LBBB WITH SGARBOSSA.
 HYPERACUTE T WAVES.

23. ISOLATED POSTERIOR WALL MI :
European Society of Cardiology (ESC) 2017 guidelines as
 Isolated ST segment depression greater than or equal to 0.5mm in leads VI-V3.
 ST elevation of 0.5 mm in leads V7-V9 with the use of posterior leads.
 Posterior wall involvement is reported to occur in 15% to al% of acute MI.
 The rate of "isolated PMI” has been reported to be approximately 3.3%.
 culprit artery: LCx/Ramus.
Missed diagnosis with ECG because:
 As posterior leads ECG was done late.
 Large back musculature was not taken into account.

24. POINTS TO REMEMBER :
 T inversions and ST depressions are manifestations of Ischemia on ECG.
 Manifestations of cardiac Injury : ST elevation.
 Manifestations of infarct : Pathological Q wave.
 Ischemia does not localize on ECG.
 T inversions and ST depressions do not localize on ECG.
 Injury and infarct localizes (ST elevations § Qwaves).
 It's a good idea to eliminate terms like "inferior ischemia"and "anterior ischemia"
from your vocabulary.
 If localized ischemia is visualized, it indicates opposite territory infarction.

25. WELLENS SYNDROME: Also known as LAD coronary T wave syndrome.
SYNDROME CRITERIA include the following:
 Characteristic T wave changesDeeply inverted or Biphasic T
waves in V2-3 (may extend to V1-6).
 History of anginal chest pain.
 Normal or minimally elevated cardiac enzyme levels.
 ECG without Q waves, without significant ST segment elevation , and
with normal precordial R wave progression .
 75% of patients develop extensive AWMI within a few weeks if they
were treated with only medical management.
DO NOT DISCHARGE WITHOUT CAG.

26. Type A – Biphasic, with initial
positivity and terminal
negativity (25% of cases)
Type B – Deeply and
symmetrically inverted (75% of
cases)
A completely normal ECG does not exclude ACS:
RisK is 4% if patients have CAD and 2% if no prior H/O CAD.
A normal ECG, has a 80 to 90% negative predictive value

27. An upsloping ST depression with tall Hyperacute T wave (rocket like).
In a patient with sepsis, shock and renal
failure, tall T waves almost certainly
indicate hyperkalemia.
In a patient who presents with acute
chest pain, it is most likely the de winter
sign.
Tall T waves of hyperkalemia are usually
narrow based where as the de winter T
waves are usually not.
DE WINTER'S T WAVE :
Reciprocal ST segment elevation
(0.5mm-1mm) in aVR

28. NON-OCCLUSION MYOCARDIAL INFARCTION (NOMI): Due to severe
single or multi-vessel disease eg: LMCA , Proximal LAD, TVD
ST elevation in aVR with ST depression in >5 Lead .
ST elevation in aVR is significant only when ST depression in
V5 & V6 are significant.
ST elevation in aVR is not significant in  LVH with Strain, BBB

29. ANTERIOR WALL MI:
ST Elevation In anterior Leads always look for Inferior Leads
IF ST depression in leads II II aVF  Proximal LAD
IF ST Elevation in Leads II III aVF wrap around LAD
IF ST Isoelectric in Leads II III aVF Distal LAD
Proximal LAD Proximal to S1 & D1
RBBB
ST Depression in Inferior Leads
ST Elevation in V1>2.5mm  V1>aVR
ST Depression in V5 & V6

32. INFERIOR WALL MI:
ST Elevation in Leads II III aVF  IWMI
aVL ST depression > aVR
ST Elevation in
Leads V1 , V2 & V3  RVMI
ST Elevation
III > II II > III
RCA OCCLUSION LCx OCCLUSION / wrap around LAD
Deep ST depression in V2 &
Isoelectric V1  PWMI
ST Elevation in II > III
ST Depression in aVR > aVL

37. ECHOCARDIOGRAPHY:
Echo usefull to know :
 Regional Wall Motion Abnormality
 LV function
 early detection of a potentially viable but stunned myocardium
 mechanical complications of MI such as ventricular thrombus,
acute mitral or tricuspid regurgitation, or ventricular septal defects
CHEST X RAY : Prominent pulmonary vascular markings on the radiograph
reflect elevated LV end-diastolic pressure.
MAGNETIC RESONANCE IMAGING: limited application during the acute
phase.
Useful in the diagnostic assessment of possible etiologies in MINOCA.
Contrast-enhanced CMR with gadolinium can accurately define areas of
myocardial necrosis.

38. NUCLEAR IMAGING: No role in the acute management of STEMI.
COMPUTED TOMOGRAPHY: CT can assess the cavity dimensions and wall
thickness, can detect LV aneurysms, and intracardiac thrombi.

39. MANAGEMENT OF STEMI

40. PREHOSPITAL MANAGEMENT:

41.  Tme to take an ECG and Diagnose STEMI < 10 mint.

42. If patient come to PCI capable center  STEMI diagnosis < 10 mint
and Time to wire cross < 60 mint
If patient come to Non PCI capable center  STEMI diagnosis < 10 mint
<120 mint then
Primary PCI < 90 mint
>120 mint then
thrombolysed < 10mint
After Lytic Bolus (ASAP)
Failed Lysis
Immediate Rescue PCI
Successful Lysis
Pharmaco Invasive PCI

43. INITIAL MANAGEMENT OF STEMI
 Insert IV line
 IV Fluid in RVMI
 Take blood for Troponins
 ECG monitoring with Defibrillator
 Oxygen if Spo2 <90%
 IV morphine for pain (IIa)

44. LOADING DOSE
Chew a non–enteric-coated tablet Aspirin 162-325mg
Clopidogrel 300mg stat if age >75yrs the 75mg
Atorvastatin 80mg /Rosuvastatin 20mg stat
If patient taken for Primary PCI then
Clopidogrel 300mg additional dose
Ticagrelor 180mg stat
Prasugrel 60mg stat

45. REPERFUSION THERAPY
Aim To Attain Normal Epicardial Coronary Flow TIMI3
Attain Normal Microvascular Flow MPG3
IF ST resolution >70% is achieved 
signifies TIMI 3 flow & MPG 3 flow

46. TMP grade 0 or no perfusion of the
myocardium is associated with the highest
rate of mortality.

47. THROMBOLYTIC AGENTS:
ALTEPLASE Bolus of 15 mg, infusion of 0.75 mg/kg for 30 minutes (maximum, 50 mg),
then 0.5 mg/kg (maximum, 35 mg) over the next 60 minutes; the total dose not to exceed
100 mg.
TENECTIPLASE Bolus of 30 mg for weight less than 60 kg, 35 mg for 60 to 69 kg, 40
mg for 70 to 79 kg, 45 mg for 80 to 89 kg, and 50 mg for 90 kg or greater.

48. CONTRAINDICATIONS TO USE OF FIBRINOLYTICS FOR TREATING
STEMI:
NEWER FIBRINOLYTICS  DESMOTEPLASE is highly fibrin specific.

49. SIGN OF REPERFUSION Hypotension with Bradycardia and relief of chest pain.
Give IV fluids for low BP
POST LYSIS ANTICOAGULATION upto 8 days of Hospital stay
upto 3 days post PCI
Preferred anticoagulant  Enoxaparin
<75yrs of age 30mg iv bolus f/b 1mg/kg sc 12hrly
>75 yrs of age (no bolus ) 0.75mg/kg sc once a day
eGFR <30 once daily dose
fondaparinux  (only with sTk) 2.5mg iv bolus f/b 2.5mg sc once daily

50. Mortality of pre hospital Lysis is less than primary PCI because time is the most
important factor.
Trials: CAPTIM, STREAM, PRAGUE-2

51. PRIMARY PCI

52. INDICATIONS FOR CORONARY ANGIOGRAPHY IN PATIENTS WHO
WERE MANAGED WITH FIBRINOLYTIC THERAPY OR WHO DID NOT
RECEIVE REPERFUSION THERAPY
<12 HRS PRIMARY PCI IS A CLASS I RECOMMENDATION

54. ADJUNCTIVE THERAPY FOR STEMI
Non Pharmacological Therapy 
 Life style modifications
 Stop smoking
 Stop alcohol and weight control
 Exercise based cardiac rehabilitation
Pharmacological Measures
 DAPT
 STATIN
 BETA BLOCKER
 ACEi /ARB
 MRA
 NITRATE

55. DUAL ANTIPLATELET THERAPY (DAPT)

56. TREATMENT ALGORITHM FOR THE DURATION OF P2Y12 INHIBITOR
THERAPY IN PATIENTS WITH RECENT ACUTE CORONARY SYNDROME
(NSTE-ACS OR STEMI)

57. STATINS High intensity statinare recommended
lipid profile within 24hrs and repeat after 4-6 wks
Target LDL <70mg/dl
ACEi / ARB The reduction in mortality with ACE inhibitors was
accompanied
by significant reductions in the development of HF.

58. RECOMMENDATIONS FOR BETA-BLOCKER THERAPY FOR STEMI
Commonly Used BB Are Carvedilol,Bisoprolol,Metoprolol

59. NITRATES
No mortality benefits
used when Uncontrolled HTN, HF,Residual Angina is present
CALCIUM CHANNEL BLOCKER No mortality benefits
used when BB is contraindicated