Myocardial infarction.

- Edward Hyde (Before 1550BC): Earliest description of angina

in the Ebers Papyrus
- William Heberden (1768): Coined the term "angina pectoris"
and also referred to it as "Heberden's asthma."
- Edward Jenner (1776): Proposed that angina is a result of
coronary artery insufficiency.
- William Osler (1912): Termed angina as the "cramp of heart
muscle."
- Nikolay Anichkov (1950): Linked coronary artery disease as
the predominant cause of angina, marking the appearance of
ischemic heart disease in textbooks.
1970: Thrombus confirmed as the cause of myocardial
infarction through post-mortem examinations.
- Eugene Braunwald (20th Century): Contributed significantly
to the understanding of ischemic heart disease, advancing
knowledge on its pathophysiology and treatment strategies.

Coronary Artery Disease (CAD):

- Refers to luminal narrowing of a coronary artery, typically

caused by atherosclerosis.
- Leading contributor to ischemic heart disease (IHD).

Ischemic Heart Disease (IHD):

- Encompasses conditions such as angina pectoris, myocardial

infarction (MI), and silent myocardial ischemia.
- Represents a spectrum of cardiovascular disorders.

Cardiovascular Disease (CVD):

- Includes a broader range of conditions beyond IHD.

 - Encompasses cardiomyopathy, heart failure (HF), arrhythmia,
hypertension, cerebrovascular accident (CVA), diseases of the
aorta, peripheral vascular disease (PVD), valvular heart
disease, and congenital heart disease.

Stable Angina:

- Defined as angina symptoms or equivalent symptoms

reproducible with consistent levels of activity.
- Relief achieved through rest.

Definition of MI: UDMI 2018

Universal definition of myocardial injury summary :

First few definitions were based on clinical features and ECG

Then came CPK MB

Then came Trop I which was optional but now it’s compulsory
Gist of the definition :

1.Myocardial Injury

2. Troponin > 99th percentile

3. Acute MI 5 types
Myocardial injury:

Elevated cardiac Troponin with at least one value above 99th Percentile
of upper reference limit

Acute - Rise or/and fall in Troponin

Chronic - Elevated above Upper limit but no rise and fall

Causes of elevated trop I :
Approach to chest pain

Typical angina has three features:

(1) substernal chest discomfort with a characteristic quality and

duration that is

(2) provoked by stress or exertion and

(3) relieved by rest or nitroglycerin.

Atypical angina has two of these three characteristics. Non-cardiac chest

pain meets one or none of these characteristics.

Chronic stable angina is reproducibly precipitated in a predictable manner

by exertion or emotional stress and relieved within 5–10 minutes by
sublingual nitroglycerin or res

Chest pain history taking -

Blood supply of heart :
Myocardial Ischaemia Background

Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two

main entities:

Non-ST-elevation myocardial infarction (NSTEMI).

Unstable angina pectoris (UAP).

Which of the following ECG findings are associated with myocardial

ischemia, except:

A) ST segment depression

B) T wave flattening

C) Peaked T waves

D) U-wave inversion

E) None

Patterns of Myocardial Ischaemia

Two main ECG patterns associated with NSTEACS:

ST segment depression

T wave flattening or inversion

While there are numerous conditions that may simulate myocardial ischaemia
(e.g. left ventricular hypertrophy, digoxin effect), dynamic ST segment and T wave

changes (i.e. different from baseline ECG or changing over time) are strongly
suggestive of myocardial ischaemia.

Other ECG patterns of ischaemia

Hyperacute (peaked) T waves or pseudonormalisation of previously inverted T waves

(i.e. becoming upright) suggest hyperacute STEMI.

Another, less well-known ECG feature of myocardial ischaemia is U-wave inversion.

MORPHOLOGY OF ST DEPRESSION

Which of the following statements regarding ST depression on an ECG is

Wrong?

A) Upsloping ST depression is highly specific for myocardial ischemia.

B) ST depression ≥ 2 mm in ≥ 3 leads indicates a high probability of

NSTEMI with significant mortality.

C) Horizontal or down sloping ST depression ≥ 1 mm at the J-point in ≥ 2

contiguous leads suggest myocardial ischemia.

D) ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads may

indicate myocardial ischemia according to the 2007 Task Force Criteria.
ST depression can be either upsloping, downsloping, or horizontal
(see diagram below).

Horizontal or down sloping ST depression ≥ 0.5 mm at the J-point in ≥

2 contiguous leads indicates myocardial ischaemia (according to
the 2007 Task Force Criteria).

ST depression ≥ 1 mm is more specific and conveys a worse

prognosis.

ST depression ≥ 2 mm in ≥ 3 leads is associated with a high

probability of NSTEMI and predicts significant mortality (35%
mortality at 30 days).

Upsloping ST depression is non-specific for myocardial ischaemia.

Examples of ST segment morphology in myocardial ischaemia

T wave inversion

T wave inversion may be considered to be evidence of myocardial

ischaemia if:

At least 1 mm deep

Present in ≥ 2 continuous leads that have dominant R waves

(R/S ratio > 1)

Dynamic — not present on old ECG or changing over time

Widespread T wave inversion due to myocardial ischaemia (most prominent in the lateral leads)
 Myocardial Infarction on ECG

Which of the following criteria is NOT typically associated with ST elevation

myocardial infarction (STEMI)?

A) New ST elevation ≥ 1 mm in two contiguous leads

B) ST elevation ≥ 2 mm in V2-V3 in men above 40 years old or ≥ 2.5 mm in

men below 40 years old.

C) ST elevation ≥ 1.5 mm in leads V2-V3 in women.

D) ST elevation ≥ 1.5 mm in V2-V3 if age below 40 years and >2mm if age

is above 40 years
DYNAMIC ST-T WAVE CHANGES

What is the primary reason for the dynamic ST-T changes observed in
myocardial infarction (MI)?

A) Abnormalities in the P wave morphology

B) Alterations in ventricular hypertrophy

C) Ischemia-induced cellular changes and electrophysiological alterations

D) Changes in atrioventricular node conduction

Pathophysiology for Dynamic ST-T wave changes :

1. Ischemia-induced cellular changes: Ischemia disrupts cellular

metabolism and ion homeostasis in cardiac myocytes, leading to altered
ion channel function and membrane potentials.

2. Electrophysiological alterations: Ischemia affects the transmembrane

ion currents responsible for action potential generation and propagation,
particularly in phases 2 and 3 of the action potential. This disruption
manifests as ST segment deviation and T wave changes on the ECG.

3. Regional myocardial injury: The specific ECG changes observed in MI

depend on the location and extent of myocardial injury resulting from
reduced blood flow in a particular coronary artery territory.

4. Temporal evolution of changes: The dynamic nature of ST-T changes

reflects the evolving nature of ischemic injury, with ST segment
elevation indicating ongoing myocardial injury and potential reperfusion
or resolution leading to normalization or decrease in ST elevation.
ECG Features of Anterior STEMI

ST segment elevation with subsequent Q wave formation in precordial

leads (V1-6) +/- high lateral leads. These changes are often preceded by
hyperacute T waves

Reciprocal ST depression in inferior leads (mainly III and aVF)

NB: The magnitude of reciprocal change in inferior leads is determined by

the magnitude of ST elevation in I and aVL (as these leads are electrically
opposite III and aVF), and hence may be minimal or absent in anterior
STEMIs that do not involve high lateral leads.

Clinical Relevance of Anterior Myocardial Infarction

Anterior STEMI usually results from occlusion of the left anterior

descending artery (LAD).

Anterior myocardial infarction carries the poorest prognosis of all infarct

locations, due to the larger area of myocardium infarct size.
A study comparing outcomes from anterior and inferior infarctions
(STEMI + NSTEMI) found that compared with inferior MI, patients with
anterior MI had higher incidences of:

In-hospital mortality (11.9 vs 2.8%)

Total mortality (27 vs 11%)

Heart failure (41 vs 15%)

Significant ventricular ectopic activity (70 vs 59%)

Lower ejection fraction on admission (38 vs 55%)

In addition to anterior STEMI, other high-risk presentations of anterior

ischaemia include left main coronary artery (LMCA) stenosis, Wellens
syndromeand De Winter T waves.

The precordial leads can be classified as follows:

 Septal leads = V1-2

 Anterior leads = V3-4
 Lateral leads = V5-6

The different infarct patterns are named according to the leads with maximal ST
elevation:

 Septal = V1-2
 Anterior = V2-5
 Anteroseptal = V1-4
 Anterolateral = V3-6, I + aVL
 Extensive anterior / anterolateral = V1-6, I + aVL

Clinically important

Other important ECG patterns to be aware of:

Anterior-inferior STEMI due to occlusion of a “wraparound” LAD

. This presents with simultaneous ST elevation in the precordial

and inferior leads, due to occlusion of a variant (“type III”) LAD
that wraps around the cardiac apex to supply both the anterior
and inferior walls of the left ventricle

Left main coronary artery stenosis: widespread ST depression with

ST elevation in aVR ≥ V1

Wellens syndrome: deep precordial T wave inversions or biphasic T waves

in V2-3, indicating critical proximal LAD stenosis (a warning sign of
imminent anterior infarction)

De Winter T waves: upsloping ST depression with symmetrically peaked T

waves in the precordial leads; a “STEMI equivalent” indicating acute LAD
occlusion.

ECG Examples

Example 1
  ST elevation and hyperacute T waves in V2-4
 ST elevation in I and aVL with reciprocal ST depression in lead III
 Q waves are present in the septal leads V1-2
 These features indicate a hyperacute anteroseptal STEMI

Example 2a

Hyperacute Anterior STEMI:

 There are hyperacute T-waves in V2-6 (most marked in V2 and V3) with loss of
R wave height.
 Normal sinus rhythm with 1st degree AV block
 There are premature atrial complexes (beat 4 on the rhythm strip) and
multifocal ventricular ectopy (PVCs of two different types), indicating an
“irritable” myocardium at risk of ventricular fibrillation
Example 2b :

Example 3

Example 4
Extensive Anterior STEMI (acute):

ST elevation in V1-6 plus I and aVL (most marked in V2-4)

Minimal reciprocal ST depression in III and aVF

Q waves in V1-2, reduced R wave height (a Q-wave equivalent) in V3-4

There is a premature ventricular complex (PVC) with “R on T’

phenomenon at the end of the ECG; this puts the patient at risk for
malignant ventricular arrhythmias

Example 5

Tombstoning of ST segment seen in Proximal LAD Occlusion

Example 6

Anterior-inferior STEMI

 ST elevation is present throughout the precordial and inferior leads

There are hyperacute T waves, most prominent in V1-3

Q waves are forming in V1-3, as well as leads III and aVF

This pattern is suggestive of occlusion occurring in “type III” or

“wraparound” LAD (i.e. one that wraps around the cardiac apex to supply
the inferior wall)
Territories

Prediction of the Site of LAD Occlusion

The site of LAD occlusion (proximal versus distal) predicts both infarct
size and prognosis.

Proximal LAD / LMCA occlusion has a significantly worse prognosis due

to larger infarct territory size and more severe haemodynamic
disturbance

The site of occlusion can be inferred from the pattern of ST changes in

leads corresponding to the two most proximal branches of the LAD:

the first septal branch (S1) and the first diagonal branch (D1)

 S1 supplies the basal part of the interventricular septum, including

the bundle branches (corresponding to leads aVR and V1)
 D1 supplies the high lateral region of the heart (leads I and aVL)
Occlusion proximal to S1

Signs of basal septal involvement:

ST elevation in aVR

ST elevation in V1 > 2.5 mm

Complete RBBB

ST depression in V5

This patient’s ECG shows several signs of a very proximal LAD occlusion (ostial LAD
occlusion septal STEMI):

Occlusion proximal to D1

Signs of high lateral involvement:

 ST elevation / Q-wave formation in aVL and I

 ST depression ≥ 1 mm in II, III or aVF (reciprocal to STE in aVL)

 There is a septal STEMI with ST elevation maximal in V1-2 (extending out to

V3).
 There is a new bifascicular block (RBBB + LAFB)
 Marked ST elevation (> 2.5 mm) in V1 plus STE in aVR — these features
suggest occlusion proximal to S1
MCQ
LATERAL STEMI
Clinical Significance of lateral STEMI

 The lateral wall of the LV is supplied by branches of the left anterior

descending (LAD) and left circumflex (LCx) arteries.

 Infarction of the lateral wall usually occurs as part of a larger territory

infarction, e.g. anterolateral STEMI.

 Isolated lateral STEMI is less common, but may be produced by occlusion of

smaller branch arteries that supply the lateral wall, e.g. the first diagonal
branch (D1) of the LAD, the obtuse marginal branch (OM) of the LCx, or
the ramus intermedius.

 Lateral STEMI is a stand-alone indication for emergent reperfusion.

 Lateral extension of an anterior, inferior or posterior MI indicates a larger

territory of myocardium at risk with consequent worse prognosis.

How to recognise a lateral STEMI

 ST elevation in the lateral leads (I, aVL, V5-6).

 Reciprocal ST depression in the inferior leads (III and aVF).
 ST elevation primarily localised to leads I and aVL is referred to as a high
lateral STEMI.
NB. Reciprocal change in the inferior leads is only seen when there is ST elevation in
leads I and aVL. This reciprocal change may be obliterated when there is concomitant
inferior ST elevation (i.e an inferolateral STEMI)
Patterns of lateral infarction

Three broad categories of lateral infarction:

 Anterolateral STEMI due to LAD occlusion.

 Inferior-posterior-lateral STEMI due to LCx occlusion.
 Isolated lateral infarction due to occlusion of smaller branch arteries such as
the D1, OM or ramus intermedius.

High Lateral STEMI

ST elevation is present in the high lateral leads (I and aVL).

There is also subtle ST elevation with hyperacute T waves in V5-6.

There is reciprocal ST depression in the inferior leads (III and aVF) with
associated ST depression in V1-3 (which could represent anterior
ischaemia or reciprocal change).

This pattern is consistent with an acute infarction localised to the

superior portion of the lateral wall of the left ventricle (high lateral
STEMI).

The culprit vessel in this case was an occluded first diagonal branch of
the LAD.
Example no.2

 There is subtle ST elevation in the high lateral leads (I and avL).

 There is a pathological Q wave in aVL plus inverted T waves in both I and aVL.
 This pattern is diagnostic of a recent (“completed”) high lateral MI.
 The patient in this case had a 90% occlusion of his obtuse marginal artery (= a
branch of the LCx supplying the lateral wall of the LV).

Example no.3

Anterolateral STEMI:

 ST elevation is present in the anterior (V2-4) and lateral leads (I, aVL, V5-6).
 Q waves are present in both the anterior and lateral leads, most prominently
in V2-4.
 There is reciprocal ST depression in the inferior leads (III and aVF).
 This pattern indicates an extensive infarction involving the anterior and lateral
walls of the left ventricle .
INFERIOR STEMI

Inferior myocardial infarction (MI) accounts for 40-50% of all MIs. It

generally has a more favourable prognosis than anterior
myocardial infarction (in-hospital mortality only 2-9%), however
certain associated features indicate a worse outcome

ECG DIAGNOSTIC CRITERIA

ST elevation in leads II, III, aVF

Hyperacute T waves may precede these changes

Reciprocal ST depression in aVL

Progressive development of Q waves in II, III, aVF

Associated features, all of which confer a worse prognosis, include:

 Concomitant right ventricular infarction (40% of patients);

these patients may develop severe hypotension in response to
nitrates
 Significant bradycardia due to second or third-degree AV
block (20%)
 Posterior infarction due to extension of infarct area
Don’t neglect Avl :

 aVL is the only lead truly reciprocal to the inferior wall, as it

is the only lead facing the superior part of the ventricle. It is
thus a sensitive marker for inferior infarction
 In patient cohorts with inferior occlusion myocardial
infarction (OMI), ST depression in aVL has been shown to be
more prevalent than STE in inferior leads
 91% of “subtle” inferior STEMIs that do not meet STEMI
criteria but show occlusion on PCI demonstrate ST depression
in aVL
Which Artery is the Culprit?

Inferior STEMI can result from occlusion of any of the three main
coronary arteries:

 Dominant right coronary artery (RCA) in 80% of cases

 Dominant left circumflex artery (LCx) in 18%
 Occasionally, a “type III” or “wraparound” left anterior descending
artery (LAD), producing the unusual pattern of concomitant
inferior and anterior ST elevation.

RCA occlusion is suggested by:

 ST elevation in lead III > lead II

 Presence of reciprocal ST depression in lead I
 Signs of right ventricular infarction: STE in V1 and V4R

Circumflex occlusion is suggested by:

 ST elevation in lead II = lead III

 Absence of reciprocal ST depression in lead I

Signs of lateral infarction: ST elevation in the lateral leads I and

aVL or V5-6
WE MUST KNOW V4 R LEAD IN IWMI

Early inferior STEMI:

 Hyperacute (peaked) T waves in II, III and aVF with relative

loss of R wave height
 Early ST elevation and Q-wave formation in lead III
 Reciprocal ST depression and T wave inversion in aVL
 ST elevation in lead III > lead II suggests an RCA occlusion; the
subtle ST elevation in V4R would be consistent with this.
Reciprocal changes of iwmi in aVL

Example 3
Massive inferolateral STEMI:

 Marked ST elevation in II, III and aVF with a “tombstone”

morphology
 Reciprocal change in aVL
 ST elevation is also present in the lateral leads V5-6, indicating an
extensive infarct of the inferior and lateral walls

Inferior STEMI with sinus node dysfunction (either sinus arrest or

extreme sinus bradycardia) and a slow junctional escape rhythm.

 Bradycardia and AV Block in inferior STEMI

 Up to 20% of patients with inferior STEMI will develop either
second- or third-degree AV block. There are two presumed
mechanisms for this:
 Ischaemia of the AV node due to impaired blood flow via the
AV nodal artery. This artery arises from the RCA 80% of the
time, hence its involvement in inferior STEMI due to RCA
occlusion.
 Bezold-Jarisch reflex = increased vagal tone secondary to
ischaemia.
Right Ventricular Infarction
DIAGNOSTIC CRITERIA

In patients with inferior STEMI, right ventricular infarction is

suggested by:

 ST elevation in V1
 ST elevation in V1 and ST depression in V2 (highly specific for
RV infarction)
 Isoelectric ST segment in V1 with marked ST depression in V2
 ST elevation in III > II
 Diagnosis is confirmed by the presence of ST elevation in the
right-sided leads (V3R-V6R)

1. V1 is the only standard ECG lead that looks directly at the

right ventricle
2. Lead III is more rightward facing than lead II and hence more
sensitive to the injury current produced by the right ventricle
Example ECG

Example 1a

Inferior STEMI. Right ventricular infarction is suggested by:

 ST elevation in V1
 ST elevation in lead III > lead II

Example 1b

Repeat ECG of the same patient with V4R electrode position:

 There is ST elevation in V4R consistent with RV infarction

Example 2

Another example of right ventricular infarction in the context of inferior STEMI:

 ST elevation in lead III > lead II

 Isoelectric ST segment in V1 with marked ST depression in V2
 There is ST elevation in V4R
Posterior Myocardial Infarction
Clinical Significance of Posterior MI

Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context

of an inferior or lateral infarction.

 Isolated posterior MI is less common (3-11% of infarcts).

 Posterior extension of an inferior or lateral infarct implies a much
larger area of myocardial damage, with an increased risk of left
ventricular dysfunction and death.
 Isolated posterior infarction is an indication for emergent coronary
reperfusion. However, the lack of obvious ST elevation in this
condition means that the diagnosis is often missed

Be vigilant for evidence of posterior MI in any patient with an inferior or lateral

STEMI.
How to spot posterior infarction

As the posterior myocardium is not directly visualised by the standard

12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal
leads V1-3.

Posterior MI is suggested by the following changes in V1-3:

 Horizontal ST depression
 Tall, broad R waves (>30ms)
 Upright T waves
 Dominant R wave (R/S ratio > 1) in V2
 In patients presenting with ischaemic symptoms, horizontal ST
depression in the anteroseptal leads (V1-3) should raise the suspicion
of posterior MI

Typical appearance of posterior infarction in V2

Explanation of the ECG changes in V1-3

The anteroseptal leads are directed from the anterior precordium

towards the internal surface of the posterior myocardium.

Because posterior electrical activity is recorded from the anterior

side of the heart, the typical injury pattern of ST elevation and Q
waves becomes inverted:
ST elevation becomes ST depression

Q waves become R waves

Terminal T-wave inversion becomes an upright T wave

The progressive development of pathological R waves in posterior

infarction (the “Q wave equivalent”) mirrors the development of Q
waves in anteroseptal STEMI.
Posterior leads
Leads V7-9 are placed on the posterior chest wall in the following
positions (see diagram below):

 V7 – Left posterior axillary line, in the same horizontal plane as V6.

 V8 – Tip of the left scapula, in the same horizontal plane as V6.
 V9 – Left paraspinal region, in the same horizontal plane as V6.

POSTERIOR LEAD PLACEMENT V7, V8, V9

THE DEGREE OF ST ELEVATION SEEN IN V7-9 IS TYPICALLY MODEST –
NOTE THAT ONLY 0.5 MM OF ST ELEVATION IS REQUIRED TO MAKE THE
DIAGNOSIS OF POSTERIOR MI!
Example ECG

Example 1a

Inferolateral STEMI. Posterior extension is suggested by:

 Horizontal ST depression in V1-3

 Tall, broad R waves (> 30ms) in V2-3
 Dominant R wave (R/S ratio > 1) in V2
 Upright T waves in V2-3

Example 1b

The same patient, with posterior leads recorded:

 Marked ST elevation in V7-9 with Q-wave formation confirms involvement of

the posterior wall, making this an inferior-lateral-posterior STEMI (= big
territory infarct!).
Example 3a

Patient presenting with chest pain:

 The ST depression and upright T waves in V2-3 suggest posterior MI.

 There are no dominant R waves in V1-2, but it is possible that this ECG was
taken early in the course of the infarct, prior to pathological R-wave
formation.
 There are also some features suggestive of early inferior infarction, with
hyperacute T waves in II, III and aVF.

Example 3b

An ECG of the same patient taken 30 minutes later:

 There is now some ST elevation developing in V6.

 With the eye of faith there is perhaps also some early ST elevation in the
inferior leads (lead III looks particularly abnormal).
Example 3c

The same patient with posterior leads recorded:

 Posterior infarction is confirmed by the presence of ST elevation >0.5mm in

leads V7-9.

Example 4a

Patient presenting with central chest pain

 Inferior STEMI with posterior extension. Extensive territory

Example 4b

The same patient with posterior leads (V8,9) recorded:

STEMI EQUIVALENT :
Wellen’s syndrome
 The pattern is usually present in the pain free state — it may be
obscured during episodes of ischaemic chest pain, when there is
“pseudonormalisation” of T waves in V2-3
 Wellens syndrome is a key example of why all patients presenting
with chest pain must have serial ECGs

Clinical significance

 Patients may be pain free by the time the ECG is taken, and have
normal or minimally elevated cardiac enzymes. However, they are
at extremely high risk for extensive anterior wall MI within the
subsequent days to weeks

 Due to the critical LAD stenosis, these patients usually require

invasive therapy, do poorly with medical management, and may
suffer MI or cardiac arrest if inappropriately stress tested

Diagnostic criteria

Rhinehart et al (2002) describe the following diagnostic criteria for Wellens

syndrome:

 Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)

 ECG pattern present in pain-free state
 Isoelectric or minimally-elevated ST segment (< 1mm)
 No precordial Q waves
 Preserved precordial R wave progression
 Recent history of angina
 Normal or slightly elevated serum cardiac markers
There are two patterns of T-wave abnormality in Wellens syndrome:

Type A – Biphasic, with initial positivity and terminal negativity (25% of

cases)

Type B – Deeply and symmetrically inverted (75% of cases)

Biphasic T Waves (Type A) Deeply Inverted T Waves (Type B)

Wellens T wave evolution

T wave changes can evolve over time from Type A to Type B pattern (Smith et al).

Evolution of T-wave inversion [A-D] after coronary reperfusion in STEMI reperfusion

and in Wellens syndrome (NSTEMI). Modified from Smith et al. Evolution of T-wave
inversion. The ECG in acute MI, 2002
Example 5

This fantastic ECG series (submitted by paramedic Andrew Bishop) shows a stuttering
pattern of LAD occlusion, reperfusion and re-occlusion in a middle aged lady with
chest pain.

The ECGs are presented in chronological order, over a 45 minute period from the
prehospital environment to the cath lab:

(a) Patient experiencing chest pain and diaphoresis

 The ECG shows a clear anterolateral STEMI, with inferior reciprocal change
 The artery is occluded at this point
(b) Resolution of pain

 The ECG now shows a typical Wellens pattern of biphasic T waves in V2-3,
plus improvement in the anterolateral ST elevation
 This indicates spontaneous reperfusion of the LAD — i.e. the artery has re-
opened
(c) Recurrence of chest pain and diaphoresis

 With recurrence of pain there is pseudo-normalisation of the precordial T

waves: the previously biphasic T waves have become prominently upright (=
“hyperacute” T waves)
 This apparent normalisation of the T waves indicates re-occlusion of the LAD
artery
(d) Ongoing ischaemic symptoms

 Following re-occlusion of the artery, there is further evolution of the

anterolateral ST changes, with evolving anterior STEMI

(e) Symptoms improving

 Once again there is reperfusion of the artery, only this time the ST changes are
slower to resolve

(f) Now Pain Free

 Now the T waves are starting to become biphasic again (Wellens Pattern A)
Original Sgarbossa Criteria
The original three criteria used to diagnose infarction in patients with LBBB are:

 Concordant ST elevation > 1mm in leads with a positive QRS complex (score
5)
 Concordant ST depression > 1 mm in V1-V3 (score 3)
 Excessively discordant ST elevation > 5 mm in leads with a -ve QRS
complex (score 2)

These criteria are specific, but not sensitive (36%) for myocardial infarction. A
total score of ≥ 3 is reported to have a specificity of 90% for diagnosing
myocardial infarction.

During right ventricular pacing the ECG also shows left bundle brach
block and the above rules also apply for the diagnosis of myocardial
infarction during pacing, however they are less specific.
ECG Examples

Example 1

Positive Sgarbossa criteria in a patient with LBBB and troponin-positive

myocardial infarction:

 This patient presented with chest pain and had elevated cardiac
enzymes.
 Previous ECG showed typical LBBB
 There is 1mm concordant ST elevation in aVL (= 5 points)
 Other features on this ECG that are abnormal in the context of
LBBB (but not considered “positive” Sgarbossa criteria) are the
pathological Q wave in lead I and the concordant ST depression in
the inferior leads III and aVF.
 This constellation of abnormalities suggests to the authors that
the patient was having a high lateral infarction
Example 2

E
Positive Sgarbossa criteria in a patient with a ventricular paced rhythm:

 There is concordant ST depression in V2-5 (= Sgarbossa positive).

 The morphology in V2-5 is reminiscent of posterior STEMI, with
horizontal ST depression and prominent upright T waves.
 This patient had a confirmed posterior infarction, requiring PCI to a
completely occluded posterolateral branch of the RCA.
PULMONARY EMBOLISM

1. What is the most common ECG finding in patients with pulmonary

embolism?

- A) Right axis deviation

- B) Right atrial

Saz a`7H ECG Features:

 Sinus tachycardia – the most common abnormality (seen in 44% of

patients with PE)
 Complete or incomplete RBBB (18%)
 Right ventricular strain pattern – T wave inversions in the right
precordial leads (V1-4) ± the inferior leads (II, III, aVF). This pattern
is associated with high pulmonary artery pressures (34%)
 Right axis deviation (16%). Extreme right axis deviation may occur,
with axis between zero and -90 degrees, giving the appearance of
left axis deviation (“pseudo left axis”)
 Dominant R wave in V1 – a manifestation of acute right ventricular
dilatation
 Right atrial enlargement (P pulmonale) – peaked P wave in lead II >
2.5 mm in height (9%)
 SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T
wave in III (20%). This “classic” finding is neither sensitive nor
specific for PE
 Clockwise rotation – shift of the R/S transition point towards V6
with a persistent S wave in V6 (“pulmonary disease pattern”),
implying rotation of the heart due to right ventricular dilatation
 Atrial tachyarrhythmias – AF, flutter, atrial tachycardia (8%)
 Non-specific ST segment and T wave changes, including ST
elevation and depression (50%)
  Simultaneous T wave inversions in the inferior (II, III, aVF) and right
precordial leads (V1-4) is the most specific finding in favour of PE,
with reported specificities of up to 99% in one study.

ECG Examples

Example 1

Massive bilateral pulmonary embolus

 Sinus tachycardia
 RBBB
 T-wave inversions in the right precordial leads (V1-3) as well as lead III

Example 2
Massive bilateral pulmonary embolus

 RBBB
 Extreme right axis deviation (+180 degrees)
 S1 Q3 T3
 T-wave inversions in V1-4 and lead III
 Clockwise rotation with persistent S wave in V6

Example 3

Massive pulmonary embolus

 Sinus tachycardia.
 Simultaneous T-wave inversions in the anterior (V1-4) and inferior
leads (II, III, aVF).
 Non-specific ST changes – slight ST elevation in III and aVF.
MANAGEMENT OF MI :
Nitrates in the management of acute coronary
syndrome

MECHANISMS OF ACTION

Potential mechanisms by which nitrates can relieve ischemic pain

include:

●Dilatation of large coronary arteries and arterioles (>100 millimicrons

[nanometers] in diameter), which may lead to increased perfusion of

ischemic zones.

●Dilatation of the venous system with decreased preload, reduction in

ventricular volume, and a fall in pulmonary capillary wedge pressure.

This effect is useful in patients with pulmonary congestion.

●Systemic arterial dilatation, which decreases afterload, also occurs but

to a lesser degree. These changes lower wall stress and oxygen

consumption and can reverse a restrictive filling pattern.

●Termination of an episode of variant angina.

●Enhanced collateral blood flow.

INTRAVENOUS NITROGLYCERIN

Intravenous nitroglycerin is typically initiated in patients with

persistent ischemic chest pain despite three sublingual nitroglycerin
tablets and other adjunctive therapies.

Dosing — An intravenous infusion permits titration of therapy according

to the blood pressure response.

● The goal of intravenous nitroglycerin therapy is relief of symptoms or a

mean arterial blood pressure 10 percent below baseline in normotensive
patients and up to 25 to 30 percent in hypertensive patients.

The blood pressure lowering should be gradual with careful attention to

signs or symptoms of hypoperfusion. The systolic pressure should not fall
below 90 mmHg or by more than 30 mmHg.

● The initial infusion rate is 5 to 10 mcg/min.

● If the above goals are not met, the infusion rate is gradually increased
at approximately 10-minute intervals by 5 to as much as 20 mcg/min.

● In general, the dose should not exceed 400 mcg/min.

Nitrates in all forms should be avoided in patients with one or more of the
following :

● Systolic blood pressure less than 90 mmHg or ≥30 mmHg below

baseline. Nitrates may induce symptomatic hypotension and can lead to
hemodynamic decompensation in the setting of cardiac ischemia.

● Marked bradycardia (heart rate less than 50 beats per minute) or

tachycardia (heart rate greater than 100 beats per minute). In this
setting nitrates may cause hemodynamic decompensation.

● Known or suspected right ventricular infarction. Nitrates should be

avoided because of the increased risk of inducing hypotension. (See
"Right ventricular myocardial infarction".)

● Patients who have taken a phosphodiesterase inhibitor for erectile

dysfunction within the last 24 hours (or perhaps as long as 48 hours with
tadalafil). Nitrates may induce severe hypotension. (See "Sexual activity
in patients with cardiovascular disease".)

● Hypertrophic cardiomyopathy. Nitrates can induce or increase outflow

tract obstruction, even in those not known to have a resting gradient.