Myocardial infarction_ Causes, Symptoms, Diagnosis, Treatment, and Pathology

Myocardial infarction
Causes, Symptoms, Diagnosis, Treatment, Pathology
Marc Imhotep Cray, M.D.

Marc Imhotep Cray, M.D..
Topics Outline
2
 Scientific foundations
 Pathology of MI
 A Clinical & Pathology Correlation Case
 Clinical Medicine Capsule (Dx & Tx)

Scientific foundations
3

Epidemiology
 Myocardial infarction is a common presentation of coronary
artery disease
 WHO estimated in 2004, that 12.2% of worldwide deaths were
from ischemic heart disease (IHD) leading cause of death in
high- or middle-income countries and  second only to lower
respiratory infections in lower-income countries
 Worldwide, more than 3 million people have STEMIs and 4
million have NSTEMIs a year
 STEMIs occur about twice as often in men as women
4

Diagnostic Classifications & Terminology
5
 Anatomic (Pathologic) Diagnosis= Atherosclerosis (ASHD)
 Etiologic Diagnosis= Coronary Heart Disease (CHD, IHD,
CAD)
 Physiologic Diagnosis= Angina Pectoris (Stable vs
Unstable vs ACS ), SOB, Atrial fibrillation, MI etc.
 Functional Diagnosis= New York Heart Association
(NYHA) functional classification Heart Failure
o Pulmonary Edema/Cardiogenic Shock major acute complication
of myocardial infarction (STEMI and NSTEMI )

NYHA Functional Classification HF
The classes (I-IV) are:
Class I: no limitation is experienced in any activities; there are no
symptoms from ordinary activities
Class II: slight, mild limitation of activity pt. comfortable at rest
or with mild exertion.
Class III: marked limitation of any activity pt. comfortable only
at rest
Class IV: any physical activity brings on discomfort and Sx occur at
rest
Note: This score documents severity of Sx and can be used to assess response
to treatment
While its use is widespread, NYHA score is not very reproducible and does not
reliably predict walking distance or exercise tolerance on formal testing
"Limitations of the New York Heart Association functional classification system and
self‐reported walking distances in chronic heart failure". Heart. 93 (4): 476–82.
6

Coronary heart disease (CHD) Defined
(Etiologic Dx)
7
 Coronary heart disease (CHD) is a condition in which
proper circulation of blood and oxygen are not
provided to heart and surrounding tissue
 Result is due to a narrowing of small blood vessels,
which normally supply heart with blood and oxygen
 Coronary heart disease, a type of cardiovascular
disease leading cause of death for both men and
women in United States

Causes (Anatomic Dx)
8
 Cause of CHD atherosclerosis, which takes place with plaque
and fatty build up on artery walls narrowing vessels

Arteriosclerosis
9
 Arteriosclerosis is a general term
for several disorders that cause
thickening and loss of elasticity in
arterial wall
 Atherosclerosis, the most common
form, is also the most serious b/c it
causes coronary artery disease and
cerebrovascular disease
 Atherosclerosis is patchy intimal
plaques (atheromas) in medium-
sized and large arteries
 plaques contain lipids, inflammatory
cells, smooth muscle cells, and
connective tissue
Atherosclerotic narrowing, microscopic
Normal coronary artery, microscopic
From: Webpath Cardiovascular Pathology image plates

Pathobiology of Atherosclerosis
10
When excess cholesterol deposits on
cells and on inside walls of blood
vessels it forms an atherosclerotic
plaque
First step of atherosclerosis is injury
to endothelium (See slide # 5) which
results in atherosclerotic lesion
formation
When plaque ruptures blood clots
form which lead to ↓ blood flow,
resulting in cardiovascular events
(ACS)
Coronary artery, severe atherosclerosis, gross
Coronary artery, mild atherosclerosis, gross
From: Webpath Cardiovascular Pathology image plates

Pathobiology of Atherosclerosis cont’d.
11
Symptoms develop when growth or
rupture of plaque reduces or
obstructs blood flow
Diagnosis is clinical and confirmed
by angiography, ultrasonography, or
other imaging tests
Treatment includes risk factor and
dietary , modification, physical
activity, antiplatelet drugs, and
antiatherogenic drugs
Image plate description: Heart and LAD coronary artery with recent thrombus, gross
 Anterior surface of heart demonstrates an opened left anterior descending coronary artery
 Within lumen of coronary can be seen a dark red recent coronary thrombosis
 Dull red color to myocardium as seen below glistening epicardium to lower right of thrombus
is consistent with underlying MI From: Webpath Cardiovascular Pathology image plates

Risk Factors for Atherosclerosis
12
Risk factors atherosclerosis include:
 Dyslipidemia
(hypercholesterolemia/LDL-C)
 diabetes
 cigarette smoking
 family history
 sedentary lifestyle
 obesity
 hypertension

CAD Risk Factors
13
1. Age (particularly 40+)
2. Diabetes
3. Genetics (heredity)
4. High blood pressure
5. High bad cholesterol
(LDL)
6. Increased levels of C-
reactive protein, fibrinogen,
or homocysteine
7. Lack of sufficient physical
activity
8. Low good cholesterol (HDL)
9. Menopause
10. Obesity
11. Smoking
 Certain conditions are considered to put an individual at
greater risk for coronary heart disease
Following are some risk factors: (same as for atherosclerosis in general)

Symptoms OF CHD
14
 Some more frequent symptoms of coronary heart
disease include:
1. Angina (ischemic pain)
2. Myocardial Infarction
3. Shortness of breath
4. Atrial fibrillation

Diagnosis
15
Diagnosis of CHD may be accomplished by a variety of
means:
1. Coronary angiography
2. Coronary arteriography
3. Coronary CT angiography
4. Echocardiogram
5. Electrocardiogram (ECG)
6. Electron-beam CT (EBCT)
7. Exercise stress test
8. Magnetic resonance angiography
9. Nuclear scan

Remember: A MI occurs when an atherosclerotic plaque slowly builds up in inner lining of
a coronary artery and then suddenly ruptures, causing catastrophic thrombus formation,
totally occluding artery and preventing blood flow downstream.
16
Online version

Areas where pain is experienced in myocardial infarction,
showing common (dark red) and less common (light red)
areas on the chest and back.
17

Criteria for Diagnosis of acute myocardial
infarction (AMI)
Criteria
 An AMI, according to current consensus, is defined by
an elevated cardiac biomarker and at least one of the
following:
 Symptoms relating to ischemia
 Changes on an electrocardiogram (ECG), such as ST segment
changes, new left bundle branch block, or Q waves
 Changes in motion of heart wall on imaging
 Demonstration of a thrombus on angiogram or at autopsy
18

Types (classification) of MI
Types
MIs are generally clinically classified into
 ST elevation MI (STEMI) and non-ST elevation MI
(NSTEMI) These are based on changes to an ECG
STEMIs make up about 25 - 40% of MIs
19

Types (classification) of MI cont’d.
 A more explicit classification system, based on
international consensus in 2012, also exists
classifies MIs into five types:
1. Spontaneous MI related to plaque erosion and/or
rupture, fissuring, or dissection
2. MI related to ischemia, such as from increased oxygen
demand or decreased supply, e.g. coronary artery spasm,
coronary embolism, anemia, arrhythmias, high blood
pressure or low blood pressure
20

Types (classification) of MI cont’d.
3. Sudden unexpected cardiac death, including cardiac
arrest, where symptoms may suggest MI, an ECG may be
taken with suggestive changes, or a blood clot is found in a
coronary artery by angiography and/or at autopsy but
where blood samples could not be obtained, or at a time
before the appearance of cardiac biomarkers in the blood
4. Associated w coronary angioplasty or stents
 Assoc. w percutaneous coronary intervention (PCI)
 Assoc. w stent thrombosis as documented by angiography or at
autopsy
5. Associated w CABG
21

Diagnosis of MI cont’d.: Cardiac biomarkers
There are a number of different biomarkers used to
determine presence of cardiac muscle damage
 Troponins (bld), are considered best, and preferred b/c
they have greater sensitivity and specificity for measuring
injury to heart muscle than other tests
 A rise in troponin occurs within 2–3 hours of injury to
heart muscle, and peaks within 1–2 days
o Gross value, as well as a change over time, useful in measuring
and diagnosing or excluding MI
o One high-sensitivity cardiac troponin is able to rule out MI as
long as ECG is normal
22

Diagnosis of MI cont’d.: ECGs
 Electrocardiograms (ECGs) are a series of leads placed on a
person's chest that measure electrical activity assoc. w
contraction of heart muscle
 Taking of an ECG is an important part in workup of an AMI,
and ECGs are often not just taken once, but may be
repeated over minutes to hours, or in response to changes
in Sn or Sx
 In addition to a rise in biomarkers, a rise in ST segment,
changes in shape or flipping of T waves, new Q waves, or a
new LBBB can be used to Dx an AMI
23

ECG cont’d.
 In addition, ST elevation can be used to Dx an ST segment
myocardial infarction (STEMI)
 A rise must be new, in two adjacent ECG leads [greater than 2 mm (0.2
mV) for males] and [greater than 1.5 mm (0.15 mV) in females ] in all
leads except for V2 and V3, where it must be greater than 1 mm (0.1 mV)
 ST elevation is assoc. w infarction, and may be preceded by
changes indicating ischemia such as ST depression or inversion
of T waves
 Abnormalities can help localize location of an infarct, based on leads that
are affected by changes
 Early STEMIs may be preceded by peaked T waves
 Other ECG abnormalities relating to complications of AMI may
also be evident such as atrial or ventricular fibrillation
24

A 12-lead ECG showing a STEMI
Elevation of ST segment can be seen in some leads(II, III, aVF)
25

Poor movement of heart due to an MI as
seen on ultrasound
26
Online version

Pulmonary edema due to an MI as seen on
ultrasound
27
Online Version

Differential diagnosis
 There are many causes of chest pain, which can originate from
the heart, lungs, gastrointestinal tract, aorta, and other
muscles, bones and nerves surrounding the chest
In addition to MI, other causes of CP include
 Angina, insufficient blood supply (ischemia) to the heart
muscles without evidence of cell death
 Gastroesophageal reflux disease (GERD)
 Pulmonary embolism (PE)
 Tumors of the lungs
 Pneumonia
 Rib fracture
 Costochondritis and other musculoskeletal injuries
28

DDx cont’d.
 Rarer severe DDx includes
 Aortic dissection
 Esophageal rupture
 Tension pneumothorax, and
 Pericardial effusion causing cardiac tamponade
 Chest pain in an MI may mimic heartburn
 Causes of sudden-onset breathlessness generally involve lungs or
heart, including
 Pulmonary edema
 Pneumonia
 Allergic reactions and asthma, and
 Pulmonary embolus, acute respiratory distress syndrome
(ARDS) and metabolic acidosis
29

Treatment
30
Coronary heart disease treatment methods may include:
(depends on presenting Physiologic Dx)
1. Angioplasty with stenting
2. Coronary artery bypass surgery (CABG)
3. Medication (Thrombolytic agents)
4. Minimally invasive heart surgery
5. Proper diet and exercise
6. Quitting smoking
7. Treatment of other comorbidities, HTN, DM, Obesity

Marc Imhotep Cray, M.D.. 31
Myocardial Infarction
Pathology
Drawing of heart showing anterior left ventricle wall infarction

Heart, left ventricle, acute myocardial
infarction, gross
32
• This is left ventricular wall which
has been sectioned lengthwise to
reveal a large recent MI
• Center of infarct contains necrotic
muscle that appears yellow-tan
• Surrounding this is a zone of red
hyperemia
• Remaining viable myocardium is
reddish- brown
Webpath Cardiovascular Pathology image plates

Heart, left ventricle and septum, MI, gross
33
• This cross section through heart
demonstrates LV on left
• Extending from anterior portion &
into septum is a large recent MI
• Center is tan with surrounding
hyperemia
• Infarction is "transmural" in that it
extends through full thickness of wall

Heart, transmural MI with rupture and
hemopericardium, gross
34
 One complication of a transmural
MI is rupture of myocardium
• most likely to occur in first week
between 3 to 5 days following initial
event, when myocardium is softest
 White arrow marks point of
rupture in this anterior-inferior MI
of left ventricular free wall and
septum
 Note dark red blood clot forming
hemopericardium
• hemopericardium can lead to
tamponade

Heart, left ventricular aneurysm, gross
35
 A cross section through
heart reveals a ventricular
aneurysm with a very thin
wall at arrow
• Note how aneurysm bulges
out
• Stasis in this aneurysm
allows mural thrombus,
which is present here, to
form within aneurysm Webpath Cardiovascular Pathology image plates

Putting it All Together_ A Clinical & Pathology
Correlation Case (Read: MI Case Scenario with annotations. pdf)
Source: Stevens A, Lowe J, Scott I. Core Pathology, 3rd Ed. St. Louis: Mosby-Elsevier, 2009; 1-3.
A. History of chest pain which improved on rest must mean that
coronary arteries are severely narrowed by atheroma, causing
partial blockage of lumen.
Diagnosis A
Diagnostic process requires an understanding of pathology
Reduction in blood supply to heart muscle
will have produced symptoms of chest pain
only on exertion, when heart is working hard
and has high blood and oxygen requirements.
It is characteristic that this type of pain
(angina of effort) disappears on resting.
Relevant pathology A
36

Clinical & Pathology Correlation Case cont’d.
B. The constant chest pain must mean that pt. now has a true
MI, and that coronary artery is completely blocked, perhaps by
a thrombus.
Relevant pathology B Diagnosis B
There will now be an area of dead heart muscle
in wall of left ventricle, and patient's life is at risk.
Thoughts in doctor’s mind
“I must look out for symptoms and signs of
immediate complications of MI. It will take about
8 weeks for infarcted heart muscle to heal by
scarring; until then he is at risk.”
37

Clinical & Pathology Correlation Case cont’d.
C. This patient's immediate complications are failure of left ventricle, leading to
reduced cardiac output (responsible for his cold, clammy skin and his low blood
pressure). Also, his damaged left ventricle is unable to empty completely at
systole, so there will be increased back pressure in the left atrium and
pulmonary veins and capillaries. Fluid will pass from pulmonary capillary blood
into his alveoli, making him very breathless (pulmonary edema).
The breathlessness and shock must mean
that the patient has a failing left ventricle.
Thoughts in doctor’s mind
“I had better begin treatment immediately
to improve output and strength of
damaged left ventricular muscle. I will give him
strong analgesia for pain and distress, and
consider thrombolysis therapy to break down
thrombus occluding his coronary artery.”
Diagnosis BRelevant pathology C
38

Clinical Medicine Capsule
(Dx & Tx)
39

Acute Coronary Syndromes (ACS)
 ACS is a spectrum of clinical syndromes caused by plaque
disruption or vasospasm  leads to acute myocardial ischemia
 Unstable angina (UA) is defined as chest pain that is
(1) new onset, is (2) accelerating (ie, occurs with less exertion, lasts
longer, or is less responsive to medications),
or (3) occurs at rest
 distinguished from stable angina pectoris by patient history
 UA signals presence of possible impending infarction based
on plaque instability
In contrast,
 NSTEMI indicates myocardial necrosis marked by elevations in
troponin I and creatine kinase–MB isoenzyme (CK-MB) without
ST-segment elevations seen on ECG
40

ACS: UA vs NSTEMI cont’d.
41
Diagnosis
 Patients should be risk stratified according to Thrombolysis
in Myocardial Infarction (TIMI) study criteria
 UA is not assoc. w elevated cardiac markers, but ST changes
may be seen on ECG
 NSTEMI is Dx by serial cardiac enzymes and ECG

Thrombolysis in Myocardial Infarction (TIMI) Risk
Score for UA/NSTEMI
42
Characteristics Point
History
Age ≥ 65 years
Three or more CAD risk factors (premature family history, DM,
smoking, HTN, ↑ cholesterol)
Known CAD (stenosis > 50%)
ASA use in past 7 days
Presentation
Severe angina (2 or more episodes within 24 hours)
ST deviation ≥ 0.5 mm
+ cardiac marker
Risk score—total points* (0–7)
1
1
1
1
1
1
1
*Patients at higher risk (risk score ≥ 3) benefit more from enoxaparin (vs
unfractionated heparin), glycoprotein IIb/IIIa inhibitors, and early angiography.
Le T, Bhushan V, Vincent L. Chen VL, King MR. First Aid for the USMLE Step 2 CK ,9th Ed. New York, NY:
McGraw-Hill Education, 2016.

ACS: UA vs NSTEMI cont’d.
43
Treatment
 Treat acute symptoms with ASA, O2, IV nitroglycerin, and IV
morphine, and consider β-blockers as hemodynamics allow
 Admit to hospital, and monitor until acute MI has been ruled
out by serial cardiac enzymes
 Pts. w CP refractory to medical therapy, a TIMI score of ≥ 3, a
troponin elevation, or ST changes > 1 mm should be given IV
heparin and scheduled for angiography and possible
revascularization (percutaneous coronary intervention [PCI] or
coronary artery bypass graft [CABG])
MNEMONIC: When your patient is MOANing from an MI, remember— MOAN
Morphine
Oxygen (to maintain saturations)
ASA
Nitrogen

ST-Elevation Myocardial Infarction (STEMI)
44
 STEMI=ST-segment elevations and cardiac enzyme release
2° to prolonged cardiac ischemia and necrosis
 History/Physical examination
 Presentation: Acute-onset substernal chest pain,
commonly described as a pressure or tightness that can
radiate to left arm, neck, or jaw
 Assoc. Sx: Diaphoresis, SOB, lightheadedness, anxiety,
N/V, and syncope
 PE: May reveal arrhythmias, hypotension (cardiogenic
shock), and evidence of new CHF
NB: The best predictor of survival is left ventricular ejection
fraction (EF)

STEMI cont’d.
45
Diagnosis
 ECG will show ST-segment elevations or new LBBB
o ST-segment depressions and dominant R waves in leads V1–V2 can also
be reciprocal change indicating posterior wall infarct
 Sequence of ECG changes: Peaked T waves →ST-segment
elevation →Q waves →T-wave inversion→ ST-segment
normalization →T-wave normalization over several hours to days
 Cardiac enzymes:
o Troponin I is most sensitive and specific cardiac enzyme
o CK-MB and CK-MB/total CK ratio (CK index) are also regularly checked
o Both troponin I and CK-MB can take up to 6 hours to rise following onset
of chest pain

Typical pattern of serum marker elevation after an acute MI
CK-MB = creatine kinase, MB isoenzyme; cTnI = cardiac troponin I; cTnT = cardiac troponin T;
LD1 = lactate dehydrogenase isoenzyme 1; MLC = myosin light chain.
46
Tintinalli JE et al. Tintinalli’s Emergency Medicine: A Comprehensive Study
Guide, 6th ed. New York, NY: McGraw-Hill; 2004.)

ST-segment abnormalities
47
 Inferior MI (involving the RCA/PDA): ST-segment elevation in
leads II, III, and aVF Obtain a right-sided ECG to look for ST
elevations in right ventricle
 Anterior MI (involving LAD and diagonal branches): ST-segment
elevation in leads V1–V4
 Lateral MI (involving LCA): ST-segment elevation in leads I, aVL,
and V5–V6
 Posterior MI: ST-segment depression in leads V1–V2 (anterior
leads) can be indicative Obtain posterior ECG leads V7–V9 to
assess for ST segment elevations

Inferior wall myocardial infarction. In this patient with acute chest pain,
ECG demonstrated acute ST-segment elevation in leads II, III, and aVF with
reciprocal ST-segment depression and T-wave flattening in leads I, aVL, and V4–V6
48

Anterior wall myocardial infarction. This patient presented with acute
chest pain. The ECG showed acute ST-segment elevation in leads aVL and
V1–V6, and hyperacute T waves.
49

STEMI Treatment
50
Initial treatment:
 Key medications: ASA, β-blockers, clopidogrel,
morphine, nitrates, and O2
 If pt. is in heart failure or in cardiogenic shock, do
not give β-blockers instead, give ACEIs provided
that pt. is not hypotensive
 In inferior wall MI avoid nitrates due to risk of
severe hypotension

STEMI Treatment cont’d.
51
Interventions:
 Emergent angiography and PCI should be performed if
possible
o If PCI cannot be performed within 90 minutes, and there are no
contraindications to thrombolysis (eg, a history of hemorrhagic
stroke or recent ischemic stroke, severe heart failure, or
cardiogenic shock), and patient presents within 3 hours of chest
pain onset, thrombolysis with tPA, reteplase, or streptokinase
should be performed instead of PCI
 Long-term treatment includes ASA, ACEIs, β-blockers, high-
dose statins (goal LDL < 100 mg/dL), and clopidogrel (if PCI
was performed)
 Modify risk factors with dietary changes, exercise, and
tobacco cessation

Complications
52
 Arrhythmia is most common complication and most common
cause of death following acute MI
 Less common complications include reinfarction, left ventricular
wall rupture, VSD, pericarditis, papillary muscle rupture (with mitral
regurgitation), left ventricular aneurysm or pseudoaneurysm, and
mural thrombi
 A timeline of common post-MI complications:
o First day: Heart failure
o 2–4 days: Arrhythmia, pericarditis
o 5–10 days: Left ventricular wall rupture (acute pericardial tamponade causing
electrical alternans, pulseless electrical activity), papillary muscle rupture
(severe mitral regurgitation)
o Weeks to months: Ventricular aneurysm (CHF, arrhythmia, persistent ST-
segment elevation, mitral regurgitation, thrombus formation)
 Dressler syndrome, an autoimmune process occurring 2–10 weeks
post-MI, presents with fever, pericarditis, pleural effusion,
leukocytosis, and ↑ ESR

See next slide for links to tools and resources for further study.
THE END
53

Further study
Putting it All Together_ A Clinical & Pathology Correlation
Case .pdf
Downloads
Autonomic and Cardiovascular Pharmacology (ACVP)
Clinical Correlate Articles. pdf_from e-Medicine
54

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