Prepared by md, PhD. Marta R. Gerasymchuk, pathophysiology department of IFNMU

2. CONTENT
1. Features of coronal circulation of blood and metabolism of
cardiac muscle.
2. Classification of coronary heart disease. CHD: determination,
reasons and terms of origin, form.
3. Ischemic heart disease. Definition of the notion, risk factors,
mechanisms of development
4. Sudden coronary death: reasons, mechanisms of origin.
5. Angina pectoris: classification, pathogenesis of displays.
6. Heart attack of myocardium: kinds, description of functional
and biochemical violations in a cardiac muscle, mechanisms of
pain syndrome.
7. Mechanisms of origin of spasms of coronary vessels.
8. Complication of heart attack of myocardium. Pathogenesis of
cardiogenic shock.
9. Experimental models of heart attack of myocardium.

3. ACTUALITY
• The term coronary heart disease (CHD) describes heart
disease caused by impaired coronary blood flow. In most
cases, CHD is caused by atherosclerosis.
• Diseases of the coronary arteries can cause angina,
angina
myocardial infarction or heart attack, cardiac
attack
dysrhythmias, conduction defects, heart failure, and
dysrhythmias defects failure
sudden death.
death
• During the past 50 years, there have been phenomenal
advances in understanding the pathogenesis of CHD and
in the development of diagnostic techniques and
treatment methods for disease.
• However, declines in morbidity and mortality have failed
to keep pace with these scientific advances, probably
because many of the outcomes are more dependent on
lifestyle factors and age than on scientific advances.
advances

4. FUNCTIONAL ORGANIZATION
OF THE CIRCULATORY SYSTEM
■ The circulatory system consists of the heart,
heart
which pumps blood; the arterial system,
system
which distributes oxygenated blood to the
tissues; the venous system, which collects
system
deoxygenated blood from the tissues and
returns it to the heart; and the capillaries,
capillaries
where exchange of gases, nutrients, and
wastes occurs.
■ The circulatory system is divided into two
parts: the low-pressure pulmonary
circulation, linking the transport function of
circulation
the circulation with the gas exchange
function of the lungs; and the high-pressure
systemic circulation, providing oxygen and
circulation
nutrients to the tissues.
■ The circulation is a closed system, so the
output of the right and left heart must be
equal over time for effective functioning of
the circulation.

5. Coronary Heart

Disease
The term coronary heart disease
(CHD) describes heart disease
caused by impaired coronary blood
flow.
 In most cases, CHD is caused by
atherosclerosis.
 Diseases of the coronary arteries can
cause angina, myocardial infarction
or heart attack, cardiac dysrhythmias,
conduction defects, heart failure, and
sudden death.
 Heart attack is the largest killer of
American men and women, claiming
more than 218,000 lives annually.
Each year, 1.5 million Americans
have new or recurrent heart attacks,
and one third of those die within the
first hour, usually as the result of
cardiac arrest resulting from
ventricular fibrillation.

6. Pathogenesis of Coronary
Heart Disease
• HDL (good) cholesterol
removes excess
cholesterol in the
blood stream.
• LDL (bad) cholesterol
enters the arterial wall
and is taken up by our
body’s scavenger
cells.
• Subsequently, they will
turn into fatty streaks
which progress into
atheromatous plaques.
• Hence, LDL
cholesterol is said to
promote
atherosclerosis.

7. Healthy Lifestyle
Well-Balanced Cholesterol Levels :
•Cholesterol readings includes:
Total cholesterol
Desirable : < 5.2 mmol/L
Borderline High : 5.2 – 6.2 mmol/L
High : ≥ 6.2 mmol/L
LDL cholesterol
Desirable : < 3.3 mmol/L
Borderline High : 3.3 – 4.1 mmol/L
High : ≥ 4.1 mmol/L

8. Healthy Lifestyle
Well-Balanced Cholesterol Levels :
HDL cholesterol
Acceptable: ≥ 0.9 mmol/L
Risky : < 0.9 mmol/L
Triglyceride
Desirable : < 2.3 mmol/L
•A healthy person should have a higher level of
HDL and a low level of LDL and triglyceride .

10. Types of chronic ischemic heart disease
and acute coronary syndromes
Coronary heart disease
Chronic ischemic heart disease Acute coronary syndrome
Stable Variant No ST-segment ST-segment
angina angina elevation elevation
Silent myocardial Unstable Q-wave
ischemia angina AMI
Non-ST-segment
elevation AMI

11. The Normal Heart - Coronary Artery Anatomy
Left Main CA
Layers of the Arterial Wall
Circumflex
Adventitia
Media
Intima
Right CA
Left Anterior Descending CA Marginal Branch Intima composed of
endothelial cells

12. Atherosclerosis:
A Progressive Process
Plaque Ischemia
Occlusive Rupture/ Unstable
Fibrous Fissure &
Fatty Atherosclerotic
Thrombosis
Angina
Normal Streak Plaque Plaque
Thrombus formation
MI
Coronary vasospasm
Coronary
Death
Stroke
PHASE I: Initiation PHASE II: Progression PHASE III: Complication
Critical Leg
Ischemia
Disease progression
Libby P. Circulation. 2001;104:365-372.

13. Complicated Fibrous
Lesion/ Plaque Intermediate
Rupture Atheroma Lesion Fatty
Foam
Streak Cells
Pathogenesis of Atherosclerosis

14. 1) FATTY
STREAK
(non-
palpable,
but a
visible
YELLOW
streak)
2) ATHEROMA
(plaque)
(palpable)
3) THROMBUS
(non-
functional,
symptomati
c)

16. Coronary Artery Pathology in Ischemic Heart Disease
Plaque
Syndrome Stenoses Disruption Plaque-Associated Thrombus
Stable angina >75% No No
Unstable angina Variable Frequent Nonocclusive, often with thromboemboli
Transmural Variable Frequent Occlusive
myocardial infarction
Subendocardial Variable Variable Widely variable, may be absent,
myocardial infarction partial/complete, or lysed
Frequent
Sudden death Usually Often small platelet aggregates or thrombi
severe and/or thromboemboli

17. The IVUS technique can detect
angiographically ‘silent’ atheroma
IVUS
Angiogram
Little
No evidence evidence of
of disease disease
anterior descending Atheroma
coronary artery
IVUS=intravascular ultrasound
Nissen S, Yock P. Circulation 2001; 103: 604–616 IVUS – intravascular ultrasaund

18. Correlation of CT angiography of the
coronary arteries with intravascular Non-calcified, soft, lipid-rich plaque in
ultrasound illustrates the ability of MDCT left anterior descending artery (arrow) .
to demonstrate calcified and non-calcified The plaque was confirmed by
coronary plaques (Becker et al., Eur J intravascular ultrasound (Kopp et al.,
Radiol 2000) Radiology 2004)

20. Pathophysiology of ISCHEMIA
 Ischemia of cardiac cells occurs when the oxygen
supply is insufficient to meet metabolic demands.
 Myocardial cells are unable to store much energy in
the form of adenosine triphosphate (ATP) and must
therefore continuously receive a supply of oxygen
for aerobic synthesis of ATP.
 ATP is essential for powering myocardial
construction as well as for cell maintenance.
Because the heart is unable to slow its activity
when ATP supplies dwindle, it is essential that a
steady flow of oxygen be provided.

21. Critical factors in meeting cellular
demands for oxygen are:
the rate of coronary perfusion the myocardial workload
can be impaired in next ways depends on
Large, stable Vasospasm Heart rate
atherosclerotic plaque
Preload
Acute platelet aggregation Poor perfusion
and thrombosis pressure Afterload
Failure of autoregulation Contractility
by the microcirculation

22. ANGINA PECTORIS
• Par oxysmal (sudden)
• Recur r ent
• 15 sec.15 min.
• Reduced perfusion, but NO infar ction
• THREE TYPES
• STABLE: relieved by rest or nitroglycerin
• PRINZMETAL: SPASM is main feature, responds to
nitro, S-T elevation
• UNSTABLE (crescendo, PRE-infarction, Q-wave
angina): perhaps some thrombosis, perhaps some
non transmural necrosis, perhaps some
embolization, but DISRUPTION of PLAQUE is
universally agreed upon

23. Chest Pain
 First symptom of those suffering myocardial
ischemia.
 Called angina pectoris (angina – “pain”)
 Feeling of heaviness, pressure
 Moderate to severe
 In substernal area
 Often mistaken for indigestion
 May radiate to neck, jaw, left arm/ shoulder
Due to :
Accumulation of lactic acid in
myocytes or stretching of myocytes

24. Stable angina pectoris
 Caused by chronic coronary obstruction
 Recurrent predictable chest pain
 Gradual narrowing and hardening of
vessels so that they cannot dilate in
response to increased demand of physical
exertion or emotional stress
 Lasts approx. 3-5 minutes
 Relieved by rest and nitrates
Stress test
shows
ST segment
depression
> 1mm

25. Prinzmetal angina pectoris
(Variant angina)
 Caused by abnormal vasospasm of normal vessels (15%) or
near atherosclerotic narrowing (85%)
 Occurs unpredictably and almost exclusively at rest.
 Often occurs at night during REM sleep
(rapid eye movement)
 May result from hyperactivity of sympathetic nervous system,
increased calcium flux in muscle or impaired production of
prostaglandin
 Vasoconstriction is due to platelet thromboxane A2 or an
increase in endothelin
This causes a pattern of ST elevation that is very similar to acute STEMI
— i.e. localised ST elevation with reciprocal ST depression occurring
during episodes of chest pain. However, unlike acute STEMI the ECG
changes are transient, reversible with vasodilators and not usually
associated with myocardial necrosis. They may be impossible to
differentiate on the ECG.
ST elevation myocardial infarction (STEMI)

26. Silent Ischemia
 Totally asymptomatic
 May be due abnormality in innervation
 Or due to lower level of inflammatory
cytokines

27. Treatment
 Pharmacologically manipulate blood
pressure, heart rate, and contractility to
decrease oxygen demands
 Nitrates dilate peripheral blood
vessels and
 Decrease oxygen demand
 Increase oxygen supply
 Relieve coronary spasm

28.   blockers:
 Block sympathetic input, so
 Decrease heart rate, so
 Decrease oxygen demand
 Digitalis
 Increases the force of contraction
 Calcium channel blockers
 Antiplatelet agents (aspirin, etc.)

29. Surgical treatment
• Angioplasty – mechanical
opening of vessels
• Revascularization – bypass
• Replace or shut around
occluded vessels

31. ACUTE CORONARY SYNDROMES
 “The acute coronary syndromes are frequently initiated
by an unpredictable and abrupt conversion of a stable
atherosclerotic plaque to an unstable and potentially life-
threatening atherothrombotic lesion through superficial
erosion, ulceration, fissuring, rupture, or deep
hemorrhage, usually with superimposed thrombosis.”

32. Unstable Angina pectoris
Lasts more than 20 minutes at rest,
or rapid worsening of a pre-existing
angina
May indicate a progression to M.I.
Pathogenesis:
Severe, fixed, multivessel
atherosclerotic disease
Disrupted plaques with or without
platelet nonocclusive thrombi

33. The ECG above belongs to a patient with unstable angina pectoris. Negative T
pectoris
waves are observed in leads C2-C5 while negative U waves are seen in leads C2-
C4. Additionally, the PR interval is above 200 msec (1st degree AV block).
Coronary angiography showed significant stenosis of the LAD and Circumflex
(Cx) arteries

34. Sudden cardiac death (SCD)
 1. Inexpected death within 1 hour after the onset of
symptoms
2. Risk factors
 a. Obesity
 b. Glucose intolerance
 c. Hypertension
 d. Recent non-Q wave myocardial infarction
 e. Smoking
3. Occurs more frequently in the morning hours when
hypercoagiilability is at its peack
4. Pathogenesis
 a. Severe atheroselerotic coronary artery disease
 b. Disrupted filimns plaques
 c. Absence of occlusive vessel thrombus (>80%; of cases)
 d. Cause of death is ventricular fibrillation.
 5. Diagnosis of exclusion after the following causes are
ruled out
 a. Mitral valve prolapse (MVP)
 b. Hypertrophic cardiomyopathy
 c. Calcific aortic stenosis
 d. Conduction system abnormalities
 e. Cocaine abuse

36. Acute myocardial infarction (AMI)
1. Epidemiology
 a. Most common cause of
death in adults in the
United States.
 b. Prominent in males
between 40 and 65 years
old
 c. No predominant sex
predilection after 65 years
old
 d. At least 25% of AMIs
are clinically unrecognized.

37. Myocar dial Ischemia
 Myocardial cell metabolic demands not met
 Time frame of coronary blockage:
 10 seconds following coronary block
 Decreased strength of contractions
 Abnormal hemodynamics
 See a shift in metabolism, so within minutes:
 Anaerobic metabolism takes over
 Get build-up of lactic acid, which is toxic within
the cell
 Electrolyte imbalances
 Loss of contractibility

38. 20 minutes after blockage
Myocytes are still viable, so
If blood flow is restored, and
increased aerobic metabolism, and
cell repair,
 →Increased contractility
About 30-45 minutes after blockage, if
no relief
Cardiac infarct & cell death

39. Myocardial infarction
 Necrosis of cardiac myocytes
– Irreversible
– Commonly affects left ventricle
– Follows after more than 20 minutes of
ischemia

40. Pathogenesis
a. Sequence
 1) Sudden disniptinn of an atheromatous
plaque
 2) Subendothelial coliagen and thrombogenic
necrotic material are exposed.
 3) Platelets adhere to the exposed material
and eventually form an occlusive platelet
thrombus.
b. Role of thromboxane A2
 1) Contributes to formation of the platelet
thrombus
 2) Causes vasospasm of the artery to reduce
blood flow

41. PATHOPHYSIOLOGY
Coronary artery cannot supply enough blood to the heart in
response to the demand due to CAD
Within 10 seconds myocardial cells experience ischemia
Ischemic cells cannot get enough oxygen or glucose
Myocardium Infarction
Ischemic myocardial cells may have decreased electrical &
muscular function
Cells convert to anaerobic metabolism.
Cells produce lactic acid as waste
Pain develops from lactic acid accumulation
Pt feels anginal symptoms until receiving demand increase
02 requirements of myocardial cells

42. PROGRESSION OF
NECROSIS
0-1/2 hr reversible injury

43. Types of myocardial infarction
a. Transmural infarction (Qwave infarction)
• 1) Involves the full thickness of the myocardium
• 2) New Q waves develop in an
electrocardiogram (ECG).
b. Subendocardial infarction (non-Q wave
infarction)
• 1) Involves the inner third of the myocardium
• 2) Q waves are absent.

45. Reperfusion injury
a. Follows thrombolytic (fibrinolytic) therapy
b. Early reperfusion salvages some injured but
viable myocytes but destroys myocytes that are
irreversibly damaged.
1) Removal of irreversibly damaged myocytes
improves short- and long-term function and
survival.
2) Prevents any further damage to myocardial cells
3) Limits the size of the infarction
c. Reperfusion histologically alters irreversibly
damaged cells.
1) Produces contraction band necrosis
2) Caused by hyporcontraction of myofibrils in dying
cells
• Due to the influx of Ca-++ into the cytosol

46. RE-PERFUSION
 Thrombolysis
 PTCA
 CABG
 Reperfusion CANNOT restore necrotic
or dead fibers, only reversibly injured
ones
 REPERFUSION “INJURY”
 Free radicals
 Interleukins

47. Consequences after acute coronary artery occlusion
Blood flow
M. Ischemia
Chest
discomfort PMVT, VF M.stunning
Heart failure
STEMI NSTEMI ,UA Sudden
Cardiogenic
Elevated Death shock
+CK,Trop-T
Cardiovascular Research & Prevention Center, Bhumibol Adulyadej hospital

48.  May hear
extra, rapid Clinical Manifestations
heart sounds
 ECG
changes:

T wave
inversion
 ST
segment
depression

49. MYOCARDIAL INFARCTION
Transmural vs. Subendocardial (inner 1/3)
DUH! EXACT SAME risk factors as atherosclerosis
Most are TRANSMURAL, and MOST are caused by
coronary artery occlusion
In the 10% of transmural MIs NOT associated with
atherosclerosis:

Vasospasm
 Emboli
 UNexplained

50. Structural, functional changes
 Decreased contractility
 Decreased LV compliance
 Decreased stroke volume
 Dysrhythmias
 Inflammatory response is severe
 Scarring results –
 Strong, but stiff; can’t contract like
healthy cells

51. Sign and Symptom
 Classic symptom of heart attack
are chest pain radiating to neck,
jaws, back of shoulder, or left arm
 The pain can be felt like:
 Squeezing or heavy pressure
 A tight band on the chest
 An elephant sitting on the chest

53. Other symptoms Cont
include:
 Shortness of
breath (SOB)
 Weakness and
tiredness
 Anxiety
 Lightheadedness
 Dizziness
 Nausea vomiting
 Sweating, which
may be profuse

54. Clinical manifestations
 Sudden, severe chest pain
 Similar to pain with ischemia, but stronger
 Not relieved by nitrates
 Radiates to neck, jaw, shoulder, left arm
 Indigestion, nausea, vomiting
 Fatigue, weakness, anxiety, restlessness and
feelings of impending doom.
 Abnormal heart sounds possible (S3,S4)

55.  Blood test show several markers:
 Leukocytosis
 Increased blood sugar
 Increased plasma enzymes
 Creatine kinase
 Lactic dehydrogenase
 Aspartate aminotransferase (AST or SGOT)
 Cardiac-specific troponin

56. Laboratory diagnosis of AMI
 I. Serial testing for creatine kinase isoenzyme MB (CK-MB)
1) CK-MB appears within 4 to 8 hours; peaks at 24 hours; disappears within 1.5 to 3 days.
 • Sensitivity and specificity 95%,
2) Reinfarction
 a) Occurs in 10% of AMIs
 b) Reappearance of CK-MB after 3 days
 II. Serial testing for cardiac troponins I (cTnl) and T (cTnT)
1) Normally regulate calcium-mediated contraction
2) cTnl and cTnT appear within 3 to 12 hours: peak at 24 hours; disappear within 7 to 10 days.
 a) Sensitivity 84% to 96%, specificity 80% to 95%
 b) False positive results are lisually related to ischemia (e.g., unstable angina),
3) CK-MB is used in conjunction with troponins to diagnose an AMI.
 a) Detects reinfarction (troponins cannot)
 b) Improves overall sensitivity and specificiry in diagnosing an AMI
 III. Lactate dehydrogenase (LDH)1-2 "flip"
1) Normally, LDH2 is higher than LDH1.
 • In AMI, LDH1 in cardiac muscle is released, causing the “flip,"
2) LDH1-2
 • Appears within 10 hours; peaks at 2 to 3 days: disappears within 7 days
3) This test has been replaced by troponins I and T.

57. Treatment
 First 24 hours crucial
 Hospitalization, bed rest
 ECG monitoring for arrhythmias
 Pain relief (morphine, nitroglycerin)
 Thrombolytics to break down clots
 Administer oxygen
 Revascularization interventions: by-
pass grafts, stents or balloon
angioplasty

58. AMI
DIAGNOSIS
• SYMPTOMS
• EKG
• DIAPHORESIS
• (10% of MIs are “SILENT” with Q-waves)
• CKMB gold standard enzyme
• Troponin-I, Troponin-T better
• CRP predicts risk of AMI in angina patients

59. Primary Management Techniques
• Heart Attack Treatment
• First you must conduct a primary survey of the casualty;
• A primary survey consists of following the DRABCD procedure, this involves;
• D = DANGER – If I find a heart attack casualty I should check for any
surrounding danger to myself first and for the casualty and others
• R = Response – I should asses whether the person is conscious or unconscious
using the COWS procedure; -Can you hear me, -Open your eyes, -What is
your name, -Squeeze my hand.
• A = Airways - After response if the casualty is unconscious I should then
check the airways for any obstructions or blockages and if there is a
blockage turn the victim onto his/her side and clear the airway.
• B = Breathing – The next step if the patient is unconscious is to check for
signs of life. Check for breathing by using look, listen and feel technique. If
breathing place the casualty in recovery position, if not give 2 rescue
breaths and...
• C = Compressions - If the casualty is unconscious with no breathing, start
compressions immediately! Give 30 compressions. At a rate of 100
compressions per minute (approx 2 compressions per second). At 1/3 depth
of the casualty’s chest.
• D = Defibrillation - If available use a defibrillator on the casualty as soon as
possible.

60. Definitions
• Cardiac Output: (Q) = HR X SV
• Cardiac Index = Q / body surface area
• Preload: (EDV) volume of the left ventricle at the end of diastole
(dependent on venous return & stretch of the cardiac muscle cells)
• Afterload: resistance to ventricular emptying during systole
(the amount of pressure the left ventricle must generate to squeeze
blood into the aorta)
• Frank Starling Law of the Heart:the heart will contract with greater
force when preload (EDV) is increased
• Myocardial Contractility: the squeezing contractile force that the
heart can develop at a given preload
• regulated by:
• sympathetic nerve activity (most influential)
• catecholamines (epinephrine norepinephrine)
• amount of contractile mass
• drugs

61. Don’t wait for a heart attack to take
an action !
Don’t wait for a second life we
are not cats!

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