Ischemic Heart Disease

and
Myocardial Infarction
Pathophysiology of Myocardial
Ischemia
Emma Angela Jacob, DPCP,
DPCC
December 13, 2009
 Global deaths from
cardiovascular causes in 1990
30 and estimated for 2020
Millions of deaths from
cardiovascular causes

25
6
20

15
5
10 19
5 9
0
1990 (developed) countries
Western 2020
Non-Western (developing) countries
Murray CJ, Lopez AD. Lancet 1997; 349: 1269–
1269–76.
 HERO-2: 30-day
15
mortality by region
13.2

10.8 11
10.2
10

% 6.7

0
Western South Eastern Russia Asia
countries America Europe (N=6,057) (N=756)
(N=2,563) (N=1,820) (N=5,877)
HERO-2 Investigators. Lancet 2001; 358: 1855–
1855–63.
 Physiology and Pathophysiology of
Coronary Blood Flow / Ischemia
 Basic Physiology / Determinants of MVO2
 Autoregulatory Mechanisms / Coronary Flow Reserve
 Pathophysiology of Coronary Ischemia
and Atherosclerosis
 Clinical Syndromes
 Stable Angina
 Acute Coronary Syndromes
 Unstable Angina
 Acute MI (UA, AMI)
Coronary Arteries
Normal Anatomy
 Left main coronary
artery (LMCA)
Left circumflex
Right coronary coronary artery(LCx)
artery (RCA)

Left anterior
descending
coronary
artery (LAD)
 Basic Principles
 myocardial cells have to do only 2 things:
contract and relax; both are aerobic, O2
requiring processes
 oxygen extraction in the coronary bed is
maximal in the baseline state; therefore to
increase O2 delivery, flow must increase
 large visible epicardial arteries are conduit
vessels not responsible for resistance to flow
(when normal)
 Basic Principles

 small, distal arterioles make up the major

resistance to flow in the normal state
 atherosclerosis affects the proximal, large
epicardial arteries
 once arteries are stenotic resistance to flow
increases unless distal, small arterioles are able to
dilate to compensate
 Myocardial Ischemia:
Occurs when myocardial oxygen demand exceeds
myocardial oxygen supply
 Myocardial Ischemia:
Occurs when myocardial oxygen demand exceeds
myocardial oxygen supply

MVO2 = Myocardial Oxygen Demand

MVO2 determined by:

Heart Rate
Contractility
Wall Tension
 MVO2 (Myocardial Oxygen Demand)

 Increases directly in proportion to heart rate

 Increases with increased contractility
 Increases with increased Wall Tension:
i.e. increases with increasing preload or
afterload
 Heart Rate

10

8
MVO2
cc/min 6
/100g
4

2
100 150 200
Heart Rate (BPM)
 Contractility
10
Norepinephrine

Control

MVO2
(cc/min 5
/100g)

Peak Developed Tension (g/cm2)

 Wall Tension

Is related to Pressure x Radius

Wall Thickness

Defined as: Force per unit area generated in the LV

throughout the cardiac cycle

Afterload - LV systolic pressure

Preload - LV end-diastolic pressure or volume
 Myocardial Ischemia:
Occurs when myocardial oxygen demand exceeds
myocardial oxygen supply
 Myocardial Oxygen Supply

Determined by:

Coronary Blood Flow & O2 Carrying Capacity

( Flow = Pressure / Resistance)

 Oxygen saturation of
the blood
 Coronary perfusion pressure
 Coronary vascular resistance  Hemoglobin content
of the blood
 Coronary Blood Flow
Proportional to perfusion pressure /
resistance
 Coronary Perfusion  Coronary Vascular
pressure resistance
=  external compression
Diastolic blood  intrinsic regulation
pressure, minus LVEDP  Local metabolites
 Endothelial factors
 Neural factors (esp.
sympathetic nervous
system)
Endocardium and CFR (Coronary Flow
Reserve)
 Endocardium vs Epicardium
 Greater shortening / thickening, higher wall
tension: increased MVO2
 Greater compressive resistance
 ? Decreased Perfusion Pressure
 Less collateral circulation
 Net Result is more compensatory arteriolar
vasodilatation at baseline and therefore
decreased CFR
 Autoregulatory Resistance
 Major component of resistance to flow
 Locus at arteriolar level
 Adjusts flow to MVO2
 Metabolic control
 Oxygen
 Adenosine , ADP
 NO (nitric oxide)
 Lactate , H+
 Histamine, Bradykinin
 Autoregulatory Resistance

Involves 3 different cells

 Myocardial muscle cell - produces byproducts of
aerobic metabolism (lactate,adenosine, etc)
 Vascular endothelial cell (arteriole) - reacts to
metabolic byproducts
 Vascular smooth muscle cell (arteriole) - signaled
by endothelial cell to contract (vessel constriction)
or relax (vessel dilation)
 Autoregulation of Coronary
Blood Flow
 Oxygen  Adenosine
 Acts as vasoconstrictor
 As O2 levels drop during
ischemia: pre-capillary
vasodilation and
increased myocardial
blood supply
 Potent vasodilator
 Prime mediator of
coronary vascular tone
 Binds to receptors on
vascular smooth muscle,
decreasing calcium entry
into cell
 Adenosine
 During hypoxemia, aerobic metabolism in
mitochondria is inhibited
 Accumulation of ADP and AMP
 Production of adenosine
 Adenosine vasodilates arterioles
 Increased coronary blood flow
 Autoregulatory Resistance
200
Adenosine
Flow
cc/100g Control
/min
100

0
60 80 100 115 130

Coronary Perfusion Pressure (mmHg)

 Autoregulators
 Other endothelial-
derived factors
contribute to
autoregulation
 Dilators include:
 EDRF (NO)
 Prostacyclin
 Constrictors include:
 Endothelin-1
 Coronary Flow Reserve

 Arteriolar autoregulatory vasodilatory capacity in

response to increased MVO2 or pharmacologic agents
 Expressed as a ratio of Maximum flow / Baseline flow
 ~ 4-5 / 1 (experimentally)
 ~ 2.25 - 2.5 (when measured clinically)
 Coronary Flow Reserve

 Stenosis in large epicardial (capacitance) vessel 

decreased perfusion pressure  arterioles downstream
dilate to maintain normal resting flow
 As stenosis progresses, arteriolar dilation becomes chronic,
decreasing potential to augment flow and thus decreasing
CFR
 Endocardial CFR < Epicardial CFR
 As CFR approaches 1.0 (vasodilatory capacity “maxxed
out”), any further decrease in PP or increase in MVO2 
ischemia
Endocardium and CFR (Coronary Flow
Reserve)
 Coronary Flow Reserve
5

4 Maximum Flow
Coronary
Blood
Flow 3

2
Resting Flow
1

0 25 50 75 100
Epicardial % Diameter Stenosis
Prevalence of CAD in Modern
Society

70
60
Age(years)
50
70%
40 <25
50% 25-40
30
>40
20
10 25%
0

Cleveland Clinic Cardiac Transplant

Donor IVUS Data-Base
 Risk Factors
 family History
 cigarette smoking
 diabetes mellitus
 hypertension
 hyperlipidemia
 sedentary life-style
 obesity
 elevated homocysteine, LP-a ?
Coronary lesions in Men and Women,
Westernized and non-Westernized diets
 Atherosclerotic Plaque
Evolution from Fatty Streak
 Fatty streaks present in
young adults
 Soft atherosclerotic
plaques most vulnerable
to fissuring/hemorrhage
 Complex interaction of
substrate with circulating
cells (platelets,
macrophages) and
neurohumoral factors
 Plaque progression….

 Fibrous cap develops

when smooth muscle
cells migrate to intima,
producing a tough
fibrous matrix which
glues cells together
Intra-vascular Ultrasound
(IVUS)
Atherosclerotic Plaque
Physiologic Remodeling
Coronary atherosclerosis
 Stable Angina - Symptoms
 mid-substernal chest pain
 squeezing, pressure-like in quality (closed fist =
Levine’s sign)
 builds to a peak and lasts 2-20 minutes
 radiation to left arm, neck, jaw or back
 associated with shortness of breath, sweating, or
nausea
 exacerbated by exertion, cold, meals or stress
 relieved by rest, NTG
Symptoms and Signs:
Coronary Ischemia
Stable Angina - Diagnosis
Exercise Treadmill Test
Stable Angina - Diagnosis
Thallium Stress Test
 Stable Angina - Treatment
 Risk factor modification (HMG Co-A Reductase inhibitors = Statins)
 Aspirin
 Decrease MVO2
 nitrates

 beta-blockers

 calcium channel blockers

 ACE-inhibitors

 Anti-oxidants (E, C, Folate, B6)?

 PCI – the most common clinical indication for PCI is ANGINA
PECTORIS, despite med tx + ischemia during a stress test
Stable Angina - Treatment
Mechanical Dilation:
Angioplasty, Stent, etc.
Treatment of Stable Angina
-STENTS
 Stable Angina - Treatment
Coronary Artery Bypass Grafting Surgery (CABG)
 Acute Coronary Syndromes:
Terminology
 Pathophysiology of all 3 is the same
 Unstable Angina (UA)
 ST depression, T Wave inversion or normal
 No enzyme release
 Non-Transmural Myocardial Infarction (NTMI or SEMI)
 ST depression, T Wave inversion or normal
 No Q waves
 CPK, LDH + Troponin release
 Transmural Myocardial Infarction (AMI)
 ST elevation
 + Q waves
 CPK, LDH + Troponin release
 Pathophysiology of the Acute
Coronary Syndromes (UA,MI)
 Plaque vulnerability and extrinsic
triggers result in plaque rupture
 Platelet adherence, aggregation and
activation of the coagulation cascade
with polymerization of fibrin
 Thrombosis with sub-total (UA, NTMI) or
total coronary artery occlusion (AMI)
Pathophysiology of Acute
Coronary Syndromes
Pathophysiology of Acute
Coronary Syndromes
“Vulnerable Plaque”
 Cross section of a
complicated plaque
Unstable Plaque
Microvascular Obstruction Following Plaque Rupture

Plaque rupture Platelet-thrombin micro-emboli

Thrombus

Cutoff TnT Curve

CK-MB
CK-MB
CK-MB
CK-MB Microvascular
CK-MB
CK-MB
1st 2nd 3rd Obstruction
embolus embolus embolus
00 03m o0 1, 5
Angiogram in unstable angina:
eccentric, ulcerated plaque
Angiogram in unstable angina:
after stent deployment
 Acute Coronary Syndrome
Unstable Angina / Myocardial Infarction
Symptoms

 new onset angina

 increase in frequency, duration or severity
 decrease in exertion required to provoke
 any prolonged episode (>10-15min)
 failure to abate with >2-3 S.L. NTG
 onset at rest or awakening from sleep
 Unstable Angina -
High Risk Features

 prolonged rest pain

 dynamic EKG changes (ST depression)
 age > 65
 diabetes mellitus
 left ventricular systolic dysfunction
 angina associated with congestive heart failure,
new murmur, arrhythmias or hypotension
 elevated Troponin i or t
Assessment algorithm for suspected
non-ST elevation ACS
 Unstable Angina / NTMI
Pharmacologic Therapy

 ASA and Heparin beneficial for acute

coronary syndromes ( UA, NTMI, AMI)
 Decrease MVO2 with Nitrates, Beta-
blockers, Ca channel blockers, and Ace
inhibitors
 consider platelet glycoprotein 2b / 3a
inhibitor and / or low molecular weight
heparin
 Anti-Platelet Therapy

 Three principle pathways of platelet

activation with >100 agonists: ( TXA2,
ADP, Thrombin )
 Final common pathway for platelet
activation / aggregation involves
membrane GP II b / III A receptor
 Fibrinogen molecules cross-bridge
receptor on adjacent platelets to form a
scaffold for the hemostatic plug
 Platelet GP IIB/ IIIA Inhibitors
with Acute Coronary Syndromes
Odds Ratios and 95% CI for Composite Endpoint
( Death,Re- MI at 30days ) Placebo (% ) Rx ( % )

PURSUIT 15.7 14.2

PRISM 7.1 5.8

(vs Heparin)

PRISM PLUS 11.9 8.7

(+ Heparin)

PARAGON 11.7 12.0

(high dose)

0.2 1 4
Rx better Placebo better
 Low Molecular Weight Heparin
in Acute Coronary Syndromes
Odds Ratios and 95% CI for Composite Endpoint UH / Placebo Rx
( Death, MI, Re-angina or Revasc at 6-14 days ) (%) (%)

FRISC 10.3 5.4

FRIC 7.6 9.3

ESSENCE 19.8 16.6

TIMI 11b 16.6 14.2

0.2 1 4
LMWH Better UH Better
 Unstable Angina
Anti-thrombotic Therapy

 Thrombolytics are not indicated

 “lytic agents may stimulate the thrombogenic
process and result in paradoxical aggravation of
ischemia and myocardial infarction”

TIMI IIIB Investigators

Circulation 1994; 89:1545-1556
 ACC/AHA GUIDELINE + 2002 UPDATE:
EARLY INVASIVE STRATEGY
Class I
An early invasive strategy in patients with UA/NSTEMI
and any of the following high-risk indicators.
d) Recurrent angina/ischemia with CHF symptoms,
S3, pulmonary edema, increasing rales, or new or
worsening MR
e) High-risk findings on noninvasive stress testing
f) Depressed LV systolic function (e.g., EF<0.40 on
noninvasive study)
g) Hemodynamic instability
h) Sustained VT
i) PCI within 6 months or prior CABG
 Prinzmetal’s Angina
clues to diagnosis
 Transient ST-segment elevation during chest
pain
 Intermittent chest pain
 often repetitive
 usually at rest

 typically in the early morning hours

 rapidly relieved by nitroglycerine

 Syncope (rare), Raynaud’s, migraine

Coronary Stenosis Severity Prior to
Myocardial Infarction

% Stenosis
68% 14% >70
18% 50-70
<50

Falk et al, Circulation 1995; 92: 657-71

 Acute Myocardial Infarction
 total thrombotic occlusion of epicardial coronary
artery  onset of ischemic cascade
 prolonged ischemia  altered myocardial cell
structure and eventual cell death (release of
enzymes - CPK, LDH, Troponin)
 altered structure  altered function (relaxation and
contraction)
 consequences of altered function often include
exacerbation of ischemia (ischemia begets
ischemia)
 Acute Myocardial Infarction

 wavefront phenomenon of ischemic evolution -

endocardium to epicardium
 If limited area of infarction  homeostasis achieved
 If large area of infarction (>20% LV )  Congestive heart failure
 If larger area of infarction (>40% LV)  hemodynamic collapse
AMI - Wavefront Phenomenon
 Acute Myocardial Infarction
 Transmural
 Non-transmural / sub-  total, prolonged
endocardial occlusion
 Non-occlusive thrombus  EKG - ST elevation
or spontaneous re-  Rx - Thrombolytic
perfusion Therapy or Cath Lab /
 EKG – ST depression PTCA
 Some enzymatic release
– troponin i most
sensitive
Cardiac enzymes: overview

Legend: A. Early CPK-MB isoforms after acute MI

B. Cardiac troponin after acute MI
C. CPK-MB after acute MI
D. Cardiac troponin after unstable angina
Markers of MI: Troponin I
Diagnosis of MI:
Role of troponin i
 Troponin I is highly
sensitive
 Troponin I may be
elevated after
prolonged
subendocardial
ischemia
 See examples
below
 Causes of Troponin elevation

 Any cause of prolonged (>15 – 20

minutes) subendocardial ischemia
 Prolonged angina pectoris
 Prolonged tachycardia in setting of CAD
 Congestive heart failure (elevated LVEDP
causing decreased subendocardial
perfusion)
 Hypoxia, coupled with CAD
 “aborted” MI (lytic therapy or spontaneous
clot lysis)
 EKG diagnosis of MI
 ST segment
elevation
 ST segment
depression
 T wave inversion
 Q wave formation
 Consequences of Ischemia
(Ischemia begets Ischemia)
 chest pain
 systolic dysfunction (loss of contraction)
 decrease cardiac output

 decrease coronary perfusion pressure

 diastolic dysfunction (loss of relaxation)

 higher pressure (PCWP) for any given volume

 dyspnea, decrease pO2, decrease O2 delivery

 increased wall tension (increased MVO2)

All 3 give rise to stimulation of sympathetic nervous system with subsequent

catecholamine release- increased heart rate and blood pressure (increased MVO2)
 Ischemic Cycle
Ischemia / infarction

Diastolic Dysfunction Systolic Dysfunction

chest pain

pulmonary LV diastolic pressure cardiac output

congestion
pO2

wall tension catecholamines

(heart rate, BP)
MVO2
Treatment of Acute Myocardial Infarction

 aspirin, heparin, analgesia, oxygen

 reperfusion therapy
 thrombolytic therapy (t-PA, SK, n-PA, r- PA)
 new combinations ( t-PA, r-PA + 2b / 3a inhib)
 cath lab (PTCA, stent)
 decrease MVO2
 nitrates, beta blockers and ACE inhibitors
 for high PCWP - diuretics
 for low Cardiac Output - pressors (dopamine, levophed,
dobutamine); IABP; early catheterization
ACC / AHA Guidelines 2004
 ACC / AHA Guidelines 2004
An invasive strategy is generally preferred if:

• Skilled PCI laboratory is available with surgical back-up

• Medical contact-to-balloon or door-to-balloon
time is <90 minutes
• (Door-to-Balloon)-Door-to-Needle) time is <1 hour

• High risk from STEMI:

• Cardiogenic shock
• Killip class ≥ 3
• Contraindications to fibrinolysis, including increased risk of
bleeding and ICH

• Late presentation
• Symptom onset was more than 3 hours ago
Complications of Acute M.I.
Left Anterior Descending Occlusion
Occlusion of
the
left anterior
descending
coronary
artery
 Experimental Data
 Canine studies – transient artery clamping or
ligation
 Balloon angioplasty studies
 Time dependent series of events
 Chest Pain as a late event
 ACUTE M.I.
THE “ISCHEMIC CASCADE”
Diastolic dysfunction
Chest pressure, etc.

Acute MI Release of CPK

Ischemic EKG changes

Localized systolic dysfunction
 ACUTE M.I.
THE “ISCHEMIC CASCADE”

1. Diastolic dysfunction
2. Localized systolic dysfunction
3. Ischemic EKG changes
4. Chest pressure, etc.
5. Release of CPK
 SYMPTOMS

SURFACE
ECG
REST 2-
D ECHO

MPI/DSE
PET
 Time course of cell death

 20 - 40 minutes to irreversible cell injury

 ~ 24 hours to coagulation necrosis
 5 - 7 days to “yellow softening”
 1 - 4 weeks: ventricular “remodeling”
 6 - 8 weeks: fibrosis completed
 Think Anatomically!!

 Left main coronary artery supplies

two-thirds of the myocardium
 LAD supplies ~ 40% of the L.V.,
including apex, septum and anterior
wall
 RCA supplies less L.V.
myocardium, but all of
the R.V. myocardium
Blood supply of the septum
 Think Anatomically!!!

 LAD supplies most of the conduction

system below the A-V node
(i.e. the His-Purkinje system)
 RCA supplies most of the conduction
system at or above the A-V node
(i.e. the A-V node and, usually, the
S-A node)
Conduction System of the Heart
 ACUTE M.I.
Anatomical correlates
LAD occlusion causes extensive
infarction associated with:

 LV failure
 High grade heart block
 Apical aneurysm formation
 Thrombo-embolic complications
 ACUTE M.I.
Anatomical correlates
RCA occlusion causes moderate
infarction associated with:

 RV failure
 Bradyarrhythmias
 Occasional mechanical complications
 ACUTE M.I.
Arrhythmias

Sinus bradycardia
 Sinus tachycardia

 Atrial fibrillation

 PVCs / ventricular tachycardia /ventricular

fibrillation
 Heart block
 Arrhythmias:
Inferior M.I.
 Sinus bradycardia -- S.A. nodal artery and
increased vagal tone
 Heart block -- A-V nodal artery
1st degree A-V block
Wenckebach 2nd degree A-V block
A-V dissociation
 Atrial fibrillation -- L.A. stretch
 Ventricular tachycardia / fibrillation --
via “re-entry” or increased
automaticity
 Arrhythmias:
Anterior M.I.
 Sinus tachycardia -- low stroke volume
 Heart block -- His-Purkinje system
Left or Right Bundle branch block
Complete Heart Block
 Ventricular tachycardia / fibrillation
due to “re-entry” or increased
automaticity
 ACUTE M.I.
Hypotension

 Identify hemodynamic subset

 Distinguish decreased preload from decreased
cardiac output
 Think about hemodynamic monitoring
 Hemodynamic subsets

 Starling curves to 6
plot “preload” versus 5
4
cardiac output Cardiac 3
2
 Identification of high Output 1
0
risk subgroups
 Definition of
cardiogenic shock L.V.E.D.P.
 3
2 .5
2 1 3
Cardiac 1 .5
Index 1
0 .5
(L/min/m2)
0 2 4

L.V.E.D.P.

Hemodynamic Subsets
 Acute M.I.
Mechanical Complications
 Rupture of free wall Tamponade

Pseudoaneurysm

 Rupture of papillary muscle

Acute Mitral regurgitation

 Rupture of intraventricular septum

Acute V.S.D.
 ACUTE M.I.
Papillary Muscle Rupture
Leading to Acute M.R.
 ACUTE M.I.
Papillary Muscle Rupture
Leading to Acute M.R.

 Systolic murmur
 Giant V - waves on PC Wedge tracing
 Echo/Doppler confirmation

 RX with Afterload reduction

 Intra-aortic balloon pump

“Flail” Mitral Leaflet
Echo/Color Doppler of Acute M.R.

LV

RA LA
Development of giant “V waves”

P. A. pressure P.C. Wedge pressure

V-wave
 Acute Mitral Regurgitation:
Treatment

 Rapid diagnosis
 Afterload reduction
 Inotropic support
 Intra-aortic balloon pump
 Surgical valve replacement
 ACUTE M.I.
Acute Ventricular Septal
Defect
•Can occur with either
anterior or inferior MI
•Peak incidence on
days 3-7
•Causes an abrupt left-
to-right “shunt”
 ACUTE M.I.
Acute Ventricular Septal
Defect
•Abrupt onset of a
harsh systolic murmur,
often with a “thrill”
•Detected by an
oxygen saturation
“step-up”
 Oxygen saturation “step-up”

IV C sat SV C sat RA sat RV sat PA sat

70% 65% 68% 88% 88%

 Acute V.S.D.:
Treatment

 Rapid diagnosis
 Afterload reduction
 Inotropic support
 Intra-aortic balloon pump
 Surgical repair of ruptured septum
Intra-Aortic Balloon Pump
 Augments coronary
blood flow during
diastole
 Decreases afterload
during systole by
deflating at the onset of
systole
 Reduces myocardial
ischemia by both
mechanisms
Intra aortic balloon pump
Intra-aortic balloon pump
 Free Wall Rupture

 Cardiac Tamponade  Pseudoaneurysm

Equalization of diastolic
pressures  Enlarged cardiac
silhouette
Hypotension
 Echocardiographic
J.V.D. diagnosis

Clear lung fields

Pulsus paradoxus
 ACUTE M.I.
Apical Aneurysm
 Associated with large,
transmural antero-apical
MI
 Can lead to LV apical
thrombus
 Is associated with
ventricular arrhythmias
 ACUTE M.I.
Apical Aneurysm
 Causes “dyskinesis” of
the apex
 Can be detected by
cardiac echo
 Can lead to systemic
emboli
 Anticoagulants may
prevent embolization
 Right Heart Failure
 Very commonly a  Cardiac causes
Pulmonic valve stenosis
sequela of Left Heart 

 RV infarction
Failure
 Parenchymal pulmonary
 LVEDP causes
 PCW  COPD
 ILD
 PA pressure
 Pulmonary vascular disease
 Right heart pressure
 Pulmonary embolism
overload  Primary Pulmonary
hypertension
 ACUTE M.I.
Right Ventricular Infarction
 Jugular venous distention with clear lungs
 Equalization of right atrial and PCW pressures
 ST elevation in right precordial leads

 Therapy with fluids

 3
2 .5
2
1 3
Cardiac 1 .5
Index 1
(L/min/m2) 0 .5
0 2 4

L.V.E.D.P.
Hemodynamic Subsets
 ACUTE M.I.
Pericarditis

Pleuritic chest pain

 Radiation to the trapezius ridge
 Fever

 Pericardial friction rub

 ACUTE M.I.
CARDIOGENIC SHOCK

 Large area of myocardial necrosis

 Consider mechanical complications

 Exclude correctable causes -- i.e.

hypovolemia or R.V. infarct
 I.A.B.P. C.A.B.G. OR P.T.C.A.
 Summary for RCA (or
circumflex) infarct

R ig h t c o r o n a r y a r t e r y

R ig h t v e n t r ic u la r in f a r c t S - A n o d a l in f a r c t P o s t e r o - m e d ia l p a p illa r y
A - V n o d a l in f a r c t m u s c le in f a r c t

H y p o te n s io n d u e t o B r a d y a r r h y t h m ia s A c u t e m it r a l r e g u r g it a t io n
d e c r e a s e d L . V . f illin g 1 s t d e g r e e A - V b lo c k ( w it h o r w it h o u t
M o b it z I 2 n d d e g r e e b lo c k p a p illa r y m u s c le r u p t u r e )
A - V d is s o c ia t io n
 Summary for LAD infarct
Left anterior descending artery

40% of LV myocardium His-Purkinje system

Cardiogenic shock due

toloss of large amount of Advanced Heart Block
myocardium (LBBB, 3rd degree A-V block
and Mobitz II 2nd degree)

Intraventricular septum Antero-apical wall

(upper two-thirds)

Acute ventricular septal defect Apical L.V. aneurysm

Ventricular Apical thrombus

arrhythmias formation

Arterial embolism
originating in the L.V.
 Summary

 Think
 Think
anatomically!!! hemodynamic
subsets!!!

 LAD vs. RCA

Watch out for

mechanical
complications
THE END