1
Atherosclerosis &
Coronary heart/artery
disease (CHD/CAD)
Myocardial blood supply & metabolism
Ethiopathogenesis of atherosclerosis
Myocardial ischemia – compensation
CAD – symptoms & outcomes
2
Heart needs a lot of energy to
continually perform as a pump
CO = SV  f
sympathetic
parasympathetic
venous return
3
Myocardial metabolism
• heart is a pump that has to
continually perform 2 processes:
• automacy = generation of
action potential in order to
perform
• contraction
• myocardium thus has a very
high demand for ATP even in
resting state
• for contraction
• actin/myosin – ATP
• Ca2+ handling (Ca2+-ATP-ase,
SERCA)
• for repolarisation
• Na+/K+-ATP-ase
• ATP is produced by oxidation of
substrates
• FFA
• glucose (glycogen)
• ketone bodies and lactate
• therefore myocardium requires
large amounts of O2 and must
be, therefore, well perfused !!
4
Oxygen extraction by various
tissues/organs
Organ CaO2 - CvO2 (vol %) % extraction
heart 10 – 12 65 – 70
skeletal muscle (resting) 2 – 5 13 – 30
kidney 2 – 3 13 – 20
intestine 4 – 6 25 – 40
skin 1 – 2 7 – 13
whole body 20 – 30 %
• Theoretically, the maximal amount of oxygen that can be extracted
is 20 vol % (if CaO2 = 200 ml O2/l )
• In reality, however, the maximal oxygen extraction is around 15 -
16 vol % because of the kinetics of oxygen dissociation from
haemoglobin
• Therefore, the heart is extracting one-half to two-thirds of the
physiologically available oxygen under normal operating conditions
5
Oxygen consumption – quantitative
aspects
• amount of oxygen supplied by the
coronary blood (VO2): ~45 ml O2/min
• VO2 = Qm  CaO2
• myocardial perfusion (Qm) = 210 – 240
ml/min in the resting state (1000 – 1200
ml/min during the exercise)
• CaO2 = 200 ml O2/l
• for PaO2 = 13.3 kPa and c[Hb] = 150 g/l
• consumption in the resting state: ~30 ml
O2/min (~65 - 70%)
• very high O2 extraction (A - VO2 difference)
compared to other organs
• therefore, the only mechanism increasing
the oxygen supply is an increase of
blood flow
• because aorta has a constant pressure, it
has to be done by vasodilatation in the
coronary bed = coronary reserve
• small scale neovascularisation is also
possible
6
Blood supply of the heart
• demand for O2 and
substrates is met by
heart blood vessels coronary
arteries branching
from the
ascendant aorta
• (1) left coronary artery
• (a) left ant. desc. branch
• supplies front part of
the LV and RV and front
part of the septum
• (b) circumflex branch
• supplies left and back
wall of the LV
• (2) right coronary artery
• supplies RV
7
8
Hypoxia
formation of
collaterals
9
Coronary blood flow – temporal pattern
• blood flow is diminished during
the systole due to:
• (1) temporal blocking of coronary
ostia by opened aortic valves
• (2) high flow during systole which
“sucks” the blood out (= Venturi
effect)
• (3) compression of vessels during
the systolic contraction
• therefore most of the coronary
flow occurs during diastole
• tachycardia shortens diastole so
there is relatively less time
available for coronary flow during
diastole to occur
• coronary arteries penetrates
myocardium from surface (epicardium)
to the internal
chamber lining (endocardium)
direction
• therefore, endocardium is more
susceptible to ischemia, especially
at
•  perfusion pressures (e.g.
atherosclerosis)
• or  intracardial pressure (e.g.
heart failure)
10
(Problematic) anatomy of
coronary arteries
11
Factors influencing myocardial O2
consumption (MVO2)
• (1) wall tension
• that’s why O2 demand
is  in pressure or
volume overload
• (2) contractility
• (3) heart rate
• that’s why (i.e. 2 & 3)
O2 demand is  during
sympathetic activation
• (4) myocardial mass
• that’s why O2 demand
is  in cardiac
hypertrophy (esp.
maladaptive)
• rough estimate of
energetic demands of
heart: tension-time
index (TTI)
• SBP x heart rate
12
Wall tension x pressure or volume
overload x MVO2
• wall tension () = tension
generated by myocytes that results
in a given intraventricular pressure
at a particular ventricular radius
• pressure and volume overload have
very various effects on MVO2
• afterload = pressure
• preload = volume (filling ~ end-diastolic
pressure)
• V = 4/3 × r3
• r = 3 V
•  = P × 3 V / d
• 100% increase in ventricular volume (V)
increases wall tension () by only 26%
• in contrast, increasing intraventricular
pressure (P) by 100% increases wall
tension () by 100%!
for detail see
previous
slide
13
Why hypertrophy does not 
O2 consumption at the end
• hypertrophy ( d) normalizes wall
tension () per gram of myocardium
in case of pressure or volume
overload
•  = P × r / d
• initially, it does reduces
MVO2 when wall tension
increases and heart has
to generate higher
pressure to overcome
V or P overload
• however, as the total
mass of myocardium
increases, consumption of O2
increases as well
• myocardial hypertrophy is not
paralleled by similar growth of coronary
bed
14
Hypertrophy development
15
Coronary blood flow - autoregulation
• autoregulation tightly coupled
to the oxygen demand
• between 60 to 200 mmHg of the
perfusion pressure (i.e. systemic
pressure) helps to maintain normal
coronary blood flow whenever
coronary perfusion pressure changes
due to changes in aortic pressure
• during exercise maximal flow can be
reached (“coronary reserve”)
• factors:
• (1) adenosine
• the most important mediator of active hyperemia
• metabolic coupler between oxygen consumption and coronary blood
flow = formed from cellular AMP by 5'-nucleotidase
• AMP is derived from hydrolysis of intracellular ATP and ADP
• (2) nitric oxide
• an important regulator of coronary blood flow, produced by endothelial
nitric oxide synthase
• (3) sympathetic activation
• 1-receptor (more than 1-receptor) activation results in coronary
vasodilation (plus increased heart rate, contractility)
• "functional sympatholysis“: sympathetic activation to the heart results in coronary
vasodilation and increased coronary flow due to increased metabolic activity (increased
heart rate, contractility) despite direct vasoconstrictor effects of sympathetic activation
on the coronaries
16
Coronary collaterals & angiogenesis
• enhancement of blood flow
to ischaemic myocardium
can result from
• (1) recruitment of preexisting
coronary collaterals
• variable density among
people?
• (2) true
angiogenesis/arteriogenesis
• angiogenesis = budding of
capillaries that leads to the
formation of new
microvessels from preexisting
vascular structures
• due to hypoxia (HIF-
1/VEGF)
• failure of concomitant
angiogenesis in
hypertrophic
myocardium
17
Consequences of O2/ATP
depletion
•  contractility (systolic dysfunction)
•  EF (ejection fraction),  SV (stroke volume)
•  diastolic relaxation (diastolic dysfunction)
•  EDP (end-diastolic pressure)
• in summary …  CO (cardiac output)
• in the most serious form = cardiogenic shock
• (auto)regulatory and systemic regulatory
mechanisms cause vasodilation in the intact
part of coronary bed - vascular steal
• stenotic arteries do not react to this
stimulation and healthy ones fjurther “steal”
the blood from already ischemic region
• accumulation of K+, lactate, serotonin and
ADP causes ischemic pain (angina)
• in the less advanced form above mentioned
processes appear only during the exercise,
later also in the rest
18
Nitrates restore „vascular steal“
by dialation of collaterals
19
Causes of myocardial ischemia
• myocardial ischemia = imbalance between supply of the oxygen (and
other essential myocardial nutrients) and the myocardial demand for
these substances
• causes:
• (1) reduced coronary blood flow due to a fixed mechanical obstruction
• coronary atherosclerosis (with or without thrombus) = coronary artery/heart
disease (CAD/CHD)
• thrombembolism
• (2) dynamic obstruction
• vascular spasm
• (3) “small vessel disease”
• diabetic angiopathy
• polyarteritis nodosa
• systemic lupus erythematodes
• (4) decrease of blood oxygenation or concentration of oxygen carrier
• hypoxic hypoxia
• anemic hypoxia
• (5) inadequately high demand for oxygen
•    cardiac output (e.g. thyreotoxicosis)
• myocardial hypertrophy (due to pressure or volume overload)
• (1) and (2) affect larger artery branches (epicardially), (3) to (5)
smaller terminal branches and very often superimpose on the previous
two processes
• myocardial ischemia is the most commonly occurs as a result of
coronary atherosclerosis (AS)
20
Vessels affected by AS
21
CAD due to AS – main facts
• AS is a degenerative process
characterised by chronic inflammation
of the vessel wall
• AS represents multifactorial disease
due to endogenous (typically with
significant genetic component) and
environmental factors
• AS can theoretically affect any vessel, in
reality AS is limited only to arteries (=
arteriosclerosis)
• due to the role of blood pressure as a
pathogenic factor
• moreover, not all arteries are equally
affected, but most often those in
predilections (bifurcations, non-laminar
flow)
• coronary and cerebral bed, renal artery,
truncus coeliacus, lower extremities artery
bifurcations
• main players in the AS ethiopathogenesis
• (1) modified lipoproteins (LDL)
• (2) monocyte-derived macrophages
• (3) normal cells of vessel wall (smooth
muscle cells)
• morphologicaly defined stages (findings)
in naturalhistory of AS:
• (1) endothelial dysfunction
• (2) fatty streak
• (3) fibrous plaque
• (4) complicated plaque
22
Cardiovascular risks
• identification of the main CV
risks by prospective
epidemiologic studies
• Framingham study =  TK, 
cholesterol,  triglycerides,  HDL,
smoking, obesity, diabetes, physical
inactivity,  age, gender (male) and
psychosocial factors
• original cohort (from 1948)
• 5,209 subjects (aged 32 – 60 yrs)
from Framingham, Massachusetts,
USA
• detail examination every 2 years
• II. cohort (from 1971)
• 5,124 adult offspring
• III. cohort
• 3,500 grandchildren of original
participants
• late clinical manifestation of longterm
untreated / decompensated
hypertension:
• heart attack, stroke (
atherosclerosis)
• heart failure ( left ventricular
hypertrophy)
• renal failure ( hyperfiltration,
nephrosclerosis)
• retinopathy
Risk factors of AS
Signif. contribution of genetics
 plasma LDL and VLDL,  HDL
 lipoprotein apo(a)
hypertension
diabetes mellitus
male gender
 plasma homocysteine
 plasma haemostatic factors (e.g.
fibrinogen, PAI, ..)
metabolic syndrome/ins. resistance
obesity
chronic inflammation
Environment / non-genetic
smoking
physical inactivity
high fat intake in diet
certain infections
23
Endothelium - physiological role of ECs
• (1) vasodilation
• smooth muscle cells (SMC) in blood
vessels - notably arterioles - work in close
association with the overlying ECs
• action of hormones, neurotransmitters
(ACh) or deformation of the ECs by flow
of blood (shear stress) trigger reactions
that influence associated SMC, these
effects operates via second messenger
systems
• phospholipase A2 (PLA2) which activate
cyclooxygenase (COX) / prostacyclin
synthase (PCS) to produce prostaglandins
(PGI2) which diffuse readily through the
tissue fluids to act on SMC
• alternatively, nitric oxide synthase
(L-arginase) (NOS) produces highly
diffusible gaseous "neurotransmitter„
NO acting on SMC either through
G-protein systems or directly on ion
channels
• (2) antiadhesive /antiinflammatory
action
• no VCAM, ICAM, selectins, …
• (3) antithrombotic, antiagregant
and fibrinolytic action
• heparansulphate
• thrombomodulin
• tPA
24
NO-mediated vasodilation
• biosynthesis of the key endogenous
vasodilator NO is principally performed
by the calcium-dependent endothelial
isoform of nitric oxide synthase (eNOS)
• this is triggered by the binding of
agonists or by shear stress (1) and
facilitated by a variety of cofactors and
the molecular chaperone heat-shock
protein 90 (HSP90)
• amino acid L-Arg is converted by eNOS
into NO (2), with L-citrulline as a
byproduct. NO diffuses into adjacent
smooth muscle cells (3) where it
activates its effector enzyme, guanylate
cyclase (GC)
• GC (4) converts GTP into the second
messenger cyclic guanosine
monophosphate (cGMP), which activates
protein kinase G (PKG) (5), leading to
modulation of myosin light chain kinase
and smooth muscle relaxation.
• PKG also modulates the activity of
potassium channels (IK; 6), thereby
increasing cell membrane
hyperpolarization and causing relaxation
25
Action of agonists on NO production
26
Endothelial dysfunction
• given the essential role of endothelial integrity in maintenance of normal
vessel morphology endothelial dysfunction act as a pro-atherogenic
factor increasing adhesivity, permeability and impairing vasodilatation
• causative factors:
• increase BP (hypertension)
• mechanical shear stress
• turbulent flow
• bifurcations
• biochemical abnormalities
• glucose
• modified proteins
• incl. LDL
• homocysteine
• oxidative stress
• oxygen radicals
• formed by smoking
• inflammation
• certain infections
• Chlamydia pneumoniae
• Helicobacter pylori
27
Effect of inflammation on EC
28
Endothelium - summary
Functional Dysfunctional
constant vasodilation due to
mechanical stimuli (shear stress)
and mediators (Ach, bradykinine)
mediated by NO, PGI2 (event.
adenosine)
increased sensitivity to paracrine
constrictive mediators
(epinephrine, norepinephrine, AT
II, serotonin) and active
formation of vasoconstrictors (ET-
1)
anti-adhezive / anti-inflammatory
state (NO, PGI2), inhibition of
expression of adhezive proteins
expression of adhesive molecules
(ICAM, VCAM, selectins),
production of cytokines (e.g.
MCP-1) attracting migration of
inflammatory cells into
subendothelial space
constant local anticoagulant
production (heparansulphate,
thrombomoduline), antiagregant
and thrombolytic state (tPA)
prothrombotic (vWf, TF), antifibrinolytic
(PAI-1) phenotype
29
(1) Initiation – formation of fatty streak
• LDLs can exist in native or
modified forms
• native LDL is recognised and bound by LDL-R
• modified LDL is uptaken by scavenger receptors
• in vivo LDL is modified by oxidation
(acetylation or glycation) in circulation
and in subendothelial space
• minimally at first (mmLDL), extensively later (oxLDL)
(oxLDL)
• mmLDL and oxLDL are cytotoxic and
pro-inflammatory, they increase
expression of adhesive molecules
(VCAM, ICAM, selectins) by EC
• monocytes and T lymphocytes
adhere to endothelium and migrates
to subendothelial space, here
monocytes transform to
macrophages
• interestingly, neutrophils that are
constant cell type present in
inflammatory lessions are completely
absent in AS, finding not entirely
understood; it might be because of
the particular cytokine spectrum –
expression of MCP-1 (monocyte
chemotactic protein) by EC
• macrophages ingest oxLDL via their
scavenger receptors (SR-A and
CD36) and form this was so called
“foam cells” (= lipid-laden macropghges)
• macroscopically seen as a yellowish dots or streaks in subendothelium, hence “fatty streaks”
• free cholesterol from oxLDL in macrophages is again esterified by ACAT-1 (acyl-CoA cholesterol
acylransferase) and stored together with lipids, inversely, it can be transform into soluble form by
hormone -sensitive lipase, inbuilt into plasma membrane and exported from the cell (by transporter
ABCA1 and HDL)
• reverse CH transport via HDL is crucial anti-atherogenic mechanism
30
Role of macrophages in AS initiation
• scavenger receptors of macrophages
for modified macromolecules play
physiologically important role in cellular
defence against cytotoxic agents, but at
the same time they can act as pathogenic
mechanisms under the:
• high CH levels
• its increased modification
• oxidation, glycation
• defective reverse CH transport
• Tangier disease (mutation in ABCA1)
• abnormal stimulation of monocytes
• scavenger receptors are part of the
innate immunity
• both natural antibodies and scavenger receptors developed
during evolution under the frequent stimulation by certain
pathogens
• (1) natural antibodies (IgM)
• against bacterial pathogen-associated
molecular patterns [PAMPs]
• (2) pattern-recognition receptors
(PPRs)
• SR-A, CD36, TLR (Toll-like receptor)
• oxidised molecules (i.e. particular
epitopes) are very often similar to
PAMP !!!
31
(2) Progression – formation of plaque
• immunologic interaction
between macrophages
and T lymphocytes
(Th1 and Th2 subpopulation)
locally
maintains the chronic
inflammation
• production of both proatherogenic
Th1
cytokines (MCP-1,
IL-6, TNF-α, …)
and anti-atherogenic
Th2 (IL-4)
• mutual balance between
Th1 and Th2 is topically
modified by many factors
• macrophages as antigenpresenting
cells help to
activate B lymphocytes
to wards production of
auto-antibodies against
oxLDL  formation of
immune complexes  inflammation
• cytokines stimulate other cells, mainly SMCs of media, to migrate into intima,
proliferate ( intima thickening) and secrete proteins of extracelullular matrix
(collagen)  fibrose plaque
• pathologic calcification of atherosclerotic vessel wall is not a passive
consequence but result of changed gene expression in macrophages
(osteopontin)
32
Macrophages in advanced AS – role in
AS progression
• M in early lesions
• majority of Ch in the form of
esters (enzyme ACAT)
• non-thrombogenic
• HDL reverse transport works
• M in advanced lesion
• accumulation of free Ch (FCH)
• highly thrombogenic
• FCH in membranes of
endoplasmic reticulum
changes its permeability and
Ca concentration inside → ER
stress → apoptosis of
macrophages → more of FCH
extracellularly → increased
thrombogenicity of atheroma
• production of MMPs
33
Haemodynamically significant stenosis manifests
ususally after a significant (>50%) reduction in
luminal diameter
34
(3) Complication – rupture and thrombosis
• plaque can grow and slowly
obstruct lumen or it can
become instable and lead to
thrombosis and acute
complete obstruction 
“complicated plaque”
• intimal macrophages and
SMC die (necrosis and
cytokine-induced apoptosis)
and establish necrotic core
of the plaque with accumulated
extracellular CH
• stimulated and hypoxic
macrophages produce
proteolytic enzymes
degrading extracellular
matrix proteins (matrix
metaloproteinases,
MMPs) which further
weaken the plaque
• plaque rupture (often eccentric and CH-rich), typically in the plaque “shoulder”
lead to exposure of accumulated lipids and tissue factors to platelets and
coagulation factors and cause thrombosis
• this can be manifested as a complete vessel occlusion and thus lead to tissue
necrosis (e.g. myocardial infarction or stroke) or incomplete occlusion as a
consequence of repeated cycles of rupture  microthrombotisation 
fibrinolysis  healing = “instable plaque”
35
Thrombosis of the plaque
• Two different mechanisms are
responsible for a thrombosis on
the plaque:
• (1) denudation of endothelium
covering the plaque
• subendothelial connective tissue is
exposed - platelet adhesion
occurs - thrombus is adherent to
the surface of the plaque
• (2) deep endothelial fissuring of
the advanced plaque with a
lipid core
• plaque cap tears (ulcerates,
fissures or ruptures), allowing
blood from the lumen to enter the
inside of the plaque itself (the
core with lamellar lipid surfaces,
tissue factor (triggering platelet
adhesion) produced by
macrophages and exposed
collagen, is highly thrombogenic
• thrombus forms within the plaque,
expanding its volume and
distorting its shape
36
37
38
Animal models of AS - mouse
• generally, it is extremely difficult to simulate AS in animals, even those
kept in captivity
• in this aspect Homo sapiens is quite unique in their susceptibility to damage of
vessel wall
• although mice is the most studied model, exp. induced AS is not
entirely similar to man
• exp. model of AS
• induced
• high CH diet + endothelial denudation + hypertension (ligation of a. renalis)
• spontaneous (knock-out)
• ApoE -/- mouse
• LDL-R -/- mouse
• exp. model spontaneous IM
• induced
• ligation of coronaries
• spontaneous
• comb. apoE/LDL-R -/+
mental stress + hypoxia
39
Clinical manifestation of CHD
• chronic ischemic heart
disease
• stable angina pectoris
• variant/vasospasctic angina
• silent myocardial ischemia
• acute coronary syndromes
• unstable angina
• myocardial infarction
• subendocardial (non-Q)
• ECG: ST-segment elevation
absent (non-STEMI)
• transmural (Q)
• ECG: ST-segment elevation
present (= STEMI)
40
Angina pectoris
• diagnosis of angina is largely based on the
clinical history
• the chest pain is generally described as
'heavy', 'tight' or 'gripping‘
• typically, the pain is central/retrosternal and
may radiate to the jaw and/or arms
• it can range from a mild ache to a most
severe pain that provokes sweating and fear,
there may be associated breathlessness
• types:
• (1) stable
• provoked by physical exertion, especially after
meals and in cold
• aggravated by anger or excitement
• pain occurs predictably at a certain level of
exertion and fades with rest (the threshold for
developing pain is variable depending on the
extent of the stenosis)
• (2) unstable
• angina of recent onset (less than 1 month)
• worsening angina (previously stable for certain
time)
• angina at rest
• (3) variant (Prinzmetal's) angina
• occurs without provocation, usually at rest or
night, as a result of coronary artery spasm
• more frequently in women
• (4) cardiac syndrome X
• personal history of angina + positive exercise
test + angiographically normal coronary arteries
• heterogeneous group (more common in women)
• due to microvascular abnormalities
41
Myocardial infarction (MI)
• result of the plaque rupture with
superadded thrombus
• occlusive thrombus consists of a
platelet-rich core ('white clot')
and a surrounding fibrin-rich
('red') clot
• irreversible changes develop 20-
40 min after complete occlusion
of the artery
• 6 hours after the onset of
infarction, the myocardium is
swollen and pale
• in 24 hours the necrotic tissue
appears deep red owing to
haemorrhage
• during the next few weeks, an
inflammatory reaction develops
and the infarcted tissue turns
grey and gradually forms a thin,
fibrous scar
• late remodelling
• alteration in size, shape and
thickness of both the infarcted
myocardium (which thins and
expands) and the compensatory
hypertrophy that occurs in other
areas of the myocardium
42
Clinical features of MI
• severe chest pain
• onset is usually sudden, often
occurring at rest, and persists fairly
constantly for some hours
• however, as many as 20% of
patients with MI have no pain
• so-called 'silent' myocardial
infarctions are more common in
diabetics and the elderly
• MI is often accompanied by
sweating, breathlessness, nausea,
vomiting and restlessness
• differential diagnosis!
• sinus tachycardia and the fourth
heart sound are common
• modest fever (up to 38°C) due to
myocardial necrosis often occurs
over the course of the first 5 days
43
Localisation and extent of MI
• branch of coronary
arteries
• LCA
• ascendant
• circumflex
• RCA
• stenosis/occlusion
• epicardial
• subendocardial
44
MI diagnosis
• requires at least two of
the following:
• a history of chest pain
• evolving ECG changes in
respective leads
• a rise in cardiac enzymes
or troponins
45
STEMI vs. non-STEMI
46
ECG changes during Q-MI
• first few minutes – tall spiked T
waves
• during first hours - ST segment
elevation develops (Parde
waves)
• after the first few hours - the T
wave inverts
• during days after onset - the R
wave voltage is decreased and
Q waves develop
• after a few days - the ST
segment returns to normal
• after weeks or months - the T
wave may return to normal
• deep Q wave remains forever
47
Cardiac markers of acute MI
• necrotic cardiac tissue releases several
enzymes and proteins into the serum:
• CK - creatinkinase
• peaks within 24hrs and is usually
back to normal by 48hrs (also
produced by damaged skeletal
muscle and brain)
• cardiac-specific isoforms (CK-MB)
allows greater diagnostic accuracy
• the size of the enzyme rise is broadly
proportional to the infarct size
• Troponins I and T
• consists of three subunits, troponin I (TnI), troponin T (TnT) and troponin C
(TnC), each subunit is responsible for part of troponin complex function
• TnI inhibits ATP-ase activity of acto-myosin. TnT and TnI are presented in cardiac
muscles in different forms than in skeletal muscles
• only one tissue-specific isoform of TnI is described for cardiac muscle tissue (cTnI)
• it is considered to be more sensitive and significantly more specific in diagnosis of
MI than the CK-MB and LDH isoenzymes
• cTnI can be detected in blood 3–6hrs after onset of the chest pain, reaching peak
level within 16–30hrs
• Myoglobin
• historically AST - aspartate aminotransferase and LDH - lactate
dehydrogenase
• AST and LDH rarely used now for the diagnosis of MI
• LDH peaks at 3-4 days and remains elevated for up to 10 days and can be useful in
confirming myocardial infarction in patients presenting several days after an episode of
chest pain
48
Complications of MI
• early phase (days after MI)
• arrhythmias
• ventricular extrasystoles
• ventricular tachycardia (may degenerate into ventricular fibrillation)
• atrial fibrillation (in about 10% of patients with MI)
• sinus bradycardia (associated with acute inferior wall MI)
• escape rhythm such as idioventricular rhythm (wide QRS complexes with a regular rhythm at 50-100
b.p.m.) or idiojunctional rhythm (narrow QRS complexes) may occur
• sinus tachycardia
• AV nodal delay (first-degree AV block) or higher degrees of block
• may occur during acute MI, especially of the inferior wall (the right coronary artery usually supplies the SA
and AV nodes)
• acute anterior wall MI may also produce damage to the distal conduction system (the His bundle or bundle
branches)
• development of complete heart block usually implies a large MI and a poor prognosis
• cardiac failure
• pericarditis
• later
• recurrent infarction
• unstable angina
• thromboembolism
• mitral valve regurgitation
• ventricular septal or free wall rupture
• late complications
• post-MI syndrome (Dressler's syndrome)
• chronic v.s. autoimmune pericarditis
• ventricular aneurysm
• recurrent cardiac arrhythmias
49
Acute interventions – stenting
& angioplasty (PTCA)
50
Follow-up interventions – bypass
surgery & transplantation
51