CORONARY ARTERY
DISEASE OVERVIEW
Pathogenesis, Clinical Features,
Diagnostic Testing and Therapy
Hank George, FALU, CLU, FLMI
“Myocardial infarction, sudden death and unstable
angina have in common a genesis of coronary
thrombosis, which develops as a result of a
ruptured vulnerable or an eroded atherosclerotic
plaque. As long as atherosclerotic lesions do not
rupture and eroded plaques do not induce
thrombosis, coronary disease may be a clinically
silent disease associated with low mortality.
Whenever plaques start to rupture and
thrombogenic material is coming into contact with
circulating blood, a situation is created
which may lead to acute coronary syndrome
associated with high mortality”
Johannes A. Schaar
Erasmus Medical College, Amsterdam
Circulation 108(2003):2636
What do we know
about atherosclerosis?
• It is a diffuse, systemic disease of
the arterial tree
• It may be present and even severe
despite the absence of recognized
clinical symptoms
• It may produce no extra mortality or
morbidity…until it destabilizes
resulting in VULNERABLE PLAQUE
What characterizes a
VULNERABLE PLAQUE?
Typically, a non-obstructive
atheroma having a central lipid
core, a thin fibrous cap and a
yellowish appearance.
What can trigger an acute coronary
event by inducing destabilization
of a vulnerable lesion?
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Temperature change
Smoking a cigarette
Sexual activity
Vigorous exercise in a deconditioned person
Acute mental stress
Pollution
Infection
Excess hydration
Day-to-day dietary changes
Severe periodontal disease
What is the “endothelium?”
The lining covering the internal
surface of blood vessels, heart
valves and bodily cavities
What is the role of the endothelium?
It protects the artery from injury
by maintaining an antithrombotic
surface, mediating vasodilation
and inhibiting inflammation
What is endothelial DYSFUNCTION?
Disruption of normal function, leading to
vasoconstriction, endothelial inflammation
and thrombus formation
What induces DYSFUNCTION?
Inflammation, excess oxidized LDL-cholesterol
and many other complex biological factors
How do we know that inflammation
occurring outside the coronary arteries
is associated with
acute coronary syndromes?
Because patients with systemic
inflammatory diseases such as
rheumatoid arthritis and SLE develop
endothelial dysfunction and have
excess CAD
Coronary Artery Disease
Four Main Presentations
SILENT ISCHEMIA
CHRONIC STABLE ANGINA PECTORIS
ACUTE CORONARY SYNDROMES
UNSTABLE ANGINA PECTORIS
MYOCARDIAL INFARCTION
SILENT ISCHEMIA
• Ischemic changes on ECGs in the
absence of clinically-recognized
symptoms
• Most common in diabetics due to
neuropathy
• As significant as chronic stable
angina in terms of the subsequent
risk of ACS events, as well as
mortality and morbidity.
CHRONIC STABLE ANGINA
• Episodes of chest pain and other
symptoms (dyspnea, fatigue) induced by
increased oxygen demand and relieved
with cessation of inciting activity or Rx
• Patients often have 2-3 times more silent
episodes than symptomatic episodes
• BEST CASES have minimal excess
mortality when compared to the general
population
How does
chronic stable angina
differ from
unstable angina?
STABLE
• Presents with typical
chest pain, induced by
typical symptoms
• May be presumptively
diagnosed by
symptoms only
• Due to fixed
obstructive disease
• Managed as
outpatient
• Treated medically or
surgically – often by
patient choice
UNSTABLE
• Presents like MI with
prolonged chest
pains, etc.
• Diagnosed by ECG
and cardiac markers
• Due to intraluminal
thrombus formation in
vulnerable disease
• Managed in hospital
• Treated by
percutaneous
coronary intervention
(PCI)
CHEST PAIN EPISODE
Underwriting Triage
• Age, gender
• CV profile
• Where did patient present? ER? GP
office?
• Were Sx typical or atypical
• What brought it on?
• What brought relief?
• Referral to non-cardiologist?
• Management
TROPONIN
• Myocardial proteins cTnT + cTnI
• Essential component of MI diagnosis
• Elevate from heart muscle damage; more
sensitive and specific than CK-MB
• Degree of elevation during/after MI key to
long term prognosis
• Elevates in other scenarios, including
after noncardiac surgeries
• These elevations are adverse mortality
predictors even in absence of
structural/functional heart damage
NT-proBNP
Finest CV Marker EVER
• Elevations due to myocardial stretch
• Elevates in all forms of cardiac disease
• Predictive of future mortality in subjects
free of known CV disease
• Independent of usual CV risk factors
• Inexpensive
• Recent report says protective value payoff from this test is FANTASTIC
• Will replace subjective (treadmill, ECG)
CV screening in underwriting
Other candidates
for CV screening
• HbA1-c
• Cystatin C
• Apolipoprotein B:A1 ratio
Diagnostic Testing in CAD
• Resting ECG
• Treadmill stress ECG
• Stress echocardiogram – exercise vs.
dobutamine (why can’t he exercise?)
• Myocardial scintigraphy (thallium,
etc.)
• Noninvasive CT angiography
• Invasive angiography (presurgical?)
Disease Assessment Parameters
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Exercise ischemia
Treadmill performance
Reversible vs. irreversible lesions
Left ventricular ejection fraction
(LVEF)
• Wall motion: hypokinesis,
dyskinesis, akinesis
• Degree of fixed obstructive disease
CAC
Coronary Artery Calcium
• Scanned for with helical and
electron beam computed tomography
• Extent of calcium quantified
• Range 0-400
• Very low risk with scores 0-10;
just the opposite with 101-400
• Readily available to consumers for
$200 = antiselection potential!
MEDICAL MANAGEMENT
• Antianginals: nitroglycerin,
isosorbide dinitrate, mononitrates
• Beta-blockers or calcium channel
blockers as alternative antianginals
• Clopidogrel, aspirin as
antithrombotic prophylaxis
• Statin prophylaxis
• Lifestyle modification
SURGICAL MANAGEMENT
• Percutaneous coronary intervention,
with or without stenting (PCI)
• Coronary artery bypass grafting
(CABG)
• CABG has less long-term cardiac
morbidity in terms of symptom
recurrence
• No difference in 10 year prospective
mortality
Bravata. Annals of Internal Medicine. 147(2007):703
Does surgical management lead to
lower subsequent mortality than
medical management?
It depends on which study you believe!
Overall, this does not matter nearly as
much as (1) the extent of heart damage
and (2) how the patient responds to the
diagnosis in terms of compliance and
lifestyle choices
What factors should be
considered in potentiallyinsurable CAD cases?
• Extent of myocardial damage
• Current myocardial function, based on
interim testing
• Nature and extent of treatment
• Compliance with Rx
• Risk factor improvement (BP, lipids)
• Health habit changes (quit smoking,
exercise)…and
…one more: whether or not the
individual is depressed, based
on symptoms, need for
treatment, etc.
Many recent studies have shown
that depressed CAD patients
have significantly greater
intermediate and longer-term
morbidity and mortality
CHEST PAIN
with normal coronary anatomy
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Mostly women
Chest pain has features of angina
Often positive stress test
Further evaluation shows no evidence of
significant obstructive coronary disease
• Microvascular disease often present
• No significant extra mortality
• Substantial excess morbidity
STRESS CARDIOMYOPATHY
• Takotsubo cardiomyopathy, apical
ballooning syndrome
• 82% postmenopausal females
• Induced by severe stress, also acute
medical illness and after surgery
• Presents like ACS
• No obstructive lesions
• Normalization of left ventricular function
in 1-3 months in most cases
• Supportive care only
• Recurrence rate 2-10%
What is the long-term mortality risk?