CORONARY ARTERY DISEASE OVERVIEW Pathogenesis, Clinical Features, Diagnostic Testing and Therapy

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CORONARY ARTERY DISEASE OVERVIEWPathogenesis,
Clinical Features, Diagnostic Testing and Therapy
Hank George, FALU, CLU, FLMI
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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

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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
  morbidityuntil it destabilizes resulting in
  VULNERABLE PLAQUE

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What characterizes aVULNERABLE PLAQUE?

• Typically, a non-obstructive atheroma having a
  central lipid core, a thin fibrous cap and a
  yellowish appearance.

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What can trigger an acute coronary event by
inducing destabilization of a vulnerable lesion?

• 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

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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
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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
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How do we know that inflammation occurring
outside the coronary arteriesis associated with
acute coronary syndromes?

• Because patients with systemic inflammatory
  diseases such as rheumatoid arthritis and SLE
  develop endothelial dysfunction and have excess
  CAD

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Coronary Artery DiseaseFour Main Presentations

• SILENT ISCHEMIA
• CHRONIC STABLE ANGINA PECTORIS
• ACUTE CORONARY SYNDROMES
• UNSTABLE ANGINA PECTORIS
• MYOCARDIAL INFARCTION

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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.

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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

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How does chronic stable angina differ from
unstable angina?
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STABLE
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)

• 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

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CHEST PAIN EPISODEUnderwriting 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

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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

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NT-proBNPFinest 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 pay-off from
  this test is FANTASTIC
• Will replace subjective (treadmill, ECG) CV
  screening in underwriting

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Other candidates for CV screening

• HbA1-c
• Cystatin C
• Apolipoprotein BA1 ratio

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Diagnostic Testing in CAD

• Resting ECG
• Treadmill stress ECG
• Stress echocardiogram exercise vs. dobutamine
  (why cant he exercise?)
• Myocardial scintigraphy (thallium, etc.)
• Noninvasive CT angiography
• Invasive angiography (presurgical?)

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Disease Assessment Parameters

• Exercise ischemia
• Treadmill performance
• Reversible vs. irreversible lesions
• Left ventricular ejection fraction (LVEF)
• Wall motion hypokinesis, dyskinesis, akinesis
• Degree of fixed obstructive disease

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CACCoronary 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!

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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

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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
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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

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What factors should be considered in
potentially-insurable 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

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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
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CHEST PAIN with normal coronary anatomy

• 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

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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?