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Syndrome
Chairman : Dr.Venkataramanappa
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In-Hospital
Antithrombotic Thrombolysis
Therapy Primary PCI
ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation
myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention.
Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.
ACS should be distinguished from stable
angina,develops during exertion and
resolves at rest. In contrast ,unstable
angina- occurs suddenly, often at rest or
with minimal exertion, or at lesser degrees
of exertion than the individual's previous
angina ("crescendo angina").
New onset angina is also considered
unstable angina, since it suggests a new
pathophysiologic process in the coronary
artery.
Angina
• Chest pain and
related symptoms
which are caused
by inadequate
blood flow and
oxygen supply to
the myocardial
cells of the heart.
Unstable Angina
• Symptoms of
angina at rest
• New onset of
exertional angina
• Increase in
severity of
previously “stable”
angina
NSTEMI
• Similar to UA
except that
ischemia is severe
enough to cause
myocardial
damage resulting
in the release of
cardiac enzymes
Who’s at risk ?
• Classical: Male > Females
until age 60
• Gender Difference
• Symptom Presentation:
– Males – primarily chest
discomfort
– Females
» Shortness of Breath 55%
» Weakness 52%
» Fatigue 40%
» No Chest Pain 40%
• Risk Factors
Gender
Cigarette smoking
Cholesterol – LDL
Hypertension
Diabetes – vascular
disease more than
blood sugar level
Activity level
Stress
PATHOPHYSIOLOGY
Decrease in O2 supply &/ increase myocardial O2 demand,
superimposed on coronary obstruction.
4 pathophysiological processes contribute to this-
(a) plaque rupture/erosion with superimposed non
occlusive thrombus.
(b) dynamic obstruction {eg: coronary spasm}
(c) progressive mechanical obstruction.
(d) secondary to other systemic conditions{ anaemia}
• Plaque disruption
• Acute thrombosis
• Vasoconstriction
Plaque disruption
– Passive plaque disruption
soft plaque with high concentration of cholesteryl esters and a thin
fibrous cap
– Active plaque disruption
macrophage-rich area with enzymes that may degrade and weaken
the fibrous cap; predisposing it to rupture
Acute Thrombosis
-- Vulnerable plaque
disrupted plaque with ulceration
occurring in 2/3 of unstable patients
exposed lipid-rich core abundant in cholesteryl ester-highly
thrombogenic
--Systemic Hypercoagulable State
disrupted plaque with erosion
occurring in 1/3 of unstable patients
Vasoconstriction
--the culprit lesion in response to arterial damage/plaque
disruption
--area of dysfunctional endothelium near the culprit lesion
--platelet-dependent and thrombin-dependent vasoconstriction,
-- --mediated by serotonin &
Process of resolution
– spontaneous thrombolysis
– vasoconstriction resolution
– presence of collateral circulation
Delayed or absence of resolution
may lead to non-Q-wave or Q-wave
myocardial infarction
The signs and symptoms may include:
• chest pain
• shortness of breath
• nausea
• vomiting
• diaphoresis (sweating)
• palpitations
• anxiety or sense of impending doom
• a feeling of being acutely ill
Chest Pain vs. Discomfort
Quality:
Heaviness Pressure
Constriction Tightness
Strangulation Indigestion
Burning Aching
Choking
Low Risk
• new-onset exertional angina
• minor chest pain during
exercise
• pain relieved promptly by
nitroglycerine
Management
• can be managed safely as an
outpatient (assuming close
follow-up and rapid
investigation)
Intermediate Risk
• prolonged chest pain
• diagnosis of rule-out MI
Management
• observe in the ER or Chest Pain Unit
• monitor clinical status and ECG
• obtain cardiac enzymes every 8 to 12 hours
High Risk
•recurrent chest pain
• ST-segment change
•hemodynamic compromise
•elevation in cardiac enzymes
Management
•monitor in the Coronary Care Unit
Therapeutic Goals
• Reduce myocardial
ischemia
• Control of symptoms
• Prevention of MI and
death
Medical Management
• Anti-ischemic therapy
• Anti-thrombotic therapy
Medical Therapy
• Anti-ischemic therapy
– nitrates, beta blockers, calcium
antagonists
• Anti-thrombotic therapy
– Anti-platelet therapy
• aspirin, ticlopidine, clopidogrel,
GP IIb/IIIa inhibitors
– Anti-coagulant therapy
• heparin, low molecular weight
heparin (LMWH), warfarin, hirudin,
hirulog
Anti-ischemic Therapy
• restrict activities
• morphine
• oxygen
• nitroglycerine
– pain relief, prevent silent ischemia, control hypertension, improve
ventricular dysfunction
– nitrate free period recommended after the first 24-48 hours
• beta-blockers
-- lowering angina threshold
-- prevent ischemia and death after MI
-- particularly useful during high sympathetic tone
• calcium antagonists
-- particularly the rate-limiting agents
-- nifedipine is not recommended without concomitant ß-blockade
Anti Thrombotic therapy
Anti-platelet Therapy
• aspirin is the “gold standard”
– irreversible inhibition of the cyclooxygenase pathway in platelets,
blocking formation of thromboxane A2, and platelet aggregation.
– in UA, ASPRIN reduced the risk of fatal or nonfatal MI by 71%
during the acute phase, 60% at 3 months, and 52% at 2 years
– bolus dose of 160-325 mg, followed by maintenance dose of 80-160
mg/d
• Thienopyridines
-- Ticlopidine (Ticlid )
-- clopidogrel (Plavix )
•Low-molecular-weight heparin
-- advantages over heparin:
-- better bio-availability
-- higher ratio (3:1) of anti-Xa to anti-IIa activity
-- longer anti-Xa activity, avoid rebound
-- induces less platelet activation
-- ease of use (subcutaneous - qd or bid)
-- no need for monitoring
1. Circulation 1994;89:81-88
2. JAMA 1996;276:811-815
Coronary Interventions
Biochemical Markers II
Biochemical Markers III
Molecular First Duration of Sensit Specif
Protein mass (kD) detection detection ivity icity
• Tachycardia
• PE w/ Right Vent: infarct
• Cardiac failure w/ myonecrosis
• Cardiac surgery
• Myocarditis
• Renal failure
Coronary Angiogram
• Observer variability
• Discordance btw severity of lesion
and physiologic effects
– Greater stenosis vs more unstable
plaques?
• 2-D picture of a 3-D problem
– Diffuse disease may limit estimation of
“abnormal segments”
• Missed lesions
Prehospital Chest Pain Evaluation
and Treatment
a. Severe CHF
Goals Recommendations
Goals Recommendations
If blood pressure is 120/80 mm Hg or greater:
Blood
pressure • Initiate lifestyle modification (weight control, physical
control: activity, alcohol moderation, moderate sodium
Goal: < 140/90 restriction, and emphasis on fruits, vegetables, and low-
mm Hg or fat dairy products) in all patients.
<130/80 mm Hg
if chronic If blood pressure is 140/90 mm Hg or greater or
kidney disease 130/80 mm Hg or greater for individuals with
or diabetes chronic kidney disease or diabetes:
Goals Recommendations
Goals Recommendations
Goals Recommendations
Goals Recommendations