Acute Coronary Syndrome
Acute Coronary Syndrome
Acute Coronary Syndrome
ACS: DEFINITION
A spectrum of clinical diagnoses comprising unstable angina, Non-STEMI, and STEMI that
share similar pathological features involving intracoronary thrombosis.
PATHOPHYSIOLOGY
atherosclerosis with superimposed coronary thrombosis
Slowly growing high-grade stenoses can progress to complete occlusion but do not usually
precipitate acute STEMI d/t collateral circulation
During development of plaques, abrupt transition can occur, resulting in
Platelet activation
Thrombin generation
Thrombus formation
Blood flow occlusion leads to imbalance between supply and demand and could lead
to myocardial necrosis
Pts with non-transmural infarction more likely to have more significan stenosis in IRA
Less severe stenosis with lipid-laden plaques and fragile caps more likely to rupture and
causing thrombsis and STEMI
Stable Angina
Progressive narrowing of coronary lumen
Stable fibrous cap
Unstable Angina
Progressive narrowing
Acute worsening of coronary lumen due to thrombus formation
NSTEMI
Acute worsening of coronary lumen due to
thrombus formation
Sub-occlusive/transient coronary thrombus with
myocardial necrosis
STEMI
Minimal prior narrowing of coronary lumen
Acute rupture of thin fibrous cap
Occlusive thrombus formation
Acute injury pattern
Myocardial necrosis
TYPE OF ACS
Angina
Definition: Discomfort in the chest/ choking, that
characteristically comes on with exertion,
relieved by rest and/or NTG
Character
Constricting
Squeezing
Burning
Heaviness
Dull ache
Knife-like, sharp
Jabs
Pleuritic
Location
Substernal
Anterior thorax
Arms, shoulders
Neck, teeth,
Interscapular
Provoking
Factors
Exertion
Excitement
Cold, meals, stress
EKG
STEMI:
Q waves , ST elevations, hyper acute T waves; followed by T wave
inversions.
Clinically significant ST segment elevations:
o than 1 mm (0.1 mV) in at least two anatomical contiguous leads
or 2 mm (0.2 mV) in two contiguous precordial leads
(V2 and V3)
Note: LBBB and pacemakers can interfere with diagnosis of MI on EKG
EKG
NSTEMI:
ST depressions (0.5 mm at least) or T wave inversions ( 1.0 mm at least) without
Q waves in 2 contiguous leads with prominent R wave or R/S ratio >1.
o Isolated T wave inversions:
can correlate with increased risk for MI
o may represent Wellens syndrome:
critical LAD stenosis
>2mm inversions in anterior precordial leads
Unstable Angina:
May present with nonspecific or transient ST segment depressions or elevations
Cardiac Enzymes
Troponin is primarily used for diagnosing MI because it has good sensitivity and specificity.
o CK-MB is more useful in certain situations such as post reperfusion MI or if
troponin test is not available
Other conditions can cause elevation in troponin such as renal failure or heart failure
The increasing troponin trend is the important thing to look for in diagnosing MI.
Order Troponin together with ECG when doing serial testing to rule out ACS.
Manifestations
Chest Pain Classification
Substernal
Exertional
Relieved with rest
Interpretation
Typical Angina: 3 criteria from above
TnT and TnI have different amino acid sequence in cardiac vs. skeletal muscle
Permits development of cardiac specific antibodies
More sensitive and specific than CKMB
Detects minimal amounts of cardiac necrosis (neg. CKMB)
o minor myocardial damage/microinfarction
Elevated in MI (pos. CKMB)
New guidelines suggest troponin is sufficient to dx MI
Other situations assoc. with increased troponin:
o CHF
o ICU
o Renal failure
o CVA
o Myocarditis/other myocardial injury
Assesses LV function
Guides treatment: PCI, CABG or medical therapy
Indications
UA/post MI with ongoing pain, ST depresssion
Hemodynamic instability
CHF, ventricular arrhythmias
Previous PCI, CABG
High risk non-invasive test
Emerging as the strategy of choice for initial evaluation of most ACS with elevated
troponins or EKG changes
o Based on FRISC II, TACTICS trials