Diagnosis of suspected acute coronary syndromes
• Acute coronary S comprises: unstable angina, non-ST
segment elevation MI. and ST segment elevation MI.
• Unstable angina defined by one of
- Crescendo angina ---- angina on excertion, occurring
over a few d with increasing frequency, provoked by
progressively less exertion.
- Angina occurring recurrently and unpredictably, without
specific provocation (short lived and relived by nitrates).
- Unprovoked and prolonged episodes of chest pain
raising suspicion of AMI without definite ECG or lab.
• Non ST segment elevation MI (NSTEMI) ---Typical chest
pain > 20-30 min. with normal or non-specific ECG
changes and high troponin with or without elevated
cardiac enzymes indicating myocardial damage.
• Both unstable angina and NSTEMI are called non-ST
segment elevation acute coronary S.
• MI as a clinical event consequent to death of cardiac
myocytes (myocardial necrosis) caused by ischemia. The
process initiated by fissuring of an atheromatus plaque in
a coronary artery causing: hge into a plaque causing it t
swell and restrict the lumen of the artery, contraction of
smooth muscle within the artery wall causing further
constriction, and thrombus formation on the surface of the
plaque causing partial or complete obstruction of the
\
lumen or distal embolism. The extent to which these
events reduce the flow to the myocardium largely
determines nature of the clinical syndrome that ensues.
Cardiac enzymes
• Routinely carried out acutely, but should not delay ttt.
• Elevations of biochemical markers diagnose cardiac inj., not
infarction (eg, HF, rapid AF, myocarditis, sepsis). Small
amounts of cardiac inj. can occur in critically ill pts. Troponin
elevations also occur in chronic kidney dis.
• Discordant enzymes — 1/3 pts with an acute coronary S
have elevated troponins but normal CK-MB.
• Aborted MIs ---- Using older assays, some STEMI pt who
rapidly reperfused not develop cardiac biomarker elevation.
Troponin T & I
• Very sensitive & specific markers of cardiac inj. High level 6-
8 h after onset of pain indicates a higher risk of further
coronary events in unstable angina & combined ST segment
depression and high troponin identifies a particularly high-
risk group for subsequent MI & sudden death (normal
values does not eliminate risk).
\ peak 18-24 for 36-48 hrs.
• Onset 3-12 hrs,
• Acute MI can be excluded in most pts by 6 h, but if there is a
high degree of suspicion of coronary S, 12-h sample should
be obtained. Very few pts become +ve after 8 h.
• It is not uncommon to measure a 2nd troponin < 6 h in pt
who are highly suspected of having ongoing NSTEMI, since
80 % of pt who rule in will do so in 2-3 h. In an occasional pt
in whom the index of suspicion for acute MI is high, but the
1st 2 troponin measurements are not elevated, a repeat
measurement at 12 - 24 h may be necessary.
• Troponin elevations persist for 1-2 w after acute MI, but
values are usually not rising or falling rapidly at this time,
allowing one to distinguish acute from more chronic events.
CKmb
• Relatively low until 4-6 h after symptom onset " if -ve in this
period not exclude infarction (some pts do not show a
biomarker" elevation for 12 h)
• Onset 3-12 h, peak 18-24 for 10 d.
• CK-MB is measured when a troponin assay is not available.
Previously, CK-MB was advocated to help diagnose re-
infarction, but now troponin has subsumed that role. Re-
infarction is diagnosed if there is ≥ 20 % increase of the
value in the 2nd sample.
Multidetector CT coronary angiography
• Recently proposed in the management. Feasible, practical,
and accurate when compared with invasive angio. Enable
DD, and can rule out obstructive coronary artery dis. Not
recommended if STEMI diagnosis is likely
Angiography
• Complete normalization of ST-segment elevation with
complete relief of symptoms after nitroglycerin
administration, suggestive of coronary spasm and/or MI.
Early angiography (within 24 h) is recommended.
• Immediate for recurrent ST elevation, chest pain episodes.
• Chest pain or discomfort.
Suspect • Hemodynamic instability or even cardiac arrest esp. in
vulnerable pts (elderly, diabetics, and PO).
• Fluid-responsive hypotensive pt with high CVP and no
congestion suggest RV infarction.
Evaluate rapidly to determine if symptoms suggestive of
acute ischemia, or other potentially life-threatening illness.
• Suggestive history (elder, ischemia, male, diabetes,
hypertension, hyperlipidemia, cocaine use, and smoking).
• Analyze pain characteristics.
• 12 lead ECG within 10 min.; repeat / 10 - 20 min. if initial
ECG is non-diagnostic but clinical suspicion remains high.
If ECG suspicious but not diagnostic, consult expert early.
- STEMI (0.1mV equals to 1mm square)
▪ ST segment elevations; measured at J-point, > 2.5, 2
mm in men < 40 , > 40 y repectively, or >1.5 mm in
women in leads V2–V3 and/or >1mm in other leads "in
absence of LV hypertrophy or LBBB".
▪ Posterior MI ---- V1- 3" ST segment depression &
dominant R wave". Confirmed by ST segment
elevation > 0.5 mm (>1mm in 40 y men) recorded in
+ posterior leads V7–V9).
▪ Presence of LBBB --- ECG diagnosis becomes difficult
but often possible (concordant ST-segment elevation >
1mm in +ve QRS leads, concordant depression > 1
mm in V1-3, and discordant elevation > 5mm in –ve
QRS leads). Pt with a clinical suspicion of ischemia
and LBBB should be managed as STEMI.
❖ Pacemaker rhythm may prevent interpretation and may
require angio. Reprogramming, allows evaluation of
ECG changes during intrinsic heart rhythm, considered
in pt who are not dependent on ventricular pacing.
❖ Earliest change in an STEMI may be the development
of a hyperacute or peaked T wave reflects localized
hyperkalemia, then ST segment elevates in leads
recording electrical activity of involved myocardium; it
has: Initially, elevation of J point and ST segment
retains its concavity. Over time, ST segment elevation
Confirm becomes more pronounced and ST segment becomes
Workup more convex or rounded upward. ST segment may
eventually become indistinguishable from T wave.
❖ Over time, ST segment gradually returns to isoelectric
baseline, R wave amplitude markedly reduced, and Q
wave deepens, and T wave becomes inverted. These
changes generally occur within 2 w, but may progress
more rapidly, within several h.
❖ Complete normalization of ECG following STEMI is
uncommon but can occur, particularly with small
infarcts and when LVEF and RWM improve. This is
usually associated with spontaneous recanalization or
good collateral circulation. In contrast, persistent Q
waves and ST elevations > several w after an infarct
correlate strongly with a severe underlying wall motion
disorder (akinetic or dyskinetic zone), although not
necessarily a frank ventricular aneurysm.
- NSTEMI or unstable angina:
▪ ST segment depressions, deep T wave inversions
without Q waves, or no changes.
- Detect site
▪ Anterior or antero-septal MI -------- V1 – 4.
▪ Inferior MI -----------II, III, and aVF.
▪ Lateral MI ---------- V5-V6 + I and aVL.
▪ RV infarct--- In inferior MI, record rt precordial leads
(V3R and V4R) seeking ST-segment elevation.
▪ Multi-Vessel ischemia ----- ST depression >1mm in >
8 surface leads (infero-lateral ST depression), coupled
with ST-segment elevation in aVR and/or V1, suggests
lt main coronary artery obstruction, particularly if pt
presents with hemodynamic compromise.
❖ Take care of other pathologies with ECG changes (DD).
Echo
• Has no role when diagnosis already apparent.
• Rule out non-cardiac chest pain & visualize RWMAs within
seconds of artery occlusion & location & extent of an infarct
& RV infarction, acute VSD, MR, and systolic dysfunction.
 Diagnosis of suspected acute coronary syndromes "continue"
Q wave
• Not required for ECG diagnosis of MI.
• When present, they may suggest the portion of lt and rt
ventricles that have been affected and size of the infarct.
• The reason why Q waves do or do not develop following
coronary occlusion is related, to size and location of the
infarct. Careful ECG-pathologic correlations have shown
that transmural infarcts can occur without Q waves.
• The following are criteria for ECG changes associated 12 leads ECG shows ST segment depression caused by myocardial ischemia caused by non
ST segment acute coronary S
with prior MI (in absence of LVH or LBBB):
- Any Q wave in leads V2 to V3 ≥0.02 s or QS complex in
V2 and V3; or Q wave ≥0.03 s and ≥ 0.1 mV deep or QS
complex in I, II, aVL, aVF; or V4 to V6 in any 2 leads of a
contiguous lead grouping (I, aVL; V1 - V6; II, III, aVF).
- R wave ≥0.04 s in V1 to V2 and R/S ≥1 with a concordant
positive T wave in the absence of a conduction defect.
• Q waves usually follow a similar distribution to the acute ST
and T wave abnormalities. Q waves can be seen in
hypertrophic cardiomyopathy.
• Pathologic Q waves may be absent in MI:
12 leads ECG shows T wav einversion in NSTEMI
- Small infarcts
- Infarction in areas that is electrically "silent," that is, in
areas that project potentials to regions on the body
surface on which there are no electrodes.
- Chronically ischemic or "hibernating" but non-infarcted.
- Resolution of Q wave. Approximately 10 % of anterior
and 25 % of inferior MIs revert to a non-diagnostic pattern
within 2 y after the infarct, and a higher percentage have
a diminution in Q wave area. Functional recovery of
stunned myocardium contributes to Q wave resolution.
- Other concomitant conduction disorders as LBBB, 12 leads shows antero-lateral STEMI
electronic ventricular pacemaker patterns, and WPW S
that obscure emergence of new Q waves.

DD of ECG abnormalities
Early repolarization
• Present on ECG when there is J-point elevation of ≥0.1 mV
in 2 adjacent leads with slurred or notched morphology.
• The ECG shows normal variant ST-segment elevations (2 -
3 mm) that are usually best seen in the mid-chest leads, 12 leads ECG shows inferior STEMI
that is V3 to V4. Reciprocal ST-depression may be present,
but limited to lead aVR. ST-elevations may be seen in the
limb leads, but are < 1 mm.
ST-segment elevation or depression
• Causes: Atherosclerotic narrowed coronary artery, coronary
artery spasm, myopericarditis, and stress cardiomyopathy.
• Acute pericarditis, typically induces diffuse ST segment
elevations, usually in most of chest leads and in leads I,
aVL, II, and aVF. Reciprocal ST-depression is seen in lead
12 leads ECG shows posterior STEMI
aVR. Presence of PR segment elevation in aVR with PR
segment depressions in other leads. Abnormal Q waves do
not occur and the ST elevation is followed by T wave
inversion after a variable time period.
• Myocarditis can, in some, simulate ECG pattern of acute
pericarditis or acute MI. May be associated with regional
ST-elevations and Q waves, elevated. Serum creatine
kinase MB fraction, and RWMAs on echo. Should be
ECG shows Q waves and prominent doming ST segment elevation in II, III, and
suspected in young pts who present with a possible MI but aVF, findings which are characteristic of an acute inferior MI. ST elevation in right
have a normal angiogram. precordial leads - V4R, V5R, and V6R - indicates RV involvement as well (arrows).
The ST depressions in leads I and aVL represent reciprocal changes.
• ST-elevation occurs in the early phase of takotsubo
cardiomyopathy. Digitalis, ventricular hypertrophy cause
.

ST-segment depression mimicking subendocardial

ischemia. Abnormal T waves: can reflect normal variants,
hyperkalemia, and cerebrovascular inj., LV volume loads
due to mitral or aortic regurgitation, among other causes.
ST elevations and tall positive T waves are also common
findings in leads V1 and V2 with LBBB or LVH patterns.
• Prominent T wave inversions can occur in ventricular
ECG shows findings typical of an evolving Q-wave anterior MI: loss of R waves in leads V1 to
hypertrophy, cardiomyopathy, myocarditis, cerebrovascular V3, ST segment elevations in V2 to V4, and T wave inversions in leads I, aVL, and V2 to V5.
inj., particularly intracranial hge, intermittent ventricular Sinus bradycardia (55 b/min) is present due to concurrent therapy with a beta blocker.

pacing intermittent left LBBB, or intermittent ventricular pre-

excitation (the latter 3 are referred as "memory T waves").
• Q waves: physiologic or positional variants, ventricular
hypertrophy, acute or chronic non-coronary myocardial inj.,
WPW pre-excitation pattern, and ventricular conduction
disorders, especially LBBB.. Classical teachings indicate
that a Q wave must be >40 msec to be considered
abnormal. Newer studies, suggest that Q waves > 30 msec Later stage in the evolution of an acute anterior myocardial infarction. There is a
in I, II, aVL, aVF, or V4 - V6 may be equally diagnostic . QS pattern in leads V1 to V3 and T wave inversion in leads V2 to V4. The ST
segment elevations in these leads have almost disappeared.