ACUTE CORONARY SYNDROME Cardiology

Dr. R. Deduyo
It takes several years until the fourth decade which is the most common
ATHEROTHROMBOSIS decade and
Acute thrombosis occurring in the presence or pre-existing If this would ruptured-complicated lesion(ACS)
atherosclerosis produces acute ischemic strokes, acute ischemic
strokes(if it affects the cerebral artery), acute ischemic syndromes of
peripheral arteries(found on patients who are chronically hypertensive ATHEROSCLEROSIS to ATHEROTHROMBOSIS
only or diabetics only or combination of DM and hypertension) and
acute coronary syndrome( patients with severe and chronic chest
discomfort) (including unstable angina, myocardial infarction (NSTEMI
and STEMI) and sudden death

Burden of Acute Coronary Syndrome

Significant public health problem both in industrialized and developing
countries

ACUTE CORONARY SYNDROME

ST Elevation Myocardial Infarction (STEMI)
o 1,680,000 hospitalization for ACS in 2001
o 30% of ACS patients have STEMI
o 500,000 STEMI events per year in USA Stable plaque
- Fibrous cap is thick
- Lipid core
- lumen

Disrupted plaque
- Thick ,rich lipid core
- Thin fibrous cap
- (+) thrombus- it can partially occlude or completely occlude the arterial
lumen.

Atherosclerosis is not a disease of butas or the lumen. It is the disease of

the arterial wall . It is not the plaque that causes the occlusion but a
ruptured plaque that releases several thrombi. It will depend on where it
will lodge : Cerebral artery stroke or CVA; Coronary Artery ACS;
Peripheral Artery peripheral arterial Diseases and whose etiology are the
same(w/c is Atherosclerosis) and the risk factors are Hypertension, DM and
genetic predisposition.

From patient with ischemic discomfort, it is not actually a pain that is

usually the complaint,and the discomfort is quite progressive,
heaviness(mabigat andg dibdib) and a foot of an elephant has landed on
the chest;Meron dagan and hindi makirot.

You will able to palpate and elicit tenderness and there will be an
inflammation , and it is contionus and last for 1-2-3 hours and even weeks,
and pag tumagal na, deads na sya!!

It is a discomfort associated with cold clammy skin, sold

sweating,pallor,face sweat and diminish peripheral pulsation.
ATHEROSCLEROSIS TIMELINE
The very first thing and unexpensive test that we can request is
From first decade of life Electrocardiogram. It is easy, accessible,(even in ambulance as patient is
o Foam cells transported to the center and even those working on 911 can access.)
o Fatty streak what to look for? Just ST segment changes.
o Growth mainly by lipid accumulation

From third decade NORMAL:

o Intermediate lesion
o Atheroma
o Growth mainly by lipid accumulation

From fourth decade

o Fibrous plaque( smooth muscle and collagen)
o Complicated lesion/rupture( thrombosis, hematoma)

Atherosclerosis starts even during the first decade of life and some of them
are offspring of diabetic and hypertensive parents.It has been studied that
in the blood vessel of newborn, they were able to find fatty streaks on the
arterial wall ( fatty streaks which are the early lesion of atherosclerosis), so
this can progress for the 1st,2nd ,3rd decade of life, and as you can see , there
is gradual growth of atherosclerotic plaque.

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 ACUTE CORONARY SYNDROME Cardiology
Dr. R. Deduyo
Pathologic and Clinical Presentation of Acute Coronary Syndromes

UNSTABLE ANGINA and NSTEMI

Abnormal findings:
(Imbalance between oxygen demand and supply)
Coronary blood supply can be impaired bec there may be thrombus
that is non occlusive (di bumabara) or vasosapasm f coronary arteries.
So, in a patient with less non occlusive thrombus, there is less severe
ischemia and myocardial damage .There is discomfort and the patient
can tolerate Unstable angina.
A combination of non occlusive thrombus and spasm of arteries is
equivalent to complete occlusion of arteries. There would be severe
ischemia and myocardial damage ST elevation MI
What is the relationship of troponin and damage? The troponin is the
marker that the myocardium has been damaged(No blood supply)

Non- occlusive thrombus less severe ischemia and myocardial

damage unstable angina cardiac markers: normal

Vasospasm severe ischemia and myocardial damage NSTEMI

cardiac markers: elevated(Troponin I, Troponin T, CKMB)

If the ST elevation is not seen, diagnosis is either unstable angina or Non ST
elevation Myocardial Infarction
If it is (+) with ST elevation, diagnosis is St elevation MI.
A biochemical cardiac marker will distinguish the two (-) for ST elevation.
It is not the LDH, CKA,etc but the TROPONIN(troponin I and T),
Unstable angina Negative(-) for St elevation and NormalTroponin and
with ischemic discomfort
Non ST elevation Myocardial InfarctionPositive(+) for troponin T and I
(w/c is in nanogram/dL; morethan 50 indicates positivity) and with an hour
of chest dicomfort.
Q wave indicates necrosis of myocardium.
history:
severe localized chest or arm pain at rest or on minimal exertion
> 20mins crescendo pattern
Chronic stable angina-angina related to activity and even at rest or no
activity, pain scale of 5-10.Sometimes the patient do not have the
luxury of discomfort pero heart Failure kagad. Presentation is not
discomfort but severe DOB with crackles all over, with Pulmonary
edema and Heart Failure(complications).Sometimes patient
presentation are dyspneic, eith mitral regurgitation, S3 gallop, crackles
which is persistent.
Unstable angina- cardiac marker is normal
NSTEMITroponi (+)
Physical exam:
pulmonary edema new or worsening MR, S3, new or worsening
rales

ECG:
transient ST segment changes (>0.05mv) new bundle branch
block, sustained ventricular tachycardia
Left Bundle Block can be considered STEMI--+ peaking of T wave
and 4-6 mm above the base line in ST segment changes.

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 ACUTE CORONARY SYNDROME Cardiology
Dr. R. Deduyo
PATHOLOGIC and ECG changes in NSTEMI PATHOLOGIC and ECG changes in STEMI

o First several days o First and second days

- Some subendocardial muscle dies(necrosis, decr perfusion, not - Transmural infarction nearly complete. Some ischemia and injury
enough blood in myocardium), lesion does not extend through the may be present at borders
entire heart wall - R wave gone or nearly gone
- R wave persists but may diminish somewhat - Significant Q wave
- Q wave not significantsinificant if it is of the height of R wave.; - ST elevation may decrease
necrosis - T wave inversion beginning
- ST often returns to baseline
- T-wave inversion may occur o After 2 or 3 days
Opposite of St elevation is depression. - Transmural infarction complete
- No R wave
T wave inversion: - Deep Twave inversion
- Marked Q wave
- ST may be at baseline

o After several weeks or months

- Infracted tissue replaced by fibrous scar, sometimes bulging
(ventricular aneurysm)
- Some R wave may return
- T wave often less inverted
- Significant Q wave usually persists
- ST elevation may persist if aneurysm _____

*necrosis is changed to fibrosis.

o After several weeks or months There is cardiomegaly and can ruptured and caused sudden death.
- Lesion heals. Some subendocardial fibrosis may occur but does not No ST elevation seen? If the whole thickness of myocardium has been
involve entire thickness of heart wall affected ; St elevation is not seen instead Q wave is seen.
- Q wave not significant Typical significance of Qwave is more than 2/3 of the height and there is
- ST segment and T wave may or may not return to normal also t wave inversion and ST elevation decreases.

o ECG changes in Unstable Angina/NSTEMI

- ST segment depression (30%) NORMAL Q WAVE:
- T-wave inversion (20%)
- Transient ST-segment elevation (5%)

ST ELEVATION MYOCARDIAL INFARCTION (STEMI)

Total occlusion

o Pathological Diagnosis
- Prolonged ischemia PATHOLOGIC Q WAVE;
- Myocyte Death
- Coagulation Necrosis
- Myocytolysis

o Clinical Diagnosis
- History
Accelerating Angina and rest pain(>30mins)
Consistricting, crushing, compressing, heaviness,
choking
Retrosternal radiating to ulnar aspect of left arm
Atypical presentation

- Physcial exam
Soft S1, S3, S4, MR due to papillary muscle dysfunction,
pericardial friction rub o STEMI ECG findings
Hypotension, tachycardia, bradycardia - At least 2mm ST segment elevation in two or more precordial leads
- ST segement elevation of at least 1 mm in two or more leads
S4(not always present); S3-decr resistance in ventricular filling
period of diastole o Myocardial Ischemia, Injury and Infarction
- QRS Complexes in Infarction
- ECG- ST Segment Elevation, Q waves(signifies necrosis) Normal QRS progression
- Cardiac Markers- Troponins (cTnT, cTnI), CK-MB mass, Height of R wave is related to thickness of viable myocardium
Myoglobin
- The golden hour is the first 4 hrs or 4-6 hrs- for fibrinoltyic o Abnormal Q waves
therapy. - Duration: > 0.04sec
- Depth: > 25% of the height of R wave

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 ACUTE CORONARY SYNDROME Cardiology
Dr. R. Deduyo
PRIMARY AND RECIPROCAL ST CHANGES IN ACUTE PHASE INFARCTION
Before Infarct In acute phase infarction (Injury)
Lead facing infarct zone ST elevation typical primary
change
Lead opposite infarct zone ST depressionTypical reciprocal
change

o T wave changes in Myocardial Infarction

- Deep symmetrical T wave inversion
- Symmetry refers to the equality of the angles of downstroke and
upstroke of the T wave
So from normal to St elevation that can happen for hours during injury,
And If you see Q wave it means that it is more than 24 hrs.
In other words the evidence that there is myocardial injury in the life of pt
is the presence of Q wave . This is the evolution of Ecg Changes in a
patient with ACS.

o Evolution of ECG changes in Acute STEMI

a. Normal
b. Hours ST elevation
c. Days Qwaves, Small R, ST elevation
d. Weeks Q waves, Small R, ST isoelectric, Deep T inversion ANTEROSEPTAL:
e. Months Q waves, small R, ST isoelectric, T wave upright

INFARCT, LOCATION AND ECG LEAD INVOLVEMENT

We are looking for ST elevation,depression,T wave, Q wave inversion. Usually
yung ST segment depression ,kung walang injury in the Left opposite side, it is
dignificant pero kung may Q wave and ST segment depression , and on the
opposite side wold be a normal St segment elevation,so RECIPRCOCAL
CHANGES.
Location of infarction Leads showing primary changes
Typical changes
Anterior Infarction
Anteroseptal V1, V2, V3
Anterior V1-V3, V4-V6
Anterolateral V4-V6, I and AVL, possibly II
Extensive Anterior V1- V6, I and AVL
High Lateral AVL (plus high precordial leads)
Inferior infarction
Inferior II, III,AVF
Inferolateral-Apical II, III, AVF, V5, V6 and sometimes
also I and AVL
Inferoseptal II, III, AVF, V1-V3
Other changes
Posterior infarction V1, V2( inverse of usual changes 2. A 65 y/o male diabetes,awakens early in the morning bec of severe
elsewhere) epigasrtric pain radiating to ant chest
Subendocardial Infarction Any lead (usually multiple leads) Comorbidity :age,obese,dm
2,3 AVF inferior wall
CASE: St segment depression
1. A 55 y/o male who experienced severe constricting chestapain AVF (always (-);if it is (+) ,positive for Right ventricular problem
radiating to the back after discussion, 3 hours later he was brought Reciprocal Change with depression
ot the ER DX: Inferior wall myocardial infarction with Reciprocal changes of
ST segment depression in lateral wall
NORMAL:

INFERIOR WALL ONLY!

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 ACUTE CORONARY SYNDROME Cardiology
Dr. R. Deduyo
A. Assess the Initial ECG
B. 12L ECG is central to triage of ACS in the ER. Classify patients as
being 1 to 3 symptoms with 10 minutes of arrival
a. STEMI
ST-segment elevation
Or new or presumably new LBBB

b. High risk unstable (UNSTEMI)

ST-segment depression
Dynamic T-wave inversion

c. Intermediate/ low risk unstable angina

Non-diagnostic ECG
ST depression 0.5-1mm
T-wave inversion or flattening or flattening in leads
with dominant R waves

Assess initial 12L ECG

A. ST elevation or new LBBB/ ST elevation AMI
3.) A 45 y/o male surgeon complaining of retrosternal apin with choking during Treatment
sensation suddenly during elevation. Start Adjunctive Treatment (within 24hrs of onset/
T wave inversion stable)
Tall R wave B-blockers
2,3 AVF Clopidogrel
Left axis deviation cardiomegaly
Heparin (UFH or LMWH)
Big r wave
ACE inhibitors (or ARB)
V5 V6
ST segment depression
clopidogrel and Aspirin- within 90mins of thrombus
Non ST elevation or unstable in lateral wall
formation, malabot yung thrombus and pwedeng
matusok at bukahin ,the lagyan ng stent! (magic! )
Yung Angioplasty walang sugat,mas madali
pero pag matagal na,tumigas na, Bypass na, mas mahal
ACUTE CORONARY SYNDROME yun!
Most common proximate cause of sudden cardiac death Why do we give beta blockers?
Chest pain It dec the HR,If Increase yung HR, more oxygen
ECG changes consumption needed and Contraindications of Beta
Cardiac markers blocker :
IF there is presence of pulmonary edema, IT is
Case NO NO NO!
- 55y/o man heavy failure
- Hypertensive, diabetic, smoker bradycardia
- High cholesterol hypotensive
- Severe substernal chest heaviness> 30 mins, crushing, squeezing complete heart block
Contraindications of Fibrinolytic therapy
What do you do? (streptokinase, Tissue plasminogen activator)
a. Assess ABCs (+) bleeding episode
b. Insert IV line CVA hemorrhage
c. Give oxygen per nasal cannula In short the patient needs to undergo
d. Get a 12 lead ECG REVASCULARIZATION

Chest pain (Suggestive of ischemia) Main t

A. Immediate assessment
- Vital sign, O2 saturation Time onset of symptoms
- IV access - >12 hours admit to monitored bed, assess risk
- 12 L ECG status
- Brief history and PE - <12 hours
- Cardiac Markers
- Electrolytes, coagulation and portable CXR Select reperfusion strategy
Be aware of reperfusion goals:
B. Immediate general treatment - Door to balloon inflation(PCI) goal of 90 min
- Oxygen 4LPM - Door to needle (fibrinolysis) goal of 30 mins
- ASA 160-325mg - Continue adjunctive therapies and HMGCoA
- Nitroglycerin SL or spray reductase inhibitor(statin)
- Morphine
- MONA Morphine, Oxygen, NTG, ASA Cardiogenic shock or contraindications to fibrinolytics,
- Notify receiving hospital PCI treatment of choice. PCI not available, use
fibrinolytics
C. Assess initial 12LECG

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 ACUTE CORONARY SYNDROME Cardiology
Dr. R. Deduyo
Primary PCI selected
- Experienced operators
- High volume centers
- Cardiac surgical capability

Fibrinolytic therapy selected

- Altapase
- Streptokinase
- APSAC

B. ST depression/ dynamic T-wave inversion (High risk UA/ non-STEMI)/

ST elevation or new LBBB/ ST-elevation AMI

C. Non-diagnostic ECG
o ST depression 0.5-1mm
o T wave inversion or flattening in leads with dominant R waves
o Intermediate/low risk unstable angina

Absolute contraindications to beta blocker therapy

o Severe LV failure and pulmonary edema
o Bradycardia(heart rate < 60bpm)
o Hypotension( SBP < 100mm Hg)
o Signs of poor peripheral perfusion
o Second or third-degree heart block

If there is ST elevation,initiate Ischemic therapy and Non dx ECG

like this type,combine ECG and serum markers
Main Objective is
to reduce necrosis that affects the myocardium
prevent major cardiac event and ventricular aneurysm,
cardiac arrhythmia, rupture of chorda tendenae and most
common complication (Heart failue) and most common
cause of death (Cardiac arrhythmia)

Start adjunct tx:

NTG
Betablocker
Clopidogrel-less expensive, for three montha
Heparin
Glycoprotein IIb/IIa

High risk subgroup:

refractory ischemic chest pain
recurrent/persistent ST deviation
Hemodynamic instability
Pump failure

Early invasive starategy includes cathetherization and revascularization.

Prevention:
Clopidogrel-less expensive,( FOR LIFE)
New antiplatelet: PRASUGREL AND BRELINTA
Statin therapy high dose(FOR LIFE)
ACE ARB(FOR LIFE)

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