ACUTE CORONARY

SYNDROME
Aarthi V
Roshan Kollipara
Aparna Nair
Case outline
28 y/o male presented with chief complaint of chest pain, which started at 9
am that day. Patient refers that he had a sudden onset of central chest
pain(6/10) along with 2 episodes of vomiting.

Troponin assay was done(11am) which came back negative.

He has no previous medical or surgical history. He refers his mother died of

myocardial infarction some years ago.

Physical examination was unremarkable.

Acute Coronary Syndrome
It’s a term used to describe a range of conditions associated with sudden,
reduced blood flow to the heart.

It is a spectrum of clinical diagnoses comprising :

- unstable angina
- Non ST elevation Myocardial Infarction(NSTEMI)
- ST elevation Myocardial Infarction(STEMI)

that share similar pathological features involving intracoronary thrombosis.

(or new LBBB)
Etiology
Atherosclerosis is the disease responsible for most cases of Acute Coronary
Syndrome. 90% of myocardial infarctions result from an acute thrombus that
obstructs an atherosclerotic artery

Non atherosclerotic causes:

● Coronary occlusion secondary to vasculitis

● Coronary artery emboli
● Vasospasm;drug use; increased oxygen demand (heavy
exertion/fever/hyperthyroidism)
● Decreased oxygen delivery(anemia, CO poisoning)
Pathogenesis
Risk Stratification
Clinical features
SYMPTOMS
● Prolonged cardiac pain +/- pain in throat,arms, neck, jaw and back.
● Anxiety and fear
● Nausea and vomiting
● Angina equivalents’ dyspnea,epigastric discomfort
● Collapse,syncope,fatigue

NOTE: Pain may be absent in patients with prior stroke, age>75 and those
with DM. Painless MI is more common in females.
NSTEMI

Chest discomfort is severe and has at least one of three features:

1. Occurs at rest (or min. exertion) lasting>10 minutes

2. Relatively recent onset (within 2 weeks)
3. Occurs with a crescendo pattern(i.e distinctly more severe, prolonged or
frequent than previous episodes)
SIGNS
● Signs of sympathetic activation- pallor, sweating, tachycardia
● Signs of vagal activation - vomiting, bradycardia
● Signs of impaired myocardial function - hypotension, oliguria,cold
peripheries, narrow pulse pressure, raised jvp, 3rd heart sound,quiet first
heart sound, diffuse apical impulse,lung crepitations
● Signs of tissue damage- fever
● Signs of complications- MR, pericarditis
INVESTIGATIONS
 Anterior wall MI -
V3,V4,V5,V6

ECG Septal MI- V2,V3

Inferior wall MI- II, III,aVF

Lateral wall MI- I, aVL, V5,V6

ECG in NSTEMI
ST segment depression

T wave inversion

Maybe accompanied by some loss of R waves in the absence of Q waves.

ECG in STEMI
Initial ECG may be normal. If normal it should be repeated every 15 minutes.

We can diagnose STEMI in the absence of LVH/LBBB if:

- New onset ST elevation at J point
- >2mm in men or >1.5mm in females
- >1mm or 0.1mV in 2 contiguous limb or chest leads.

May show pathological Q waves after a few hours. This suggests that MI has
fully evolved and there is a full thickness infarct.

● New onset LBBB also suggests MI.

 In unstable angina there is no
Plasma Cardiac detectable rise in cardiac
biomarkers or enzymes.
Biomarkers MI causes rise in plasma
concentration of enzymes and
proteins that are normally
concentrated in the cardiac cells.
Cardiac creatine kinase ( CK MB)

Lactate dehydrogenase (LDH)

Myoglobin

Cardiac Troponins

Aspartate aminotransferase (AST)

Other enzymes - ischemic modified

albumin, N terminal Pro BNP, suPAR,
glycogen phosphorylase iso enzyme
BB
Echocardiography
Useful for assessing ventricular function and for detecting complications.

Abnormalities of wall motion on 2D echo are almost always present in a

STEMI. (RMWA)
Radionuclide Imaging
Not used commonly because they lack sensitivity and specificity. Myocardial
perfusion imaging with thallium-201 or technetium-99m sestamibi can show
uptake defects (cold spots) due to infarction.

It cannot distinguish between old and new infarcts.

Coronary Angiography
It can identify the site of block and allow percutaneous coronary intervention.

Cardiac MRI
MI can be accurately detected with high resolution cardiac MRI using a
technique called late enhancement.
Chest X-ray
May show evidence of pulmonary edema.

Heart size is usually normal but there may be cardiomegaly due to previous
myocardial damage or pericardial effusion.
Other Investigations
● Leukocytosis with a peak on the first day
● ESR will be raised and may remain so for days.
● Raised CRP
● H-FABP (Heart type fatty acid binding protein) as a plasma marker for the
diagnosis of patients presenting with chest pain suggestive of MI.
● Renal function tests
● Serum electrolytes
● Serum glucose and lipid profile.
Treatment of ACS
When looking into treatment of ACS, treatment varies based on the type
of ACS being handled. In case of unstable angina and NSTEMI- treatment
can be categorized as follows:

- Anti-ischemic drugs
- Anti- thrombotic drugs
- Plaque stabilizing drugs
- Pain relief and prophylaxis

When considering STEMI, in addition to all the above treatment modalities,

emergency interventions must also be taken into consideration.
NSTEMI management
1. Anti- ischemia drugs

1. Nitrates
2. Beta blockers
3. Calcium channel blockers
4. Oxygen
2.Anti- Thrombotic drugs
1. Anti-platelet drugs like Aspirin and P2Y12 receptor antagonists like
clopidogrel.
2. Anticoagulant drugs like:
a. Unfractionated heparin
b. Low molecular weight heparin
c. Direct Thrombin inhibitors like
d. Direct factor Xa inhibitors like fondaparinux
3. Plaque stabilizing drugs
ACE inhibitors

ARBs in people who dont tolerate ACE inhibitors

4. Pain relief and Prophylaxis
- If pain isnt relieved with the use of anti-ischemia drugs, Morphine
sulphate may be administered for pain relief.

When morphine is administered, appropriate management of potential side

effects should also be considered- like use of laxatives to treat opioid induced
constipation, etc.

- Prophylaxis against further such events is by the use of all the above
mentioned drugs to minimize the risk of development of thrombi/
impaired perfusion. To this list of prophylactic drugs- statins can be
added.
STEMI management
Emergency interventions
In case of STEMI management- the major difference lies in the emergency
interventions that need to be done.

As in case of STEMI- there is severe myocardial ischemia leading to death of

myocardium in the area of distribution of the occluded vessel- the primary
aim is to minimize further damage.

How is this done??

Minimize “Door- to- needle time”
What is door to needle time? Time taken to administer thrombolytic therapy
to a patient who has had a STEMI

Thrombolytic checklist needs to be cross referenced first along with the

patient’s TIMI flow grade.

Acceptable door- to - needle time is 30 min or less.

TIMI score for risk stratification of a patient
Management according to TIMI risk status
Low risk: drug therapy and appropriate surgical therapy reserved for those
refractory to drug therapy

Medium risk to high risk: Treat with multidrug therapy and early coronary
angiography and appropriate surgical intervention.
Minimize “door- to- balloon time”
In patients that have presented with STEMI to the hospital, with or without
thrombolysis- percutaneous intervention should ideally be done as soon as
possible.

If not preceded by thrombolysis- it is referred to as primary PCI.

This is essentially just percutaneous balloon catheterization of the occluded

vessel to relieve block.
Percutaneous coronary intervention
Coronary artery bypass grafting
Complications in ACS
- Ventricular dysfunction
- Hypovolemia
- Congestive heart failure
- Cardiogenic shock
- Arrthymias (ventricular premature beats, vtach, vfib, svt, sinus tachy and
brady cardia, conduction disturbances)
- Recurrent chest disorder
- Pericarditis
- LV aneurysm
- Thromboembolism
Case outline
28 y/o male presented with chief complaint of chest pain, which started at 9
am that day. Patient refers that he had a sudden onset of central chest pain
along with 2 episodes of vomiting.

Troponin assay was done(11am) which came back negative.

He has no previous medical or surgical history. He refers his mother died of

myocardial infarction some years ago.

Physical examination was unremarkable.

Case outline
28 y/o male presented with chief complaint of chest pain, which started at 9
am that day. Patient refers that he had a sudden onset of central chest pain
along with 2 episodes of vomiting.

Troponin assay was done(11am) which came back negative.

He has no previous medical or surgical history. He refers his mother died of

myocardial infarction some years ago.

Physical examination was unremarkable.