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ACS
What We All Should Know
assit. prof Dr Tanvir Hussain Chowdhury
 CAD
• CAD is a pathological process characterized by
atherosclerotic plaque accumulation in
epicardial arteries weather obstructive or non
obstructive
• It can have long stable period but also become
unstable at any time if rupture or erosion of
atheromatous plague
• It can be catagorized as either ACS or CCS
 ANGINA
• Typical ischemic type of chest pain
• Aggrabate during exertion and relieve by rest
or GTN
• Due to imbalace between supply-Demand
mismatch
• The myocardia oxygen demand transiently
exceeds the myocardia oxygen supply which
often leads to the menifestation of symptoms
 Acute Coronary Syndrome

• ACS is an unifying term represents a common

end Result of Acute Myocardial ischemia.
• It Encompasses----
1. Acute MI
- ST segment elevation
- Non ST segment elevation
2. Unstable angina
 Unstable Angina-
• Definition- Depends on the presence of one or more
of the following feature accompanied by ECG
change.
1. Typical ischaemic chest pain at rest
2. Angina pectoris of recent onset (Usually within 1
month which is brought on by minimum exertion)
3. Crescendo angina – Rapid deteriation of previously
stable angina.That is angina occurs in increase in
frequency,intensity or both.
4. Angina not relieved with nitroglycerin.
Pathophysilogy of MI
Fate of coronary thrombus
 Risk factor Of ACS
A.Non Modifiable -
 Age
Sex
gender
genetic
high fibrinogen
etnicity
B.Modifiable -
 Smoking
 physical inactivity
 obesity
 Hypertension
 dyslipidemia
 diabetes Mellitus
 Alcohol
 Unhealthy Diet
 social Deprivation
 Classification Of MI-
1. Anatomical Classification-
– Transmural
– Sub endocardial
2. According to ST segment-
– STEMI
– NON STEMI
3. According to location-
– Anterior
– Inferior
 – Posterior (infero basal)
– Lateral
– Septal
– Right ventricular
4. Clinical classification-
A. Type 1 –
Spontaneous MI related to ischaemia from
a coronary plug rupture or dissection.
B.Type 2-
MI due to ischaemia resulting from increase
oxygen demand or decrease supply.
C.Type 3-
Sudden cardiac death with symptom of
ischaemia,new ST elevation or LBBB or coronary
thrombus.
D.Type 4a-
MI associated with PCI
E. Type 4b-
MI associated with stent throbosis.
F.Type 5-
MI associated with CABG.
 Clinical Features Of MI-
A.Precipitating Factors-
 Usually heavy exercise & emotional stress can
precipitate MI.
 Circadian periodicity –
Peak incidence of events occuring in the morning
probably due to increase platelet aggregation, increase
sympatho adrenegic discharge (increase
catecholamine & cortisol level)
 A sudden fall BP may produce an attack. Eg- as a result
of shock,haemorrage/following a operation.
B.Symptoms-
 Severe crushing central chest pain describe as
squeezing or constricting sensation with frequent
radiation to the left arm,often associated with an
impending sense of doom.
 Usually more than 20min not relieved with rest or
GTN.
 Acute MI may painless,usually an elderly patient
with diabetes,post operative patient.
2.Associated Symptoms-
Nausea,Vomiting,Fatigue,Profound
sweating,Palpitation,Dyspnoea,Acute Confusion
3.Atypical Features-
 Only dyspnoea without pain
 Atypical location of pain
 Acute indigestion
 Sudden mania or psychosis
 Apprehension & nervousness
 Syncope
Physical Signs-
Class1
 Investigations-
ECG-
 It is the central to confirming the diagnosis but
maybe difficult to interupt if there is bundle branch
block or previous MI.
 Initial ECG is maybe normal.Repeated ECG is
important specially where there is highly clinical
suspicious of MI or typical symptom
 Earliest ECG chamnge is ST segment deviation or
new onset LBBB is seen initially.Subsequently
development of Q wave & T wave maybe inverted
ECG in ACS
ECG change in STEMI
ECG change in Non-ST-ACS
2.Serum Marker Of Cardiac Damage-
Myoglobin
Troponin I & T
Creatinin kinase (CK)& its myocardial band(CK-
MB)
Aspartate amino transferase
Lactate dehydrogenase
High sensitive troponin
3.Echocardiograph-
 Useful for assessing ventricular function & for
detecting important complications such as
mural thrombus,cardiac
rupture,VSD,MR,pericardial effusion.
4.CxR-
 Pulmonary oedema
 Prominent vascular marking
5.Other blood tests-
 Serum Lipid – During 24-48hrs after admission,gradually fall
(fall of HDL cholesterol after STEMI greater then fall of total
cholesterol)
Then 8weeks after the infarction has occurred is gradually
increased

 WBC- Elevated usually occur within 2hrs & peak 2-3days &
return to normal in 1week.

 ESR- Usually normal 1-2days then rise to a peak on the 4-5th

days & remain elevated for several weeks
 Others

• NT-pro BNP-Should be consider for prognostic

Information(class iia)
• S.creatinine ,eGFR
• CBC
• FBS
• HBA1C
• D dimar
• CXR
 Invasive

6.CAG- Gold standard investigation

-All pt with SYTEMI
-High risk Patient with NSTEMI
 Complications-
A.Early complication(Less than 1week)-
1.HF- LVF,RVF,Biventricular failure
2.Cardiogenic shock
3.Arrythmia
4.Mechanical complication-
 Rupture of papillary muscle causes MR
 Rupture of IVS causes VSD
 Rupture of ventricular wall
5.Pericarditis
6.Pericardial temponade
7.Post MI angina
8.Mural thrombus
9.Pulmonary systemic embolism
B.Late Complications(More than 1week)-
1.Dresslers Syndrome
2.Left ventricular aneurysm
3.Frozen shoulder
4.Post MI psychosis
5.Late arrythmia
 Treatment Of MI-
A.Initial management-
1.Admission in CCU
2.Complete bed rest
3.02 inhalation-4l/min,specially in patient with
clinically significnt hypoxaemia (SPO2 less than
90%),HF ,Dyspnoea
4.IV assess
5.Monitoring of ECG,Pulse,BP,Urine output,Lung
base.
6.Loading dose of Ecosprine,Clopidrogel
7.Tab.Atorvastatin 80mg continue with 40mg
8.S/L Nitrate-1-2puffs S/L repeated if necessary 5mint
interval.
9.IV Morphin 2-4 mg IV slowly 1mg/min with
increments of 2-8mg IV repeated at 5-8mg if
necessary
10.Continue
Atorvastatin,Ecosprin(75mg),Clopidrogel(75mg)at
anti anginal drugs
11.A proton pump inhibitor in combination with
dual anti platelet therapy(DAPT) is
recommended in patient with GIT
haemorrhage/ PUD
12.Anti anginal drugs
 Oral/IV nitrate treatment is indicated to relieve
angina.
 IV nitrate is recommended in patient with
recurrent angina &/sign of HF/HTN
 Oral beta blocker is treatment for all patient in
absence of contraindication
 CCB is recommended for anginal relief if
patient is already receiving nitrate/Beta
blocker & patient with contraindication to
beta blocker
 Consider oral beta blocker,ACE
inhibitor(haemodynamically stable patient)as
early as possible
 B.Reperfusion :
consider primary PCI/thrombolysis In
STEMI
1. Protocol for thrombolysis
a.Indication- Fibrinolytic therapy is indicated in
all patients with a symptom STEMI less than
12hrs & persistent ST elevation/new onset
LBBB.
 Thrombolytic Agents-
-STK(fibrin non specific)
-Tenecteplase
-Reteplase
-T-PA
-Alteplase
Percutaneous Coronary Intervention
(PCI)
 Late Management of MI
• Risk stratification and further investigation lifestyle
modification
– Cessation of smoking
– Regular exercise
– Diet (weight control, lipid-lowering)
• Secondary prevention drug therapy
– Antiplatelet therapy (aspirin and/or clopidogrel)
– β-blocker
– ACE inhibitor
– Statin
– Additional therapy for control of diabetes and hypertension
– Aldosterone receptor antagonis
• Rehabilitation devices: Implantable cardiac defibrillator
(high-risk patients)
Thank You