MANAGMENT OF ACUTE

CORONARY SYNDROME

Presenter – Dr. Abhishek Kumar

Guide – Dr. Abhay Kumar

Reference
Harrison’s Internal Medicine, 19th edition
Braunwald’s Heart Disease, 10th edition
AHA/ACC Guideline for the Management of ACS
Ischemic heart disease – a real burden
IHD due to inadequate supply of
blood and oxygen to a part of
heart according to its demand.

It is m/c chronic life-threatening

illness.

In 50% block basal flow normal

but no increase when demands
increases.
In 80% block blood flow is
decreased even at rest leading to
acute coronary syndrome.

Determinant of demand – HR, Contractility and Wall tension(stress)

Determinant of supply – O2 conc, Pulm function, Hb conc and Blood flow
Categorize the Chest Pain

Typical angina
1. Retrosternal component with radiation
2. Brought on by stress or exercise
3. Relieved promptly by rest or NTG

Atypical angina
 2 of above 3 criteria

Non-anginal chest pain

 1 of above 3 criteria
CHARACTERISTICS OF TYPICAL ANGINAL CHEST
PAIN

CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF

ANGINA

TYPE OF PAIN DULL SHARP/STABBING

PRESSURE/CRUSHING
PAIN
DURATION 2-5 MIN, <20 MIN SECONDSTO
HOURS/CONTINUOUS

ONSET GRADUAL RAPID

LOCATION/CHEST WALL SUBSTERNAL, NOT LATERAL CHEST

TENDERNESS TENDER TO PALP. WALL/TENDER TO PALP.
REPRODUCIBALITY WITH WITH
EXERTION/ACTIVITY BREATHING/MOVING

AUTONOMIC SYMPTOMS PRESENT USUALLY ABSENT

Chest Pain Differential

Angina Esophageal

Pericarditis reflux/spasm
Pleuritis Peptic/biliary/colonic

Pulmonary
referred pain

Embolism Chest wall pain

Aortic dissection Neurogenic pain

DEFINITIONS
 CAD is a continuum of disease….

 Stable angina -> unstable angina -> AMI -> sudden cardiac
death

 Acute coronary syndrome encompasses unstable angina,

NSTEMI, STEMI

 Stable angina – transient episodic chest pain d/t myocardial

ischaemia, reproducible with exertion, frequency constant
over time.usually relieved with rest/NTG.

 Classification of angina – Canadian Cardiovascular Society

classification.
Canadian Cardiovascular Association
Classification of Angina
CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY

CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY –

PAIN OCCURS WITH WALKING, CLIMBING
STAIRS,STRESS

CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY – PAIN

OCCURS ON MINIMAL EXERTION

CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT

PAIN, PAIN AT REST
NSTE-ACS
Unstable Angina is defined as angina pain or ischemic
discomfort with at least one of three features:
 It occurs at rest (or with minimal exertion), usually lasting
>10 minutes
 It is of relatively recent onset (i.e., within the prior 2 weeks)

 It occurs with a crescendo pattern (i.e., distinctly more severe,

prolonged, or frequent than previously).

 The diagnosis of NSTEMI is established if a patient with

the clinical features of UA develops evidence of myocardial
necrosis, as reflected in elevated cardiac biomarkers and
ECG changes.
Ref - Harrison’s Internal Medicine, 19 edition, chapter 294
th
STE - ACS
ST Elevation MI
Prolonged R/S chest pain > 20 minutes with

Persisting ST elevation despite NTG

At least 1 mm in 2 adjacent limb leads
At least 2 mm in 2 adjacent precordial leads
New onset LBBB (for purpose of thrombolysis)

Evolution of new q waves (excluding LBBB scenario)

Enzyme or bio-marker elevation
BIOCHEMICAL MARKERS

IDEAL MARKER:
 High concentration in myocardium
 Myocardium specific
 Released early in injury
 Proportionate to injury
 Non expensive testing

 Troponins
 CKMB
 Myoglobin
 Other markers
BIOCHEMICAL MARKERS
Troponin T vs I
 Both equivalent in diagnostic and prognostic abilities
( except in renal failure – Trop T less sensitive)
 Elevation starts~ 3hrs to 12hrs
 Remain elevated for 7 to 10 days
 Meta-analysis (Heindereich et al) – odds of death increased
3 to 8 fold with positive troponins in ACS.

MYOGLOBIN
 Rapid release within 2 hours
 Not cardiac specific
 Rule out for STEMI rather than rule in.

Ref - Harrison’s Internal Medicine, 19th edition, chapter 294

BIOCHEMICAL MARKERS

 CKMB

 Useful in diagnosing re-infarction

 Aim – to exclude MI within 6hrs of symptom onset
 2 hour delta CKMB mass
 Determine changes in serum marker levels over certain
time intervals –Delta values
 Increasing values while still within normal range
suggestive of ischaemia – more rapid anti- ischaemic
mxn.
 Used in conjunction with troponins
Management of ST Elevation MI

Pre hospital care

The time for the patient to recognize the seriousness of the

problem and seek medical attention.

Prehospital evaluation, treatment, and transportation.

the time for diagnostic measures and initiation of treatment

in the hospital e.g., “door-to-needle” time for patients
receiving a fibrinolytic agent.
Management in ER

 Control of cardiac pain and anxiety.

 Reduction of infarct size.

Analgesics
Nitrates
Beta blockers
Oxygen

Ref-Braunwald’s Heart Disease, 10th edition, chapter 52

Analgesics
Morphine, meperidine, pentazocin, NSAIDS.

Morphine is the analgesic of choice.

Reduction of anxiety with successful analgesia diminishes the

patient’s restlessness and the activity of the autonomic nervous
system, with a consequent reduction in the heart’s metabolic
demands.
4 to 8 mg iv stat

Repeat 2 to 4 mg every 5 to 15 mins after checking side effects –

hypotension, resp depression and severe vomiting
Morphine very beneficial in pul edema, tachypnea and
tachycardia.
Nitrates
Enhance coronary blood flow by coronary vasodilatation and
decrease ventricular preload by increasing venous capacitance
Sublingual, oral , spray and IV

All patients having chest pain should be given sublingual

nitrates to reduce pain except – suspected right vent infraction,
hypotension (SBP< 90 mmHg) and bradycardia (HR< 60).
IV nitrates in raised BP, pul edema and waxing & waning chest
pain.
Frequent monitoring of BP is necessary.
Nitrates
Sublingual or spray form
GTN (nitroglycerine) – 0.5 mg
Isosorbide dinitrate – 5 mg or 10 mg
Can be repeated for three times for persisting pain.

IV Nitroglycerine
5 μg/min is recommended to start with.
Increase the rate 10 μg/min every 5 min until symptoms are relieved, systolic
arterial pressure falls to <100 mmHg, or the dose reaches 200 μg/min.
Replace IV nitroglycerin with oral nitrates when the patient has been
painfree for 12–24 h.

The only absolute contraindications to the use of nitrates are hypotension or

the use of sildenafil or other phosphodiesterase-5 inhibitors within the previous
24–48 h.
Beta blockers

Aid in the relief of ischemic pain, reduce the need for

analgesics in many patients, and reduce infarct size and
life-threatening arrhythmias.
Oral and IV

Oral beta blockers to all except in heart failure killip class

II or more, hypotension, bradycardia and AV block.
Pre- reperfusion era routine iv use for all persons but now
if patient has hypertension and tachyarrhythmia
(COMMIT trial)
Beta blockers
Exclude patients with heart failure, hypotension (systolic
blood pressure <90 mm Hg), bradycardia (heart rate <60
beats/min), or significant atrioventricular (AV) block.
Administer metoprolol in three 5-mg intravenous boluses

Observe the patient for 5 minutes after each bolus, and if the
heart rate falls below 60 beats/min or systolic blood pressure
falls below 100 mm Hg, do not administer any further drug.
If hemodynamic stability continues 15 minutes after the last
intravenous dose, begin oral metoprolol tartrate, 25 to 50 mg
every 6 hours for 2 days as tolerated, and then switch to 100
mg twice daily.
Beta blockers
Contraindications
 Asthma
 COPD
 AV conduction disturbance
 Bradycardia
 Raynaud’s phenomena
 Intermittent claudication.

Infusion of an extremely short-acting beta blocker, such as

esmolol, (t 1/2 9 mins.) 50 to 250 mg/kg/ min, may be useful in
patients with relative contraindications like mild asthma,
mild bradycardia, mild HF and first degree heart block.
Oxygen Therapy
Hypoxemia can occur in patients with STEMI and generally
results from ventilation-perfusion abnormalities that are
sequelae of left ventricular failure; concomitant intrinsic
pulmonary disease may be an additional cause of hypoxemia.
Treating all patients hospitalized for STEMI with oxygen for at
least 24 to 48 hours is common practice based on the empiric
assumption of hypoxia and evidence that increased oxygen in
the inspired air may protect ischemic myocardium.
Arterial oxygen saturation can be estimated by pulse oximetry,
and oxygen therapy can be omitted if the oximetric findings are
normal
Reduction of infract size

Most imp is reperfusion therapy which includes

thrombolysis and PCI.

Rest – physical and emotional

Severe anemia

LVF

Infection and fever

Tachycardia
Fibrinolysis or Thrombolysis

 The principal goal of fibrinolysis is prompt restoration of

coronary blood flow

 It acts by promoting the conversion of plasminogen to plasmin,

which subsequently lyses fibrin thrombus.

 Door-to-needle time 30 min.

 Thrombolysis in myocardial infarction (TIMI)grading system.

TIMI 0

TIMI 1

TIMI 2

TIMI 3
Contraindication of Fibrinolysis

Ref-Braunwald’s Heart Disease, 10th edition

Contraindication of Fibrinolysis

Ref-Braunwald’s Heart Disease, 10th edition

STREPTOKINASE
1.5 MU infusion over 1hour.

tPA (Tissue plasminogen activator)

15mg IV bolus, 0.75mg/kg over 30 min, 0.5mg/kg
over 1hr

TENECTEPLASE (VELIX)
30 mg or 0.5 mg/kg iv bolus within 10 secs.

RETEPLASE (rPA)
10 MU IV bolus, followed by 10 MU IV after 30
min
Ref-Braunwald’s Heart Disease, 10th edition, page 1105
General measures

Diet
Bowel movement
Sedation
 Diazepam (5mg)
 Oxazepam (20mg)
 Lorazepam (0.5-1mg)
Activity
 First 12 hrs.
 12 to 24 hrs.
 After one day
 After two day
Anticoagulation therapy

It is imp for maintaining patency of the infarct-related artery,

regardless of whether a patient receives fibrinolytic therapy.
It also prevents deep venous thrombosis, pulmonary
embolism, ventricular thrombus formation, and cerebral
embolization.

Unfractionated heparin
Direct thrombin inhibitors – Hirudin and Bivalirudin
LMWH
Anticoagulation therapy

Unfractionated heparin

In pre-fibrinolysis era

The most serious complication is bleeding especially
intracranial hemorrhage, when fibrinolytic agents are
prescribed.
6o IU/kg iv bolus then 12 IU/kg/hr
Infusions of unfractionated heparin are cumbersome to
administer.
Provide unreliable levels of anticoagulation
Require frequent measurements of the APTT
risk for heparin-induced thrombocytopenia
Anticoagulation therapy
LMWH
 Stable, reliable anticoagulant effect, high bioavailability permitting
administration via the subcutaneous route.

 A high anti-Xa–to–anti-IIa ratio producing blockade of the

coagulation cascade in an upstream location and resulting in a
marked decrement in thrombin generation.

 In the ASSENT 3 trial, with enoxaparin has shown mortility and

reinfarction benefit.
 30-mg intravenous bolus, followed by subcutaneous injections of 1
mg/kg every 12 hours for at least 8 days.
Ref-Braunwald’s Heart Disease, 10th edition
Antiplatelet therapy

A sound scientific basis exists for inhibiting platelet

aggregation in all patients with STEMI, regardless of
the reperfusion management strategy.

Aspirin
Clopidogrel
Prasugrel
Ticagrelor
Aspirin – If not taken before the loading dose of 325 mg then
75 to 162 mg once daily in maintenance phase. (ISIS 2 study)

Clopidogrel – Loading dose of 300 mg if patient is not

receiving primary PCI therapy and 600 mg if primary PCI is
planned followed by 75 mg daily in maintenance phase.
(COMMIT and CLARITY-TIMI 28 trials.)

Prasugrel administered as an oral loading dose of 60 mg and

10 mg daily.

Ticagrelor administered as an oral loading dose of 180 mg and

90 mg twice daily
Inhibition of Renin-Angiotensin-Aldosterone
system
Inhibition of RAAS has favourable impact on
 ventricular remodelling
 improvement in hemodynamics
 reduction in the incidence of congestive heart failure and
 recurrent infarction.

The mortality benefit is additive to aspirin and beta blockers.

Current recommendations is after administration of aspirin

& beta blockers, regardless of fibrinolysis status all patients
with STEMI should be considered for inhibition of the RAAS.
ACE Inhibitors
ARBs
Aldosterone blockers

High risk STEMI patients should receive lifelong treatment with

ACEIs. While rest can be given short term therapy for 4 to 6 weeks.

Those patients who develops side effects of ACEIs should be

switched to ARBs.

Long term aldosterone blockers should be given in high risk patient

in STEMI along with beta blockers and ACEIs after ruling out
contraindications.
Ranolazine
A newer strategy attempts to increase the efficiency of oxygen
utilization by shifting the energy substrate preference of the heart
from fatty acids to glucose. Drugs that may act by this mechanism
are termed partial fatty acid oxidation inhibitors (pFOX
inhibitors) and include ranolazine and trimetazidine. However,
more recent evidence suggests that the major mechanism of
action of ranolazine is inhibition of late sodium current.

Ivabradine
Another new group of antianginal drugs selectively reduces heart
rate with no other detectable hemodynamic effects. It act by
inhibition of the sinoatrial pacemaker current, If.
Complications of MI
Ventricular dysfunction
 In patients with LVEF < 40%, regardless of whether HF
present or not, ACEIs or ARBs should be given.
 Avoidance of hypoxemia, diuresis, inotropic support,
nitrates.
Shock
 Prompt steps to reduce infract size.
 Norepinephrine – 2 microgm/min up to 15 microgm/min
 Dopamine – 5 microgm/kg/min up to 15 microgm/kg/min
 Dobutamine – 2.5 microgm/kg/min up to 10
microgm/kg/min
Complications of MI
Arrhythmia
 Due to autonomic nervous system disturbance, electrolyte
disturbances and instability of myocytes due to ischemia.

 Ventricular premature beats

 Prophylactic antiarrhythmic not needed.

 Ventricular tachycardia and fibrillation

 For sustained VT, intravenous regimen of amiodarone (bolus of 150 mg over
10 min, followed by infusion of 1.0 mg/min for 6 h and then 0.5 mg/min)
 An unsynchronized discharge of 200–300 J (monophasic wave form;
approximately 50% of these energies with biphasic wave forms) when
ventricular tachycardia causes hemodynamic deterioration.
 Implantation of a cardioverter/defibrillator (ICD)
Complications of MI
 Supraventricular arrythmia
Most common is sinus tachycardia
Treat the secondary cause (anaemia, HF, fever and metabolic
disturbances).
If with sympathetic overdrive use of beta blockers or calcium
channel blockers.
In atrial fibrillation with heart failure digoxin is used.
If hemodynamic deterioration and instabilty is present atrial fib
should be treated with electroshock.

 AV conduction disturbances
Temporary and permanent pacemakers.
Anterior vs Inferior wall MI.
Complications of MI
Thromboembolism
 Cause 25% of MI deaths.
 More common with ant. wall infarction
 For Echo documented LV clots systemic anticoagulation is
given for 3 to 6 months
Pericarditis
 Pericardial rub and pericardial pain.
 pain radiating to either trapezius muscle
 Usually be managed with aspirin (650 mg 4 times daily).
 Anticoagulants potentially could cause tamponade in the
presence of acute pericarditis (as manifested by either pain
or persistent rub) and therefore should not be used unless
there is a compelling indication.
Management of NSTE-ACS

General measures
 Rest, Continuous ECG monitoring, Diet, Ambulation
Invasive versus Conservative Strategy
Anti-ischemic Treatment
 Nitrates, Beta blockers and Calcium channel blockers
Anti Thrombotic Therapy
 Antiplatelets and anticoagulants.
Long Term Therapy
Risk Stratification: TIMI score
NSTEMI or unstable angina are risk stratified:
 Age>=65
 >= 3 CAD risk factors:
 HTN, hyperlipidemia, diabetes, smoker, family hx of early MI
 Documented CAD with >=50% stenosis
 ST segment deviation
 ≥ 2 anginal episodes in past 24 hours
 Aspirin use in the past week (marker for more severe case)
 Elevation of cardiac enzymes

Stratify risk based on number of variables

Risk:
 0-2: Low 3-4: Intermediate 5-7: High risk
Management of NSTE-ACS

General measures
 Rest, Continuous ECG monitoring, Diet, Ambulation
Invasive versus Conservative Strategy
Anti-ischemic Treatment
 Nitrates, Beta blockers and Calcium channel blockers
Anti Thrombotic Therapy
 Antiplatelets and anticoagulants.
Secondary prevention
SECONDARY PREVENTION

 INCREASED FOCUS ON SECONDARY PREVENTION:

 SMOKING CESSATION

 DIET MODIFICATION/WT CONTROL

 BP CONTROL

 LIPID MANAGEMENT

 EXERCISE

 DIABETES MANAGEMENT
Thank You