ACUTE CORONARY SYNDROME (ACS)

Comprehensive Long Answer Question Notes

Chapter 1: Cardiology

These notes cover STEMI, NSTEMI, Unstable Angina, Complications, Investigations, Management, Thrombolysis,
PCI, CABG, Aftercare and Rehabilitation — structured for exam long-answer questions.

<b>SECTION</b>
<b>TOPIC</b> <b>PAGE</b>

1 ST-Elevation Myocardial Infarction (STEMI) 2

2 Types of Myocardial Infarction 2

3 Non-ST-Elevation Myocardial Infarction (NSTEMI) 3

4 Acute Coronary Syndrome (ACS) — Overview & Classification 3

5 Clinical Features of ACS 4

6 Complications of Acute Coronary Syndrome 5

7 Investigations 7

8 Management of ACS 9

9 Antiplatelet Therapy & Anticoagulants 10

10 Thrombolytic (Fibrinolytic) Therapy 11

11 Percutaneous Coronary Intervention (PCI) 12

12 Coronary Artery Bypass Grafting (CABG) 13

13 Reperfusion Options for STEMI 13

14 Aftercare and Rehabilitation 14

15 Non-STEACS, Unstable Angina, Right Ventricular MI 15

1. ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)

Definition & Etiology

STEMI is due to the formation of an occlusive thrombus at the site of rupture of an atheromatous plaque in
a coronary artery. Usually there is minimal prior narrowing of coronary lumen.

Causes:
• Primary cause: Occlusive thrombus on ruptured atheromatous plaque.
• Coronary spasm (rarely), coronary emboli.
• Aortitis, hypercoagulable state, use of cocaine.
• Congenital anomalies (e.g., origin of left anterior descending from pulmonary artery) — may cause MI in
infancy; very rare in adults.
• 50% coronary stenosis → ischemia with exertion; 80% coronary stenosis → ischemia at rest or minimal stress.

2. TYPES OF MYOCARDIAL INFARCTION

<b>Type</b> <b>Description</b>

Type 1 Spontaneous MI with ischemia due to primary coronary event (plaque erosion/rupture, fissuring, dissection)

Type 2 MI due to oxygen demand-supply mismatch secondary to ischemia from increased demand or decreased supply (cor

Type 3 Diagnosis of MI resulting in sudden cardiac death

Type 4a MI after percutaneous coronary intervention (PCI) — post-PCI related

Type 4b Infarction from stent thrombosis

Type 5 MI after coronary artery bypass graft (CABG) — post-coronary artery bypass graft

Transmural infarct: Involves full thickness of myocardium. Subendocardial infarct: Involves subendocardial
region only. Silent infarct: Infarct without symptoms, only ECG changes.

3. NON-ST-ELEVATION MYOCARDIAL INFARCTION (NSTEMI)

Causes
Most commonly caused by an imbalance between oxygen supply and demand. This imbalance results from a
partially occluding thrombus forming on a disrupted atherothrombotic coronary plaque or on eroded coronary artery
endothelium.

Other causes:
• Dynamic obstruction: Coronary spasm (Prinzmetal's variant angina)
• Severe mechanical obstruction: Progressive coronary atherosclerosis
• Increased myocardial oxygen demand: Fever, tachycardia, thyrotoxicosis in presence of fixed epicardial
coronary obstruction
• Severe ischemia or myocardial necrosis may develop due to reduction of coronary blood flow by partially
occluding thrombus and by downstream embolization of platelet aggregates and/or atherosclerotic debris.

Diagnosis of NSTEMI
Clinical presentation: Based on at least one of three features:
1. Occurs at rest (or with minimal exertion) lasting >10 minutes
2. Relatively recent onset (i.e., within prior 2 weeks)
3. Occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previous episodes)
Evidence of myocardial necrosis: If a patient with above clinical features shows evidence of myocardial
necrosis, as reflected in abnormally elevated levels of biomarkers of cardiac necrosis — NSTEMI is established.
 4. ACUTE CORONARY SYNDROME (ACS) — OVERVIEW &
CLASSIFICATION
Ischemic heart disease (IHD) forms a spectrum of diseases and consists of stable angina and acute coronary
syndromes (includes STEMI, NSTEMI, and unstable angina).
Acute Coronary Syndrome (ACS) is a term used for spectrum of clinical presentations due to acute myocardial
ischemia.

ACS includes:
• ST-elevation myocardial infarction (STEMI): Majority of STEMI has Q-wave MI (QwMI) (Flowchart 1.3)
• Non-ST-elevation myocardial infarction (NSTEMI): A small percentage of STEMI and majority of NSTEMI
have non-Q-wave MI (NQwMI, previously known as subendocardial infarction). However, the terms Q-wave or
non-Q-wave infarctions are not used at present.
• Unstable angina (UA): Includes patients with ACS but with normal ECG, without elevation of cardiac injury
markers and no ST elevation in the ECG. Management of unstable angina and NSTEMI is similar.

Spectrum of Ischemic Heart Disease:

<b>Ischemic Heart Disease</b>

Chronic Coronary Artery Disease (CAD) with Stable

Acute
Angina
Coronary Syndrome (ACS)

STEMI NSTEMI + Unstable Angina (UA)

5. CLINICAL FEATURES OF ACUTE CORONARY SYNDROME

Symptoms
• Prolonged cardiac pain: Myocardial ischemia causes chest discomfort termed angina pectoris. Classic
manifestation is angina — heavy chest pressure or squeezing, a burning feeling, or difficulty breathing.
• The discomfort often radiates to the left shoulder, neck, or arm. It typically builds in intensity over a few
minutes.
• The pain may begin with exercise or psychological stress, but ACS most commonly occurs without obvious
precipitating factors.
• Pain may be absent in patients with prior cardiac, prior stroke, age >75 years, and diabetes mellitus. Painless
MI is more common in females compared to males.
• Any patient with severe chest pain lasting >20 minutes may be suffering from a myocardial infarction. This pain
usually does not respond to sublingual GTN.
• Other features: Anxiety, fear of impending death, nausea and vomiting, breathlessness, collapse, syncope.

Physical Signs
Sometimes infarction occurs without any physical signs.

Table: Various signs of acute coronary syndrome and causes

<b>Type</b> <b>Complication</b>

Ischemic Infarct extension, reinfarction, and angina

Mechanical Cardiogenic shock, cardiac failure, mitral regurgitation, ventricular aneurysm, cardiac rupture (papillary mu

Arrhythmic Atrial or ventricular arrhythmia, dysfunction of sinus or atrioventricular node

Thromboembolic Left ventricular mural thrombus, CNS embolus (stroke) and peripheral embolus

Inflammatory Pericarditis

6. COMPLICATIONS OF ACUTE CORONARY SYNDROME

Major mechanical and structural complications occur only with significant, often transmural MI.
A. Arrhythmias
Many patients with acute coronary syndrome may develop arrhythmia and they are transient in most cases and are
of no hemodynamic or prognostic importance. Relief of pain, rest, and correction of hypokalemia may prevent
arrhythmias.

Ventricular Fibrillation (VF):

• Develops in 5–10% of patients and appears to be the major cause of death in those who die before receiving
medical attention.
• Treatment: Immediate synchronized DC shock. In other cases, digoxin or beta-blocker is given.

Atrial Fibrillation:
• Common but usually transient; does not need emergency treatment.
• If it produces a rapid ventricular rate with hypotension or circulatory collapse → prompt cardioversion by
immediate synchronized DC shock.
• In other cases, digoxin or beta-blocker is given.

Bradycardia:
• Usually does not need treatment.
• If hypotension or hemodynamic deterioration → atropine 0.6–1.2 mg IV may be given.

Various arrhythmias in ACS (Box 1.26):

• Atrial fibrillation
• Atrial tachycardia
• Bradycardia (especially after inferior MI) and tachycardia
• Atrioventricular heart blocks
• Ventricular fibrillation
• Ventricular tachycardia
• Accelerated idioventricular rhythm
• Ventricular ectopic beats

B. Cardiogenic Shock
Causes:
• Arrhythmia
• Hypovolemia due to excessive diuretic therapy or recurrent vomiting
• Extensive myocardial damage (has bad prognosis)
Risk factors: Older age, hypertension, diabetes mellitus, multivessel coronary artery disease, anterior MI, prior MI
or angina, prior heart failure, STEMI, and left bundle branch block.

C. Left Ventricular Failure

It commonly leads to pulmonary edema.

D. Mechanical Complications
Myocardial rupture:
Part of the necrotic muscle in a fresh infarct can result in tear or cardiac rupture. Most frequent during 3 to 7 days
after transmural infarcts.

Rupture of the ventricular free wall:

It is the most common and results in hemopericardium and cardiac tamponade. It is usually fatal.

Rupture of the ventricular septum:

Less common and can lead to acute VSD and left-to-right shunt. Presents with sudden hemodynamic deterioration
and produces a new loud pansystolic murmur radiating to the right sternal border.
Rupture of papillary muscle:
Can lead to acute severe mitral regurgitation, presenting with a pansystolic murmur and third heart sound.

E. Embolism
Thrombus may form on the endocardial surface of freshly infarcted myocardium due to local abnormality in
myocardial contractility (causing stasis) and endocardial damage (creating a thrombogenic surface). This can lead
to systemic thromboembolism and occasionally causes a stroke. Venous thrombosis and pulmonary embolism
may also develop. Now less common with prophylactic anticoagulants and early mobilization.

F. Ventricular Aneurysm
After acute transmural infarction, the affected ventricular wall may bulge outward during systole resulting in
ventricular aneurysm. It develops as a late complication of large transmural infarcts.

G. Pericarditis
Early pericarditis:
A transmural MI → can involve the pericardium → cause fibrinous or fibrinohemorrhagic pericarditis. Usually
develops on second or third day.

Delayed form — Postmyocardial Infarction Syndrome (Dressler Syndrome):

Develops 2–10 weeks after infarction. Characterized by fever, pericarditis, and pleurisy. Probably immunologically
mediated reaction to necrotic muscle. Treatment: aspirin or other NSAIDs or corticosteroids.

Treatment of Pericarditis:
Aspirin 650 mg QID and withhold anticoagulants.

H. Right Ventricular Myocardial Infarction

Right ventricular myocardial infarction is seen with an acute inferior MI secondary to complete occlusion of the
proximal RCA.
Clinical triad: Hypotension, elevation of venous pressure, and clear lung fields in a patient with inferior STEMI
should prompt evaluation for massive pulmonary embolism.
One-mm ST elevations in V4R or V1 are the most sensitive marker of RV involvement.
Initial therapy: IV fluids. If hypotension persists → inotropic support with dobutamine and mechanical support may
be necessary.

I. Cardiogenic Shock — Killip Classification

<b>Class</b>
<b>Based on Clinical Examination (Killip's)</b> <b>Mortality</b>

I Rales and S3 absent 6%

II Crackles, S3 Gallop, elevated jugular venous pressure 17%

III Frank pulmonary edema 38%

IV Shock, SBP <90 mm Hg 81%

J. Complications — Complications Table (Table 1.41)

<b>Cause of Sign</b> <b>Sign</b>

Tissue damage Mild fever

Sympathetic activation Pallor, sweating, and tachycardia

Impaired myocardial function Hypotension, oliguria, cold peripheries, narrow pulse pressure, raised JVP, third heart sound, soft f

Vagal activation Vomiting and bradycardia

Complication Systolic murmur due to mitral regurgitation or uncommonly due to VSD; pericardial friction rub due
7. INVESTIGATIONS

A. Electrocardiogram (ECG)
The 12-lead ECG is central to confirming the diagnosis and should be done and interpreted within 10 minutes of
arrival. The initial ECG may be normal or nondiagnostic in about 30% of cases. Repeated ECGs are needed,
especially where the diagnosis is uncertain.

Changes in ECG:
Characteristic changes are observed in leads that 'face' the ischemic or infarcted area (anteroseptal, anterolateral,
strict anterior, inferior, and posterior wall infarction).

STEMI — ST-segment changes:

• ST-segment deviation is the earliest ECG change. With proximal occlusion of a major coronary artery,
ST-segment elevation (or new bundle branch block) is observed initially.
• Later, there is diminution in the size of the R wave and, in transmural (full-thickness) infarction, development of a
Q wave.
• Subsequently, the T wave becomes inverted and persists after the ST segment has returned to normal.

NSTEMI and Unstable Angina:

• Due to partial occlusion of a major vessel or complete occlusion of a minor vessel, causing unstable angina or
partial-thickness (subendocardial) MI.
• They usually produce ST-segment depression, and T-wave changes.
• When infarction is present, there may be some loss of R waves in the absence of Q waves.

B. Plasma Cardiac Biomarkers (Biochemical Markers of Cardiac Injury)

• Unstable angina: There is no detectable rise in cardiac biomarkers or enzymes. The initial diagnosis is made
from clinical history and ECG only.
• Myocardial infarction: Causes arise in the plasma concentration of enzymes and proteins normally
concentrated within cardiac cells: creatine kinase (CK), aspartate aminotransferase (AST), lactate
dehydrogenase (LDH), myoglobin, and troponins (troponin I and troponin T). These markers leak from necrotic
myocardial cells into the blood circulation.

Table: Characteristics of plasma biomarkers for acute MI (Table 1.42)

<b>Marker Protein</b> <b>Elevation after AMI (h)</b>
<b>Peak plasma conc. (h)</b>
<b>Normalization (days)</b>

Myoglobin 2–3 6–12 1–2

Cardiac troponin I 3–8 12–24 7–10

Cardiac troponin T 3–8 12–24 7–10

Creatine kinase MB 2–6 12–24 2–3

Cardiac Creatine Kinase (CK):

• A nonspecific enzyme marker. Present in brain, myocardium, and skeletal muscle. Has two isoforms: M and B.
• MB form of CK (CK-MB) is sensitive but not specific (also raised in skeletal muscle injury).
• CK-MB levels rise within 4 to 6 hours of MI onset, peaks at 12 hours, returns to normal within 72 hours.
• Total CK is also raised in diseases of skeletal muscle (polymyositis, muscular dystrophies), hypothyroidism, and
stroke.

Lactate Dehydrogenase (LDH):

Not a specific marker. Starts rising after 24–48 hours. Remains for many days and returns to normal in 7–14
days. An elevated LDH (isoenzyme of LDH) is a more sensitive indicator of myocardial infarction than total LDH.

Myoglobin:
An oxygen-carrying respiratory protein found only in skeletal and cardiac muscle. It is an earliest marker of MI.
Level rises within 1–3 hours, peaks in about 8–12 hours and return to normal in about 24–36 hours.
Cardiac Troponins:
Proteins involved in heart muscle contraction. Increased plasma levels establish the diagnosis of myocardial
infarction. Cardiac-specific proteins are of two types: cardiac Troponins I (cTnI) and Troponins T (cTnT). They
are the most sensitive and specific markers of myocardial injury. Increased plasma levels establish diagnosis
and peak at 48 hours.
Levels begin to rise at 4–6 hours; therefore, this assay is particular useful. Elevated troponin values may remain
for 7–10 days after acute MI. About one-third of patients with unstable angina also have elevated cTn, which
classifies them to non-ST-elevation MI.

Aspartate Aminotransferase:
Starts to rise by about 12 hours and reaches a peak on the first or second day.

Other enzymes:
(1) Ischemia modified albumin; (2) N terminal Pro BNP; (3) suPAR (soluble urokinase-type plasminogen activator
receptor); (4) Glycogen phosphorylase isoenzyme BB.

C. Other Blood Tests

• Leukocytosis: With a peak on first day.
• Erythrocyte sedimentation rate (ESR): Raised and may remain so for days.
• C-reactive protein: Elevated.
• Heart-type fatty acid-binding protein (H-FABP): As a plasma marker for diagnosis of patients presenting with
chest pain suggestive of MI (within 2 hours) after onset of symptoms. However, its use as a diagnostic tool for
MI is limited.

D. Chest X-ray
• May show evidence of pulmonary edema not evident on clinical examination.
• Heart size is usually normal but there may be cardiomegaly due to previous myocardial damage or pericardial
effusion.

E. Echocardiography
Useful for assessing ventricular function and for detecting complications (mural thrombus, cardiac rupture,
ventricular septal defect, mitral regurgitation, pericardial effusion).

F. Radionuclide Scanning
Helps to detect the site of necrosis and the extent of damage to ventricular function.
8. MANAGEMENT OF ACUTE MYOCARDIAL INFARCTION

Immediate Management
The first 24–48 hours, patients should be admitted immediately to hospital. During first 24–48 hours the risk for
fatal arrhythmia is highest and as a result, there is a significant risk of death or recurrent myocardial ischemia.
Patients are best treated in an intensive coronary care unit (ICU).

Initial Treatment — General Treatment ('MONAC')

Admit in intensive coronary care unit, attach a cardiac monitor, and secure an intravenous line.

M — Morphine:
2–4 mg q 5–10 minutes to control chest pain.

O — Oxygen:
4 L/minute. Hypoxemia in uncomplicated MI is usually due to ventilation-perfusion abnormalities and may be
exacerbated by CHF. Oxygen is given to patients suspected of having an acute coronary syndromes and oxygen
saturation <90%.

N — Nitroglycerine (NTG):
Sublingual or spray, followed by infusion for persistent chest pain.

A — Aspirin:
160–325 mg chew and swallow or/and

C — Clopidogrel:
300 mg oral.

Confirm Diagnosis — Investigations:

• Electrocardiogram (ECG)
• Plasma cardiac biomarkers: Troponin T or I and CK-MB

Specific Therapy:
• Thrombolysis or percutaneous coronary interventions (PCI)
• Beta-blockers unless contraindicated
• Treat complications (arrhythmias, congestive failure, and shock)

9. ANTIPLATELET THERAPY & ANTICOAGULANTS

Control of Pain by Analgesics

Proper control of pain is necessary not only to relieve distress but also to lower adrenergic drive which reduces
vascular resistance, BP, infarct size, and susceptibility to ventricular arrhythmias.
• Intravenous opiates: Initially, morphine 2–4 mg or diamorphine 2.5–5 mg along with antiemetics
(metoclopramide 10 mg), repeated until patient is comfortable.
• Beta-blockers, nitroglycerine, and thrombolysis may also help in reducing the pain.

Antiplatelet Therapy
Aspirin:
• In ACS, oral aspirin (75–325 mg daily) improves survival and reduces mortality.
• First dose (300 mg) should be given orally within the first 12 hours and should be continued indefinitely if no side
effects.

Combination Therapies:
 • Combination of aspirin and an ADP-receptor blocker (clopidogrel, prasugrel, or ticagrelor) is recommended in
patients with STEMI who are undergoing primary PCI (up to 12 months) or (clopidogrel) fibrinolysis.
• In acute coronary syndrome without ST-segment elevation, ticagrelor (180 mg, followed by 90 mg twice daily) is
found to be more effective than clopidogrel in reducing vascular death, MI, stroke, and other causes of death.

Glycoprotein IIb/IIIa Receptor Antagonists:

• Powerful inhibitors of platelet aggregation and prevent thrombus formation.
• Examples: tirofiban, eptifibatide, and abciximab.
• Abciximab is a monoclonal antibody which binds tightly with a long half-life.
• Beneficial in patients who undergo PCI, those with recurrent ischemia, and those with high risk (diabetes mellitus
and raised troponin).

Anticoagulants (Antithrombin Therapy)

Prophylactic anticoagulants are given to prevent deep vein thrombosis and pulmonary embolism in patients who do
not receive fibrinolytic agents. They reduce the risk of thromboembolic complications and prevent reinfarction in the
absence of reperfusion therapy or after successful thrombolysis.

Unfractionated Heparin (UFH):

Given as an initial bolus dose of 60 IU/kg (maximum 4,000 units) followed by an initial infusion of 12 IU/kg/hour
(maximum 1,000 units/hour). Dose adjusted to attain activated partial thromboplastin time at 1.5–2 times control.
Given before the completion of infusion of rt-PA or tenecteplase or patients receiving STK.

Low-Molecular Weight Heparin (LMWH):

Used as an adjunct to thrombolytics. Produces higher reperfusion rate and lower reocclusion rate compared to
unfractionated heparin. Dose of 5,000 units is given twice a day subcutaneously.

Direct Thrombin Inhibitors:

Appear better than the unfractionated heparin in patients undergoing PCI. Include hirudin and bivalirudin.
Pentasaccharides (subcutaneous fondaparinux 2.5 mg daily) are safe and effective. However, fondaparinux is not
used as sole agent and contraindicated if PCI is planned.
Antithrombin preparations should be continued for at least 48 hours and preferably for 8 days or till discharge or
coronary revascularization.

Statins
High-dose statins are recommended in all patients during the first 24 hours of admission for STEMI, irrespective of
patient's cholesterol concentration, if there are no contraindications (allergy, active liver disease). They are
recommended during the early phase of therapy up to at least 4 weeks.

Advantages:
• Statins lower cholesterol and have direct effects on endothelial function, oxidative stress, inflammation,
thrombosis, and plaque stabilization.
• High-dose atorvastatin (40–80 mg) or rosuvastatin (20–40 mg) therapy before emergency percutaneous
coronary intervention has following advantages:
– Reduce periprocedural inflammatory response
– Reduce myocardial dysfunction
– Prevent contrast-induced nephropathy
10. THROMBOLYTIC (FIBRINOLYTIC) THERAPY IN ACUTE CORONARY
SYNDROME
Fibrinolytic therapy should be initiated within 30 minutes (door-to-needle time or first medical
contact-to-needle time).

Thrombolytic Agents
These include plasminogen activators, i.e., streptokinase (STK), urokinase (UK), human tissue plasminogen
activator (tPA-alteplase), recombinant plasminogen activator (rPA-reteplase), tenecteplase, anisoyated
plasminogen streptokinase activator complex (AP-SAC, anistreplase), and single-chain urokinase plasminogen
activator (scu-PA).

Mechanism of Action
Thrombolytic or fibrinolytic agents lyse thrombi/clot to recanalize the occluded vessels (mainly coronary arteries) by
the activation of plasminogen to form plasmin. They are curative rather than prophylactic.

Fibrin-specific fibrinolytics:
They generate fibrin-specific fibrinolytics at the site of thrombus/clot. Examples include rPA (reteplase),
tenecteplase (TNK), and scu-PA. They have lower mortality rate compared with STK and also lack the significant
acute side effects of hypotension and allergy caused by STK.

Generation plasmin in the systemic circulation:

These agents generate plasmin in systemic circulation producing a systemic lytic state. This leads to reduction in
blood viscosity, and produces strong anticoagulant and antiplatelet effects. Examples include streptokinase (STK)
and urokinase (UK). STK use is associated with lower incidence of intracranial hemorrhage, especially in older
individuals.
Thrombolytic therapy is not recommended for patients with NSTEMI and unstable angina.

Indications for Thrombolysis (Box 1.27)

<b>Category</b> <b>Indication</b>

Definitely beneficial • ST-segment elevation >0.1 mV in two or more contiguous leads, with time to therapy 12 hours or less
• Left bundle branch block (LBBB) obscuring ST-segment analysis and history/analysis of acute MI <12

Some benefit • ST-segment elevation with time to therapy 12–24 hours

Not indicated • ST-segment depression only (unless leads V7–V9 show ST depression related to posterior wall MI)
• Time to therapy >24 hours

Contraindications to Thrombolytic Therapy (Box 1.29)

Absolute:
• History of cerebrovascular hemorrhage anytime in life
• History of nonhemorrhagic stroke or other cerebrovascular event within the past 1 year
• Uncontrolled marked hypertension (systolic BP >180 mm Hg, diastolic BP >110 mm Hg) — However, STK can
be given
• Suspected aortic dissection
• Active internal bleeding (excluding menses)
• Known intracranial aneurysm/AVM/malformation/neoplasm (primary or metastatic)
• Intracranial/spinal surgery within last 3 months

Relative:
• Current use of anticoagulants (INR ≥2)
• Recent (<2 weeks) invasive or surgical procedure, prolonged (>10 min) CPR
• Known bleeding diathesis
 • Recent trauma (including traumatic resuscitation)
• Pregnancy
• Hemorrhagic ophthalmic condition
• Active peptic ulcer disease
• History of severe hypertension that is currently controlled

Signs of Reperfusion (Box 1.28)

• Immediate relief of chest pain
• Reduction of the initial ST-segment elevation by 50% within 60–90 minutes of fibrinolytic therapy
• Onset of reperfusion arrhythmias (accelerated idioventricular rhythm and frequent ventricular ectopics)
• Early peaking of CK-MB enzyme

Complications of Thrombolytic Therapy

• Hemorrhage: Most common complication. Most common site is region of puncture sites, genitourinary system,
and intracranial hemorrhage (about 0.5% of patients).
• Allergic reactions: May develop with use of STK and APSAC.
• Hypotension: May develop if STK is infused rapidly.

TIMI Grading System (Thrombolysis in Myocardial Infarction — Box 1.30)

<b>Grade</b> <b>Description</b>

TIMI 0 Absence of antegrade flow beyond a coronary occlusion

TIMI 1 Faint antegrade coronary flow beyond the occlusion, although filling of the distal coronary bed is incomplete

TIMI 2 Flow is delayed or sluggish antegrade flow with complete filling of the distal territory

TIMI 3 Flow is normal which fills the distal coronary bed completely

Thrombolytic Agents and their Doses (Table 1.44)

<b>Thrombolytic agent</b> <b>Dose</b>

Alteplase (tPA) 15 mg bolus followed by 50 mg intravenously over the first 30 min, followed by 35 mg over the next 6

Streptokinase (STK) 1.5 million units (MU) intravenous infusion over 1 hour

Tenecteplase (TNK) Given as a single weight-based intravenous bolus of 0.53 mg/kg over 10 seconds

Reteplase (rPA) Double-bolus regimen consisting of a 10 MU bolus given over 2–3 minutes, followed by second 10-M
11. PERCUTANEOUS CORONARY INTERVENTION (PCI)
Percutaneous coronary intervention is the treatment of choice, provided it is performed promptly by a qualified
interventional cardiologist in an appropriate facility.

Indications for PCI

Patients with STEMI with following features:
• Symptoms of ischemia of less than 12 hours duration.
• Symptoms of ischemia of less than 12 hours duration who have contraindications to fibrinolytic therapy,
irrespective of the time delay from first medical contact.
• Cardiogenic shock or acute severe heart failure (HF), irrespective of time delay from MI onset.
• It may be recommended if there is clinical and/or ECG evidence of ongoing ischemia between 12 and 24 hours
after symptom onset.
• Maximum acceptable delay: For primary PCI from presentation to balloon inflation is 90 minutes if a patient
presents within 1 hour of symptom of onset or 60 minutes if a patient presents later.

Types of PCI
Primary PCI:
In which PCI is used solely in acute MI. It is indicated in cardiogenic shock, and in patients in whom thrombolytic
therapy is contraindicated. It is generally preferred with following conditions:
• Skilled PCI laboratory is available with good surgical backup.
• Door-to-balloon time is ≤90 minutes.
• Door-to-balloon time minus door-to-needle time is ≤1 hour.

High-risk STEMI:
• Cardiogenic shock
• Killip class CHF ≥3
• Contraindications to fibrinolysis including increased risk of bleeding and intracranial hemorrhage.
• Late presentation (>3 hours after symptom onset).

Rescue PCI:
Combination of PCI with thrombolytic therapy and PCI is performed within 12 hours after failed
thrombolysis/fibrinolysis for patients with continuing or recurrent myocardial ischemia.
Indications: STEMI in aged <75 years who received fibrinolytic therapy and have cardiogenic shock, severe
congestive heart failure (Killip class III), or hemodynamically compromising ventricular arrhythmias.

Facilitated PCI:
In this type PCI is done following initial pharmacological regimen aimed at improving patency of coronary arteries
before PCI.
The pharmacological regimens include GB IIB/IIIa inhibitors, full-dose or reduced-dose of fibrinolytic therapy, and
combination of a GP IIb/IIIa inhibitor, and a reduced-dose fibrinolytic/thrombolytic agent. However, this type of
reperfusion may be inferior to thrombolysis alone or primary PCI and is usually not recommended in most patients
with STEMI.
Glycoprotein IIb/IIIa inhibitors (e.g., abciximab and tirofiban) may be used in patients undergoing percutaneous
coronary interventions.

12. CORONARY ARTERY BYPASS GRAFTING (CABG)

Recommended in:
• Failed PCI with persistent pain or hemodynamic instability in patients with coronary anatomy suitable for surgery.
• Persistent or recurrent ischemia refractory to medical therapy in patients who have coronary anatomy suitable
for surgery, and are not candidates for PCI or fibrinolytic therapy.
 • Patients with STEMI at the time of operative repair of mechanical defects.

13. REPERFUSION OPTIONS FOR STEMI

Fibrinolysis
It is usually preferred in the following situations:
• Early presentation (≤3 hours from symptom of onset)
• In patients where primary PCI cannot be done because of the following:
– Catheterization laboratory occupied/unavailable
– Vascular access difficulties
– Lack of access to a skilled PCI laboratory
• Delay to primary PCI:
– Door-to-balloon time minus door-to-needle time is >1 hour
– Door-to-balloon time is >90 minutes

Primary PCI
In which PCI is used solely in acute MI. It is indicated in cardiogenic shock, and in patients in whom thrombolytic
therapy is contraindicated.

Generally preferred with following conditions:

• Skilled PCI laboratory is available with good surgical backup.
• Door-to-balloon time is ≤90 minutes.
• Door-to-balloon time minus door-to-needle time is ≤1 hour.

High-risk STEMI:
• Cardiogenic shock
• Killip class CHF ≥3
• Contraindications to fibrinolysis including increased risk of bleeding and intracranial hemorrhage.
• Late presentation (>3 hours after symptom of onset).
14. AFTERCARE AND REHABILITATION
Physical activities:
To be restricted for 4–6 weeks because replacement of infarct by fibrous tissue takes 4–6 weeks. Advised gradual
mobilization and return to work over 6 weeks. Exercise and sexual activity within the limits.

Complications:
Patients who had complications, the regimen depends on the type of complication.

Lifestyle and risk factor modification:

Control of risk factors such as obesity by regular exercises, cessation of smoking, lifestyle modifications, and
control of plasma lipids by diets and drugs.

Secondary Prevention Drug Therapy

Aspirin and Clopidogrel:
• Low-dose aspirin (75–150 mg daily) unless there is any contraindication. Clopidogrel (75 mg daily) for up to 12
months, particularly after stent implantation.
• May be given as an alternative when aspirin is contraindicated, or in combination with aspirin particularly in
patients with unstable angina or recurrent cardiac events.

Beta-Blocker:
Oral beta-blockers are continued indefinitely (unless any contraindications). Carvedilol, bisoprolol, or metoprolol
(extended release) are given to patients with heart failure. Role of beta-blockers in secondary prevention in
unstable angina is not known.

ACE Inhibitor:
ACE inhibitor is given early after an acute coronary syndrome. Long-term treatment with ACE inhibitor (e.g.,
enalapril 10 mg twice daily or ramipril 2.5–5 mg twice daily) is found to counteract ventricular remodeling, prevent
the onset of heart failure, and reduce recurrent MI.

Statin Therapy:
Started in the hospital for all patients with coronary artery disease.

Warfarin:
After myocardial infarction is given to patients having a high-risk of systemic thromboembolism due to atrial
fibrillation, mural thrombus, congestive heart failure, or previous embolization.

Nitrates:
Short-acting nitrates for chest pain. Long-acting nitrates are given for relief of symptom when beta-blocker alone is
unsuccessful or is contraindicated.

Aldosterone Antagonist:
Eplerenone is given early after myocardial infarction to patients who have LVEF ≤40%, despite optimum dose of
ACE inhibitors and beta-blockers, and have either CHF or diabetes.

Device Therapy:
Implantable cardiac defibrillators can prevent sudden cardiac death in patients who have severe left ventricular
impairment (ejection fraction ≤30%) after MI.

15. NON-ST-SEGMENT-ELEVATION ACS (NSTEACS), UNSTABLE

ANGINA & RIGHT VENTRICULAR MI

Non-ST-Segment-Elevation Acute Coronary Syndrome (NSTEACS)

Includes unstable angina (UA) and non-ST-elevation myocardial infarction (NSTEMI). Both are caused by coronary
artery spasm, progression of underlying coronary artery disease (CAD), or hemorrhage into a nonoccluding
atheromatous plaque with subsequent thrombosis producing coronary obstruction over a period of few hours.
Difference between UA and NSTEMI:
Whether or not the ischemia is sufficient to cause myocardial necrosis and a rise in serum troponin.

Non-ST-Elevation MI (NSTEMI)
• It usually shows ST depression and T inversion.
• Myocardial function (as shown by ejection fraction) may be impaired in NSTEMI early as well as late reinfarction
rates are higher.

Unstable Angina (UA)

Three principal presentations include:
• Rest angina: Angina occurring at rest and prolonged, usually more than 20 minutes.
• New-onset angina: New onset angina of at least Canadian Cardiovascular Society (CCS) class II severity.
• Increasing angina: Previously diagnosed angina that has become distinctly more frequent, longer in duration,
or lower in threshold (i.e., increased by ≥1 CCS class to at least CCS Class III).
• Normal ECG (no ST elevation), without elevation of cardiac injury markers (normal level of cardiac enzymes).
• Patients with UA have a high risk of developing death when compared to patients with stable angina, hence they
need aggressive treatment in the hospital.
Classification of risk categories in NSTEMI management are mentioned in Table 1.46.

Prinzmetal's Variant Angina

In 1959 Prinzmetal et al. described a syndrome of transient ST-segment elevation.

Etiology:
• Focal spasm of an epicardial coronary artery: Causing transient myocardial ischemia and occasionally
infarction.
• The cause of the spasm is not well defined, but various agents such as adrenergic vasoconstrictors,
leukotrienes, etc. may be responsible.
QUICK REVISION — KEY MNEMONICS & HIGH-YIELD POINTS
<b>Mnemonic / Concept</b> <b>Details</b>

MONAC Morphine, Oxygen, Nitroglycerine, Aspirin, Clopidogrel

(Initial Treatment)

Earliest marker of MI Myoglobin (rises 1–3 h, peaks 8–12 h)

Most sensitive & specific marker Cardiac Troponin I and T (rise 3–8 h, peak 12–24 h, remain 7–10 days)

TIMI 3 Normal flow — goal of reperfusion

Door-to-needle time <30 min (thrombolysis)

Door-to-balloon time ≤90 min (primary PCI)

Killip Class IV mortality 81%

Most common arrhythmia-related deathVentricular fibrillation (5–10%)

Free wall rupture Most common mechanical complication, usually fatal

Dressler syndrome 2–10 weeks post MI; fever + pericarditis + pleurisy; treat with NSAIDs

NSTEMI not for thrombolysis Thrombolysis is NOT recommended for NSTEMI and UA

Statins in STEMI Start within 24 h, high-dose atorvastatin (40–80 mg) or rosuvastatin (20–40 mg)

Aspirin dose 160–325 mg initial; 75–150 mg daily long-term

Troponin peak 48 hours; remains elevated 7–10 days

CK-MB Rises 4–6 h, peaks 12 h, returns to normal 72 h

End of ACS Notes — Chapter 1: Cardiology