Acute Myocardial Infarction (AMI)

Diagnostic Criteria for STEMI

1. Persistent ST-segment elevation in two contiguous leads:
   • ≥2.5 mm in men <40 years.
   • ≥2 mm in men >40 years.
   • ≥1.5 mm in women of any age.
2. Elevated cardiac biomarkers (e.g., troponins) indicative of myocardial necrosis.
   
   

ECG findings localise myocardial injury

• Anterior wall: Leads V1-V4.
• Inferior wall: Leads II, III, aVF.
• Lateral wall: Leads I, aVL, V5-V6.
  
  

Atherosclerotic Causes

• Atherosclerosis is the underlying cause of the vast majority of MIs
• Involves progressive accumulation of lipids, inflammatory cells, and fibrous elements in coronary arteries, forming plaques
• MI occurs when plaques disrupt, triggering thrombosis and arterial occlusion

Plaque Rupture

• Exposes the thrombogenic lipid core
• Activates platelets and the coagulation cascade
• Common in plaques with thin fibrous caps and high inflammatory activity

Plaque Erosion

• Endothelial damage leads to thrombus formation without overt rupture

Plaque Dissection or Fissuring

• Mechanical disruption increases the risk of thrombus development

Atherothrombotic Embolism

• Thrombotic fragments obstruct downstream microvasculature, causing ischaemia

Vascular Remodelling

• Inward arterial remodelling narrows the lumen, worsening flow restriction under stress

Triggers for Plaque Disruption

• Sudden surges in blood pressure or heart rate (e.g., during emotional stress or exertion)
• Mechanical stress at high shear force areas, especially near arterial bifurcations

Classification of Myocardial Infarction

 Type 1 MI

• Spontaneous MI from plaque rupture, erosion, or fissuring
• Typically causes complete coronary occlusion, often presenting as STEMI

Type 2 MI

• Caused by oxygen supply–demand mismatch without plaque disruption
• Common causes: anaemia, hypotension, tachyarrhythmias, systemic illness

Type 3 MI

• Sudden cardiac death with clinical evidence of myocardial ischaemia
• Confirmed post-mortem by thrombus or necrosis

Type 4 MI

• Related to PCI
  • Type 4a: MI during PCI
  • Type 4b: MI due to stent thrombosis

Type 5 MI

• Occurs post-CABG
• Typically linked to perioperative complications

Non-Atherosclerotic Causes

 Coronary Artery Anomalies

• Congenital: aberrant origin, myocardial bridges
• Acquired: coronary aneurysms (e.g., Kawasaki disease)

Coronary Vasospasm

• Transient spasm causing ischaemia
• Associated with Prinzmetal angina
• Triggered by cold, stress, drugs (e.g., cocaine)

Coronary Artery Dissection

• Spontaneous (SCAD), common in younger women, often peripartum
• Intramural haematoma compresses lumen

Coronary Embolism

• Sources:
  • Atrial fibrillation, left atrial thrombus
  • Endocarditis, septic emboli
  • Cholesterol or fat emboli

Inflammatory and Systemic Conditions

• Vasculitides (e.g., Takayasu arteritis, PAN) affect coronary arteries
• Autoimmune conditions (e.g., SLE) predispose to inflammation and thrombosis

Trauma

• Blunt chest trauma or iatrogenic injury during procedures

Substances and Environmental Exposures

• Cocaine and amphetamines → vasospasm, thrombosis
• Carbon monoxide poisoning, acute pulmonary conditions → hypoxia

Risk Factors and Precipitants

 Non-modifiable Risk Factors

• Age: Increased risk with age due to vascular ageing
• Sex: Men at higher risk pre-menopause; postmenopausal risk equalises
• Family History: Especially early-onset CAD
• Congenital Conditions: Marfan syndrome, Kawasaki disease

Modifiable Risk Factors

• Lifestyle Factors: Smoking, inactivity, poor diet
• Metabolic Disorders: Diabetes, hypertension, dyslipidaemia
• Obesity: Especially central obesity
• Psychosocial Stress: High stress, type A traits
• Hypercoagulable States: Thrombophilia, antiphospholipid syndrome

Paediatric Considerations

• Rare, but possible causes include:
  • Coronary artery anomalies (e.g., anomalous left coronary origin)
  • Kawasaki disease causing aneurysms or stenosis
  • Intrauterine/neonatal causes: congenital stenosis, perinatal asphyxia

Formation and Progression of Atherosclerotic Plaques

 Early Plaque Development

• Initiated by accumulation of low-density lipoprotein (LDL) cholesterol and saturated fats in the intima
• Macrophage adhesion to endothelium allows migration into the intima
• Macrophages engulf lipids, forming foam cells
• Foam cells release proinflammatory mediators, amplifying inflammation
• Results in a "fatty streak," a reversible early lesion

Advanced Plaques

• Smooth muscle cells migrate from the media and proliferate
• Deposit extracellular matrix components (proteoglycans, collagen)
• Plaques calcify and initially remodel outward (positive remodelling)
• Later encroach on the lumen, restricting blood flow under stress → angina
• Vulnerable plaques have thin fibrous caps, lipid-rich cores, and inflammatory cell infiltration → prone to rupture or erosion

Acute Coronary Events

 Plaque Rupture or Erosion

• Disruption of the plaque exposes thrombogenic contents
• Leads to platelet adhesion, aggregation, and coagulation cascade activation
• Thrombus forms, causing coronary occlusion

ST-Elevation Myocardial Infarction (STEMI)

• Complete occlusion causes transmural ischaemia
• Presents as ST-segment elevation on ECG
• Untreated, necrosis progresses from subendocardium to subepicardium in a "wavefront" pattern

Microvascular Dysfunction

• Acute ischaemia impairs microvascular function
• Perfusion may remain reduced even after recanalisation

Myocardial Injury and Cellular Changes

 Ischaemic Cascade

• Oxygen deprivation impairs myocardial contractility within seconds
• Irreversible injury occurs within 20–40 minutes
• Timing influenced by collateral flow and metabolic demand

Cellular Changes

• ATP depletion disrupts ionic gradients
• Leads to calcium overload and cellular oedema
• Coagulative necrosis develops, releasing markers such as troponin

Ventricular Remodelling

 Healing and Fibrosis

• Necrotic tissue is cleared and replaced by fibrous scar
• Ventricular dilation and spherical remodelling may follow large infarctions
• Reduced contractility predisposes to heart failure

Regulated Remodelling

• Beta-blockers and ACE inhibitors help prevent adverse remodelling
• Preserve left ventricular function

Reperfusion Injury

 Paradoxical Damage

• Reperfusion after ischaemia may worsen injury
• Mechanisms include oxidative stress, calcium overload, and inflammation
• Can result in arrhythmias, microvascular dysfunction, and additional cell death

Potential Therapies

• Investigational strategies include antioxidants and ischaemic preconditioning
• Definitive treatments remain unproven

Stunned and Hibernating Myocardium

 Stunned Myocardium

• Transient left ventricular dysfunction after ischaemia
• Occurs despite restored blood flow
• Recovery typically within hours to days

Hibernating Myocardium

• Chronic hypoperfusion leads to reversible contractile dysfunction
• Improves with revascularisation

Key Pathophysiological Features of MI

 Coronary Thrombosis

• Atherothrombosis is the predominant cause
• Initiated by plaque disruption → platelet activation and clot formation

Wavefront Phenomenon

• Necrosis begins in subendocardium and progresses outward
• Underscores urgency of early reperfusion

Ischaemia-Induced Arrhythmias

• Acute ischaemia disrupts cardiac electrical activity
• Increases risk of ventricular fibrillation and sudden death

Global Perspective

 CVD Mortality and Morbidity

• Cardiovascular disease (CVD) accounts for ~32% of global deaths
• Ischaemic heart disease (IHD) causes 38% of CVD-related deaths in women and 44% in men
• ~5.8 million new IHD cases occur annually across European Society of Cardiology (ESC) countries

Disparities Between Regions

• Developed nations have seen declines in MI incidence and mortality due to better healthcare and prevention
• Developing and transitional countries are witnessing rising MI rates due to aging, urbanisation, and lifestyle changes (e.g., smoking, poor diet, inactivity)

CVD in Developing Nations

• Regions such as Sub-Saharan Africa, Latin America, and parts of Asia face surging CVD mortality
• CVD deaths rose from 9 million in 1990 to an estimated 20 million by 2020
• Key drivers include socioeconomic transitions, Westernised diets, hypertension, and dyslipidaemia

INTERHEART Study Insights

• Identified nine modifiable risk factors accounting for over 90% of acute MI risk globally:
  • Smoking
  • Abnormal lipid levels
  • Hypertension
  • Diabetes
  • Obesity
  • Poor diet
  • Physical inactivity
  • Alcohol use
  • Psychosocial stress
• These factors are consistent across populations, regardless of sex or region

Regional Statistics

 United States

• Coronary artery disease (CAD) is the leading cause of death (500,000–700,000 deaths annually)
• ~1.5 million MIs occur yearly (550,000 new, 200,000 recurrent cases)
• Age-adjusted MI mortality has declined since the 1970s, but total deaths remain stable due to aging demographics
• Men have three times higher MI incidence before age 75; disparity narrows with age
• Black Americans have higher MI mortality than White or Hispanic individuals

Europe

• CAD remains the top cause of death
• Western Europe: 30% decline in death rates since mid-1960s
• Eastern Europe: Rise in 1990s followed by decline
• UK: Cardiovascular mortality leads to ~1.2 million hospitalisations annually; overall prevalence is ~3%

Asia

• Japan has low CAD mortality due to dietary and lifestyle factors and strong healthcare systems
• China shows increasing CAD burden, driven by smoking and urbanisation

 Global Trends

• STEMI incidence has declined in developed countries due to early interventions and improved care
• NSTEMI cases have increased due to improved detection and awareness

Sex Differences

• Postmenopausal women experience increased MI incidence, narrowing the sex gap
• Women under 60 have higher 30-day mortality after STEMI than men, even when adjusting for comorbidities

COVID-19 Impact

• UK saw a 16% increase in MI cases in 2021–2022 compared to the prior year
• Attributed to delayed care and reduced healthcare access during the pandemic

Age and Socioeconomic Factors

• Average age of first MI: 65.1 years (men), 72 years (women) in the US
• Socioeconomic disparities in healthcare access and education lead to worse MI outcomes in lower-resource settings
• Higher mortality and poorer long-term recovery observed in disadvantaged populations

Presenting Symptoms

 Chest Pain: The hallmark symptom in MI

• Character: Typically retrosternal, crushing, squeezing, or pressure-like
• Radiation: May extend to the neck, jaw, shoulders, left arm, or upper abdomen
• Duration: Commonly unremitting for 30–60 minutes
• Aggravating/Relieving Factors: Often persists despite rest or nitroglycerin

Associated Symptoms

• Nausea and vomiting, particularly in inferior MI due to vagal stimulation
• Profuse sweating (diaphoresis) linked to sympathetic activation
• Shortness of breath from left ventricular dysfunction or pulmonary congestion
• Lightheadedness, syncope, or fatigue reflecting poor perfusion
• Anxiety or a sense of impending doom

Atypical Presentations

• More common in women, elderly individuals, and patients with diabetes
• May present with fatigue, dyspnoea, or palpitations rather than chest pain
• Discomfort may be localised to the epigastrium, neck, or back
• Frequently mistaken for indigestion or musculoskeletal pain

Prodromal Symptoms

• Patients may experience fatigue, malaise, or intermittent chest discomfort in the hours or days before MI

Circadian Variation

• MI incidence peaks in early morning hours
• Related to morning increases in sympathetic tone, blood pressure, heart rate, and coagulability

Risk Factor Assessment

 Cardiovascular Risk Profile

• Smoking, hypertension, diabetes, hyperlipidaemia, obesity
• Family history of premature coronary artery disease (male <45 years, female <55 years)
• Sedentary lifestyle, poor diet, psychosocial stress

• Cocaine use or stimulant drugs
• Autoimmune or inflammatory disorders

Medical History

• Prior chest discomfort or coronary artery disease
• Previous PCI or CABG
• Comorbidities: CKD, peripheral arterial disease, atrial fibrillation

Social History

• Substance use, especially cocaine or amphetamines
• Occupational or socioeconomic stress

Risk Assessment Tools in MI

TIMI Risk Score (Thrombolysis in Myocardial Infarction)

• Predicts 14-day mortality and recurrent ischaemic risk in ACS
• Scoring factors include:
  • Age ≥65 years
  • ≥3 CAD risk factors (e.g., smoking, hypertension, diabetes)
  • Known coronary stenosis ≥50%
  • Aspirin use in past 7 days
  • ≥2 anginal episodes in past 24 hours
  • Elevated cardiac biomarkers
  • ST-segment deviation ≥0.5 mm
• Score range: 0–7; higher scores correlate with increased risk

GRACE Risk Score (Global Registry of Acute Coronary Events)

• Predicts in-hospital and post-discharge outcomes in ACS
• Parameters include:
  • Age
  • Heart rate and systolic blood pressure
  • Serum creatinine
  • Signs of heart failure or cardiogenic shock
  • Cardiac arrest on admission
  • Elevated cardiac biomarkers
  • ST-segment deviation on ECG
• Utility: Supports treatment planning and invasive management decisions

CHA₂DS₂-VASc-CF Risk Score

• Adapted from AF risk score; includes smoking and family history
• Components:
  • Congestive heart failure, hypertension, age ≥75 (2 points), diabetes
  • Stroke/TIA history (2 points), vascular disease, age 65–74, female sex
  • Smoking, family history of CAD
• Predictive power: Score >3 indicates high sensitivity (78.4%) and specificity (76.4%) for long-term cardiovascular mortality

Practical Considerations in History-Taking

 Time Since Symptom Onset

• Critical for selecting appropriate reperfusion therapy
• Patients may provide approximate timings; detailed clarification needed

Challenges

• Elderly or cognitively impaired may not report symptoms clearly
• Stoic or high-threshold individuals may minimise or underreport pain

Practical Tips

• Do not dismiss MI based on symptom relief with nitrates
• Always utilise serial ECGs and cardiac biomarkers to support diagnosis

General Appearance

• Patients with ongoing ischaemia often appear pale, diaphoretic, and anxious
• Severe cases may show respiratory distress or altered consciousness due to hypoperfusion or cardiogenic shock

Vital Signs

 Heart Rate

• Tachycardia: Common from sympathetic stimulation or pain
• Bradycardia: May indicate inferior MI, conduction block, or sinus node dysfunction
• Irregular Pulse: Suggests arrhythmias (e.g., atrial fibrillation, ventricular ectopy)

Blood Pressure

• Hypertension: May be initial response to anxiety, adrenergic drive, or pain
• Hypotension: Sign of cardiogenic shock, extensive infarction, or right ventricular MI

Respiratory Rate

• Elevated due to pulmonary congestion, hypoxaemia, or anxiety

Temperature

• Fever within 24–48 hours reflects inflammatory response and tracks with CK levels

Cardiovascular Examination

 Jugular Venous Pressure (JVP)

• Elevated JVP suggests right ventricular infarct, heart failure, or tamponade

Heart Sounds

• S3 Gallop: Suggests left ventricular dysfunction and elevated filling pressures
• S4 Gallop: Associated with stiff ventricles or diastolic dysfunction

New Murmurs

• Mitral Regurgitation: Suggests papillary muscle dysfunction or rupture
• Ventricular Septal Defect: Holosystolic murmur at left sternal edge with palpable thrill
• Pericardial Friction Rub: Indicates post-MI pericarditis

Pulse Examination

• Weak, thready pulses indicate low cardiac output
• Asymmetric pulses or inter-arm BP differences raise concern for aortic dissection

Pulmonary Examination

• Crackles or Rales: Reflect pulmonary oedema from left ventricular failure
• Wheezing: May occur in acute pulmonary oedema (“cardiac asthma”)
• Dullness to Percussion: May indicate pleural effusion in advanced cardiac failure

Abdomen

• Hepatomegaly: Sign of systemic venous congestion from right heart failure
• Hepatojugular Reflux: Suggests elevated right atrial pressure
• Abdominal Aneurysm: Pulsatile mass may indicate an aortic aneurysm

Extremities

• Cyanosis or Pallor: Reflect poor peripheral perfusion
• Cool, Clammy Skin: Caused by vasoconstriction during shock
• Delayed Capillary Refill: Suggests reduced cardiac output
• Oedema: May occur with right-sided or chronic heart failure

Key Signs of Complications

 Cardiogenic Shock

• Hypotension, cool extremities, oliguria, altered mentation, rapid thready pulse

Heart Failure

• Orthopnoea, paroxysmal nocturnal dyspnoea, pulmonary crackles, elevated JVP

Mechanical Complications

• Papillary Muscle Rupture: Acute pulmonary oedema with new systolic murmur
• Ventricular Septal Rupture: Harsh murmur with haemodynamic collapse
• Left Ventricular Free Wall Rupture: Sudden tamponade and pulseless electrical activity

Pericardial Tamponade

• Beck’s Triad: Hypotension, muffled heart sounds, elevated JVP

Practical Considerations

• Subtle Findings: Early MI may present with a normal physical exam
• Serial Examinations: Essential to detect evolving complications
• Corroborate Findings: Always combine with ECG, biomarkers, and imaging for accurate diagnosis

Initial and Critical Investigations

 Electrocardiogram (ECG)

•  Purpose:
  • Primary diagnostic tool for ACS
  • Must be performed within 10 minutes of first medical contact
• Key Features in STEMI
  • Persistent ST-segment elevation in two contiguous leads:
    • ≥1 mm in most leads
    • ≥2.5 mm in men <40 years
    • ≥2 mm in men >40 years
    • ≥1.5 mm in women in V2–V3
  • New left bundle branch block (LBBB) in appropriate clinical context
• Advanced Patterns
  • Posterior STEMI: ST depression in V1–V3; confirmed with ST elevation ≥0.5 mm in leads V7–V9
  • Right Ventricular Infarction: ST elevation ≥1 mm in V4R or aVR
  • Left Main Coronary Artery Obstruction: ST depression in ≥6 leads with concurrent ST elevation in aVR
• Serial ECGs:
  • Recommended in equivocal cases or when symptoms fluctuate
• Special Considerations
  • Use Sgarbossa criteria to diagnose STEMI in LBBB
  • Evaluate for residual ST elevation or pathological Q waves in previous silent MI

Cardiac Biomarkers

•  Troponin I and T:
  • Preferred markers of myocardial necrosis
  • High-sensitivity assays detect levels within 2–3 hours of symptom onset
  • Diagnostic criterion: rise and/or fall above the 99th percentile of the upper reference limit
• Timing:
  • Measure at presentation and again at 3–6 hours
  • Interpret changes alongside clinical and ECG findings
• Other Markers:
  • CK-MB: Less specific; now rarely used
  • Myoglobin: Rises early but lacks cardiac specificity

Coronary Angiography

•  Indications:
  • All STEMI patients within 12 hours of symptom onset
  • Primary PCI within 120 minutes where available
  • Consider in late presenters (>12 hours) if:
    • Evidence of ongoing ischaemia
    • Haemodynamic instability
    • Life-threatening arrhythmias
• Access:
  • Radial artery access preferred to reduce vascular complications
    
    

Supporting Investigations

 Laboratory Tests

• Full Blood Count (FBC):
  • Check for anaemia, leukocytosis, thrombocytopenia
• Electrolytes, Urea, Creatinine:
  • Assess renal function
  • Correct electrolyte imbalances (e.g., potassium, magnesium)
• Glucose:
  • Identify hyperglycaemia, even in non-diabetics
• C-Reactive Protein (CRP):
  • Reflects inflammation; not used in acute MI decision-making
• Serum Lipids:
  • Helps assess long-term risk
  • Repeat 30–60 days post-MI due to transient acute-phase reductions

Imaging

 Chest X-Ray

• Rule out alternative causes (e.g., aortic dissection, pulmonary oedema, cardiomegaly)
• Not diagnostic for MI

Transthoracic Echocardiogram (TTE)

• Detect regional wall motion abnormalities
• Evaluate for valvular dysfunction, pericardial effusion, or thrombus
• Helpful in atypical presentations or unclear ECG findings

Computed Tomography (CT)

• Used to exclude differential diagnoses such as aortic dissection or pulmonary embolism
• Not routinely employed for MI diagnosis

Emerging Diagnostic Modalities

 Cardiac Myosin-Binding Protein C (cMyC)

• Detectable earlier than troponin
• Potential for future rapid MI diagnosis
• Not yet in widespread clinical use

Common Cardiac Mimics of MI

Unstable Angina

• Clinical Features:
  • Chest pain similar to MI but less severe and shorter in duration
  • Pain occurs at rest, with minimal exertion, or with increasing frequency
• Investigations:
  • ECG shows non-specific ST-segment and T-wave changes without persistent ST elevation
  • Cardiac biomarkers are normal
• Key Point:
  • Unstable angina is a clinical diagnosis based on symptoms and absence of biomarker elevation

Myocarditis

• Clinical Features:
  • Often follows a viral illness or occurs in autoimmune diseases
  • Chest pain, fatigue, and signs of heart failure
• Investigations:
  • Cardiac MRI shows epicardial or mid-myocardial delayed enhancement
  • Elevated inflammatory markers (CRP, ESR)

Pericarditis

• Clinical Features:
  • Sharp, pleuritic chest pain relieved by sitting forward
  • May be associated with viral or autoimmune conditions
• Investigations:
  • ECG shows diffuse ST-segment elevation and PR-segment depression
  • Echocardiography may show pericardial effusion

Takotsubo Cardiomyopathy (Stress Cardiomyopathy)

• Clinical Features:
  • Sudden onset of LV dysfunction after emotional or physical stress
  • Mimics acute MI in presentation and ECG
• Investigations:
  • Coronary angiography shows no significant obstruction
  • Echocardiography reveals apical ballooning

Prinzmetal (Vasospastic) Angina

• Clinical Features:
  • Episodic chest pain at rest, often at night or early morning
  • Pain resolves spontaneously or with nitrates
• Investigations:
  • Transient ST-segment elevation on ECG during episodes
  • Coronary angiography is typically normal

Spontaneous Coronary Artery Dissection (SCAD)

• Clinical Features:
  • Common in younger women without traditional risk factors
  • Chest pain with ACS-like symptoms
• Investigations:
  • Coronary angiography shows intimal disruption or intramural haematoma
  • Intravascular ultrasound or OCT helps confirm diagnosis

Other Cardiac and Vascular Causes

Aortic Dissection

• Clinical Features:
  • Sudden, tearing chest or back pain
  • Pulse asymmetry or blood pressure discrepancy
• Investigations:
  • CT angiography shows dissection flap and true/false lumens
  • Chest X-ray may show widened mediastinum

Pulmonary Embolism (PE)

• Clinical Features:
  • Acute pleuritic chest pain, dyspnoea, and hypoxaemia
• Investigations:
  • ECG may show sinus tachycardia or S1Q3T3 pattern
  • Elevated D-dimer
  • Confirmed by CT pulmonary angiography

Gastrointestinal and Musculoskeletal Mimics

Gastroesophageal Reflux Disease (GORD)

• Clinical Features:
  • Burning retrosternal pain
  • Typically relieved by antacids
• Investigations:
  • Normal ECG and cardiac biomarkers
  • OGD may reveal oesophagitis or erosions in refractory cases

Oesophageal Spasm

• Clinical Features:
  • Squeezing retrosternal pain
  • Sometimes relieved by nitrates
• Investigations:
  • Oesophageal manometry or barium swallow detects dysmotility

Costochondritis

• Clinical Features:
  • Localised chest wall tenderness
  • Pain worsens with movement or palpation
• Investigations:
  • Normal ECG, cardiac biomarkers, and imaging

Respiratory Causes

Pneumothorax

• Clinical Features:
  • Sudden pleuritic chest pain and dyspnoea
• Investigations:
  • Chest X-ray shows visceral pleural line and absent lung markings

Pneumonia

• Clinical Features:
  • Fever, cough, and pleuritic chest pain
• Investigations:
  • Chest X-ray shows consolidation
  • Elevated white blood cell count

Psychiatric Causes

Anxiety or Panic Disorder

• Clinical Features:
  • Palpitations, hyperventilation, and chest discomfort
• Investigations:
  • Normal ECG, cardiac biomarkers, and imaging

Urgent Initial Management

 Immediate Actions

• Diagnosis: Make a clinical diagnosis of STEMI based on symptoms and ECG findings (persistent or increasing ST-segment elevation in two or more contiguous leads).
• Aspirin: Administer a loading dose of 300 mg unless contraindicated due to hypersensitivity. Use an alternative (e.g., clopidogrel) if aspirin is contraindicated.
• Do Not Delay: Initiate treatment immediately without waiting for cardiac troponin levels.

Assess and Stabilise

• Reperfusion Therapy: Determine eligibility for primary PCI or fibrinolysis.
• Monitoring: Establish intravenous access, start hemodynamic monitoring, and continuous pulse oximetry.
• Pain Management: Use intravenous opioids (e.g., morphine) with an anti-emetic to manage symptoms and prevent vomiting.
• Oxygen Therapy: Administer oxygen only if SpO2 <90%, respiratory distress, or signs of hypoxemia.

Reperfusion Therapy

• Primary PCI: Preferred reperfusion strategy for most patients, ideally performed within 120 minutes of diagnosis.
• Fibrinolysis: Indicated when PCI is not available within 120 minutes. Administer fibrinolysis alongside anticoagulation (e.g., enoxaparin or unfractionated heparin).

Antiplatelet Therapy

• Dual antiplatelet therapy (DAPT) should include:
  • Aspirin.
  • A P2Y12 inhibitor:
    • Prasugrel: For PCI if not on oral anticoagulation.
    • Ticagrelor: An alternative to prasugrel.
    • Clopidogrel: Use in patients on oral anticoagulants or with high bleeding risk.

Seek Specialist Input

• Engage the interventional cardiology team early for decision-making and escalation of care.

Pharmacological Management

 Intravenous Nitrates

• Indicated for persistent chest pain, hypertension, or heart failure.
• Avoid in:
  • Hypotension (e.g., systolic BP <90 mmHg).
  • Right ventricular infarction.
  • Recent use of phosphodiesterase-5 inhibitors (e.g., sildenafil).

Anticoagulation

• Initiated during reperfusion therapy but avoid pre-procedural anticoagulation if PCI is planned.
• Preferred agents:
  • Unfractionated Heparin: Standard during PCI.
  • Enoxaparin: For fibrinolysis or when heparin is contraindicated.
  • Fondaparinux: Limited to fibrinolysis with streptokinase.

Beta-Blockers

• Begin once the patient is hemodynamically stable to reduce myocardial oxygen demand.

ACE Inhibitors or ARBs

• Start within 24–48 hours for all patients unless contraindicated by hypotension or renal impairment.
• Titrate to maximum tolerated doses.

High-Intensity Statins

• Initiate during hospitalisation to reduce LDL and stabilise plaques.

Aldosterone Antagonists

• Add for patients with heart failure or reduced ejection fraction (<40%) after stabilisation.

SGLT2 Inhibitors

• Consider for patients with heart failure irrespective of left ventricular ejection fraction.

Reperfusion Strategies

 Primary PCI

• Ideal for patients presenting within 12 hours of symptom onset.
• Prioritise when PCI can be performed within 120 minutes of diagnosis.
• Drug-eluting stents are preferred to minimise restenosis risks.
• Transfer to a PCI-capable center if not available onsite.

Fibrinolysis

• Recommended for patients unable to access PCI within 120 minutes.
• Use fibrin-specific agents (e.g., tenecteplase, alteplase).
• Administer anticoagulation concurrently and assess success via ECG within 60–90 minutes.
• Arrange angiography within 2–24 hours following successful fibrinolysis.

Rescue PCI

• Indicated if fibrinolysis fails (<50% ST-segment resolution at 60–90 minutes).

Late Presenters

• PCI is still recommended if ongoing ischemia or high-risk features (e.g., cardiogenic shock, arrhythmias) are present.

Management for Special Scenarios

 Cardiac Arrest Survivors

• STEMI Post-ROSC: Proceed with immediate PCI.
• No STEMI Post-ROSC: Exclude non-cardiac causes and perform echocardiography. Consider angiography if ischemia is suspected.

Patients Without Reperfusion Eligibility

• Provide medical therapy, including DAPT, anticoagulation, beta-blockers, ACE inhibitors/ARBs, and statins.
• Perform echocardiographic assessment of left ventricular function.

Patients on Oral Anticoagulation

• Avoid fibrinolysis; primary PCI is the preferred strategy.

Secondary Prevention and Long-Term Management

 Antiplatelet Therapy

• Continue DAPT (aspirin + P2Y12 inhibitor) for up to 12 months.
• Transition to single antiplatelet therapy (aspirin or a P2Y12 inhibitor) thereafter.

Lifestyle and Risk Factor Modification

• Smoking cessation, dietary changes, physical activity, weight management, and alcohol moderation.

Cardiac Rehabilitation

• Structured programs including exercise, education, and psychological support.

Medication Adherence

• Continue beta-blockers, ACE inhibitors/ARBs, statins, and aldosterone antagonists as indicated.

Timing Targets for STEMI Management (ESC 2023)

• First medical contact to ECG: <10 minutes
• STEMI diagnosis to primary PCI: <120 minutes
• STEMI diagnosis to fibrinolysis (if indicated): <10 minutes
• Fibrinolysis to assessment of success (ECG): 60–90 minutes
• Successful fibrinolysis to coronary angiography: 2–24 hours

General Prognosis

 Mortality Rates

• Acute MI is associated with a 30% mortality rate, with approximately half of deaths occurring before hospital arrival.
• In-hospital mortality for STEMI is approximately 9%.
• An additional 5–10% of survivors die within the first year post-MI.

Long-Term Outcomes

• Approximately 50% of MI patients are rehospitalised within a year.
• Long-term prognosis depends heavily on left ventricular function and the success of reperfusion therapy.

Key Determinants of Prognosis

Improved Prognosis

• Early and successful reperfusion (e.g., PCI within 90 minutes of arrival or fibrinolysis within 30 minutes).
• Preserved left ventricular function (ejection fraction >40%).
• Adherence to evidence-based therapies (e.g., beta-blockers, ACE inhibitors, aspirin).

Worsened Prognosis

• Advanced age, diabetes, prior vascular disease.
• Delayed or failed reperfusion.
• Poorly preserved left ventricular function.
• Presence of heart failure (Killip classification ≥II) or cardiogenic shock (Killip IV).

Risk Stratification Tools

 Killip Classification

• The Killip classification stratifies patients based on the severity of heart failure at presentation, correlating with 30-day mortality risk:
  • Class I: No heart failure (mortality ~6%).
  • Class II: Rales/crackles, S3 gallop, elevated jugular venous pressure (mortality ~17%).
  • Class III: Frank pulmonary edema (mortality ~38%).
  • Class IV: Cardiogenic shock or hypotension with evidence of low cardiac output (mortality ~81%).

TIMI Risk Score for STEMI

• The TIMI (Thrombolysis in Myocardial Infarction) risk score predicts 30-day mortality:
• Scoring Factors:
  • Age ≥75 years (3 points); age 65–74 years (2 points).
  • Diabetes, hypertension, or angina (1 point).
  • Systolic BP <100 mmHg (3 points).
  • Heart rate >100 bpm (2 points).
  • Killip class II–IV (2 points).
  • Weight <150 lbs (1 point).

Risk Categories

• Low (0–4 points): 30-day mortality ~2.5%.
• Medium (5–9 points): 30-day mortality ~5–10%.
• High (>9 points): 30-day mortality >10%.

Prognostic Biomarkers

 Troponin Levels

• Elevated troponin levels correlate with increased risk of mortality and adverse outcomes.

B-Type Natriuretic Peptide (BNP)

• Higher BNP levels predict heart failure and increased long-term mortality.

High-Sensitivity C-Reactive Protein (hs-CRP)

• Elevated levels indicate systemic inflammation and correlate with worse outcomes.

ECG Findings

• Involvement of lead aVR is associated with higher mortality.
• Persistent ST-segment elevation post-reperfusion suggests larger infarct size.

Factors Impacting Prognosis

 Clinical Factors

• Age, diabetes, hypertension, and prior cardiovascular disease worsen outcomes.
• Depression post-MI is linked to poorer recovery and higher mortality.

Management Factors

• Delays in reperfusion or suboptimal therapy increase mortality risk.
• Major bleeding (e.g., as defined by TIMI or BARC criteria) is associated with higher one-year mortality.

Infarct Characteristics

• Anterior wall infarctions carry higher mortality compared to inferior or lateral wall infarctions due to greater myocardial damage.

Prognosis-Improving Interventions

 Timely Reperfusion

• Achieving reperfusion within guideline-directed timelines (e.g., PCI <90 minutes, fibrinolysis <30 minutes) improves survival.

Evidence-Based Medical Therapy

• Long-term use of beta-blockers, ACE inhibitors/ARBs, statins, and aspirin is associated with reduced mortality.

Cardiac Rehabilitation

• Exercise training and risk factor modification significantly enhance quality of life and reduce recurrent events.

Secondary Prevention

• Lifestyle changes, including smoking cessation, dietary improvements, weight management, and physical activity, improve outcomes.

Arrhythmic Complications

 Sinus Bradycardia and Atrioventricular Blocks

• Sinus Bradycardia: Common in inferior MI due to increased vagal tone. Usually transient; treat symptomatic cases (heart rate <50 bpm) with intravenous atropine.
• First-Degree and Type I Second-Degree AV Block: Often benign; may not require intervention unless symptomatic.

Complete Heart Block

• Anterior MI: Due to necrosis of the bundle branches, often requires urgent transvenous pacing and frequently permanent pacemaker placement.
• Inferior MI: Typically caused by vagal stimulation; may resolve with atropine. Temporary pacing is rarely required.

Ventricular Arrhythmias

• Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF):
  • Can occur acutely during ischemia or reperfusion or later due to scar-related reentry circuits.
  • Manage with defibrillation for VF and anti-arrhythmic therapy for sustained VT.
  • Implantable cardioverter-defibrillator (ICD) placement is indicated for patients with left ventricular ejection fraction (LVEF) <35% after 3 months of optimal medical therapy.

Mechanical Complications

 Papillary Muscle Rupture and Mitral Regurgitation

• Posteromedial Papillary Muscle: More commonly affected due to single blood supply (inferior MI).
• Results in severe mitral regurgitation, acute pulmonary edema, and cardiogenic shock.
• Requires urgent surgical repair or valve replacement.

Ventricular Septal Rupture (VSR)

• Occurs 2–8 days post-MI, commonly in anterior infarctions.
• Leads to left-to-right shunting, worsening heart failure, and cardiogenic shock.
• Requires emergent surgical repair; mortality exceeds 70% without intervention.

Ventricular Free Wall Rupture

• A catastrophic event causing hemopericardium and cardiac tamponade.
• More common in first-time anterior MIs and women.
• Requires emergency surgical repair, though mortality exceeds 80%.

Left Ventricular (LV) Aneurysm

• Chronic complication associated with large anterior infarctions.
• Can lead to heart failure, arrhythmias, and thromboembolism.
• Rarely requires surgical correction.

Right Ventricular (RV) Infarction

• Occurs in ~30% of inferior MIs.
• Presents with hypotension, elevated jugular venous pressure, and clear lung fields.
• Managed with volume expansion and inotropic support. Avoid nitrates and diuretics.

Inflammatory Complications

 Pericarditis

• Acute Pericarditis:
  • Develops within 1–4 days of MI due to inflammation of overlying pericardium.
  • Presents with pleuritic chest pain and pericardial friction rub; treat with aspirin.
• Dressler’s Syndrome (Post-MI Pericarditis):
  • Autoimmune pericarditis occurring weeks after MI.
  • Treat with high-dose aspirin; avoid NSAIDs unless necessary.
• Post-Infarction Pericardial Effusion:
  • May progress to tamponade, requiring pericardiocentesis or surgical intervention.

Thromboembolic Complications

 Left Ventricular Thrombus

• Common in large anterior MIs, especially with LV dysfunction or apical akinesis.
• Anticoagulation with vitamin K antagonists reduces embolic risk.

In-Stent Thrombosis

• Often caused by premature cessation of dual antiplatelet therapy (DAPT).
• Ensure strict adherence to DAPT for at least 12 months post-PCI.

Heart Failure and Remodeling

 Acute Heart Failure

• Results from reduced LV function due to myocardial damage or ischemia.
• Treat with diuretics, beta-blockers, ACE inhibitors, or ARBs, and aldosterone antagonists.
• Consider biventricular pacing for advanced heart failure with LVEF <35%.

Chronic Heart Failure

• Develops due to maladaptive LV remodeling. Aggressive medical management and risk factor modification are crucial.

Psychological and Long-Term Complications

 Recurrent Ischemia and Reinfarction

• Treat as a new event; modify risk factors aggressively.
• Persistent angina may require repeat angiography and PCI.

Depression

• Affects ~20% of post-MI patients and worsens outcomes.
• Screen routinely; manage with cognitive behavioral therapy, exercise, and pharmacotherapy when appropriate.

Prognosis and Risk Factors for Complications

 High-risk patients include those with

• Delayed reperfusion or large infarct size.
• LVEF <40%.
• Advanced age or comorbidities (e.g., diabetes, chronic kidney disease).
• Elevated BNP or hs-CRP levels.

Mortality Rates for Mechanical Complications

• Ventricular free wall rupture: >80%.
• Ventricular septal rupture: ~70%.
• Papillary muscle rupture with severe mitral regurgitation: 30-day survival ~24%.

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