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

1. Plaque Rupture:
   • Plaque rupture exposes the thrombogenic lipid core, activating platelets and the coagulation cascade.
   • Common in plaques with a thin fibrous cap and high inflammatory activity.
2. Plaque Erosion:
   • Endothelial damage leads to thrombus formation even without overt plaque rupture.
3. Plaque Dissection or Fissuring:
   • Mechanical disruption of the plaque increases the likelihood of thrombus development.
4. Atherothrombotic Embolism:
   • Thrombotic fragments dislodge and obstruct downstream microvasculature, leading to ischemia.
5. Vascular Remodeling:
   • Inward remodeling of coronary arteries narrows luminal diameter, exacerbating flow restriction under stress.
     
     

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

Classification of Myocardial Infarction

1. Type 1 MI:
   • Spontaneous MI caused by atherothrombotic events such as plaque rupture, erosion, or fissuring.
   • Typically results in complete coronary occlusion, often manifesting as STEMI.
2. Type 2 MI:
   • Secondary to a mismatch between oxygen supply and demand, without acute plaque disruption.
   • Common causes include anemia, hypotension, tachyarrhythmias, or severe systemic illnesses.
3. Type 3 MI:
   • Sudden cardiac death with clinical symptoms suggestive of myocardial ischemia.
   • Confirmed post-mortem by evidence of coronary thrombus or myocardial necrosis.
4. Type 4 MI:
   • MI associated with PCI (Type 4a) or stent thrombosis (Type 4b).
5. Type 5 MI:
   • MI following coronary artery bypass grafting (CABG), often linked to perioperative complications.
     
     

Non-Atherosclerotic Causes

1. Coronary Artery Anomalies:
   • Congenital anomalies such as aberrant coronary artery origin or myocardial bridges.
   • Acquired conditions like coronary artery aneurysms (e.g., Kawasaki disease).
2. Coronary Vasospasm:
   • Transient spasm of coronary arteries leads to ischemia, typically associated with Prinzmetal (variant) angina.
   • Often triggered by cold exposure, stress, or drugs (e.g., cocaine).
3. Coronary Artery Dissection:
   • Spontaneous coronary artery dissection (SCAD) disproportionately affects younger women, often in the peripartum period.
   • Disruption of the arterial wall results in intramural hematoma and vessel lumen compression.
4. Coronary Embolism:
   • Embolic events from non-coronary sources, such as:
     • Atrial fibrillation or left atrial thrombus.
     • Endocarditis or septic emboli.
     • Cholesterol or fat emboli.
5. Inflammatory and Systemic Conditions:
   • Vasculitides (e.g., Takayasu arteritis, polyarteritis nodosa) can compromise coronary arteries.
   • Autoimmune diseases (e.g., systemic lupus erythematosus) predispose to coronary inflammation and thrombosis.
6. Trauma:
   • Direct coronary artery trauma, as seen in blunt chest injury or iatrogenic injury during invasive cardiac procedures.
7. Substances and Environmental Exposures:
   • Recreational drugs such as cocaine and amphetamines cause vasospasm and pro-thrombotic states.
   • Hypoxia from carbon monoxide poisoning or acute pulmonary disorders decreases myocardial oxygen delivery.
     
     

Risk Factors and Precipitants

• Age: Risk increases with age due to progressive atherosclerosis and vascular aging.
• Sex: Men are at higher risk before menopause; postmenopausal women’s risk equals men’s.
• Family History: Genetic predisposition, especially early-onset coronary artery disease.
• Congenital Conditions: Conditions such as Marfan syndrome and Kawasaki disease predispose to coronary pathology.
  
  

• Lifestyle Factors: Smoking, physical inactivity, and poor dietary habits.
• Metabolic Disorders: Diabetes mellitus, hypertension, and dyslipidemia.
• Obesity: Central (abdominal) obesity is particularly linked to increased cardiovascular risk.
• Psychosocial Stress: High stress levels and type A personality traits.
• Hypercoagulable States: Inherited thrombophilia or antiphospholipid syndrome.
  
  

Paediatric Considerations

• Coronary artery anomalies, such as anomalous origin of the left coronary artery.
• Kawasaki disease, leading to coronary aneurysms or stenosis.
• Intrauterine or neonatal conditions, including congenital coronary stenosis or perinatal asphyxia.
  
  

Formation and Progression of Atherosclerotic Plaques

1. Early Plaque Development:
   • Initiated by the accumulation of low-density lipoprotein (LDL) cholesterol and saturated fats in the intima of blood vessels.
   • Adhesion of macrophages to endothelial cells facilitates diapedesis, enabling their migration into the intima. Here, macrophages engulf lipids, transforming into foam cells.
   • Foam cells release proinflammatory mediators, amplifying the local inflammatory response. This stage, termed the "fatty streak," is often reversible with lifestyle modifications and medical therapy.
2. Advanced Plaques:
   • Smooth muscle cells migrate from the media and proliferate, depositing extracellular matrix components such as proteoglycans and collagen.
   • Plaques calcify as they evolve, initially expanding outward (positive remodeling). Over time, they encroach on the arterial lumen, restricting blood flow under increased myocardial demand, leading to angina.
   • Vulnerable plaques develop a thin fibrous cap overlying a lipid-rich necrotic core infiltrated by inflammatory cells. These plaques are prone to rupture or erosion.
     
     

Acute Coronary Events

1. Plaque Rupture or Erosion:
   • Catastrophic disruption of a plaque exposes the thrombogenic core to circulating blood.
   • Platelet adhesion and aggregation, coupled with activation of the coagulation cascade, result in thrombus formation and coronary artery occlusion.
2. ST-Elevation Myocardial Infarction (STEMI):
   • A complete occlusion leads to transmural ischemia, manifesting as ST-segment elevation on an ECG.
   • If untreated, myocardial necrosis extends from the subendocardium to the subepicardium in a "wavefront" pattern.
3. Microvascular Dysfunction:
   • Acute ischemia also disrupts microvascular function, reducing perfusion even after large-vessel recanalisation.
     
     

Myocardial Injury and Cellular Changes

1. Ischemic Cascade:
   • Within seconds of blood flow interruption, myocardial oxygen supply becomes inadequate, impairing contractility.
   • Irreversible injury occurs within 20–40 minutes, depending on collateral circulation and metabolic demand.
2. Cellular Changes:
   • Loss of adenosine triphosphate (ATP) compromises ionic gradients, leading to intracellular calcium overload and cellular edema.
   • Coagulative necrosis ensues, with release of cellular contents such as troponin into the circulation.
     
     

Ventricular Remodeling

1. Healing and Fibrosis:
   • Necrotic myocardium undergoes inflammatory clearance and replacement by fibrous scar tissue.
   • Ventricular dilation and spherical remodeling can occur, especially after large anterior infarctions, leading to reduced contractility and heart failure.
2. Regulated Remodeling:
   • Medical therapies (e.g., beta-blockers, angiotensin-converting enzyme inhibitors) mitigate adverse remodeling and preserve left ventricular function.
     
     

Reperfusion Injury

1. Paradoxical Damage:
   • Restoration of blood flow after ischemia can exacerbate myocardial injury via oxidative stress, calcium overload, and inflammatory mediator release.
   • This phenomenon, termed reperfusion injury, may cause arrhythmias, microvascular dysfunction, and further cell death.
2. Potential Therapies:
   • Experimental approaches, including antioxidants and ischemic preconditioning, aim to minimise reperfusion injury, though definitive therapies remain elusive.
     
     

Stunned and Hibernating Myocardium

1. Stunned Myocardium:
   • Transient post-ischemic left ventricular dysfunction persists despite restored perfusion, recovering over hours to days.
2. Hibernating Myocardium:
   • Chronic hypoperfusion leads to reduced contractility, which can be reversed with revascularisation.
     
     

Key Pathophysiological Features of MI

1. Coronary Thrombosis:
   • Atherothrombosis remains the most common cause of MI. Plaque disruption initiates a cascade of platelet aggregation and clot formation.
2. Wavefront Phenomenon:
   • Myocardial necrosis begins in the subendocardium and progresses outward, emphasising the critical need for timely intervention.
3. Ischemia-Induced Arrhythmias:
   • Acute ischemia disrupts electrical stability, increasing the risk of fatal arrhythmias such as ventricular fibrillation.
     
     

Global Perspective

1. CVD Mortality and Morbidity:
   • CVD accounts for approximately 32% of global deaths, with ischemic heart disease responsible for 38% of CVD-related deaths in women and 44% in men.
   • The annual global incidence of ischemic heart disease includes approximately 5.8 million new cases across European Society of Cardiology (ESC) countries.
2. Disparities Between Regions:
   • Developed countries have seen significant declines in MI incidence and mortality over the past three decades due to improved healthcare access and preventive strategies.
   • In contrast, developing and transitional countries experience increasing MI rates, attributed to population aging, urbanisation, and lifestyle changes such as higher smoking rates, poor diets, and reduced physical activity.
3. CVD in Developing Nations:
   • Developing regions, including Sub-Saharan Africa, Latin America, and parts of Asia, are projected to face a dramatic rise in CVD-related mortality, with numbers increasing from 9 million in 1990 to 20 million by 2020.
   • Factors include socioeconomic shifts, adoption of Westernized diets, and increasing prevalence of cardiovascular risk factors like hypertension and dyslipidemia.
4. INTERHEART Study Insights:
   • This global study identified nine modifiable risk factors—smoking, abnormal lipid levels, hypertension, diabetes, obesity, poor diet, physical inactivity, alcohol use, and psychosocial stress—that account for over 90% of acute MI risk worldwide.
   • These risk factors are consistent across diverse populations, regardless of sex or geographic region.
     
     

Regional Statistics

• Coronary artery disease (CAD) is the leading cause of death, responsible for 500,000–700,000 deaths annually.
• Approximately 1.5 million MI cases occur each year, with 550,000 new cases and 200,000 recurrent cases.
• Age-adjusted death rates from MI have declined since the 1970s, yet the total number of MI-related deaths remains stable due to an aging population.
• Men experience MI three times more frequently than women before age 75, but this disparity diminishes in older age groups.
• Black Americans have higher MI mortality than White or Hispanic individuals.
  
  

• CAD remains the leading cause of death, accounting for significant morbidity and mortality.
• Death rates have declined by 30% since the mid-1960s in Western Europe, but Eastern Europe experienced increased rates during the early 1990s, followed by a subsequent decline.
• Cardiovascular mortality in the UK accounts for approximately 1.2 million hospitalisations annually, with an overall prevalence of 3%.
  
  

• Japan exhibits significantly lower CAD mortality compared to Western countries, reflecting differences in diet, lifestyle, and healthcare systems.
• China faces a rising CAD burden, driven by risk factors such as smoking and urbanisation.
  
  

Trends in MI Incidence and Mortality

1. Global Trends:
   • STEMI incidence has been declining over the past two decades in developed countries due to early intervention and improved management strategies.
   • Non-ST-Elevation Myocardial Infarction (NSTEMI) cases have increased, partly due to heightened awareness and diagnostic advancements.
2. Sex Differences:
   • MI incidence increases in postmenopausal women, narrowing the gender gap observed in younger populations.
   • Women under 60 have higher 30-day mortality rates following STEMI than men, even after adjusting for comorbidities and interventions.
3. COVID-19 Impact:
   • In the UK, the number of MI cases increased by 16% in 2021–2022 compared to the previous year, partly due to delayed care and altered healthcare access during the pandemic.
     
     

Age and Socioeconomic Factors

• The average age of first MI is 65.1 years in men and 72 years in women in the United States.
• Socioeconomic factors such as healthcare access and education significantly influence MI outcomes, with individuals in lower-resource settings experiencing higher mortality rates and poorer long-term outcomes.
  
  

Presenting Symptoms

• Chest Pain: The hallmark symptom in MI.
  • Character: Typically described as retrosternal, crushing, squeezing, or pressure-like.
  • Radiation: May radiate to the neck, jaw, shoulders, left arm, or upper abdomen.
  • Duration: Often unremitting for 30–60 minutes.
  • Aggravating/Relieving Factors: Pain may persist despite rest or nitroglycerin use.
• Associated Symptoms:
  • Nausea and vomiting, especially in inferior wall MI due to vagal stimulation.
  • Profuse sweating (diaphoresis) linked to sympathetic activation.
  • Shortness of breath due to left ventricular dysfunction or pulmonary congestion.
  • Lightheadedness, syncope, or fatigue, often indicative of poor perfusion.
    • Anxiety or an overwhelming sense of impending doom.
      
      

Atypical Presentations

• Common in women, older adults, or patients with diabetes.
  • Symptoms may include fatigue, dyspnea, or palpitations rather than chest pain.
  • Discomfort may be localised to the epigastrium, neck, or back and mistaken for non-cardiac causes like indigestion or musculoskeletal pain.
    
    

Prodromal Symptoms

• Patients may report fatigue, malaise, or intermittent chest discomfort in the days or hours preceding the acute event.
  
  

Circadian Variation

• MI incidence peaks in the early morning hours.
  • Likely linked to increased sympathetic tone, morning surges in blood pressure and heart rate, and heightened coagulability.
    
    

Risk Factor Assessment

1. Cardiovascular Risk Profile:
   • Evaluate traditional risk factors that predispose patients to MI:
     • Smoking, hypertension, diabetes, hyperlipidemia, obesity.
     • Family history of premature coronary artery disease (male <45 years, female <55 years).
     • Sedentary lifestyle, unhealthy diet, or psychosocial stress.
   • Non-traditional risk factors:
     • Cocaine use or other stimulants.
     • History of autoimmune or inflammatory diseases.
2. Medical History:
   • Previous episodes of chest discomfort or coronary artery disease.
   • Prior interventions like stenting or bypass surgery.
   • Co-existing conditions such as chronic kidney disease, peripheral arterial disease, or atrial fibrillation.
3. Social History:
   • Substance use, particularly cocaine or amphetamines.
   • Occupational stressors or poor socioeconomic support.
     
     

Risk Assessment Tools in MI

• Developed to predict 14-day mortality and risk of recurrent ischemic events in patients with ACS.
• Factors include:
  • Age ≥65 years.
  • At least three risk factors for CAD (e.g., smoking, hypertension, diabetes).
  • Known coronary stenosis ≥50%.
  • Use of aspirin in the past 7 days.
  • Severe anginal episodes in the past 24 hours.
  • Elevated cardiac biomarkers.
  • ST-segment deviation ≥0.5 mm on ECG.

• Total score ranges from 0–7; higher scores predict greater risk of mortality and adverse events.
  
  

• A widely validated tool for predicting in-hospital and post-discharge outcomes in ACS.
• Factors include:
  • Age.
  • Heart rate and systolic blood pressure at presentation.
  • Serum creatinine (as a marker of kidney function).
  • Presence of congestive heart failure or cardiogenic shock.
  • Cardiac arrest on admission.
  • Elevated cardiac biomarkers.
  • ST-segment deviation on ECG.

• Offers continuous risk stratification and is used to guide treatment, including decisions about invasive strategies.
  
  

• Modified from the atrial fibrillation risk score to include smoking and family history of CAD.
• Useful in predicting long-term cardiovascular death following MI.

• Congestive heart failure, hypertension, age ≥75 years, diabetes, stroke history, vascular disease, age 65–74, female sex, smoking, and family history.

• A score >3 demonstrates high sensitivity (78.4%) and specificity (76.4%) for long-term cardiovascular mortality.
  
  

Practical Considerations in History-Taking

1. Time Since Symptom Onset:
   • Critical for determining the appropriate reperfusion strategy.
   • Patients often approximate symptom onset, requiring careful questioning to discern the timeline.
2. Challenges:
   • Elderly or cognitively impaired patients may fail to articulate symptoms clearly.
   • Patients with stoic outlooks or high pain thresholds may downplay chest discomfort.
3. Practical Tips:
   • Do not rely solely on symptom relief after nitrates as definitive evidence against MI.
   • Always consider serial ECGs and cardiac biomarkers for diagnostic confirmation.
     
     

General Appearance

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

Vital Signs

1. Heart Rate:
   • Tachycardia: Common due to sympathetic activation or pain.
   • Bradycardia: May occur with inferior-wall MI, conduction blocks, or sinus node dysfunction.
   • Irregular Pulse: Indicative of arrhythmias such as atrial fibrillation or ventricular ectopy.
2. Blood Pressure:
   • Hypertension: Seen initially in response to adrenergic stimulation, anxiety, or pain.
   • Hypotension: Suggestive of cardiogenic shock, large infarcts, or right ventricular MI.
3. Respiratory Rate:
   • Increased in response to pulmonary congestion, hypoxemia, or anxiety.
4. Temperature:
   • Fever develops within 24–48 hours due to the inflammatory response and parallels creatine kinase (CK) levels.
     
     

Cardiovascular Examination

1. Jugular Venous Pressure (JVP):
   • Elevated JVP: Suggests right ventricular infarction, heart failure, or pericardial tamponade.
2. Heart Sounds:
   • S3 Gallop: Indicates left ventricular dysfunction and elevated filling pressures.
   • S4 Gallop: Associated with reduced ventricular compliance.
   • New Murmurs:
     • Mitral Regurgitation Murmur: Suggests papillary muscle dysfunction or rupture.
     • Ventricular Septal Defect Murmur: Holosystolic murmur at the left sternal border, often with a thrill.
   • Pericardial Friction Rub: Suggests pericarditis, a late complication of MI.
3. Pulse Examination:
   • Weak, thready pulses indicate low cardiac output.
   • Asymmetric pulses or blood pressure differences between arms suggest aortic dissection.
     
     

Pulmonary Examination

• Crackles or Rales: Indicative of pulmonary congestion or edema due to left ventricular dysfunction.
• Wheezing: May be present in acute pulmonary edema.
• Dullness to Percussion: Suggestive of pleural effusion in extensive cardiac failure.
  
  

Abdomen

• Hepatomegaly: Reflects systemic venous congestion in right-sided heart failure.
• Hepatojugular Reflux: Seen in elevated right atrial pressure.
• Abdominal Aneurysm: Pulsatile abdominal masses could suggest an aortic aneurysm as a differential.
  
  

Extremities

• Cyanosis or Pallor: Indicative of poor peripheral perfusion.
• Cool, Clammy Skin: Suggests peripheral vasoconstriction secondary to shock.
• Delayed Capillary Refill: Indicates reduced cardiac output.
• Oedema: Peripheral edema may occur with right ventricular failure or chronic cardiac dysfunction.
  
  

Key Signs of Complications

1. Cardiogenic Shock:
   • Signs include hypotension, cool extremities, oliguria, altered consciousness, and a rapid, thready pulse.
2. Heart Failure:
   • Orthopnea, paroxysmal nocturnal dyspnea, elevated JVP, and pulmonary crackles.
3. Mechanical Complications:
   • Papillary Muscle Rupture: New systolic murmur with acute pulmonary edema.
   • Ventricular Septal Rupture: Harsh murmur with hemodynamic instability.
   • Left Ventricular Free Wall Rupture: Sudden tamponade with pulseless electrical activity.
4. Pericardial Tamponade:
   • Beck’s Triad: Hypotension, muffled heart sounds, and elevated JVP.
     
     

Practical Considerations

• Subtle Findings: A normal examination does not exclude MI, especially in early presentations.
• Serial Examinations: Monitor for evolving complications such as shock, heart failure, or arrhythmias.
• Corroborate Findings: Pair examination with ECG, cardiac biomarkers, and imaging for accurate diagnosis.
  
  

Initial and Critical Investigations

• 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, or ≥1.5 mm in women in V2-V3.
  • New left bundle branch block (LBBB) in the appropriate clinical context.
• Advanced Patterns:
  • Posterior STEMI: ST depression in V1-V3 with posterior lead confirmation (ST elevation ≥0.5 mm in 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 for equivocal cases or symptom fluctuation.
• Special Considerations:
  • Use Sgarbossa criteria for diagnosing STEMI in patients with LBBB.
  • Evaluate for residual ST elevation or pathological Q waves in prior silent MI cases.
    
    

• Troponin I and T:
  • Preferred markers for myocardial necrosis, with high-sensitivity assays detecting levels within 2–3 hours of symptom onset.
  • Diagnostic criteria include a rise and/or fall above the 99th percentile of the upper reference limit.
• Timing:
  • Serial measurements at presentation and 3-6 hours after symptom onset.
  • Interpret trends in conjunction with clinical and ECG findings.
• Other Markers:
  • Creatine kinase-MB (CK-MB): Less specific and rarely used.
  • Myoglobin: Early marker but lacks specificity for cardiac injury.
    
    

• Indications:
  • All STEMI patients within 12 hours of symptom onset.
  • PCI within 120 minutes for eligible cases.
  • Consider angiography in late presentations (>12 hours) if evidence of ongoing ischemia, hemodynamic instability, or life-threatening arrhythmias exists.
• Access:
  • Radial arterial access preferred to minimise complications.
    
    

Supporting Investigations

• Full Blood Count (FBC):
  • Evaluate for anaemia, leukocytosis (inflammatory response), and thrombocytopenia (monitor for heparin-induced thrombocytopenia).
• Electrolytes, Urea, and Creatinine:
  • Assess renal function and electrolyte imbalances (potassium, magnesium) to prevent arrhythmias.
• Glucose:
  • Detect hyperglycemia, which is common even in non-diabetic patients with MI.
• C-Reactive Protein (CRP):
  • May indicate the inflammatory phase of MI but not used for acute decision-making.
• Serum Lipids:
  • Assess risk factor profile; lipid levels should be repeated 30–60 days post-MI due to transient reductions during the acute phase.
    
    

Imaging

1. Chest X-Ray:
   • Rule out alternative diagnoses (e.g., aortic dissection, pulmonary edema, or cardiomegaly).
   • Not diagnostic for MI but aids in identifying complications.
2. Transthoracic Echocardiogram (TTE):
   • Detect left ventricular regional wall motion abnormalities, valvular defects, pericardial effusion, or thrombus.
   • Useful for atypical presentations or when ECG findings are equivocal.
3. Computed Tomography (CT):
   • Primarily for ruling out differential diagnoses like aortic dissection or pulmonary embolism in chest pain cases.
   • Not routinely used for diagnosing MI.
     
     

Emerging Diagnostic Modalities

• Characteristics:
  • More rapidly detectable than troponin in early myocardial injury.
  • Potential future role in rapid MI diagnosis, though not yet in clinical use.
    
    

Common Cardiac Mimics of MI

• Clinical Features:
  • Chest pain similar to MI but less severe and often of shorter duration.
  • Pain occurs at rest, with minimal exertion, or with increasing frequency.
• Investigations:
  • ECG may show non-specific ST-segment and T-wave changes, but no persistent ST-segment elevation.
  • Cardiac biomarkers are normal, distinguishing it from NSTEMI.
• Key Point: Unstable angina is a clinical diagnosis based on symptoms and lack of biomarker elevation.
  
  

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

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

• Clinical Features:
  • Sudden onset of left ventricular dysfunction triggered by emotional or physical stress.
  • Symptoms and ECG findings mimic acute MI.
• Investigations:
  • Coronary angiography shows no significant obstructions.
  • Echocardiography reveals apical ballooning.
    
    

• Clinical Features:
  • Episodic chest pain at rest, often occurring at night or early morning.
  • Symptoms may resolve spontaneously or with nitrates.
• Investigations:
  • Transient ST-segment elevation on ECG during episodes.
  • Coronary angiography often normal.
    
    

• Clinical Features:
  • Occurs more often in younger women without traditional risk factors.
  • Presents with chest pain and features of ACS.
• Investigations:
  • Coronary angiography shows intimal disruption or intramural hematoma.
  • Intravascular ultrasound or optical coherence tomography aids diagnosis.
    
    

Other Cardiac and Vascular Causes

• Clinical Features:
  • Sudden, tearing chest or back pain, often with asymmetric pulses.
• Investigations:
  • CT angiography demonstrates a dissection flap and true/false lumens.
  • Chest X-ray may show a widened mediastinum.
    
    

• Clinical Features:
  • Acute pleuritic chest pain, dyspnea, and hypoxemia.
• Investigations:
  • ECG may show sinus tachycardia or S1Q3T3 pattern.
  • D-dimer levels elevated; confirm with CT pulmonary angiography.
    
    

Gastrointestinal and Musculoskeletal Mimics

• Clinical Features:
  • Burning retrosternal pain, often relieved by antacids.
• Investigations:
  • Normal ECG and cardiac biomarkers.
  • Oesophagogastroduodenoscopy may show oesophagitis or erosions in refractory cases.
    
    

• Clinical Features:
  • Squeezing retrosternal discomfort, sometimes relieved by nitrates.
• Investigations:
  • Oesophageal manometry or barium swallow to confirm dysmotility.
    
    

• Clinical Features:
  • Localised chest wall tenderness exacerbated by movement.
• Investigations:
  • Normal ECG, cardiac biomarkers, and imaging.
    
    

Respiratory Causes

• Clinical Features:
  • Sudden pleuritic chest pain and dyspnea.
• Investigations:
  • Chest X-ray reveals a visceral pleural line and absence of lung markings.
    
    

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

Psychiatric Causes

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

Urgent Initial Management

1. 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.
2. 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.
3. 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).
4. 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.
5. Seek Specialist Input:
   • Engage the interventional cardiology team early for decision-making and escalation of care.
     
     

Pharmacological Management

1. 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).
2. 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.
3. Beta-Blockers:
   • Begin once the patient is hemodynamically stable to reduce myocardial oxygen demand.
4. ACE Inhibitors or ARBs:
   • Start within 24–48 hours for all patients unless contraindicated by hypotension or renal impairment.
   • Titrate to maximum tolerated doses.
5. High-Intensity Statins:
   • Initiate during hospitalisation to reduce LDL and stabilise plaques.
6. Aldosterone Antagonists:
   • Add for patients with heart failure or reduced ejection fraction (<40%) after stabilisation.
7. SGLT2 Inhibitors:
   • Consider for patients with heart failure irrespective of left ventricular ejection fraction.
     
     

Reperfusion Strategies

1. 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.
2. 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.
3. Rescue PCI:
   • Indicated if fibrinolysis fails (<50% ST-segment resolution at 60–90 minutes).
4. Late Presenters:
   • PCI is still recommended if ongoing ischemia or high-risk features (e.g., cardiogenic shock, arrhythmias) are present.
     
     

Management for Special Scenarios

1. 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.
2. Patients Without Reperfusion Eligibility:
   • Provide medical therapy, including DAPT, anticoagulation, beta-blockers, ACE inhibitors/ARBs, and statins.
   • Perform echocardiographic assessment of left ventricular function.
3. Patients on Oral Anticoagulation:
   • Avoid fibrinolysis; primary PCI is the preferred strategy.
     
     

Secondary Prevention and Long-Term Management

1. Antiplatelet Therapy:
   • Continue DAPT (aspirin + P2Y12 inhibitor) for up to 12 months.
   • Transition to single antiplatelet therapy (aspirin or a P2Y12 inhibitor) thereafter.
2. Lifestyle and Risk Factor Modification:
   • Smoking cessation, dietary changes, physical activity, weight management, and alcohol moderation.
3. Cardiac Rehabilitation:
   • Structured programs including exercise, education, and psychological support.
4. Medication Adherence:
   • Continue beta-blockers, ACE inhibitors/ARBs, statins, and aldosterone antagonists as indicated.
     
     

General Prognosis

1. 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.
2. 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.
3. 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

• 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%).
  
  

• 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

1. Troponin Levels:
   • Elevated troponin levels correlate with increased risk of mortality and adverse outcomes.
2. B-Type Natriuretic Peptide (BNP):
   • Higher BNP levels predict heart failure and increased long-term mortality.
3. High-Sensitivity C-Reactive Protein (hs-CRP):
   • Elevated levels indicate systemic inflammation and correlate with worse outcomes.
4. ECG Findings:
   • Involvement of lead aVR is associated with higher mortality.
   • Persistent ST-segment elevation post-reperfusion suggests larger infarct size.
     
     

Factors Impacting Prognosis

1. Clinical Factors:
   • Age, diabetes, hypertension, and prior cardiovascular disease worsen outcomes.
   • Depression post-MI is linked to poorer recovery and higher mortality.
2. 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.
3. Infarct Characteristics:
   • Anterior wall infarctions carry higher mortality compared to inferior or lateral wall infarctions due to greater myocardial damage.
     
     

Prognosis-Improving Interventions

1. Timely Reperfusion:
   • Achieving reperfusion within guideline-directed timelines (e.g., PCI <90 minutes, fibrinolysis <30 minutes) improves survival.
2. Evidence-Based Medical Therapy:
   • Long-term use of beta-blockers, ACE inhibitors/ARBs, statins, and aspirin is associated with reduced mortality.
3. Cardiac Rehabilitation:
   • Exercise training and risk factor modification significantly enhance quality of life and reduce recurrent events.
4. Secondary Prevention:
   • Lifestyle changes, including smoking cessation, dietary improvements, weight management, and physical activity, improve outcomes.
     
     

Arrhythmic Complications

1. 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.
2. 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

1. 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.
2. 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.
3. 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%.
4. Left Ventricular (LV) Aneurysm:
   • Chronic complication associated with large anterior infarctions.
   • Can lead to heart failure, arrhythmias, and thromboembolism.
   • Rarely requires surgical correction.
5. 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

1. 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.
2. Post-Infarction Pericardial Effusion:
   • May progress to tamponade, requiring pericardiocentesis or surgical intervention.
     
     

Thromboembolic Complications

1. Left Ventricular Thrombus:
   • Common in large anterior MIs, especially with LV dysfunction or apical akinesis.
   • Anticoagulation with vitamin K antagonists reduces embolic risk.
2. 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

1. 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%.
2. Chronic Heart Failure:
   • Develops due to maladaptive LV remodeling. Aggressive medical management and risk factor modification are crucial.
     
     

Psychological and Long-Term Complications

1. Recurrent Ischemia and Reinfarction:
   • Treat as a new event; modify risk factors aggressively.
   • Persistent angina may require repeat angiography and PCI.
2. 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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