ABIM - Myocardial Infarction

Here are key facts for American Board of Internal Medicine (ABIM) Examination from the Myocardial Infarctions: Diagnosis & Treatment tutorial, focusing on clinical management and treatment decision-making that are essential for board certification. See the tutorial notes for further details and relevant links.

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1. Evolving trends: Incidence of myocardial infarctions is declining in high-income countries but rising in middle- and low-income countries. 2. Demographic variations: Incidence after age 35, from highest to lowest: Black males > Black females > White males > White females. 3. Gender differences: MI occurs approximately 10 years earlier in men than women, possibly related to risk factors like smoking and hyperlipidemia. 4. Mortality patterns: Although overall mortality has declined, rates remain higher in women than men, especially for young and minority women. 5. Disease progression: Myocardial infarction is an important cause of heart failure, which is itself a significant cause of death. 1. Major modifiable risk factors: Dyslipidemia, diabetes mellitus, hypertension, smoking (including e-cigarettes), obesity, psychosocial stress, alcohol consumption, poor diet (low in fruits and vegetables). 2. Patient awareness challenges: Many patients, especially women, are unaware of risk factors and symptoms—a significant obstacle to prevention and treatment. 3. Pre-infarction symptoms: Prodromal symptoms may occur days, weeks, or even months prior to the actual heart attack. 4. Risk factor management: Long-term treatment focuses on reducing risk factors through improved diet, exercise, and medications for hypertension and hyperlipidemia. 5. Special populations: Understanding demographic-specific clinical presentations improves risk assessment and management. 1. Diagnostic definition: Myocardial infarction is defined as myocardial injury with ischemia. 2. Presentation spectrum:

• Typical symptoms: Chest pain/angina (dull, sharp, squeezing, pressure, or discomfort) radiating to arms, neck, jaw, or back
• Atypical presentations: Common in women, elderly, and diabetics
• Silent MI: No noticeable symptoms

3. Associated symptoms: Gastrointestinal issues (nausea, vomiting, indigestion), extreme fatigue, sleep disturbances, headaches, dizziness, lightheadedness, shortness of breath, anxiety, sense of impending doom. 4. Diagnostic challenges: Absence of chest pain and/or young age often leads to missed or delayed diagnosis, associated with worse outcomes. 5. Clinical assessment: Initial evaluation should include history, physical examination, ECG, and cardiac biomarkers. 1. ECG interpretation:

• Should be obtained as soon as possible when MI is suspected
• Distinguishes between STEMI and NSTEMI, which influences treatment strategies
• Should be repeated frequently to observe the evolution of the infarction
• Q-wave abnormalities may indicate size/location of current MI or evidence of prior MI

2. ECG localization:

• Lateral infarction: Leads I and aVL; left circumflex artery
• Apical infarction: Leads V5 and V6; left circumflex or right coronary arteries
• Anterior infarction: Leads V3 and V4; left anterior descending artery
• Anterior septal infarction: Leads V1 and V2; proximal left anterior descending artery
• Inferior infarction: Leads II, aVF, and III; right coronary artery or left circumflex artery
• Right ventricular infarction: Requires additional leads V3R through V6R
• Posterolateral infarction: Requires additional leads V7-V9; right coronary or left circumflex artery

3. Cardiac biomarkers:

• Essential for diagnosis, especially cardiac troponin
• Help distinguish between NSTEMI and unstable angina
• Both troponin I and CK-MB peak within 24 hours of the MI and fall to normal levels over time

4. Imaging considerations: Although not explicitly detailed in the tutorial, integration with clinical findings and laboratory data is essential. 5. Differential diagnosis: Consider alternative causes of chest pain and elevated biomarkers. 1. Timing principles: Treatment should begin as soon as possible, ideally even before hospital arrival, to reduce the extent of myocardial necrosis. 2. Pre-hospital management:

• Oxygen administration when oxygen saturation is less than 90%
• Aspirin for antiplatelet effects
• Nitrates for chest pain (morphine is an option if nitrates are ineffective)

3. Reperfusion strategies:

• Vary by severity of infarction
• Include percutaneous coronary intervention (angioplasty), coronary bypass grafting, or fibrinolytic drugs
• STEMI patients should receive emergency PCI; if unavailable, fibrinolytic drugs must be given as soon as possible
• Unstable, complicated NSTEMI often requires immediate PCI or CABG
• Uncomplicated NSTEMI patients may wait longer, and revascularization may not be necessary
• Fibrinolytic drugs generally not recommended for NSTEMI (risks outweigh benefits)

4. Pharmacological therapy:

• Antiplatelets (aspirin, clopidogrel, or others)
• Anticoagulation drugs (unfractionated or low molecular weight heparin)
• Beta-blockers (or calcium-channel blockers)
• Statins
• ACE-inhibitors

5. Secondary prevention: Long-term management focuses on risk factor reduction through improved diet, exercise, and medications for hypertension and hyperlipidemia.

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1. Symptom variability: Chest pain or angina is variably described as dull, sharp, squeezing, pressure, or simply discomfort—understanding this spectrum improves recognition. 2. Pain radiation patterns: May radiate from the chest to arms, neck, jaw, or back—radiation patterns can help confirm diagnosis. 3. Non-chest pain presentations: Not all patients experience angina; absence increases risk of missed diagnosis, especially in women and elderly. 4. Prodromal symptoms: May occur days, weeks, or even months before the acute event—recognition can enable earlier intervention. 5. Psychological manifestations: Anxiety or sense of impending doom may precede or accompany MI—should not be dismissed as purely psychiatric. 1. Serial assessment: ECGs should be repeated frequently to observe the evolution of infarction patterns. 2. STEMI vs. NSTEMI distinction: Critical for determining appropriate reperfusion strategy. 3. Localization significance: Different lead changes indicate specific coronary artery territories:

• Anterior (V3-V4): Left anterior descending artery
• Anteroseptal (V1-V2): Proximal left anterior descending artery
• Lateral (I, aVL): Left circumflex artery
• Apical (V5-V6): Left circumflex or right coronary arteries
• Inferior (II, III, aVF): Right coronary artery (or less frequently left circumflex)

4. Extended lead sets: Right ventricular (V3R-V6R) and posterior (V7-V9) infarctions require additional leads. 5. Q-wave significance: May indicate size/location of current MI or evidence of prior MI. 1. Diagnostic utility: Cardiac biomarkers, especially troponin, are key to diagnosing myocardial infarction. 2. Differential diagnosis: Biomarker values help distinguish between NSTEMI and unstable angina—only NSTEMI shows rising/falling troponin. 3. Temporal patterns: Both cardiac troponin I and CK-MB peak within 24 hours of MI and gradually return to normal. 4. Sampling protocols: Serial measurements provide more diagnostic value than single determinations. 5. Integration with clinical findings: Biomarkers should be interpreted in the context of symptoms and ECG findings. 1. STEMI management: Emergency PCI recommended; if unavailable, fibrinolytic drugs must be given as soon as possible. 2. NSTEMI approach: Timing of intervention based on risk stratification:

• Unstable/complicated cases: Immediate PCI/CABG
• Uncomplicated cases: May wait longer; revascularization may not be necessary

3. Fibrinolytic therapy: Generally not recommended for NSTEMI as potential risks outweigh benefits. 4. Time-sensitive decisions: Treatment should begin as soon as possible to reduce myocardial necrosis. 5. Pre-hospital initiation: Treatment ideally begins before hospital arrival with oxygen (when indicated), aspirin, and nitrates. 1. Gender differences: Women experience MI approximately 10 years later than men, often with atypical symptoms, and have higher mortality rates. 2. Racial/ethnic variations: Significant differences in MI incidence across populations, with Black males having highest incidence after age 35. 3. Young patients: Absence of chest pain and young age often leads to missed diagnosis—maintain high index of suspicion. 4. Awareness disparities: Many patients, especially women, are unaware of risk factors and symptoms—patient education is crucial. 5. Risk factor clustering: Combinations of risk factors like smoking, dyslipidemia, and diabetes significantly increase MI risk.

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Below is information not explicitly contained within the tutorial but important for the American Board of Internal Medicine Examination. 1. TIMI Risk Score: Predicts 14-day and 1-year mortality risk in STEMI/NSTEMI patients. 2. GRACE Risk Score: Predicts in-hospital and 6-month mortality for ACS patients. 3. HEART Score: Stratifies chest pain patients in the emergency department for early discharge consideration. 4. Bleeding risk assessment: CRUSADE score for NSTEMI and HAS-BLED for anticoagulated patients. 5. Long-term risk prediction: ASCVD risk calculator for secondary prevention intensity. 1. Pharmaco-invasive approach: Pre-hospital fibrinolysis followed by early angiography in certain settings. 2. P2Y12 inhibitor selection: Clopidogrel vs. ticagrelor vs. prasugrel based on patient characteristics. 3. Anticoagulant options: UFH, LMWH, fondaparinux, or bivalirudin based on clinical scenario. 4. Complete vs. culprit-only revascularization: Strategies for multivessel disease in STEMI. 5. Optimal timing of non-culprit lesion intervention: Immediate vs. staged approach. 1. Mechanical complications: Recognition and management of papillary muscle rupture, ventricular septal defect, and free wall rupture. 2. Cardiogenic shock: Early recognition, hemodynamic support, and revascularization strategies. 3. Post-MI arrhythmias: Acute management and long-term risk stratification. 4. Right ventricular infarction: Special management considerations including volume resuscitation. 5. Post-infarction pericarditis: Differentiation from reinfarction and appropriate therapy. 1. Optimal medical therapy: Evidence-based medication regimens and dosing. 2. Cardiac rehabilitation: Structured programs to improve outcomes and reduce readmissions. 3. Implantable device considerations: ICD and CRT evaluations post-MI. 4. Return to activities: Evidence-based guidance for driving, physical activity, and work. 5. Long-term monitoring: Appropriate use of testing for residual ischemia and ventricular function assessment. 1. Core quality metrics: Door-to-ECG time, door-to-needle time, door-to-balloon time. 2. Regional STEMI systems: Network organization and transfer protocols. 3. Discharge planning: Medication reconciliation, follow-up arrangements, and transition of care. 4. Readmission reduction: Evidence-based strategies to prevent 30-day readmissions. 5. Healthcare disparities: Recognition and addressing gaps in MI care and outcomes.