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Lecture Notes: Myocardial Infarction (MI)

1. Definition

 Myocardial Infarction (MI), commonly called a heart attack, is the irreversible necrosis
of heart muscle (myocardium).

 Caused by prolonged ischemia due to reduced or complete obstruction of blood flow in


the coronary arteries.

 Leads to loss of contractile function and may result in heart failure, arrhythmias, or
sudden death.

2. Etiology / Causes

 Atherosclerosis of coronary arteries (most common).

 Rupture of an atherosclerotic plaque with subsequent thrombus (blood clot)


formation.

 Coronary artery spasm (Prinzmetal’s angina).

 Embolism from the left atrium or ventricle.

 Rare causes: coronary dissection, trauma, or vasculitis.

3. Pathophysiology

 Coronary artery narrowed by plaque → rupture/erosion exposes lipid core → platelet


aggregation + thrombus formation.

 Complete or partial occlusion → ↓ blood supply to myocardium.

 Within 20–30 minutes: irreversible myocardial cell injury begins.

 1–2 hours: coagulative necrosis progresses.

 Transmural MI: full thickness of wall affected (STEMI).

 Subendocardial MI: inner wall affected, not full thickness (NSTEMI).

 Healing leads to scar formation over weeks to months.


4. Epidemiology / Risk Factors

 Leading cause of death worldwide.

 Risk factors:

o Hypertension, diabetes mellitus, hyperlipidemia.

o Smoking, obesity, sedentary lifestyle.

o Family history of coronary artery disease.

o Male gender and increasing age.

5. Clinical Features

 Typical symptoms:

o Severe, crushing chest pain (retrosternal, radiates to left arm, jaw, back).

o Pain lasts >20 minutes, not relieved by rest or nitroglycerin.

o Associated with sweating, nausea, vomiting, anxiety, shortness of breath.

 Atypical symptoms (common in elderly, women, diabetics): fatigue, indigestion-like


discomfort, syncope.

 Physical exam: tachycardia, hypotension, pallor, weak pulse.

6. Complications

 Immediate: arrhythmias (ventricular tachycardia/fibrillation), cardiogenic shock, acute


left ventricular failure, cardiac arrest.

 Early (days): pericarditis, mural thrombus, extension of infarct.

 Late (weeks–months): ventricular aneurysm, chronic heart failure, recurrent MI.

7. Diagnosis

 Clinical history + ECG + cardiac biomarkers = gold standard.

 ECG:

o STEMI: ST-segment elevation, pathological Q waves, T-wave inversion.


o NSTEMI: ST depression or T-wave changes.

 Cardiac biomarkers:

o Troponin I/T → most specific, rises 3–6 hrs, peaks 24 hrs, stays elevated 7–10
days.

o CK-MB → rises 4–6 hrs, peaks 18–24 hrs, returns to normal in 2–3 days.

 Imaging: echocardiography (wall motion abnormalities), coronary angiography.

8. Management

a. Emergency/Initial Management (MONA protocol):

 Morphine → pain relief & anxiety reduction.

 Oxygen → if hypoxemic.

 Nitrates → vasodilation, reduces workload of heart.

 Aspirin → antiplatelet to prevent further clot formation.

b. Definitive Management:

 Reperfusion therapy:

o Thrombolysis (tPA, streptokinase) → dissolve clot.

o Percutaneous Coronary Intervention (PCI) → balloon angioplasty & stent


placement.

 Adjunct medications:

o Beta-blockers, ACE inhibitors, statins, anticoagulants (heparin).

c. Long-term Management:

 Lifestyle modifications: diet, exercise, stop smoking.

 Secondary prevention: aspirin, statins, beta-blockers, ACE inhibitors for life.

9. Prognosis

 Mortality highest in the first 24 hours (mainly due to arrhythmias).

 Early reperfusion greatly improves survival.


 Prognosis depends on infarct size, location, and speed of treatment.

10. Key Exam Points

 Definition: irreversible myocardial necrosis due to ischemia.

 Risk factors: hypertension, diabetes, smoking.

 Diagnosis: ECG changes + elevated troponin.

 Complications: arrhythmia, shock, ventricular aneurysm.

 Management: MONA, reperfusion (PCI/thrombolysis), secondary prevention.

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