Myocardial infarction (MI) refers to ischemic necrosis of myocardial tissue. The most common underlying cause is coronary artery disease. Type 1 myocardial infarction occurs when an unstable plaque ruptures, leading to occlusion of a coronary artery. Type 2 myocardial infarction occurs when there is a mismatch between oxygen supply and demand (due to e.g., systemic hypotension, vasospasm). MI manifests clinically with acute coronary syndrome (ACS), a potentially lethal condition. Diagnosis is based on typical clinical features, ECG findings, and elevation of cardiac biomarkers. Definitive diagnosis requires cardiac catheterization, which serves both diagnostic and therapeutic purposes. All patients suspected of having ACS should be considered for emergency revascularization; additional aspects of treatment include anticoagulation, antiplatelet therapy, statin therapy, and other adjunctive measures. Secondary prevention consists of dual antiplatelet therapy, the initiation of beta blocker and/or ACE inhibitors, statin therapy, and addressing any modifiable risk factors.
The acute management of acute coronary syndrome, including its diagnosis and treatment, is described elsewhere.
Myocardial infarction (MI) 
- Type 1 myocardial infarction: MI caused by atherosclerotic plaque disruption or acute coronary thrombosis
Type 2 myocardial infarction: MI secondary to an oxygen supply/demand mismatch 
- Less common form (14%)
- Occurs predominantly in women and in individuals with comorbidities (e.g., diabetes, previous NSTEMI)
- Not due to plaque rupture; caused by a condition other than coronary artery disease
- Ischemia is caused by increased oxygen demand (e.g., anemia) or decreased coronary blood supply (e.g., coronary artery spasm) 
- Type 3 myocardial infarction: MI resulting in death when biomarker values are unavailable
- Type 4 myocardial infarction: MI related to percutaneous coronary intervention
- Type 5 myocardial infarction: MI related to coronary artery bypass grafting
- Suspicion or confirmed presence of acute myocardial ischemia and/or myocardial infarction
- Further classified as unstable angina, NSTEMI, and STEMI
- See “Acute coronary syndrome.”
Epidemiological data refers to the US, unless otherwise specified.
- Coronary artery disease: most common cause (see “”)
- Coronary artery vasospasm (e.g., Prinzmetal angina, cocaine use)
- Coronary artery dissection
- Coronary artery embolism (e.g., due to prosthetic heart valve, atrial fibrillation)
- Takotsubo cardiomyopathy
- Thrombophilia (e.g., polycythemia vera)
- Vasculitis (e.g., polyarteritis nodosa, Kawasaki syndrome)
- Myocardial oxygen supply-demand mismatch, e.g., due to the following:
Coronary artery occlusion 
- Partial coronary artery occlusion
- Complete coronary artery occlusion
Atherosclerotic plaque disruption (type 1 MI) 
- For plaque formation, see “ ” and “ .”
- Stable atherosclerotic plaque: manifests as stable angina (symptomatic during exertion)
- Unstable plaques are lipid-rich and covered by thin fibrous caps : high risk of rupture and acute coronary syndrome
- Inflammatory cells in the plaque (e.g., macrophages) secrete matrix metalloproteinases → breakdown of extracellular matrix → weakening of the fibrous cap → minor stress → rupture of the fibrous cap → exposure of highly thrombogenic lipid core → thrombus formation → coronary artery occlusion
Oxygen supply and demand mismatch (type 2 MI) 
- Can occur in patients with or without underlying
- Decreased oxygen supply
- Increased oxygen demand (e.g., sustained tachyarrhythmia)
Nonischemic myocardial injury 
Classic presentation 
Acute retrosternal chest pain
- Typical: dull, squeezing pressure and/or tightness
- Commonly radiates to left chest, arm, shoulder, neck, jaw, and/or epigastrium
- Precipitated by exertion or stress
- Symptom relief after administration of nitrates is not a diagnostic criterion for cardiac ischemia. 
- The peak time of occurrence is usually in the morning.
- See “ .”
- Dyspnea (especially with exertion)
- Nausea, vomiting
- Diaphoresis, anxiety
- Dizziness, lightheadedness, syncope
- Acute retrosternal chest pain
- Other findings
- Atypical presentations: more likely in elderly, diabetic individuals, and women ; 
- More common in inferior wall infarction
- A 12-lead is the initial test in every patient with suspected myocardial ischemia.
- Findings include pathological Q waves, ST-segment shifts, and T-wave inversions (see “” and “”).
- Dynamic changes require serial ECG evaluation.
- Compare to prior ECGs (if available).
Localization of myocardial infarct on ECG 
|ECG leads affected||Infarct location||Vessel involved |
|II, III, aVF|| |
Infarction of the anterior wall is caused by obstruction of the LAD or its branches. Depending on the extent of anterior wall infarction, it results in ECG changes in the anterior wall leads (V1–6) and/or I and aVL. Infarction of the inferior wall is caused by obstruction of the LCX or RCA or their branches, and ECG changes are seen in leads II, III, and aVF.
Cardiac biomarkers 
- Cardiac troponin (cTn) is the most important biological marker of myocardial necrosis.
- All cardiac biomarkers require clinical context for interpretation (e.g., troponin can also be elevated in other cardiac and noncardiac conditions; see “ ”).
- Values and time references may vary based on the precise laboratory methods employed.
|Overview of cardiac biomarkers|
|Troponin T/I|| || || |
|CK-MB|| || || || |
|Myoglobin|| || || || |
Serum troponin T is the most important cardiac-specific marker.
The timing of a detectable rise in cardiac troponin levels depends (among other factors) on the assay used by the laboratory.
Additional laboratory studies 
- Elevated inflammatory markers: ↑ WBC, CRP
- BNP or NT-proBNP: may be elevated, especially in concurrent heart failure 
- LDH and AST: may be elevated due to cell necrosis
- Urine toxicology screening: Consider in suspected use of cocaine or methamphetamines. 
- Best test for definitive diagnosis of acute coronary occlusion to identify site and degree of vessel occlusion
- Can be used for concurrent intervention (e.g., ; with stent placement)
- Indications include:
- Transthoracic echocardiography
- Cardiac CT with IV contrast
Histopathological findings of MI 
|Time interval post-infarction||Histopathological findings|
| || |
2 weeks to several months
- See “Ischemia” in “.”
- Mechanism: blood flow restored → damaged myocytes release reactive oxygen species (ROS); → mitochondrial permeability transition pores are formed → cell swelling → cell death → Ca2+ entry into the cytosol → hypercontraction of myocytes → contraction band necrosis and increase in infarct size 
- Microscopic findings: neutrophilic infiltration, capillary obstruction, and contraction band necrosis of the myocardium
General principles 
- Revascularization: all patients with suspected acute coronary syndrome should be considered for emergency percutaneous coronary intervention (PCI)
- Serial 12-lead ECG
- Continuous cardiac monitoring
- Serial serum troponin measurement
- Antiplatelet therapy and anticoagulation: See “Antiplatelet therapy and anticoagulation in STEMI” and “Antiplatelet therapy and anticoagulation in NSTE-ACS.”
Adjunctive therapy: See “Adjunct medical therapy in ACS.”
- Sublingual or intravenous nitrate (nitroglycerin or ISDN)
- Morphine IV or SQ
- Beta blockers (avoid in patients with hypotension, features of heart failure, and/or risk of cardiogenic shock)
- Statins: early initiation of high-intensity statin (e.g., atorvastatin) regardless of baseline cholesterol, LDL, and HDL levels
- Oxygen: only in case of cyanosis, severe dyspnea, or SpO2 < 90% 
- Secondary prophylaxis: See “,” “; ,” and “ .”
- See “.”
0–24 hours post-infarction
Sudden cardiac death (SCD)
- Definition: A sudden death presumably caused by cardiac arrhythmia or hemodynamic catastrophe, which occurs either within an hour of symptom onset in patients with cardiovascular symptoms, or within 24 hours of being asymptomatic in patients with no cardiovascular symptoms. 
- Pathophysiology: : Fatal ventricular arrhythmia is considered to be the underlying mechanism of SCD. 
- Underlying conditions
- Prevention: : installation of the implantable cardioverter-defibrillator device 
- Arrhythmias (a common cause of death in MI patients in the first 24 hours)
- Acute left heart failure: death of affected myocardium → absence of myocardial contraction → pulmonary edema
- Cardiogenic shock
1–3 days post-infarction
- Early infarct-associated pericarditis
3–14 days post-infarction
Papillary muscle rupture
- Usually occurs 2–7 days after myocardial infarction
- Can lead to acute mitral regurgitation
- Rupture of the posteromedial papillary muscle due to occlusion of the posterior descending artery is most common.
- Clinical features
Ventricular septal rupture
- Usually occurs 3–5 days after myocardial infarction
- Pathophysiology: macrophagic degradation of the septum → ventricular septal defect → blood flow from LV to RV following the pressure gradient (left-to-right shunt) → increased pressure in RV and increased O2 content in the venous blood
- Most commonly due to LAD infarction (septal arteries arise from LAD)
- Clinical features
- Treatment: emergency surgery and revascularization (often via CABG)
Left ventricular free wall rupture
- Usually occurs 5–14 days after myocardial infarction
- Greatest risk during macrophage-mediated removal of necrotic tissue
- LV hypertrophy and tissue fibrosis from previous MI decrease the risk of free wall rupture.
- Clinical features: chest pain, dyspnea, signs of cardiac tamponade (e.g., Beck triad)
- Complications: cardiac tamponade; , sudden cardiac death (if the rupture occurs acutely)
- Left ventricular pseudoaneurysm
2 weeks to months post-infarction
Atrial and ventricular aneurysms
- Clinical features
- Diagnosis: echocardiography
- Treatment: anticoagulation, possibly surgery (see “ ” for details)
Postmyocardial infarction syndrome (Dressler syndrome): pericarditis occurring 2–10 weeks post-MI without an infective cause
- Thought to be due to circulating antibodies against cardiac muscle cells (autoimmune etiology)
- Clinical features
- Treatment: NSAIDs (e.g., aspirin), colchicine
- Complications (rare): hemopericardium, pericardial tamponade
- Arrhythmias (e.g., AV block)
- Congestive heart failure (e.g., due to ischemic cardiomyopathy)
We list the most important complications. The selection is not exhaustive.
Primary prevention 
- Treatment/avoidance of modifiable risk factors for atherosclerosis (e.g., smoking cessation, treatment of hypertension)
- Healthy, plant-based diet 
- Regular physical activity and exercise
- Low-dose aspirin is beneficial for certain high-risk groups.
- For detailed information on primary prevention see “ASCVD prevention.”
Secondary prevention of myocardial infarction 
- Lifestyle modification and treatment of modifiable risk factors (see “Primary prevention” above and “ ”)
- Lifelong low-dose aspirin: 75–100 mg/day 
- Dual antiplatelet therapy (DAPT)
- Beta blockers: Unless contraindicated, all patients should be started on a beta blocker, which has been shown to confer a mortality benefit.
- Statin: All patients should be started on a high-intensity statin (e.g., atorvastatin).
- ACE inhibitor/ARB are recommended if any one of the following are present: ; 
- Aldosterone antagonist: in addition to ACE inhibitors in patients with heart failure, LVEF < 40%, or diabetes mellitus
- One-Minute Telegram 6-2020-3/3: Statins underprescribed in patients with PAD
- One-Minute Telegram 5-2020-3/3: Aspirin discontinuation with continued P2Y12 inhibitors may be beneficial for select patients after PCI
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