MI
Myocardial Infarction
Myocardial infarction is irreversible injury and death of cardiac muscle caused by prolonged myocardial ischemia. It most commonly results from acute coronary artery thrombosis following disruption of an atherosclerotic plaque.
RegionThorax
SystemCardiovascular System
Myocardial infarction (MI) is irreversible injury and death of cardiac muscle resulting from prolonged myocardial ischemia. It occurs when the oxygen supply to a region of myocardium becomes inadequate for long enough to produce cardiomyocyte necrosis.
The most common mechanism is acute reduction of coronary blood flow caused by thrombosis over a disrupted atherosclerotic plaque. The affected myocardial territory depends on the coronary artery involved, the location and duration of obstruction, collateral circulation, and individual variations in coronary anatomy.
Myocardial infarction can impair ventricular contraction, disrupt the cardiac conduction system, alter valve function, and produce life-threatening complications such as arrhythmias, acute heart failure, cardiogenic shock, or mechanical rupture.
Coronary Circulation
The myocardium receives its arterial blood supply primarily from the right and left coronary arteries, which arise from the ascending aorta immediately superior to the aortic valve.
These vessels and their branches travel over the surface of the heart before giving rise to smaller branches that penetrate the myocardium.
Right Coronary Artery
The right coronary artery (RCA) arises from the right aortic sinus and travels within the coronary sulcus.
Its branches commonly supply portions of the right atrium, right ventricle, inferior aspect of the left ventricle, and components of the cardiac conduction system, although the exact distribution varies with coronary dominance.
Left Coronary Artery
The left coronary artery arises from the left aortic sinus and usually divides into the anterior interventricular artery and circumflex artery.
These branches supply much of the left ventricle, interventricular septum, and left atrium.
Anterior Interventricular Artery
The anterior interventricular artery, commonly called the left anterior descending artery or LAD, travels in the anterior interventricular sulcus toward the apex.
It typically supplies the anterior wall of the left ventricle, the apex, and much of the anterior interventricular septum.
Circumflex Artery
The circumflex artery travels within the left portion of the coronary sulcus.
It supplies portions of the lateral and posterior left ventricular myocardium, with its exact territory depending partly on coronary dominance.
Posterior Interventricular Artery
The posterior interventricular artery travels within the posterior interventricular sulcus.
In right-dominant circulation it usually arises from the RCA, while in left-dominant circulation it arises from the circumflex artery.
Coronary Dominance
Coronary dominance is defined by the artery that gives rise to the posterior interventricular artery.
Most individuals have right-dominant circulation, while smaller proportions have left-dominant or codominant patterns.
Myocardial Oxygen Demand
The myocardium has a continuous requirement for oxygen because cardiac muscle contracts throughout life and has limited capacity to tolerate interruption of blood flow.
Myocardial oxygen demand is influenced by heart rate, contractility, ventricular wall stress, and other hemodynamic factors.
Coronary Blood Flow
Coronary perfusion, particularly of the left ventricular myocardium, occurs predominantly during diastole.
During systole, contraction of the ventricular wall compresses intramyocardial vessels and limits flow, especially within the subendocardium.
Myocardial Ischemia
Myocardial ischemia occurs when myocardial oxygen supply is insufficient for metabolic demand.
Ischemia initially produces reversible cellular dysfunction, but prolonged severe ischemia can progress to irreversible injury and necrosis.
From Ischemia to Infarction
Loss of adequate coronary perfusion disrupts aerobic metabolism and reduces cellular ATP production.
As ischemia persists, abnormalities of ion gradients, membrane function, contractility, and cellular integrity develop. Severe prolonged ischemia eventually causes irreversible cardiomyocyte injury.
Most Common Mechanism
Most acute myocardial infarctions are related to coronary atherosclerosis complicated by acute plaque disruption and thrombosis.
A previously present atherosclerotic plaque may rupture or erode, exposing thrombogenic material to circulating blood.
Plaque Rupture
Plaque rupture disrupts the fibrous cap covering an atherosclerotic lesion.
Exposure of the lipid-rich and thrombogenic plaque interior promotes platelet adhesion, activation, aggregation, and activation of the coagulation cascade.
Plaque Erosion
Acute coronary thrombosis can also occur through plaque erosion, in which endothelial injury permits thrombus formation without classic rupture of the fibrous cap.
Coronary Thrombosis
A thrombus forming at the site of plaque disruption can partially or completely obstruct the coronary artery.
The degree and persistence of obstruction strongly influence the extent of downstream myocardial ischemia and injury.
Progression of Acute Coronary Occlusion
The common sequence can be represented as:
Atherosclerotic plaque → Plaque disruption → Platelet activation and coagulation → Coronary thrombus → Reduced coronary flow → Myocardial ischemia → Myocardial necrosis
Other Mechanisms of Myocardial Infarction
Not every myocardial infarction results from acute atherothrombosis.
Myocardial injury can occur when oxygen supply and demand become severely imbalanced, and coronary embolism, spontaneous coronary artery dissection, severe coronary spasm, and other abnormalities can also produce infarction.
Type 1 Myocardial Infarction
Type 1 myocardial infarction results from an acute atherothrombotic coronary event, typically involving plaque rupture or erosion with superimposed thrombosis.
Type 2 Myocardial Infarction
Type 2 myocardial infarction results from an imbalance between myocardial oxygen supply and demand that is not caused by acute coronary atherothrombosis.
Potential settings include severe anemia, hypoxemia, marked tachyarrhythmia, severe hypertension, hypotension, shock, or coronary vasomotor abnormalities.
ST-Elevation Myocardial Infarction
ST-elevation myocardial infarction (STEMI) is an acute myocardial infarction associated with characteristic persistent ST-segment elevation or equivalent electrocardiographic patterns indicating acute coronary occlusion in the appropriate clinical context.
It frequently reflects abrupt severe or complete obstruction of an epicardial coronary artery.
Non-ST-Elevation Myocardial Infarction
Non-ST-elevation myocardial infarction (NSTEMI) is myocardial infarction without the persistent ST-elevation pattern used to identify STEMI.
Diagnosis depends on evidence of acute myocardial injury together with clinical evidence of myocardial ischemia.
STEMI Versus NSTEMI
| Feature | STEMI | NSTEMI |
|---|---|---|
| ECG pattern | Persistent ST elevation or recognized equivalent pattern | No persistent diagnostic ST elevation |
| Coronary obstruction | Often acute complete or near-complete occlusion | Frequently incomplete, intermittent, or downstream obstruction, although mechanisms vary |
| Myocardial necrosis | Present | Present |
| Cardiac troponin | Elevated with myocardial injury | Elevated with myocardial injury |
Subendocardial Myocardium
The subendocardium is particularly vulnerable to ischemia because it experiences substantial intramural pressure during ventricular contraction and lies furthest from epicardial coronary blood supply.
Ischemic injury often begins in this region when coronary perfusion becomes critically reduced.
Transmural Infarction
With prolonged severe coronary occlusion, necrosis can extend from the subendocardium toward the epicardial surface.
When injury involves most or all of the thickness of the ventricular wall in a vascular territory, it is described morphologically as a transmural infarction.
Wavefront of Necrosis
Myocardial necrosis following severe coronary occlusion develops progressively over time rather than occurring throughout the entire threatened territory at once.
Irreversible injury generally begins in the subendocardium and advances outward toward the epicardium if adequate blood flow is not restored.
Importance of Reperfusion
Restoration of coronary blood flow can salvage myocardium that is ischemic but not yet irreversibly injured.
For acute coronary occlusion, the amount of myocardium preserved is strongly influenced by how rapidly effective reperfusion is achieved.
Infarct Size
The extent of myocardial necrosis depends on several anatomical and physiological factors.
- Location of coronary obstruction
- Duration and completeness of obstruction
- Size of the vascular territory
- Presence of collateral circulation
- Myocardial oxygen demand
- Timing and effectiveness of reperfusion
Anterior Myocardial Infarction
An anterior infarction commonly results from obstruction of the LAD or one of its major branches.
The affected territory may include the anterior left ventricular wall, apex, and anterior interventricular septum.
Inferior Myocardial Infarction
An inferior myocardial infarction commonly involves the inferior wall of the left ventricle.
In right-dominant circulation it is frequently associated with RCA obstruction, although circumflex occlusion can produce an inferior infarction in other coronary anatomical patterns.
Lateral Myocardial Infarction
Lateral left ventricular infarction may result from obstruction of circumflex branches, diagonal branches of the LAD, or other vessels supplying the lateral wall.
Posterior Myocardial Infarction
Infarction of the posterior region of the left ventricle can occur with obstruction of vessels supplying the posterior myocardial territory.
The responsible artery depends on coronary dominance and individual branching patterns.
Right Ventricular Infarction
Right ventricular infarction commonly accompanies some inferior infarctions, particularly when a proximal RCA obstruction compromises branches supplying the right ventricle.
Significant right ventricular dysfunction can reduce left ventricular preload and systemic cardiac output.
Coronary Artery and Typical Territory
| Artery | Common Myocardial Territory |
|---|---|
| LAD | Anterior left ventricle, apex and anterior interventricular septum |
| Circumflex artery | Lateral and posterolateral left ventricle, depending on anatomy |
| RCA | Right ventricle and inferior left ventricle in common right-dominant anatomy |
| Posterior interventricular artery | Inferior and posterior septal territories |
Electrocardiographic Changes
The electrocardiogram is central to the initial evaluation of suspected acute myocardial infarction.
Ischemia and myocardial injury can alter ventricular depolarization and repolarization, producing changes in the ST segment, T waves, and sometimes QRS complexes.
ST-Segment Elevation
Acute transmural ischemic injury can produce ST-segment elevation in ECG leads facing the affected myocardial territory.
The distribution of ST changes can help localize the region of acute ischemia.
ST-Segment Depression
ST-segment depression can occur with subendocardial ischemia or as a reciprocal change in leads electrically opposite a region of ST elevation.
T-Wave Changes
Myocardial ischemia can alter ventricular repolarization and produce changes in T-wave morphology.
T-wave inversion may occur during the evolution of an ischemic event.
Pathological Q Waves
Some infarctions produce pathological Q waves as electrical forces change following loss of electrically active myocardium.
Not every myocardial infarction produces persistent Q waves.
ECG Territories
| Territory | Commonly Relevant Leads |
|---|---|
| Septal | V1 to V2 |
| Anterior | V3 to V4 |
| Lateral | I, aVL, V5 to V6 |
| Inferior | II, III, aVF |
Cardiac Biomarkers
Injury to cardiomyocytes releases intracellular proteins into the circulation.
Measurement of cardiac biomarkers, particularly cardiac troponin, is fundamental to detecting myocardial injury.
Cardiac Troponin
Cardiac troponin I and cardiac troponin T are highly sensitive markers of myocardial injury.
A rise and/or fall in cardiac troponin with at least one value above the relevant upper reference limit supports acute myocardial injury, while the diagnosis of myocardial infarction additionally requires evidence that the injury is ischemic in origin.
Creatine Kinase-MB
Creatine kinase-MB (CK-MB) was historically used extensively in the diagnosis of myocardial infarction.
Cardiac troponin has largely replaced CK-MB as the preferred biomarker because of its greater cardiac specificity and sensitivity.
Symptoms
Clinical presentation varies substantially. Typical myocardial ischemic symptoms can include central chest pressure, heaviness, squeezing, or discomfort.
Symptoms may radiate to the arm, shoulder, neck, jaw, back, or epigastric region.
Associated Symptoms
- Shortness of breath
- Diaphoresis
- Nausea or vomiting
- Weakness
- Lightheadedness
- Palpitations
- Syncope in some cases
Silent and Atypical Presentations
Not all myocardial infarctions cause classic chest discomfort.
Older adults, people with diabetes, and other patients may present with dyspnea, weakness, nausea, altered mental status, or relatively subtle symptoms.
Immediate Functional Consequences
Ischemic myocardium rapidly loses contractile function.
Depending on infarct size and location, this can reduce stroke volume and ejection fraction and increase ventricular filling pressures.
Regional Wall Motion Abnormalities
Myocardial regions affected by ischemia or infarction may contract weakly or fail to contract.
Echocardiography can demonstrate these regional wall motion abnormalities and help assess overall ventricular function.
Ventricular Remodeling
After myocardial infarction, the ventricle can undergo changes in size, shape, wall thickness, and tissue composition.
This process, called ventricular remodeling, can influence long-term ventricular function and the development of heart failure.
Infarct Healing
Necrotic myocardium triggers an inflammatory response that removes dead tissue.
Granulation tissue subsequently develops, followed by deposition of collagen and formation of a fibrous scar.
Scar Tissue
Cardiac muscle lost through infarction is not replaced by normal contractile myocardium in the adult heart.
The healed infarct is therefore largely composed of noncontractile fibrous scar tissue.
Complications of Myocardial Infarction
Complications can result from electrical instability, loss of contractile myocardium, mechanical disruption, inflammation, or thrombosis.
Arrhythmias
Ischemic and injured myocardium has abnormal electrical properties.
Myocardial infarction can therefore produce atrial or ventricular arrhythmias, conduction blocks, ventricular tachycardia, or ventricular fibrillation.
Heart Failure
Loss of functioning ventricular myocardium can reduce cardiac output and elevate filling pressures.
Large infarctions or infarctions occurring in an already impaired heart can produce acute or chronic heart failure.
Cardiogenic Shock
Cardiogenic shock occurs when cardiac pump failure becomes severe enough to cause inadequate systemic perfusion.
Extensive left ventricular injury is an important cause, although mechanical complications and right ventricular infarction can also produce severe hemodynamic compromise.
Papillary Muscle Dysfunction
Ischemia or infarction involving a papillary muscle can interfere with normal mitral valve support.
This can cause or worsen mitral regurgitation.
Papillary Muscle Rupture
Mechanical rupture of a papillary muscle is an uncommon but severe complication of myocardial infarction.
Loss of chordal support can produce abrupt severe mitral regurgitation and acute pulmonary edema or cardiogenic shock.
Ventricular Septal Rupture
Infarcted tissue within the interventricular septum can rupture during the period when necrotic myocardium is structurally weakened.
This creates an acute ventricular septal defect and a left-to-right intracardiac shunt.
Free Wall Rupture
Rupture of an infarcted ventricular free wall can allow blood to enter the pericardial cavity.
Rapid accumulation of blood can cause hemopericardium and cardiac tamponade.
Pericarditis
Inflammation involving the pericardium can occur after a transmural myocardial infarction extends to the epicardial surface.
A later immune-mediated pericardial syndrome can also occur after myocardial injury.
Left Ventricular Aneurysm
A healed transmural infarction can produce a thinned, scarred ventricular wall that bulges outward during systole.
A chronic ventricular aneurysm can contribute to heart failure, arrhythmias, and mural thrombus formation.
Mural Thrombus
Abnormal wall motion and damaged endocardial surfaces can promote thrombus formation within the ventricle.
Fragments of a left ventricular mural thrombus can enter the systemic circulation and cause arterial embolism.
Recurrent Ischemia
Patients with myocardial infarction may have residual atherosclerotic disease or unstable coronary lesions.
Recurrent ischemia or reinfarction can produce additional myocardial damage.
Major Complications
| Complication | Mechanism or Effect |
|---|---|
| Arrhythmias | Electrical instability in ischemic or scarred myocardium |
| Heart failure | Loss of contractile myocardium |
| Cardiogenic shock | Severe reduction in effective cardiac output |
| Papillary muscle rupture | Acute severe mitral regurgitation |
| Septal rupture | Acute ventricular septal defect |
| Free wall rupture | Hemopericardium and cardiac tamponade |
| Ventricular aneurysm | Scarred and remodeled ventricular wall |
| Mural thrombus | Risk of systemic embolization |
Diagnosis
Diagnosis of acute myocardial infarction integrates the clinical presentation, electrocardiographic findings, cardiac biomarkers, and, when appropriate, cardiac imaging or direct assessment of the coronary arteries.
Echocardiography
Echocardiography can assess regional and global ventricular function, chamber size, ejection fraction, valve function, and mechanical complications.
It is particularly useful when hemodynamic deterioration raises concern for acute structural complications.
Coronary Angiography
Coronary angiography visualizes the coronary arterial lumen using contrast material.
It can identify obstructive lesions and acute coronary occlusion and can be followed immediately by catheter-based intervention when appropriate.
Reperfusion Therapy
The central goal in an acute coronary occlusion is restoration of blood flow before additional myocardium becomes irreversibly injured.
Reperfusion can be achieved with percutaneous coronary intervention or, in selected circumstances, fibrinolytic therapy.
Percutaneous Coronary Intervention
Percutaneous coronary intervention (PCI) uses catheter-based techniques to restore flow through an obstructed coronary artery.
Balloon dilation and placement of an intracoronary stent are commonly used to reopen and maintain the affected vessel.
Fibrinolytic Therapy
Fibrinolytic medications promote breakdown of fibrin within thrombi.
They may be used in selected patients with acute STEMI when timely primary PCI is not available and contraindications are absent.
Antiplatelet Therapy
Platelet activation is central to coronary thrombosis after atherosclerotic plaque disruption.
Antiplatelet medications reduce platelet-mediated thrombus formation and are important components of treatment for acute coronary syndromes.
Anticoagulation
Anticoagulant medications reduce activity of the coagulation cascade.
They are used in selected acute coronary syndrome settings to limit propagation of thrombosis.
Secondary Prevention
After myocardial infarction, long-term management aims to reduce recurrent ischemic events, limit ventricular remodeling, manage cardiovascular risk factors, and treat residual coronary disease.
Strategies may include lipid lowering, blood pressure control, smoking cessation, physical rehabilitation, antithrombotic therapy, and medications selected according to ventricular function and clinical circumstances.
Key Features of Myocardial Infarction
| Feature | Key Point |
|---|---|
| Definition | Myocardial necrosis caused by ischemia |
| Most common mechanism | Atherosclerotic plaque disruption with coronary thrombosis |
| Most vulnerable myocardial region | Subendocardium |
| Major biomarker | Cardiac troponin |
| Primary electrical test | Electrocardiogram |
| Common culprit vessels | LAD, RCA and circumflex artery |
| Major immediate goal in coronary occlusion | Rapid restoration of coronary blood flow |
| Important complications | Arrhythmias, heart failure, shock and mechanical rupture |
Anatomical and Physiological Importance
Myocardial infarction demonstrates the direct relationship between coronary anatomy and cardiac function. Obstruction of a coronary artery deprives its downstream myocardial territory of oxygen, and the location of the obstruction determines which ventricular walls, septal regions, papillary muscles, or conduction tissues are placed at risk.
Because irreversible injury progresses over time from the most vulnerable subendocardial regions toward more superficial myocardium, rapid restoration of coronary flow can substantially reduce the amount of myocardium that ultimately becomes necrotic.
The consequences extend beyond loss of contractile tissue. Infarction can disrupt electrical conduction, alter ventricular geometry, damage valve-supporting structures, weaken the ventricular wall, and create scar tissue that affects long-term mechanical and electrical function of the heart.
Published on September 29, 2026
Last updated on September 29, 2026
Last updated on September 29, 2026