Myocardial infarction

Article written and reviewed by Dr Luca Moretti

Myocardial infarction is ischemic necrosis of part of the myocardium. It is not defined by pain alone, a single electrocardiographic abnormality, or an elevated troponin value, but by integration of acute myocardial injury with evidence demonstrating its ischemic nature; this distinction is essential because numerous diseases cause troponin release without infarction.
The Fifth Universal Definition distinguishes myocardial injury from infarction. Injury is present when at least one cardiac troponin value exceeds the sex-specific 99th percentile of the upper reference limit; it is acute when there is a rise or fall. Myocardial infarction additionally requires symptoms, ECG findings, imaging, or coronary findings demonstrating acute ischemia.

Myocardial infarction is classified by clinical context and etiological mechanism as primary, secondary, or procedure-related. Primary infarction occurs spontaneously because of acute coronary pathology; secondary infarction results from a supply-demand imbalance caused by another acute condition; procedure-related infarction results from a complication of a percutaneous or surgical cardiac procedure within 30 days.
The classification into STEMI and NSTEMI, by contrast, describes the electrocardiographic presentation and guides the urgent strategy. It does not coincide with the universal types and is not a direct measure of transmurality. An early-reperfused STEMI may produce limited necrosis, whereas an NSTEMI may be extensive or result from an unrecognized occlusion.

Myocardial infarction remains a leading global cause of mortality, heart failure, and disability. Estimates change with troponin thresholds, population aging, and access to care. In systems with primary PCI, acute mortality has decreased, but the post-infarction burden includes recurrence, ischemic cardiomyopathy, arrhythmias, functional loss, and the need for lifelong therapy.
Final injury depends on ischemia duration, the mass at risk, collateral circulation, metabolic demand, and the microcirculation. Early reperfusion limits the wavefront of necrosis, but epicardial patency does not guarantee capillary perfusion. Edema, microembolization, no-reflow, and intramyocardial hemorrhage may reduce salvage.

Myocardial infarction is therefore not a single uniform disease but a pathological outcome shared by different mechanisms. The clinical objective is to identify rapidly an occlusion requiring reperfusion, document the diagnostic criteria, assign the correct clinical category, and treat both the cause and the consequences for the myocardium and the patient as a whole.

Etiology, risk factors, pathogenesis, and pathophysiology

In primary atherothrombotic myocardial infarction, an atherosclerotic plaque is complicated by rupture, erosion, or a calcified nodule and triggers intraluminal thrombosis. Platelets, thrombin, and fibrin abruptly reduce flow. Occlusion may be complete, partial, or intermittent and produce STEMI or NSTEMI according to territory, collateral circulation, and dynamics.
Plaque rupture exposes the necrotic core and tissue factor through a disrupted cap. It is favored by lipid burden, inflammation, and local mechanical stress, but not every plaque with high-risk features ruptures. Clinical risk depends on the interaction between the lesion and the systemic thrombotic state.

In erosion, the endothelial surface is lost without evident cap rupture. Thrombus adheres to a matrix rich in proteoglycans and smooth-muscle cells. Disturbed flow, innate immunity, and neutrophils are involved, but the OCT diagnosis remains an operational in vivo definition.
Secondary myocardial infarction occurs when another acute condition causes an imbalance between oxygen supply and demand in the absence of primary acute coronary pathology. Coronary artery disease may be present and lower the ischemic threshold but is not by itself the immediate mechanism. The precipitating factor must be identified and corrected.

Among conditions that may cause secondary infarction, severe anemia reduces arterial oxygen content, hypoxemia lowers oxygen saturation, hypotension and shock reduce perfusion pressure, while tachyarrhythmias shorten diastole and increase myocardial oxygen consumption.
Severe hypertension may increase demand, wall stress, and afterload, particularly in the presence of ventricular hypertrophy. Severe bradyarrhythmia may reduce cardiac output. Spasm, dissection, and embolism are instead acute coronary pathologies and, when they cause infarction, fall under primary myocardial infarction.

The type 3 category has been removed from the Fifth Universal Definition. In sudden death in which myocardial infarction is a plausible cause, the event is classified as primary, secondary, or procedure-related according to the clinical context and any post-mortem findings; if assessment is insufficient, the etiology may remain uncertain.
Procedure-related myocardial infarction is considered when a coronary complication occurs within 30 days of a percutaneous or surgical cardiac procedure and acute myocardial injury is accompanied by clinical or electrocardiographic evidence of ischemia. Diagnosis does not depend on a single fixed troponin threshold and requires confirmation by evidence of the coronary complication and/or cardiac imaging according to the procedural context.

Stent thrombosis may cause procedure-related myocardial infarction when it occurs as a complication within 30 days of the procedure; after 30 days it is classified as acute coronary pathology responsible for primary myocardial infarction. Event timing and intravascular imaging help define the correctable mechanism.
Restenosis or recoil may cause procedure-related myocardial infarction if it constitutes a complication within 30 days; after 30 days, restenosis responsible for acute coronary pathology falls under primary myocardial infarction. Asymptomatic restenosis alone is not myocardial infarction.

Procedure-related myocardial infarction after CABG is diagnosed when a complication of cardiac surgery within 30 days causes acute myocardial injury and the clinical, electrocardiographic, angiographic, and imaging criteria of the Fifth Universal Definition are met. A fixed diagnostic troponin threshold of 10 times the 99th percentile is not required.
Procedural injury is not synonymous with procedure-related myocardial infarction. An isolated troponin rise after a procedure documents cardiomyocyte injury, but the Fifth Universal Definition does not use a single fixed diagnostic threshold: a procedural complication and/or new ischemic imaging findings are required according to the clinical context.

Whatever the mechanism, ischemia reduces oxidative phosphorylation, depletes ATP, and shifts metabolism toward anaerobic glycolysis with accumulation of lactate and protons. Ion pumps lose efficiency, intracellular sodium and calcium increase, and contractility ceases rapidly.
Calcium overload, reactive radicals, and mitochondrial dysfunction promote hypercontracture, opening of mitochondrial pores, and cell death. Loss of sarcolemmal integrity allows structural proteins, including cardiac troponins, to enter the circulation.

In persistent coronary occlusion, necrosis progresses as a wavefront from the subendocardium toward the subepicardium over hours of ischemia. The subendocardium has greater relative consumption, intramural pressure, and dependence on diastolic perfusion. Collateral circulation and intermittent reperfusion slow progression.
The area at risk is the territory dependent on the compromised vessel; final infarct size is the portion that is not salvaged. Proximal occlusion, poor collateral circulation, and prolonged duration increase necrosis. Peak biomarker levels provide an imperfect estimate and also depend on reperfusion.

Reperfusion limits infarction but induces changes termed reperfusion injury. Radicals, inflammation, calcium, and mitochondrial pore opening may kill already critically injured cells. There is nevertheless no clinical justification for delaying reperfusion to avoid this component.
The microcirculation may remain obstructed by emboli, edema, endothelial injury, cellular aggregates, and vasoconstriction. Intramyocardial hemorrhage results from severe capillary destruction; these phenomena explain part of the prognostic variability despite equally restored epicardial flow.

The inflammatory response removes dead cells through neutrophils and macrophages. It is necessary for healing, but an excessive response extends matrix degradation and promotes remodeling. Fibroblasts and myofibroblasts subsequently deposit collagen and form the scar.
Activation of the sympathetic and renin-angiotensin-aldosterone systems initially supports pressure and output but increases consumption, afterload, and retention. Persistent neurohormonal activation promotes dilation, fibrosis, and heart failure and is a therapeutic target in patients with ventricular dysfunction.

Risk factors for primary atherothrombotic myocardial infarction reflect atherosclerosis: elevated apoB and LDL, Lp(a), smoking, hypertension, diabetes, kidney disease, age, and genetics. Risk of secondary infarction also depends on the likelihood of developing systemic precipitants and on available coronary and myocardial reserve.
Microvascular dysfunction may reduce reserve and contribute to infarction with nonobstructive coronary arteries. Prolonged epicardial or microvascular vasospasm causes severe ischemia. Etiological diagnosis often requires CMR, intracoronary imaging, and selected functional tests.

MINOCA currently denotes a working diagnosis of myocardial injury with nonobstructive coronary arteries. Nonobstructive plaque, dissection, embolism, and spasm may lead to a final diagnosis of primary myocardial infarction, while myocarditis and Takotsubo syndrome are frequent alternative causes of myocardial injury. The term remains a working diagnosis until the cause is defined.
Perioperative myocardial infarction may result from atherothrombosis, supply-demand imbalance, or procedural complications. Analgesia and sedation may obscure symptoms, making ECG and troponin important in selected high-risk patients. Classification must be based on the mechanism, not on the surgical context alone.

The pathophysiological consequence integrates contractile loss, diastolic stiffness, electrical instability, and the systemic response. When the necrotic mass exceeds compensatory capacity, low output develops; increased filling pressures produce congestion; electrical heterogeneity generates arrhythmias, and tissue fragility prepares the way for rupture.

Pathological anatomy, classification, and evolution

During the first minutes of ischemia, glycogen loss, myofibrillar relaxation, and sarcolemmal changes appear and are visible only ultrastructurally. Mitochondrial changes occur early, while macroscopic necrosis requires time and may not be evident in very rapid deaths.
Coagulative necrosis becomes histologically recognizable through hypereosinophilia and loss of nuclei and striations. Neutrophils infiltrate tissue early, followed by macrophages that remove debris. The chronology varies with reperfusion, duration, and survival.

Contraction-band necrosis is associated mainly with reperfusion and calcium overload. Cardiomyocytes show transverse eosinophilic bands from hypercontracture. The finding alone does not establish the clinical cause of infarction.
Infarction may be subendocardial, involving the inner layers without extending through the full thickness, or transmural in part of the wall. This dichotomy does not correspond rigidly to NSTEMI and STEMI, particularly in the era of early reperfusion.

An anteroseptal infarction often involves the left anterior descending territory; an inferior infarction more often depends on the right coronary artery; a lateral infarction on the circumflex or diagonal branches. Dominance, branches, and collateral circulation make the correspondence variable.
Posterior infarction involves the inferobasal wall and may be electrically hidden on the standard 12-lead ECG. CMR describes the true distribution more precisely than historical electrocardiographic terminology and quantifies transmurality.

The universal classification into primary, secondary, or procedure-related myocardial infarction must be distinguished from STEMI/NSTEMI classification, anatomical location, and size. A complete description may therefore simultaneously include the clinical category, mechanism, ECG pattern, territory, complications, and mode of reperfusion.
Primary myocardial infarction may be STEMI or NSTEMI and includes all spontaneous acute coronary pathologies, including atherothrombosis, spontaneous coronary artery dissection, embolism, and vasospasm. Absence of a visible thrombus does not exclude an atherothrombotic cause because the thrombus may lyse or be removed. Diagnosis integrates all available data.

Secondary myocardial infarction is not a residual diagnosis for any troponin elevation. It is considered when another acute condition causes supply-demand imbalance with acute myocardial injury and signs of ischemia; when coronary or cardiac imaging is feasible, the diagnosis is confirmed by obstructive coronary disease without acute coronary pathology and/or a new regional abnormality or loss of viable myocardium of ischemic origin. If ischemia is absent, the correct classification is myocardial injury.
The type 3 category is no longer used. In sudden deaths, myocardial infarction is assessed from the clinical history, ECG when available, and post-mortem findings, assigning a primary, secondary, or procedure-related classification when the mechanism can be defined; without sufficient evidence, the diagnosis remains uncertain.

Procedure-related myocardial infarction is not defined by fixed troponin thresholds because coronary procedures and surgery frequently cause myocardial injury. Diagnosis requires that the infarction result from a complication of a cardiac procedure within 30 days and be confirmed by evidence of the coronary complication and/or ischemic imaging according to the context. Distinction from isolated procedural injury is important for prognosis, quality assessment, and comparability of studies.
A new infarction during the first weeks after the index event must be classified by its mechanism as primary, secondary, or procedure-related, without a separate diagnostic category based on a 28-day threshold. If troponin remains elevated but stable or falling, a new rise in values, together with ischemic criteria, supports a new infarction.

Silent or unrecognized myocardial infarction may be suspected in the presence of new pathological Q waves and should be confirmed, when available, by imaging of an ischemic scar in the absence of a nonischemic cause. The absence of recalled symptoms does not prove that the event was truly asymptomatic.
During the first days, necrotic tissue is degraded and the wall reaches a phase of maximum fragility; this explains the classic timing of mechanical ruptures. Early reperfusion has reduced their incidence but has not eliminated them.

Infarct expansion is dilation and thinning of the infarcted region without new necrosis. It may begin early and increases stress on noninfarcted myocardium. Extensive anterior infarctions are particularly predisposed.
Ventricular remodeling comprises changes in the shape, volume, and function of the entire ventricle. Neurohormonal activation, wall stress, and matrix loss promote dilation. Reperfusion, ACE inhibition, and heart-failure therapy modify its natural history.

The collagen scar matures over the following weeks and replaces contractile tissue. It does not recover function but stabilizes the wall. The distribution of fibrosis creates electrically heterogeneous borders that may sustain re-entrant ventricular tachycardia.
Stunned myocardium is reversible dysfunction of reperfused but viable tissue. It may make initial function appear severely impaired and recover gradually. Serial assessment prevents premature definitive decisions based on a single echocardiogram.

Myocardial edema shown by CMR contributes to wall swelling and defines the acutely involved territory, but quantification of the area at risk is sensitive to timing. Late enhancement identifies necrosis and fibrosis according to gadolinium distribution.
Microvascular obstruction appears as a hypoenhancing core within late enhancement and indicates absent capillary perfusion. Intramyocardial hemorrhage may be detected with iron-sensitive sequences. Both are associated with an unfavorable prognosis.

An anterior apical infarction with akinesia promotes blood stasis and ventricular thrombus. The damaged endocardial component and hypercoagulability complete the thrombotic triad. Embolic risk depends on thrombus morphology, mobility, and persistence.
A true aneurysm is a scarred dilation containing wall layers, with a low risk of late rupture but possible heart failure, arrhythmias, and thrombus. A pseudoaneurysm is a contained rupture and has different surgical implications.

Papillary muscle scarring and remodeling may cause chronic ischemic mitral regurgitation. The mechanism is often leaflet tethering caused by papillary muscle displacement, not primary valve disease. Severity may change with loading and exercise.
Repeated infarctions cause cumulative myocardial loss and ischemic cardiomyopathy. Even small events may have a major impact if they affect critical residual territory or conduction. Prevention of recurrence is therefore part of preserving function.

Anatomical evolution must be correlated with the clinical presentation. Troponin, ECG, echocardiography, and CMR measure different aspects: cellular injury, electrical activity, mechanics, and tissue. No single test alone describes extent, age, mechanism, and prognosis.

Clinical manifestations

The history must reconstruct ischemic onset, including time, duration, course, and associated symptoms. Abrupt-onset persistent pain suggests occlusion, but prodromal episodes may precede the event. The time of the last definitely asymptomatic period is useful when onset is unclear.
The classic symptom is intense or uncomfortable retrosternal pressure, often radiating to the left or right arm, shoulders, jaw, neck, back, or epigastrium. The patient may describe it as a weight, squeezing, or burning. The term pain must not be interpreted narrowly.

Duration is usually longer than in stable angina, and rest does not ensure relief. A persistent character increases suspicion, but intermittent occlusion may generate fluctuating episodes. Intensity does not predict the extent of necrosis.
Dyspnea may accompany or replace pain, particularly in older patients and those with diabetes. It may result from ventricular dysfunction, increased filling pressures, mitral regurgitation, or arrhythmia. Hypoxemia also requires consideration of pulmonary causes.

Sweating, pallor, nausea, and vomiting indicate autonomic activation and are common in inferior infarction. Vagal hyperactivity may cause bradycardia and hypotension. Vomiting may reduce absorption of oral drugs during the most critical phase.
Syncope and presyncope suggest hemodynamic instability, arrhythmia, or a conduction disorder. Cardiac arrest from ventricular fibrillation may be the first manifestation of infarction. Resuscitation must not await etiological diagnosis.

Myocardial infarction may be silent or paucisymptomatic, particularly in diabetes, advanced age, and autonomic neuropathy. It may later be discovered through Q waves, an imaging scar, or complications. Not every ischemic scar, however, establishes the date of the event.
Women may report typical pain together with dyspnea, nausea, fatigue, or multiple symptoms. Use of the label atypical may contribute to underdiagnosis. Assessment must be based on overall probability rather than rigid male models.

In secondary myocardial infarction, symptoms of the precipitant may predominate: fever and hypotension in sepsis, dyspnea in hypoxemia, palpitations in tachyarrhythmia, and bleeding in anemia. Evidence of ischemia must be distinguished from manifestations of the systemic disease.
Procedure-related myocardial infarction may present during or after PCI with pain, ST-segment changes, side-branch loss, or no-reflow. Sedation and analgesia may attenuate symptoms. The angiographic complication and imaging therefore assume particular importance.

In procedure-related myocardial infarction after cardiac surgery, pain and ECG findings are difficult to interpret after sternotomy and anesthesia. Instability, new Q waves, graft loss, new regional dysfunction, and the troponin course point toward perioperative myocardial infarction, distinct from expected surgical injury.
On examination, the first assessment concerns vital status, consciousness, breathing, pulse, blood pressure, oxygen saturation, perfusion, and temperature. Treatment of cardiac arrest, pulmonary edema, or shock proceeds in parallel. Apparently normal blood pressure does not exclude compensated hypoperfusion.

Cold skin, delayed capillary refill, oliguria, and confusion indicate low output. Tachycardia may be compensatory or arrhythmic. Lactate complements but does not replace clinical signs of hypoperfusion.
A third heart sound, crackles, and increased jugular venous pressure indicate congestion. Killip class retains prognostic value. Sudden pulmonary edema disproportionate to apparent function should raise suspicion of acute mitral regurgitation.

Hypotension, distended jugular veins, and relatively clear lung fields suggest right ventricular infarction. Kussmaul sign may be present. Echocardiography distinguishes right ventricular dysfunction, tamponade, and pulmonary embolism.
A new holosystolic murmur after infarction may result from a septal defect or acute mitral regurgitation. Location is not always reliable, and the murmur may be faint in shock. Any sudden deterioration requires immediate echocardiography.

A pericardial friction rub and pleuritic pain may occur with post-infarction pericarditis. Pain varies with position and breathing, but clinical overlap is possible. A new effusion requires exclusion of contained rupture.
Inferior infarction may produce transient nodal block, whereas anterior infarction may cause bundle branch or infranodal atrioventricular blocks associated with extensive necrosis. Rate and hemodynamic stability determine the need for pacing.

Premature beats are frequent, but ventricular tachycardia and fibrillation indicate electrical instability. Early arrhythmias related to ischemia have a different significance from late scar-related arrhythmias. Time of onset must be documented.
A neurological deficit may result from embolism, hypoperfusion, or treatment-related hemorrhage. Concomitant chest pain and neurological deficit should also raise concern for aortic dissection. Fibrinolysis is dangerous if this diagnosis is not excluded.

In a young patient without traditional risk factors, a history of the puerperium, intense stress, connective-tissue disease, or arteriopathy points toward spontaneous dissection. Atrial fibrillation, valve disease, and endocarditis instead suggest coronary embolism.
Recurrence of pain after PCI may indicate acute thrombosis, dissection, spasm, or simple vessel stretch. New ST-segment changes and instability require immediate reassessment. Attribution to benign procedural pain must be cautious.

During the following days, hypotension, recurrent pain, fever, and respiratory deterioration must be interpreted in relation to timing. The phase of myocardial fragility predisposes to rupture, while infections and iatrogenic complications become progressively more likely.
Functional assessment includes mobilization, dyspnea, residual angina, and capacity for daily activities. Apparent stability at rest may conceal limited reserve. Rehabilitation enables safe progression and identifies persistent symptoms.

The psychological component includes fear of recurrence, depression, and post-traumatic symptoms, particularly after cardiac arrest or shock; these manifestations influence adherence, sleep, and return to activity and must be assessed as part of the post-infarction course.

Investigations and diagnosis

Diagnosis begins with an urgent ECG, repeated if the first tracing does not explain the symptoms. Persistent ST-segment elevation or an occlusion equivalent requires reperfusion without waiting for troponin. Posterior and right-sided leads complete the tracing when indicated.
High-sensitivity troponin is the biomarker of choice. A value above the sex-specific 99th percentile demonstrates injury, while a serial change indicates acuity. Thresholds and deltas are assay-dependent and must not be transferred between platforms.

The Fifth Universal Definition establishes official clinical criteria. An isolated elevated value is insufficient: acute ischemic injury is required. The context must be reconstructed before assigning the clinical category and etiological mechanism.

Fifth Universal Definition criteria for primary myocardial infarction

• Rise and/or fall in cardiac troponin with at least one value above the sex-specific 99th percentile of the upper reference limit.
• Presence of at least one of the following: symptoms of acute myocardial ischemia, new or presumably new ischemic ECG changes, or development of pathological Q waves; the diagnosis is confirmed by identification of acute coronary pathology or a new or presumably new regional abnormality and/or loss of viable myocardium with an ischemic pattern.

Secondary myocardial infarction is considered when another acute condition causes a supply-demand imbalance associated with acute myocardial injury and symptoms or electrocardiographic signs of ischemia. When coronary or cardiac imaging is feasible, the diagnosis is confirmed by obstructive coronary disease without acute coronary pathology and/or a new regional abnormality or loss of viable myocardium with an ischemic pattern.

Fifth Universal Definition criteria for secondary myocardial infarction

• Rise and/or fall in cardiac troponin with at least one value above the sex-specific 99th percentile of the upper reference limit.
• Presence of an alternative acute condition causing an imbalance between myocardial oxygen supply and demand, with symptoms of ischemia, new or presumably new ischemic ECG changes, or development of pathological Q waves.
• When coronary or cardiac imaging is feasible and appropriate, confirmation by obstructive coronary artery disease without acute coronary pathology or by a new or presumably new regional abnormality or loss of viable myocardium with an ischemic pattern.

If troponin is elevated but not dynamic, injury may be chronic. If it is dynamic without ischemia, the condition is acute nonischemic myocardial injury; this distinction avoids overdiagnosis in patients with sepsis, heart failure, pulmonary embolism, kidney failure, or myocarditis.
The type 3 category has been removed. After sudden death, myocardial infarction is assessed using clinical data and, when available, ECG, post-mortem imaging, or autopsy; final classification is primary, secondary, or procedure-related when the mechanism can be defined.

In procedure-related myocardial infarction, diagnosis is not based on a fixed troponin threshold. Within 30 days of a cardiac procedure, when a coronary complication is suspected and acute myocardial injury is accompanied by clinical or electrocardiographic evidence of ischemia, confirmation requires angiographic evidence of the complication and/or a new regional abnormality or loss of viable myocardium with an ischemic pattern according to the timing and context of the procedure.
Stent thrombosis, early restenosis, or recoil may constitute procedure-related myocardial infarction if they occur as a complication within 30 days; after 30 days, stent thrombosis or restenosis responsible for the event falls under primary myocardial infarction. Coronary angiography and intravascular imaging are fundamental.

After CABG, procedure-related myocardial infarction is defined by the same principles applied to percutaneous procedures and does not require a fixed diagnostic troponin threshold. Diagnosis is confirmed by evidence of the surgical complication and/or a new regional abnormality or loss of viable myocardium with an ischemic pattern according to the procedural context.
The ECG distinguishes urgency and location. Regional ST-segment elevation suggests acute occlusion, but pericarditis, early repolarization, hypertrophy, and aneurysm may mimic it. Bundle branch blocks and pacing require specific criteria and comparison with previous tracings.

Pathological Q waves may document previous necrosis or evolution of the event, but early reperfusion may prevent their development. Electrical normalization does not eliminate the scar, while Q waves do not always equal complete transmurality.
Echocardiography looks for new regional abnormalities, global function, right ventricular infarction, mitral regurgitation, septal defect, effusion, and thrombus. A pre-existing finding may confound interpretation, so comparison with previous examinations is valuable.

Coronary angiography documents occlusion, thrombus, dissection, embolism, and residual anatomy. A patent artery does not exclude a previously lysed thrombus. OCT and IVUS may demonstrate a complicated plaque or occult dissection and improve PCI optimization.
CMR distinguishes a subendocardial or transmural ischemic pattern from nonischemic myocarditis patterns and identifies Takotsubo syndrome, edema, microvascular obstruction, and thrombus. It is particularly important in MINOCA and unexplained troponin elevation.

Coronary CT may exclude significant coronary artery disease in selected low- or intermediate-risk patients but does not replace coronary angiography in instability or high probability. CCTA must not delay reperfusion of an evident occlusion.
Complete blood count, kidney function, glucose, electrolytes, coagulation, and lipid profile define precipitants, safety, and prevention. Anemia must be quantified and its cause investigated; creatinine and weight are required for anticoagulant dosing.

The differential diagnosis of primary myocardial infarction includes myocarditis, Takotsubo syndrome, pulmonary embolism, aortic dissection, and injury from sepsis or heart failure. The finding that best protects against error is coherence among the biomarker, ischemia, and mechanism, not troponin alone.
When secondary myocardial infarction is suspected, it must be established whether the physiological imbalance is sufficient to cause ischemia and whether coronary disease is present. Modest tachycardia with elevated troponin does not prove causality. Severity, duration, and temporal relationship must be plausible.

MINOCA denotes a working diagnosis of myocardial injury with nonobstructive coronary arteries, meaning no stenosis of 50% or greater. It does not require myocardial infarction to have already been confirmed and is not a final diagnosis. Etiological investigation combines early CMR, angiographic review, intracoronary imaging, and selected vasomotor testing.
For an early new infarction, when troponin is stable or falling, renewed growth in values together with ischemic evidence supports the diagnosis. If values continue to rise from the initial event, the biochemical dynamic alone is insufficient.

A previous unrecognized infarction may be suspected from pathological Q waves in the absence of a nonischemic cause and should be confirmed, when available, by imaging showing loss of viable myocardium with an ischemic pattern; it may also be established by pathological findings. Dating a chronic scar by ECG alone is imprecise.
Prognostic quantification uses Killip class, ejection fraction, kidney function, shock, and validated scores. CMR infarct size and microvascular obstruction add information but are not required in every patient for initial diagnosis.

The final diagnosis must report the clinical category, mechanism, ECG pattern, location, vessel, procedure, and complications. Writing only infarction loses decisive information and may lead to inappropriate treatment. Classification may be updated when new examinations clarify the mechanism.

Treatment and prognosis

The first decision is to recognize a time-dependent occlusion. In STEMI and occlusion equivalents, primary PCI must be performed rapidly; if it is unavailable within recommended times and onset is recent, fibrinolysis followed by transfer is the appropriate alternative.
In primary atherothrombotic NSTEMI, aspirin, a P2Y12 inhibitor, anticoagulation, and an invasive strategy are adapted to risk and anatomy. Hemodynamic instability, refractory ischemia, and arrhythmias require immediate angiography; in other cases timing follows risk stratification.

Radial access reduces bleeding and complications during PCI. Contemporary drug-eluting stents are the standard, while intravascular imaging guides treatment of complex lesions. Routine thrombus aspiration does not improve outcomes and remains a selective bailout measure.
In primary atherothrombotic myocardial infarction, default DAPT lasts 12 months if bleeding risk is not high, but it may be shortened or modified. Chronic anticoagulation, bleeding, age, kidney function, and stent complexity determine an individualized strategy.

Treatment of secondary myocardial infarction centers on the cause: control of tachyarrhythmia, treatment of hypoxemia and sepsis, correction of hypotension, and management of anemia or a hypertensive crisis. There is no evidence for automatically applying DAPT and anticoagulation as in primary atherothrombotic myocardial infarction.
The search for underlying coronary disease in secondary myocardial infarction depends on age, symptoms, ECG, function, and probability. Significant coronary disease may require prevention and, in selected cases, revascularization, but it does not prove that the event was atherothrombotic.

After cardiac arrest, resuscitation, defibrillation, and immediate treatment of the suspected cause take priority. After return of spontaneous circulation, persistent ST-segment elevation indicates urgent coronary angiography. Without ST-segment elevation, the strategy depends on instability and coronary probability.
Procedure-related myocardial infarction after PCI is treated by correcting the procedural complication: side-branch occlusion, dissection, no-reflow, thrombosis, or embolization. Intravascular imaging and selected intracoronary drugs guide the solution. Troponin elevation alone without an ischemic complication does not require repeat PCI.

In stent thrombosis, urgent revascularization restores flow and corrects underexpansion, malapposition, or dissection. Adherence and pharmacological response should be assessed in the clinical context. Imaging avoids treating only the thrombus while leaving the mechanical mechanism uncorrected.
In procedure-related myocardial infarction after CABG, the decision among surgical revision, PCI, and medical therapy depends on instability, the occluded vessel or graft, the territory at risk, and feasibility. Transesophageal echocardiography and coronary angiography may be urgently required.

Supportive therapy includes oxygen only for hypoxemia, nitrates when not contraindicated, and cautious analgesia. Morphine is reserved for refractory pain and may delay P2Y12 absorption. Symptomatic treatment must not divert time from reperfusion.
A high-intensity statin is started early in primary atherothrombotic myocardial infarction and atherosclerotic coronary disease. Ezetimibe and anti-PCSK9 or other nonstatin therapies are added according to LDL and risk. The lipid profile is rechecked after 4-8 weeks.

Smoking cessation requires counseling and treatment of dependence. Blood pressure, diabetes, weight, physical activity, and diet are addressed systematically. Prevention is not generic advice but part of causal treatment of atherosclerotic disease.
ACE inhibitors or ARBs are indicated especially with ventricular dysfunction, heart failure, hypertension, or diabetes. Beta-blockers have early and chronic roles in defined indications, while being avoided in shock, bradycardia, and unstabilized acute heart failure. Lifelong use is not identical in every phenotype.

Mineralocorticoid receptor antagonists are indicated after infarction with reduced ejection fraction associated with heart failure or diabetes, in the absence of hyperkalemia and severe kidney failure. Heart-failure therapy is then completed according to guidelines and tolerability.
Ventricular thrombus requires individualized anticoagulation and follow-up imaging, balanced against concomitant antiplatelet therapy. CMR is more sensitive than noncontrast echocardiography. Duration and regimen depend on resolution and embolic risk.

In shock, revascularization of the culprit vessel is urgent. Norepinephrine is generally preferred to support blood pressure, while inotropes and mechanical support depend on phenotype. Routine immediate multivessel PCI is avoided.
Mechanical complications require echocardiographic diagnosis and selected surgical or percutaneous correction. Vasopressors, ventilation, and support devices are bridges. Timing balances instability and tissue fragility, but medical treatment alone is inadequate.

Rehabilitation begins before discharge and integrates exercise, education, nutrition, smoking, mental health, and return to usual roles. It improves function and reduces new events. Home-based programs are an alternative when in-person programs are inaccessible.
Ejection fraction must be measured and, if reduced, reassessed after optimization and recovery. An implantable defibrillator for primary prevention is not decided from function during the first hours, except for secondary indications or arrhythmias not attributable to the reversible phase.

Prognosis of primary infarction depends mainly on infarct size, shock, cardiac arrest, ventricular function, and the possibility of causal treatment. Secondary myocardial infarction often carries high mortality because of comorbidities and the responsible illness, but its event profile and preventive strategy differ.
Elevated dynamic troponin has prognostic value, but the value must not be interpreted without the assay, timing, and reperfusion. Microvascular obstruction, right ventricular function, mitral regurgitation, and scar burden refine long-term estimates.

Risk of recurrence is highest during the first months and persists for years. Multivessel disease, diabetes, kidney disease, Lp(a), smoking, and uncontrolled LDL identify residual risk. Adherence is as important as the initial prescription.
Follow-up must assess angina, dyspnea, arrhythmias, bleeding, kidney function, and recovery. Return to work, driving, exercise, and sexual activity is planned according to individual risk, not through indefinite restrictions. Communication reduces fear and inactivity.

Correct attribution of the clinical category and mechanism has prognostic and therapeutic consequences. Avoiding both overdiagnosis and underdiagnosis enables causal care: reperfusion and antithrombotic therapy in atherothrombosis, physiological correction in secondary infarction, a technical solution in procedure-related infarction, and prevention consistent with the substrate.

Complications

Ventricular arrhythmias are frequent during the first hours because of ischemia, conduction heterogeneity, and catecholamines. Ventricular fibrillation and pulseless tachycardia require immediate defibrillation. Late scar-related arrhythmias have greater implications for persistent risk.
Sinus bradycardia and atrioventricular block are common in inferior infarction and often reversible with reperfusion. Anterior infranodal blocks reflect more extensive septal necrosis. Pacing is guided by symptoms, location, and risk of progression.

Heart failure results from loss of contractile mass, stunned myocardium, residual ischemia, or mitral regurgitation. It may present with mild congestion, pulmonary edema, or low output. Initial function may improve after reperfusion.
Cardiogenic shock involves hypoperfusion and organ dysfunction. It may result from left ventricular failure, right ventricular infarction, a mechanical complication, or arrhythmia. Determining the phenotype avoids inappropriate support or fluid administration.

Free-wall rupture causes tamponade and often sudden death. It may be complete or subacute and contained. A new effusion with echogenic material, hypotension, and pulseless electrical activity requires immediate treatment.
A septal defect produces a left-to-right shunt, right ventricular overload, and reduced output. The murmur may be loud but may diminish in shock. Doppler echocardiography quantifies the lesion and guides the interventional and surgical team.

Papillary muscle rupture causes acute mitral regurgitation, pulmonary edema, and shock. The posteromedial muscle is more vulnerable because of its single blood supply. Transesophageal echocardiography is often necessary and correction is urgent.
Ischemic mitral regurgitation may also result from papillary dysfunction and tethering without rupture. Severity is dynamic and depends on loading conditions. It may improve with revascularization and remodeling or become a chronic complication.

Ventricular thrombus forms on akinetic segments, particularly at the apex after anterior infarction. It may cause stroke or peripheral embolism. Contrast echocardiography and CMR increase sensitivity and allow resolution to be followed.
Early pericarditis is associated with transmural necrosis; Dressler syndrome occurs later as an immune-mediated phenomenon. Pain and ST-segment elevation must be distinguished from reinfarction. Anti-inflammatory drugs are selected with consideration of healing and antithrombotic therapy.

A pseudoaneurysm is a contained rupture with a wall formed by pericardium and fibrous tissue, whereas a true aneurysm contains scarred ventricular wall. The former has a greater risk of rupture and requires timely surgical assessment.
A true aneurysm may cause heart failure, arrhythmias, and thrombus. Persistent ST-segment elevation on the ECG may mimic acute ischemia. Echocardiography, CT, and CMR define the neck, wall, and contents.

Infarct expansion and remodeling dilate the ventricle and increase wall stress. Heart failure, functional mitral regurgitation, and reduced survival follow. Early reperfusion and neurohormonal therapy are preventive.
Microvascular obstruction sustains hypoperfusion despite a patent artery and increases infarct size. Intramyocardial hemorrhage represents a severe phenotype. Both predict remodeling and arrhythmias beyond ejection fraction.

Reinfarction may result from reocclusion, stent thrombosis, or a new plaque. During residual troponin release, it requires a new dynamic and ischemic evidence. Urgent revascularization depends on the clinical and angiographic presentation.
Stent thrombosis is often catastrophic and may be acute, subacute, late, or very late. DAPT interruption, underexpansion, malapposition, and neoatherosclerosis contribute according to timing. Imaging identifies the correctable target.

Bleeding from antithrombotic agents or vascular access increases mortality, anemia, and treatment interruption. Prevention includes radial access, correct dosing for weight and kidney function, gastric protection, and reduction of triple therapy.
Acute kidney injury results from hypoperfusion, congestion, contrast, and drugs. It is particularly frequent in shock and worsens prognosis. Hemodynamic correction and reduction of avoidable contrast are central interventions.

Stroke may be embolic from ventricular thrombus or atrial fibrillation, procedural, or hemorrhagic. An acute deficit requires urgent brain imaging and reassessment of antithrombotic therapy. After fibrinolysis, intracranial hemorrhage is a specific feared complication.
Atrial fibrillation may occur because of ischemia, increased pressures, and inflammation. It worsens output and increases embolic risk. Anticoagulation and antiplatelet therapy must be integrated while minimizing the duration of triple therapy.

Ischemic cardiomyopathy is the chronic consequence of a large infarction or repeated necrosis. It causes heart failure, mitral regurgitation, arrhythmias, and risk of sudden death. Heart-failure therapy, appropriate revascularization, and devices improve selected outcomes.
Sudden cardiac death may result from early ventricular fibrillation or late scar-related tachycardia. Late risk depends on ejection fraction, scar, arrhythmias, and syncope. Stratification must not be completed solely during initial stunning.

Infections, delirium, acquired weakness, and respiratory complications accompany complex hospitalizations. Deconditioning reduces independence and adherence, particularly in older people. Early mobilization and rehabilitation are part of preventing disability.
Depression and anxiety after infarction worsen quality of life and may reduce adherence. Fear of recurrence sometimes leads to inactivity and isolation. Screening, education, and psychological support must be integrated into follow-up.

Finally, progression of coronary disease and persistence of causal factors maintain a systemic atherothrombotic risk. Even complete revascularization does not eliminate plaques, Lp(a), diabetes, or smoking. Lifelong secondary prevention is the decisive measure against new complications.