ST-segment elevation myocardial infarction, or STEMI, is the electrocardiographic presentation of an acute coronary occlusion that causes severe and persistent regional ischemia. The working diagnosis is made in the presence of compatible symptoms and ST-segment elevation in contiguous leads or an occlusion equivalent, and it activates an immediate reperfusion strategy.
STEMI is a time-dependent diagnosis initially based on the ECG. Troponin documents acute myocardial injury and, together with evidence of ischemia, completes the diagnosis of myocardial infarction, but it may still be normal in the early stages. Waiting for the result when the tracing is diagnostic increases delay and reduces the amount of salvageable myocardium.
The most frequent cause is atherosclerotic thrombosis over a complicated plaque, generally caused by rupture or erosion. Spontaneous dissection, embolism, prolonged vasospasm, and other non-atherothrombotic occlusions are less common but important because they alter treatment and may affect people without the traditional risk profile.
ST-segment elevation reflects an injury vector produced by severe ischemia, but it does not directly measure the final transmural extent. Very early reperfusion may limit necrosis to subendocardial layers; conversely, an occlusion may present without classic criteria, particularly in a posterior location, with conduction blocks, or in specific patterns.
In countries with established catheterization laboratory networks, the incidence and mortality of STEMI have decreased, but shock and cardiac arrest continue to carry a poor prognosis. Patient- and system-related delays remain modifiable determinants. The principle that time is myocardium encompasses the entire interval from symptom onset to guidewire passage across the culprit vessel.
Primary PCI is the preferred reperfusion strategy when it can be achieved within 120 minutes of the electrocardiographic diagnosis. If this target is not realistic, symptom onset occurred within 12 hours, and there are no contraindications, immediate fibrinolysis followed by transfer to a PCI center is a validated strategy.
Care continues beyond reopening the vessel: microvascular perfusion, ventricular function, multivessel disease, and complications must be assessed. Secondary prevention begins during hospitalization with appropriate antithrombotic therapy, intensive reduction of atherogenic lipoproteins, risk-factor control, and rehabilitation.
In most cases, the mechanism is a complicated plaque with an occlusive thrombus. Rupture exposes the necrotic core to blood; erosion denudes the endothelial surface; a calcified nodule may protrude into the lumen. All activate platelets and coagulation against different underlying morphologies.
Platelets adhere through von Willebrand factor and collagen, become activated, and release ADP and thromboxane. The IIb/IIIa receptor changes conformation and binds fibrinogen, creating bridges between platelets. Aspirin and P2Y12 inhibitors block complementary pathways in this response.
Tissue factor initiates thrombin generation, which amplifies platelet activation and converts fibrinogen into fibrin. Parenteral anticoagulation limits propagation during PCI or fibrinolysis. The thrombus contains variable proportions of platelets, fibrin, and erythrocytes and changes over time.
Plaque rupture is more frequent in fibroatheromas with a large core and thin cap, but morphological vulnerability does not reliably predict the fate of an individual lesion. Mechanical stress, inflammation, and a systemic prothrombotic state contribute to clinical transition.
Surface erosion often involves less lipid-rich, matrix-rich plaques. Neutrophils, toll-like receptors, and disturbed flow contribute to endothelial injury. OCT can identify a compatible phenotype, but it does not directly visualize the endothelium and the diagnosis remains operational.
A calcified nodule occurs in severely calcified, tortuous segments. Protruding fragments disrupt luminal continuity and promote thrombosis. The anatomy often requires calcium modification to achieve adequate stent expansion.
The thrombus may undergo spontaneous lysis, fragment, or reform. This dynamic explains episodes of pain, ST-segment changes, and partially patent arteries at coronary angiography. Temporarily restored flow does not eliminate the risk of reocclusion without definitive treatment.
Spontaneous coronary artery dissection compresses the lumen through an intramural hematoma or false lumen. It is an important cause in young women and during the peripartum period. PCI may be technically complex and propagate the dissection, so it is reserved for persistent ischemia, a large territory, or impaired flow.
Coronary embolism may arise from atrial fibrillation, endocarditis, prosthetic valves, intracardiac thrombi, or paradoxical embolism. Selective aspiration can sometimes restore flow, but the source must be treated and thrombotic material distinguished from septic or neoplastic material.
Prolonged vasospasm may cause ST-segment elevation and necrosis even without fixed stenosis. Cocaine, amphetamines, and vasoconstrictive drugs may precipitate it. Resolution with nitrates does not exclude myocardial infarction because sufficiently prolonged ischemia leaves demonstrable necrosis.
Causal factors for atherosclerosis include exposure to apoB and LDL, Lp(a), smoking, hypertension, diabetes, kidney disease, and genetic predisposition. They determine plaque burden and the probability of a complicated plaque. Control after STEMI reduces events throughout the vascular tree, not only in the treated segment.
Smoking increases platelet aggregation, vasoconstriction, oxidative stress, and endothelial dysfunction. It is often the predominant factor in early STEMI. Complete cessation produces a rapid and substantial benefit; merely reducing the number of cigarettes is not equivalent to abstinence.
Diabetes promotes diffuse atherosclerosis, microangiopathy, and platelet activation and may attenuate symptoms through neuropathy. It is associated with multivessel disease, no-reflow, and a worse prognosis. Acute hyperglycemia is a risk marker even in people without diabetes.
Kidney disease increases calcification, inflammation, anemia, and bleeding risk; these patients should receive the same reperfusion strategy when indicated, with dose and contrast adjustments. Excluding them solely because of concern about kidney injury may worsen prognosis.
Occlusion interrupts supply and triggers an ischemic cascade: oxidative phosphorylation and relaxation cease, contractility decreases, membrane potentials and conduction change, and pain and ST-segment abnormalities appear. The order may vary and symptoms may be absent.
The injury current between ischemic and normal tissue produces ST-segment elevation. Distribution and polarity depend on location and vector. The tracing is an electrical representation, not a direct image of the coronary artery or the thickness of necrotic tissue.
Cell death progresses as a wavefront from the subendocardium toward the epicardium. A proximal occlusion exposes more myocardium, whereas collateral circulation, low demand, and intermittent reperfusion slow necrosis. Every delay reduces the potential benefit, particularly during the first hours.
The subendocardium is more vulnerable because of wall tension, systolic compression, and dependence on diastolic perfusion. Tachycardia and hypotension aggravate the deficit. In right ventricular infarction, reduced left ventricular preload creates a specific hemodynamic vulnerability.
Reperfusion may produce stunning, transient arrhythmias, free radicals, and calcium overload. Salvaged tissue remains temporarily dysfunctional but viable. Initial function should therefore not be considered irreversible without reassessment.
Microembolization of thrombus and plaque occludes the microcirculation. Edema, cellular aggregates, endothelial injury, and vasoconstriction maintain hypoperfusion. Routine thrombus aspiration, however, has not improved outcomes in large trials.
In no-reflow, the epicardial coronary artery is open but tissue perfusion is inadequate. Poor ST-segment resolution and reduced blush are indicators. CMR demonstrates microvascular obstruction and possible intramyocardial hemorrhage, both associated with remodeling.
The inflammatory response removes necrotic tissue and prepares the scar. Neutrophils and macrophages degrade the matrix, creating a phase of structural weakness; fibroblasts and collagen subsequently stabilize the wall. This balance influences rupture and dilation.
Sympathetic activation increases heart rate, blood pressure, and oxygen consumption, while the renin-angiotensin-aldosterone system promotes retention and remodeling; this neurohormonal response initially supports perfusion but becomes harmful if persistent.
The necrotic mass reduces cardiac output and increases filling pressures. If extensive, cardiogenic shock develops; involvement of the papillary muscles or septum may cause a mechanical complication. Ischemia also impairs electrical stability and predisposes to ventricular fibrillation.
The final pathophysiology therefore integrates epicardial occlusion, necrosis, the microcirculation, the inflammatory response, and ventricular adaptation. PCI resolves the first component, but the clinical result also depends on all the others; this explains different outcomes despite an apparently equally patent artery.
Anterior STEMI usually results from occlusion of the left anterior descending artery. ST-segment elevation involves V1-V4 and may extend to the lateral leads. A proximal location places the septum, anterior wall, and apex at risk and increases the likelihood of shock, conduction block, thrombus, and rupture.
Inferior STEMI causes ST-segment elevation in II, III, and aVF and is most often caused by the right coronary artery and less often by the circumflex artery. The ratio of elevation in III and II, reciprocal changes, and lateral leads are helpful, but coronary angiography defines the vessel.
Right ventricular involvement often results from proximal right coronary artery occlusion and is identified with V3R and V4R. It causes increased right-sided pressures and reduced left ventricular filling. Right ventricular function may recover substantially after reperfusion.
Posterior infarction involves the inferobasal wall, often in the circumflex territory. In the anterior leads it appears as reciprocal ST-segment depression and a prominent R wave. Leads V7-V9 demonstrate elevation and prevent delayed reperfusion.
Lateral STEMI involves I, aVL, V5, and V6 and is associated with the circumflex, marginal, or diagonal branches. Small branches may produce a limited territory, whereas a proximal occlusion may combine with an anterior or posterior pattern.
The historical term transmural infarction is not a perfect synonym for STEMI. Reperfusion may interrupt the wavefront before full transmurality, and CMR shows a continuous distribution of the percentage of wall involved. The ECG describes the acute phenotype.
Broad, regional hyperacute T waves may precede ST-segment elevation, particularly very early. The ST segment then rises, R waves may decrease, Q waves appear, and T-wave inversion follows. Treatment may alter or interrupt this sequence.
ST-segment resolution after reperfusion reflects electrical and microvascular recovery. A reduction of at least 50% after fibrinolysis is a practical marker of success, whereas persistence suggests failure and the need for rescue PCI.
A Q wave on arrival may indicate that onset was not recent but must not, by itself, preclude reperfusion. Persistent symptoms, instability, and total elapsed time are more important. After healing, Q waves may persist or partially regress.
Aborted myocardial infarction is a historical concept referring to very early reperfusion with minimal necrosis despite a diagnostic ECG. With high-sensitivity troponin assays, complete absence of biomarker release is rare. Clinical success is measured primarily by the myocardium salvaged.
Epicardial flow is classified as TIMI 0-3. TIMI 0 indicates absent flow and TIMI 3 normal flow, but angiographic velocity does not fully describe capillary perfusion. Myocardial blush adds a tissue-level index.
A fibrin-rich red thrombus and a more platelet-rich thrombus represent extremes of variable composition. Thrombus age and intermittent flow alter its structure. Composition cannot be inferred reliably from the color of aspirated material alone.
The culprit lesion may show rupture, erosion, calcification, or dissection. OCT has high superficial resolution; IVUS assesses diameter, plaque burden, and calcium depth. Imaging guides sizing and optimization, especially in complex anatomy.
Early necrosis appears histologically as coagulative necrosis, edema, and neutrophilic infiltration. Reperfusion may cause hemorrhage and contraction bands. During the following days, macrophages remove tissue and the wall becomes fragile.
Infarct expansion causes thinning and dilation without new necrosis. It is favored by extensive anterior infarction and failure to reperfuse. It increases stress on the remaining tissue and prepares the way for global remodeling.
Remodeling changes ventricular volume and geometry during the following weeks and months. A more spherical shape worsens efficiency and mitral regurgitation. Reperfusion, ACE inhibition, and heart-failure therapy limit progression.
Stunned myocardium remains viable but hypocontractile after flow is restored. It may recover progressively and explain an initially low ejection fraction. Necrotic tissue, by contrast, is replaced by scar and does not regain contractility.
Microvascular obstruction is often located at the center of the reperfused infarct. Its presence on CMR predicts dilation and a worse prognosis. Intramyocardial hemorrhage indicates severe capillary injury and influences scar organization.
The scar creates a substrate for ventricular re-entry. Channels of surviving myocardium conduct slowly and may sustain monomorphic tachycardia. Late risk depends on ejection fraction, fibrotic burden, arrhythmias, and syncope.
Anterior apical infarction promotes ventricular thrombus through akinesia, endocardial injury, and hypercoagulability. The thrombus may be laminated or protruding. CMR and contrast echocardiography improve detection.
Involvement of the papillary muscles may cause transient regurgitation, geometric displacement, or rupture. The posteromedial muscle is more vulnerable because of its single blood supply. Complete or partial rupture causes severe acute mitral regurgitation.
Septal necrosis may progress to septal rupture with a left-to-right shunt. The abrupt increase in pulmonary flow and right ventricular overload cause low output. Doppler identifies the site and direction even when the murmur is faint.
Free-wall rupture causes hemopericardium or is contained as a pseudoaneurysm. A true aneurysm, by contrast, is a scarred dilation with continuity of the wall layers. The anatomical distinction determines risk and treatment.
Healing produces a permanent fibrous scar. Final size depends on time, the affected vessel, collateral circulation, reperfusion, and the microcirculation. The amount of scar, more than the label STEMI itself, determines long-term function and risk.
Anatomical, electrical, and clinical classifications must remain integrated: territory, vessel, universal type, function, and complications describe different dimensions. A complete definition avoids reducing the event to ST-segment elevation alone.
The history must identify the time of onset or the last time the patient was definitely symptom-free. Persistent pain, prodromal episodes, and delays in calling for help are reconstructed without interrupting ECG acquisition and stabilization; this timing guides the strategy but does not replace assessment of clinical viability.
The classic symptom is pressing, constricting, or heavy retrosternal discomfort, often radiating to the arms, shoulders, neck, jaw, back, or epigastrium. It may be described as burning or indigestion. Intensity does not quantify the myocardial mass at risk.
The symptom often lasts more than 20 minutes and does not resolve completely with rest. An intermittent course may reflect occlusion and recanalization. Relief with nitrates does not distinguish STEMI from other causes of pain.
Dyspnea may be the predominant symptom because of ventricular dysfunction, pulmonary edema, or mitral regurgitation. In older patients or those with diabetes, it may occur without obvious pain. A silent presentation increases delay and reduces myocardial salvage.
Sweating, nausea, vomiting, and pallor reflect autonomic activation. They are particularly common in inferior infarction, in which a vagal reflex may cause bradycardia and hypotension. Repeated vomiting impairs absorption of oral P2Y12 inhibitors.
Syncope suggests an arrhythmia, conduction block, hypotension, or a mechanical complication. It may be the initial manifestation of inferior infarction with block or extensive anterior infarction. Monitoring with immediate defibrillation capability is required.
Cardiac arrest may precede recognized pain. Ventricular fibrillation is common in the early stages, whereas pulseless electrical activity requires consideration of rupture, shock, or alternative diagnoses. After ROSC, persistent ST-segment elevation indicates primary PCI.
Women may present with chest pain together with dyspnea, nausea, and weakness; older patients more often present with confusion or syncope. Labeling these as nonclassic symptoms must not reduce urgency. Any delay caused by stereotypes worsens prognosis.
In young patients, the puerperium, extreme stress, arterial disorders, and absence of atherosclerosis point toward SCAD. Cocaine and stimulants suggest vasospasm or thrombosis. Atrial fibrillation, endocarditis, or prosthetic valves suggest embolism.
On arrival, airway and breathing, oxygen saturation, heart rate, blood pressure, consciousness, and perfusion are assessed. Cardiac arrest, pulmonary edema, and shock are treated in parallel with activation of the catheterization laboratory. Internal transport must not interrupt monitoring or defibrillation capability.
Pallor, cold skin, confusion, oliguria, and delayed capillary refill indicate hypoperfusion. Blood pressure may still be preserved in the early stages. Lactate helps track severity but does not replace clinical assessment.
Crackles, a third heart sound, and hypoxemia suggest left-sided heart failure. Sudden pulmonary edema may result from acute mitral regurgitation. Urgent echocardiography distinguishes global dysfunction, a mechanical complication, and other causes.
In right ventricular infarction, hypotension and distended jugular veins with relatively clear lungs are typical. Nitrates, diuretics, and positive-pressure ventilation may further reduce preload. Fluids must be administered cautiously with reassessment.
A new systolic murmur with deterioration indicates papillary muscle or septal rupture until proven otherwise. In shock, the murmur may be faint. Echocardiography, including transesophageal echocardiography, must not be postponed.
A difference in blood pressure between the arms, tearing back pain, or aortic regurgitation suggests aortic dissection. Administration of a fibrinolytic agent in this condition may be fatal. The alternative diagnosis must be excluded rapidly when suspicion is substantial.
Pleuritic pain, hypoxemia, and signs of venous thrombosis suggest pulmonary embolism, which may cause troponin elevation and right-sided abnormalities. Pneumothorax, pericarditis, and esophageal rupture complete the main emergency differential diagnoses.
Bradycardia in inferior infarction may result from vagal tone or nodal ischemia and often responds to reperfusion. An anterior infranodal block is more threatening. Symptoms, QRS morphology, and location guide atropine administration and pacing.
Ventricular tachycardia may cause palpitations, syncope, or cardiac arrest. If sustained and associated with instability, it requires immediate cardioversion. After correction, persistent ischemia, electrolyte abnormalities, and reperfusion failure must be sought.
Recurrence of pain and ST-segment elevation after PCI suggests reocclusion, stent thrombosis, dissection, or no-reflow. A new tracing must be obtained immediately. Symptoms without electrocardiographic changes still require clinical assessment.
After fibrinolysis, pain relief and reperfusion arrhythmias may accompany success, but the principal measure is ST-segment resolution. Persistence beyond 90 minutes, pain, or instability indicates failure and the need for rescue PCI.
During the following days, pleuritic pain and a friction rub suggest early pericarditis. Recurrent pressure-like pain requires exclusion of reinfarction. Low-grade fever may accompany necrosis, whereas persistent high fever points toward infection.
Sudden hemodynamic collapse during the phase of tissue fragility requires investigation for rupture, mitral regurgitation, septal defect, tamponade, and arrhythmia. Simply attributing it to progression of shock may miss a correctable cause.
Before discharge, residual angina, dyspnea, ability to mobilize, and signs of congestion are assessed. Ventricular function guides treatment and follow-up, but it may improve as stunning resolves and must be reassessed.
Anxiety, depression, and fear of sexual or physical activity are common. Rehabilitation enables a gradual and safe return to activity. Avoiding exertion indefinitely without an indication may worsen functional capacity, weight, and mental health.
The clinical presentation evolves rapidly, so examination must be serial. Blood pressure, perfusion, rhythm, oxygen saturation, urine output, murmurs, and congestion are reassessed after every intervention. Change is often the first sign of a complication.
A 12-lead ECG must be recorded and interpreted within 10 minutes of first medical contact. A diagnostic tracing immediately activates the PCI network. Prehospital transmission allows the center to be alerted and the emergency department to be bypassed when this is part of the organized pathway.
ST-segment elevation is measured at the J point using standard calibration. The working diagnosis requires an ischemic context and at least two contiguous leads. Thresholds differ in V2-V3 by sex and age and apply in the absence of left ventricular hypertrophy or left bundle branch block.
ESC electrocardiographic criteria for a working diagnosis of STEMI
Suspected posterior infarction requires V7-V9; ST-segment elevation of at least 0.5 mm supports the diagnosis, with a threshold of at least 1 mm in young men according to the specific criteria. ST-segment depression in V1-V3 with an upright terminal T wave is an important reciprocal sign.
In inferior infarction, V3R and V4R are recorded to identify right ventricular involvement. Elevation in V4R is particularly useful but may be transient, so the leads must be obtained early. The finding changes preload management and prognosis.
If the first ECG is nondiagnostic, serial tracings at short intervals and during pain may document evolution. Hyperacute T waves, the de Winter pattern, and transient ST-segment elevation may precede or replace the classic pattern. Suspicion of persistent occlusion justifies urgent angiography.
A new or presumably new left bundle branch block is not diagnostic by itself. ST-segment concordance, excessive discordance according to the modified Sgarbossa criteria, symptoms, and instability increase suspicion. Uncertainty must not delay coronary angiography when ischemia is persistent.
Interpretation may be difficult during ventricular pacing and in right bundle branch block. Concordance criteria, comparison with previous tracings, and echocardiography are helpful, but the strategy remains clinical. A nonclassic pattern does not exclude an occluded artery.
High-sensitivity troponin is measured, but it must not delay reperfusion. The final diagnosis of myocardial infarction requires a rise or fall in troponin with at least one value above the sex-specific 99th percentile and evidence of ischemia, typically already provided by symptoms and the ECG.
Criteria from the Fifth Universal Definition applicable to acute primary myocardial infarction
Complete blood count, creatinine, electrolytes, blood glucose, and coagulation tests define risk and safety. A lipid profile is obtained early to establish preventive treatment. None of these tests should delay transfer to the catheterization laboratory.
Bedside echocardiography identifies regional abnormalities, right ventricular dysfunction, mitral regurgitation, septal defect, and effusion. It is essential in instability and useful when tracings are equivocal, but it must not delay PCI when ECG findings and symptoms are clear.
Urgent coronary angiography confirms the vessel, defines the anatomy, and allows PCI. It may show thrombus, occlusion, dissection, or embolism. A mild stenosis after recanalization does not exclude the mechanism and may require OCT or IVUS.
OCT characterizes the plaque surface, thrombus, dissection, stent expansion, and apposition; IVUS assesses diameter, plaque burden, and deep calcium. Imaging is recommended for complex lesions and is useful when mechanisms are ambiguous, while unjustified delays must be avoided.
ST-segment resolution is assessed after reperfusion. An insufficient reduction indicates inadequate tissue perfusion; after fibrinolysis, less than 50% resolution at 60-90 minutes defines practical failure and indicates rescue PCI.
TIMI flow and myocardial blush describe epicardial and tissue-level results. TIMI 3 does not exclude no-reflow. Persistent pain, instability, arrhythmias, and poor ST-segment resolution must take precedence over a reassuring angiographic impression.
CMR is not part of the initial decision, but it quantifies infarct size, transmurality, area at risk, microvascular obstruction, hemorrhage, and thrombus. In cases with nonobstructive coronary arteries, it distinguishes infarction, myocarditis, and Takotsubo syndrome.
The differential diagnosis of ST-segment elevation includes pericarditis, early repolarization, ventricular aneurysm, hypertrophy, hyperkalemia, Brugada syndrome, and Takotsubo syndrome. Urgent angiography is often appropriate when occlusion cannot be safely excluded.
An aortic dissection may involve a coronary ostium and mimic STEMI. Back pain, pulse asymmetry, aortic regurgitation, or pericardial effusion increase suspicion. Fibrinolysis is contraindicated and urgent aortic imaging becomes the priority.
Pulmonary embolism and myocarditis may cause troponin elevation and ST-segment abnormalities, but their distribution, echocardiographic findings, and imaging differ. An alternative diagnosis must be sought without lowering the threshold for coronary angiography in an unstable patient.
Documentation must record symptom onset, first medical contact, ECG time, diagnosis, fibrinolytic bolus, or guidewire passage; these intervals measure network quality. Failure to meet a target requires process analysis, not merely a clinical justification.
The diagnosis must specify location and vessel, function, universal type, reperfusion, and complications. STEMI is most often a primary myocardial infarction caused by atherothrombosis, but SCAD, embolism, and vasospasm are also possible causes of primary myocardial infarction with the same ECG phenotype. Etiological attribution follows the anatomy and test results.
A late-presenting patient requires assessment of symptoms and viability. Between 12 and 48 hours, a PCI strategy may still be considered; beyond 48 hours, routine PCI of a persistently occluded vessel in an asymptomatic patient is not indicated, whereas persistent ischemia or instability changes the decision.
Before discharge, ejection fraction, valves, the right ventricle, and complications are assessed. In large anterior infarctions, apical thrombus is sought with contrast echocardiography or CMR if necessary. Residual anatomy and the revascularization plan must be explicit.
Finally, prognostic assessment integrates Killip class, kidney function, shock, cardiac arrest, ejection fraction, infarct location, and the microcirculation. The troponin value is informative but does not replace timing, anatomy, and hemodynamic status. Prognosis is updated throughout hospitalization.
The first intervention is immediate activation of the reperfusion system. The patient is monitored with a defibrillator available, the ECG is obtained, and the PCI center is alerted. Transfer must avoid stops and handoffs that add no clinical value.
Oxygen is reserved for patients with oxygen saturation below 90%. It does not improve outcomes in normoxemic patients. Noninvasive ventilation may help pulmonary edema, with attention to its hemodynamic effects on preload.
Nitrates reduce pain and congestion when blood pressure and preload permit. They are avoided in hypotension, preload-dependent right ventricular infarction, and after PDE5 inhibitors. They do not replace reperfusion, and the response does not confirm the mechanism.
Morphine is titrated only for severe persistent pain because it may delay absorption of P2Y12 inhibitors and cause nausea and hypotension. Reassurance, treatment of ischemia, and rapid PCI are fundamental components of symptom control.
Aspirin is administered promptly as a chewable loading dose unless there is severe allergy or active bleeding. A P2Y12 inhibitor is added: ticagrelor or prasugrel is preferred to clopidogrel in appropriate patients undergoing PCI.
Prasugrel is contraindicated after stroke or TIA and requires caution in older age or low body weight. Ticagrelor may cause dyspnea and bradycardia. Clopidogrel remains necessary with fibrinolysis, anticoagulation, or when the more potent agents are inappropriate.
Anticoagulation during primary PCI uses unfractionated heparin or selected alternatives. With fibrinolysis, enoxaparin or heparin is given according to age and kidney function. Parenteral therapy must not be prolonged without an indication after a successful procedure.
Primary PCI is superior to fibrinolysis when performed promptly and reduces death, reinfarction, and stroke. The organizational target is guidewire passage within 120 minutes of diagnosis, with even shorter intervals for patients already at a PCI center.
If PCI cannot be achieved within 120 minutes, fibrinolysis must be started rapidly, ideally within 10 minutes of diagnosis, if symptoms began less than 12 hours earlier and there are no contraindications. Bleeding risk increases with age and comorbidity.
Fibrin-specific agents, particularly tenecteplase, are used according to weight-based protocols. In patients aged at least 75 years, a reduced dose of tenecteplase decreases intracranial hemorrhage. The choice must follow regulatory authorization and the network protocol.
Absolute contraindications to fibrinolysis include previous intracranial hemorrhage, known intracranial vascular lesions or neoplasms, recent ischemic stroke, active bleeding, and suspected aortic dissection. History and blood pressure must be checked without causing avoidable delay.
After the bolus, transfer to a PCI center is immediate. Rescue PCI is indicated for less than 50% ST-segment resolution at 60-90 minutes, persistent pain, recurrent ischemia, or hemodynamic or electrical instability.
After successful fibrinolysis, a pharmacoinvasive strategy includes coronary angiography within 2-24 hours. Recurrence is not awaited. Clopidogrel is the P2Y12 inhibitor administered with fibrinolysis; in patients subsequently undergoing PCI, switching to ticagrelor or prasugrel may be considered after 48 hours according to ischemic and bleeding risks.
Radial access is the standard when feasible. Contemporary drug-eluting stents reduce restenosis and repeat revascularization. Lesion preparation and intravascular imaging improve expansion and apposition in complex anatomy.
Routine thrombus aspiration is not recommended because TOTAL and other studies showed no overall benefit and reported an increase in stroke. Aspiration may be used as a bailout measure in selected thrombus or embolism.
In stable patients with multivessel disease, complete revascularization of significant stenoses reduces new events. It may be performed during the index procedure or as a staged procedure according to anatomy, kidney function, and complexity, generally within the early pathway defined by guidelines.
In cardiogenic shock, initial PCI must treat the culprit vessel; immediate routine PCI of the other vessels increases risk. Vasopressors, inotropes, and support devices are selected according to phenotype. A microaxial flow pump may be reasonable in selected patients at experienced centers.
Oral beta-blockers are started early in the absence of acute heart failure, low output, bradycardia, or risk of shock. Intravenous metoprolol may be considered before PCI in stable patients without heart failure and with systolic blood pressure above 120 mmHg, but it is not routine for all patients.
ACE inhibitors or ARBs are particularly indicated with anterior infarction, reduced ejection fraction, heart failure, diabetes, or hypertension. Mineralocorticoid receptor antagonists are indicated with an ejection fraction no higher than 40% and heart failure or diabetes, if kidney function and potassium permit.
A high-intensity statin is started immediately, with early addition of ezetimibe when the target cannot be achieved with a statin alone. The 2026 US guidelines recommend LDL below 55 mg/dL and non-HDL cholesterol below 85 mg/dL for very-high-risk secondary prevention, using combination therapy according to distance from target and response.
DAPT is maintained for 12 months as the default strategy in the absence of high bleeding risk. Shortened duration, P2Y12 monotherapy, or de-escalation is reserved for selected patients. Chronic anticoagulation requires a short course of triple therapy.
Cardiac rehabilitation is prescribed before discharge. It addresses exercise, smoking, nutrition, adherence, psychological support, and return to usual roles. A home-based program is a valid alternative when an in-person program is not accessible.
In-hospital prognosis depends on shock and cardiac arrest, anterior location, delay, kidney function, age, and Killip class. Reperfusion dramatically reduces risk, but no-reflow, mechanical complications, and arrhythmias may negate a good epicardial result.
Long-term determinants include ejection fraction, scar burden, multivessel disease, diabetes, bleeding, and lipid control. Function is reassessed after stunning has resolved before primary-prevention devices are considered.
Stable patients presenting after 48 hours with a persistently occluded vessel do not benefit from routine reopening in the absence of ischemia. Persistent symptoms, arrhythmias, instability, or a large viable territory instead require a specific invasive assessment.
Early discharge is possible only in selected low-risk patients who have undergone successful reperfusion, have no arrhythmias or complications, and have organized follow-up. Continuity of care includes lipid testing at 4-8 weeks and clear instructions regarding DAPT.
Ventricular fibrillation is the leading cause of early sudden death. Ischemia creates dispersion of refractoriness and slowed conduction. Prompt defibrillation and rapid access to emergency care determine survival even before PCI.
Polymorphic ventricular tachycardia is often related to active ischemia, whereas late monomorphic tachycardia uses the scar as a circuit. Arrhythmias during the first 48 hours do not have the same prognostic significance as unprovoked late arrhythmias.
Bradycardia and atrioventricular block are common in inferior STEMI and often transient. Infranodal block in anterior STEMI indicates extensive septal injury. Temporary pacing is indicated when bradycardia causes instability or there is a high risk of progression.
Acute heart failure ranges from mild congestion to pulmonary edema. Contractile loss, stunning, mitral regurgitation, and arrhythmias contribute. Diuretics, vasodilators, ventilation, and reperfusion are selected according to blood pressure and mechanism.
Cardiogenic shock carries high mortality and requires urgent revascularization of the culprit vessel. The phenotype may be left-sided, right-sided, biventricular, or mechanical. Lactate, echocardiography, and, when necessary, invasive hemodynamics guide support.
No-reflow sustains tissue ischemia after PCI and is associated with a large infarct, diabetes, delay, and high thrombus burden. Intracoronary vasodilators may be attempted, but no single therapy is universally effective. Prevention remains fundamental.
Right ventricular infarction causes hypotension and venous congestion with preload dependence. Excess fluid dilates the right ventricle and worsens ventricular interdependence. Sinus rhythm, reperfusion, and blood-pressure support are central.
Free-wall rupture causes hemopericardium, tamponade, and pulseless electrical activity. It may be immediately fatal or subacute. Urgent echocardiography and surgery are required; pericardiocentesis is only a selected bridge.
A septal defect causes an acute left-to-right shunt, right ventricular overload, and low output. A new murmur and deterioration must prompt Doppler assessment. Circulatory support and surgical or percutaneous closure are determined by a multidisciplinary team.
Papillary muscle rupture causes acute mitral regurgitation, pulmonary edema, and shock. The posteromedial muscle is more vulnerable. Ejection fraction may appear normal or high because the ventricle ejects into the low-pressure atrium, masking severity.
Ischemic mitral regurgitation without rupture results from papillary dysfunction and remodeling. It may be dynamic and worsen with exertion or loading conditions. Revascularization, heart-failure therapy, and selected valve intervention address its different mechanisms.
Ventricular thrombus is more frequent after a large anterior apical infarction. It may embolize and requires anticoagulation balanced against DAPT. Follow-up imaging confirms resolution and guides duration.
Early pericarditis causes pleuritic pain and a friction rub during the following days; Dressler syndrome occurs later and is immune-mediated. Both must be distinguished from reinfarction and contained rupture.
A true ventricular aneurysm results from a dilated scar and may cause heart failure, arrhythmias, and thrombus. A pseudoaneurysm is a contained rupture with a greater risk of rupture. CT and CMR complement echocardiography.
Adverse remodeling dilates the ventricle and increases wall stress, promoting heart failure and mitral regurgitation. Extensive infarction, no-reflow, and delay are determinants. Neurohormonal therapy and early reperfusion limit it.
Stent thrombosis may cause early or late reinfarction. Interruption of DAPT, underexpansion, malapposition, and edge dissection are important factors. Repeat PCI must correct the mechanism, using imaging when possible.
Reinfarction requires new ischemia and a renewed troponin dynamic if the biomarker remains elevated. A new rise in serial values from stable or falling levels supports the diagnosis; the change must be interpreted in an assay-specific manner together with new evidence of ischemia. Persistent pain alone is insufficient.
Major bleeding results from fibrinolysis, antithrombotic agents, or vascular access and worsens prognosis. Intracranial hemorrhage is the most feared complication of fibrinolysis. Blood-pressure control, correct selection, and adjusted dosing reduce risk.
Acute kidney injury is promoted by shock, congestion, and contrast. It reduces therapeutic options and increases mortality. Hemodynamic stability, the minimum necessary contrast volume, and correct dosing are the most practical interventions.
Stroke may be embolic from ventricular thrombus or atrial fibrillation, procedural, or hemorrhagic after fibrinolysis. An acute neurological deficit requires immediate imaging and coordination between cardiology and neurology.
Atrial fibrillation worsens cardiac output and increases embolic risk. Anticoagulation must be integrated with DAPT while limiting triple therapy. Rhythm or rate control depends on stability and duration.
Ischemic cardiomyopathy results from a large scar or repeated infarctions. It causes chronic heart failure, arrhythmias, and sudden death. Ejection-fraction-guided therapy, appropriate revascularization, and selected devices modify prognosis.
Depression, anxiety, and deconditioning impair recovery after a major event. Fear of exertion may lead to inactivity and isolation. Rehabilitation addresses safety, physical capacity, and mental health simultaneously.
The risk of recurrent events persists because of non-culprit plaques, LDL, Lp(a), diabetes, and smoking. Revascularizing the lesion does not cure the entire atherosclerotic process. Intensive secondary prevention and adherence are essential.
Death may result from arrhythmia, shock, rupture, reinfarction, or progressive heart failure. Their relative importance changes over time: electrical complications predominate during the first hours, mechanical complications during the following days, and remodeling over the long term.
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