Coronary thrombosis

Article written and reviewed by Dr Luca Moretti

Coronary thrombosis is the formation of a clot within a coronary artery. In most acute coronary syndromes, thrombus arises on rupture, erosion, or a calcified nodule of an atherosclerotic plaque, a mechanism addressed in dedicated monographs; here the focus is in situ thrombosis without a causal atherosclerotic substrate. Thrombosis on stents or devices is also included; this boundary avoids confusing a common finding, thrombus, with a single etiology.
A local thrombus must be distinguished from an embolus arriving from a distant site and from dissection, in which a hematoma or false lumen compresses the vessel. It must also be separated from pure spasm, although prolonged spasm may promote thrombosis through stasis and endothelial injury; mechanism-based diagnosis requires angiography and intracoronary imaging. Aspiration of thrombotic material alone does not identify its origin. Embolic sources and systemic conditions must be sought in parallel.

Nonatherosclerotic forms are heterogeneous and rare, so dedicated treatment trials are lacking. Evidence comes from acute coronary syndrome guidelines, hematology documents, recommendations for antiphospholipid syndrome, cancer studies, and device consensus statements. Etiologic heterogeneity prevents a single therapy beyond initial reperfusion. Antiplatelet drugs, anticoagulants, and mechanical correction have different indications. Overtreatment may cause hemorrhage without preventing the responsible mechanism.
The clinical presentation is often STEMI or NSTEMI, but nonocclusive thrombi may cause intermittent ischemia or dissolve before coronary angiography. Absence of residual stenosis does not automatically prove embolism or exclude a transient local event; the coronary wall must be interrogated when the answer changes therapy. OCT reveals superficial lesions and struts. IVUS defines expansion, hematoma, and deeper architecture in a complementary manner.

Etiology, risk factors, pathogenesis, and pathophysiology

Thrombosis emerges from the interaction among vascular surface, blood, and flow. Endothelial activation exposes tissue factor and adhesion molecules; platelets adhere, activate, and aggregate; thrombin converts fibrinogen to fibrin. Stasis or recirculation permits local accumulation of activated factors; the thrombogenic triad can operate without plaque rupture. One factor rarely explains everything. Infection, drugs, cancer, and coronary geometry may converge in the same event.
Antiphospholipid antibody syndrome is an acquired thrombophilia capable of causing arterial, venous, and microvascular thrombosis. Lupus anticoagulant, anticardiolipin, and anti-beta2-glycoprotein I antibodies promote endothelial, platelet, monocyte, complement, and coagulation activation; a triple-positive profile identifies high risk. One test during infarction does not confirm APS. Laboratory persistence and the clinical criterion require specialist interpretation.

Myeloproliferative neoplasms, particularly polycythemia vera and essential thrombocythemia, combine hyperviscosity, platelet and leukocyte activation, inflammation, and endothelial interactions. JAK2 V617F is associated with particular thrombotic risk, but platelet count alone does not measure danger; clonal thrombosis may precede hematological diagnosis. Persistent erythrocytosis, thrombocytosis, or leukocytosis requires assessment. Extreme thrombocytosis may coexist with acquired von Willebrand disease and bleeding.
Paroxysmal nocturnal hemoglobinuria promotes thrombosis through intravascular hemolysis, nitric oxide depletion, platelet activation, and complement. Unusual venous sites are more characteristic, but arterial events may occur. Cytopenias, hemolysis, dark urine, or atypical thrombosis guide flow cytometry; subclinical PNH should not be sought indiscriminately after every infarction. Yield rises with consistent hematological abnormalities. A positive diagnosis changes hematological therapy and prognosis.

Cancer increases arterial risk through tissue factor, thrombin, neutrophil extracellular traps, cytokines, platelet activation, and endothelial injury. Risk varies with site, stage, and proximity to diagnosis. Cisplatin, fluoropyrimidines, VEGF inhibitors, some tyrosine kinase inhibitors, and hormonal therapies add specific mechanisms; cancer-associated thrombosis is not always responsive to anticoagulation. Thrombocytopenia and bleeding lesions complicate management. Trials do not support universal anticoagulant prevention of arterial events in outpatients.
Combined estrogen-progestin contraceptives and estrogen therapy alter coagulation and fibrinolytic factors. Absolute arterial risk remains low in healthy young women but rises with age, smoking, hypertension, migraine with aura, and thrombophilias. Preparations and doses do not have identical profiles; estrogen-related risk is multiplicative, not isolated. Pregnancy and puerperium add physiological hypercoagulability. In a woman with infarction, SCAD and vasospasm, which are more common than pure thrombosis, must also be considered.

Severe COVID-19 may produce systemic inflammation, endotheliopathy, platelet activation, complement, neutrophil extracellular traps, and stasis. Early STEMI cohorts observed greater thrombus burden, multivessel thrombosis, and stent thrombosis, but were observational studies from a specific pandemic phase; the thrombotic signal does not always demonstrate a plaque-free vessel. Concomitant infection may destabilize existing atherosclerosis. Treatment must avoid generalizing from selected cases.
Cocaine and amphetamines combine vasoconstriction, tachycardia, hypertension, platelet activation, and endothelial injury. Severe spasm reduces flow and may provide a substrate for local thrombosis. Ergot derivatives and other vasoconstrictors less often produce a similar sequence; substance-related thrombosis requires a nonjudgmental history and targeted tests. A positive toxicology result does not exclude plaque or dissection. Isolated nonselective beta-blockade during cocaine intoxication remains problematic.

Coronary ectasia and aneurysm create recirculation and stasis, promoting mural thrombus and occlusion even without plaque rupture. Vasculitis, previous Kawasaki disease, connective tissue disorders, and congenital anomalies may alter wall and flow. Local compression or trauma may also activate coagulation; coronary stasis is a recognizable anatomical mechanism. Treatment depends on diameter, thrombus, and ischemia. Evidence for chronic anticoagulation in isolated ectasia remains limited.
A stent introduces a surface and changes vascular geometry and healing. Underexpansion, malapposition, edge dissection, uncovered struts, fracture, and residual thrombus promote early thrombosis. Interruption or poor response to antiplatelet drugs increases risk; stent thrombosis is a multifactorial failure. Neoatherosclerosis and acquired malapposition emerge in very late cases. Intracoronary imaging permits correction of the mechanical cause, not merely the clot.

Catheters and guidewires may injure the intima, create dissection, arrest flow, or introduce thrombus. Inadequate procedural anticoagulation, long procedure times, and insufficient flushing increase risk. After surgery or structural interventions, inflammation and interruption of antithrombotic therapy may contribute; iatrogenic thrombosis arises locally and must be distinguished from material embolized by a device. Timing helps but is insufficient. Angiographic review clarifies origin and mechanism.

Pathological anatomy, classification, and progression

Arterial thrombus is often platelet-rich in high-shear regions and contains fibrin, erythrocytes, neutrophils, and extracellular material. The erythrocyte component increases in stagnant portions. A simplistic distinction between white arterial and red venous thrombus does not describe this heterogeneity; thrombus composition varies within the same clot. Time, therapy, and location alter histology. Gross aspirate color does not reliably identify the cause.
A thrombus may be mural and nonocclusive, subtotal, or completely occlusive. It may propagate proximally and distally, oscillate within the lumen, or fragment. Ischemic territory depends on location and collaterals, while distal embolization damages the microcirculation even after epicardial reopening; thrombus burden guides technique and no-reflow risk. Angiography may underestimate its volume. OCT sees superficial detail, but the thrombus itself may obscure the wall.

Nonatherosclerotic in situ thrombosis may be classified by substrate: systemic hypercoagulability, inflammatory or toxic endothelial injury, anatomical stasis, prolonged spasm, procedural trauma, and intracoronary devices; this taxonomy is mechanistic and categories are not mutually exclusive; the dominant substrate guides prevention. A cancer patient may also have an underexpanded stent. Attributing everything to the systemic state would leave the local defect unresolved.
Fresh thrombus contains fibrin networks trapping cells and platelets. If flow is restored, it may dissolve through endogenous fibrinolysis and treatment; if it persists, macrophages, fibroblasts, capillaries, and organization intervene. Late canalization may produce multiple lumens on imaging. Thrombus organization indicates persistence, not necessarily embolism. A layered structure may mimic plaque or dissection. Correlation with history and surrounding wall prevents error.

ARC classification of stent thrombosis

• Definite thrombosis: angiographic confirmation of thrombus arising in the stent or within 5 mm of its margins, associated with acute ischemic symptoms, new ischemic ECG changes, or a typical biomarker pattern, or pathological confirmation of recent thrombus in the stent.
• Probable thrombosis: unexplained death within 30 days of implantation, or infarction in the treated vessel territory without angiographic confirmation and no other evident cause.
• Possible thrombosis: unexplained death more than 30 days after implantation, a sensitive but poorly specific category intended mainly for study adjudication.
• Acute thrombosis: within 24 hours; subacute: after 24 hours and up to 30 days; late: after 30 days and up to one year; very late: after one year.

ARC definitions standardize endpoints but do not replace individual clinical diagnosis. Possible thrombosis assigns every late unexplained death to the stent and has low specificity; definite thrombosis is specific but misses events without angiography or autopsy; ARC certainty describes documentation, not severity. Temporal classification suggests different mechanisms. Every real case requires review of the index procedure, adherence, and current imaging.
Acute and subacute thrombosis mainly involves underexpansion, edge dissection, residual thrombus, compromised inflow or outflow, and uncovered struts. Neoatherosclerosis, neointimal rupture, acquired malapposition, and fracture gain importance in late or very late forms; the temporal mechanism is probabilistic and not exclusive. An underexpanded stent may thrombose years later. OCT and IVUS identify combinations unresolved by angiography.

Microvascular thrombosis may accompany sepsis, COVID-19, catastrophic antiphospholipid syndrome, and disseminated intravascular coagulation. Myocardial injury may then result from microinfarctions without visible epicardial occlusion. Positive troponin does not automatically equal focal coronary infarction; coronary microthrombosis is rarely demonstrated in vivo. Magnetic resonance imaging and systemic context provide clues. Autopsy or biopsy is exceptional and not routine.
Favorable evolution includes lysis, restoration of TIMI 3 flow, and microvascular recovery. Unfavorable courses include propagation, reocclusion, distal embolization, stenotic organization, and recurrence due to a persistent cause. An excellent final angiographic result does not remove later systemic risk; late stability requires control of the mechanism. APS, an MPN, or cancer remain active beyond PCI. A mechanically corrected stent still requires adequate antiplatelet adherence.

Clinical manifestations

The typical manifestation is acute chest pain with ST elevation or depression and a dynamic troponin rise. Complete occlusion more often produces STEMI, while partial or intermittent thrombus may cause NSTEMI or unstable angina. No symptom reveals a nonatherosclerotic substrate; the acute coronary syndrome must be treated before etiology is complete. Young age and otherwise normal coronary arteries raise suspicion but do not justify less urgent care.
Dyspnea, nausea, sweating, and syncope accompany extensive ischemia or arrhythmias. Shock and cardiac arrest may be the first sign of left main, proximal-vessel, or stent thrombosis in an already compromised territory. Hemodynamic instability dominates diagnostic priorities. Rapid echocardiography seeks dysfunction and mechanical complications. Samples for hematological studies may be collected without delaying angiography and support.

Nonocclusive thrombosis may cause recurrent episodes, a variable threshold, or silent ischemia. Spontaneous lysis may leave nonobstructive arteries at examination and provisionally place the case on a MINOCA pathway; this proves neither a microvascular nor embolic disorder; a transient thrombus may leave OCT signs. Magnetic resonance imaging confirms the ischemic pattern. Timing and drugs given before angiography must be reconstructed.
APS may present with infarction at a young age, previous venous or arterial thrombosis, recurrent miscarriage, livedo, thrombocytopenia, or lupus. A prolonged aPTT may appear paradoxical in a thrombotic patient because lupus anticoagulant affects phospholipid-dependent tests; the antiphospholipid phenotype does not require every sign. A normal aPTT does not exclude APS. Diagnosis must not rest on antibody positivity during the emergency alone.

Myeloproliferative neoplasms may feature headache, erythromelalgia, aquagenic pruritus, splenomegaly, or previous thrombosis, but infarction may precede recognized symptoms. Hematocrit, leukocytes, and platelets may be abnormal; dehydration and the acute phase change values; the hematological signal requires confirmation after stabilization. Reactive thrombocytosis is common and not equivalent to an MPN. Driver mutations are tested in the appropriate specialist pathway.
In cancer, coronary thrombus may occur near diagnosis, during chemotherapy, or in advanced disease. Chest pain may be muted or confused with anemia, infection, or drug toxicity. Thrombocytopenia does not prevent the event and increases treatment risk; the cardio-oncology presentation requires shared decisions. Cancer prognosis does not automatically justify conservative care. Platelet count, tumor site, and planned procedures affect antithrombotics and revascularization.

Stent thrombosis often presents as STEMI, sudden death, or infarction in the treated territory. Date and type of implant, lesion complexity, and antiplatelet therapy are essential. Recent interruption for bleeding or surgery increases probability but does not prove sole causality; the previous stent must be located from documentation. Several stents may lie in one vessel. Angiography and imaging identify the segment generating thrombus.
COVID-19, sepsis, or catastrophic APS may produce multivessel thrombosis and multiorgan dysfunction. Pain may be absent in ventilated or sedated patients, and metabolic disturbances may confound the ECG. Troponin elevation is common in critical illness from nonthrombotic causes; the systemic context simultaneously raises and lowers specificity. An occluded artery confirms an epicardial target. Without occlusion, infarction criteria and imaging are required, not automatic inference.

Investigations and diagnosis

ECG, high-sensitivity troponin, complete blood count, renal function, electrolytes, and coagulation tests form the initial assessment. Primary PCI for STEMI proceeds without awaiting thrombophilia tests. Echocardiography defines territory, function, and complications but does not detect coronary thrombus sensitively; the urgent diagnosis is anatomical and clinical. Pretreatment samples may help if care is not delayed. The acute phase alters many hemostatic parameters.
Angiography shows a filling defect, cutoff, contrast around thrombus, stasis, or occlusion. A large burden with few atherosclerotic signs suggests but does not prove a nonatherosclerotic form. Multivessel distribution may reflect hypercoagulability, multiple emboli, or complicated diffuse spasm; the angiographic pattern guides the procedure. Intracoronary nitrate tests reversibility of constriction. After thrombus reduction, the wall can be assessed more accurately.

OCT distinguishes plaque rupture and identifies findings compatible with erosion, such as adherent thrombus on an intact cap or luminal irregularity without visible rupture. It may also recognize a calcified nodule, dissection, and thrombus on an apparently intact wall. In devices it measures expansion, apposition, strut coverage, and neoatherosclerosis. High OCT resolution is decisive at the surface. Residual thrombus causes shadowing and limits diagnosis. Contrast flushing may be unsuitable in instability or severe renal failure.
IVUS visualizes the entire wall, vessel area, deep plaque, intramural hematoma, and stent expansion and margins. It distinguishes subtle surface changes less well but needs less lumen clearing and penetrates some tissues better than OCT. IVUS imaging is particularly useful for underexpansion and sizing. An apparently normal wall reduces the plausibility of atherothrombosis. It does not itself prove systemic thrombophilia.

Differentiation from embolism requires a search for a cardiac or paradoxical source using echocardiography, rhythm monitoring, and selected imaging. A sharp distal cutoff and normal vessel after aspiration favor embolism; a documented local lesion favors in situ thrombosis; the origin-site distinction may remain probabilistic. APS and cancer can cause both local thrombi and emboli. Aspirate histology offers clues but often shows only fibrin and platelets.
SCAD may mimic smooth stenosis, distal occlusion, or thrombus. OCT or IVUS identifies a false lumen, flap, or hematoma, but instrumentation may extend dissection. Resolution after intracoronary nitrate supports epicardial spasm; if spasm has already caused thrombus, both coexist; the vascular differential diagnosis guides procedural caution. Ectasia and aneurysm are evident on angiography and IVUS. Vasculitis requires systemic signs and wall imaging, not autoimmune tests alone.

APS testing includes lupus anticoagulant, IgG or IgM anticardiolipin, and IgG or IgM anti-beta2-glycoprotein I. Positivity must persist at least 12 weeks to support diagnosis; anticoagulants, inflammation, and the acute phase may interfere; the antiphospholipid laboratory requires hematological interpretation. The 2023 ACR/EULAR criteria are for research classification. Clinical diagnosis remains distinct and integrates context, titer, and persistence.
BSH guidelines discourage routine inherited testing after adult arterial thrombosis because factor V Leiden, the prothrombin variant, and natural anticoagulant deficiencies have weak associations and rarely change management. In young people without atherosclerosis, acquired causes that alter therapy are prioritized; indiscriminate thrombophilia screening produces incidental results. MTHFR must not be requested as a thrombotic test. Selective testing is scheduled when acute conditions and drugs will not distort interpretation.

Repeat blood count, smear, ferritin, and erythropoietin guide assessment for an MPN; JAK2, CALR, and MPL mutations follow hematological algorithms. With consistent cytopenias or hemolysis, flow cytometry for GPI-deficient clones assesses PNH; these are not universal indiscriminate first-line panels; the hematological pathway starts from persistent abnormalities. Hemoconcentration may mimic erythrocytosis. Inflammation, iron, and drugs alter counts and require context.
Extensive cancer investigation is not indicated after every coronary thrombosis. History, examination, blood count, biochemistry, and age-recommended screening guide further testing. Weight loss, recurrent thrombosis, thrombocytosis, or focal findings justify targeted imaging; the cancer search must avoid unjustified overdiagnosis. Cancer drugs are reconstructed with dates and doses. Cardio-oncology distinguishes vasospastic, thrombotic, and myocardial toxicity.

Cardiac magnetic resonance imaging confirms ischemic necrosis and quantifies edema, microvascular obstruction, and scar. When arteries have reopened, it distinguishes myocarditis and Takotsubo syndrome; subendocardial or transmural distribution supports infarction. It does not always determine whether thrombus was local or embolic; tissue characterization complements coronary anatomy. Timing affects edema sensitivity. Instability and incompatible devices may preclude early imaging.

Treatment and prognosis

The acute phase follows coronary syndrome guidelines: primary PCI for STEMI, a risk-based invasive strategy for NSTEMI, and antiplatelet and procedural anticoagulant therapy unless contraindicated. Causal investigation must not delay reperfusion. High bleeding risk changes drugs and access; timely reperfusion saves myocardium regardless of etiology. The plan is then narrowed to the documented mechanism. A nonatherosclerotic diagnosis may reduce unnecessary long-term therapy.
During PCI, the wire and microcatheter cross thrombus cautiously. Manual aspiration is not routine but may be considered with a large burden, absent flow, or diagnostic need. IIb/IIIa inhibitors are reserved for bailout in thrombotic complications or no-reflow; thrombus reduction permits wall imaging. Balloon and stent are not mandatory without a residual lesion. Excess manipulation increases distal embolization and bleeding.

In stent thrombosis, flow is restored with ballooning, selective aspiration, and antithrombotic therapy. OCT or IVUS should be strongly considered after stabilization to identify underexpansion, malapposition, fracture, edge dissection, or neoatherosclerosis; mechanical correction is essential against recurrence. High-pressure post-dilation treats underexpansion when safe. A new stent is used only for a precise indication, avoiding unnecessary layers.
Adherence, interruption, dose, and interactions of P2Y12 therapy are checked immediately. If possible, a more potent agent is considered for unexplained thrombosis, balanced against bleeding. Genetic or platelet function tests are not universally recommended but may be considered in selected recurrent cases. Antiplatelet therapy requires individualized duration. Recent surgery needs coordination. Indefinite DAPT extension alone does not correct an underexpanded stent.

For a first arterial thrombosis in APS, EULAR recommends a vitamin K antagonist with INR 2 to 3 or 3 to 4 according to thrombotic and bleeding risk. Rivaroxaban must not be used in triple-positive patients, and DOACs are not preferred in arterial APS; APS prevention may include aspirin in selected cases. Recurrence at therapeutic INR requires adherence review and specialist reassessment. A higher target, aspirin addition, or heparin are individualized options.
In MPNs, treatment of the coronary event is combined with disease control. Polycythemia vera requires hematocrit below 45 percent; low-dose aspirin and cytoreduction are indicated according to risk, diagnosis, and bleeding. Essential thrombocythemia is stratified by age, thrombosis, and mutation; hematological cytoreduction reduces the systemic substrate. Extreme thrombocytosis with acquired von Willebrand disease may temporarily contraindicate aspirin. Hematology and cardiology coordinate antithrombotic and clonal therapy.

In cancer, PCI and antiplatelet therapy remain central to the arterial event when appropriate. Platelet count, tumor site, bleeding, and planned procedures determine strategy. Trial meta-analysis does not support universal prophylactic anticoagulation to prevent arterial events in oncology outpatients. Cancer therapy may be stopped or modified when causally implicated. Anticoagulation is used for a specific indication, not cancer alone. Decisions consider prognosis without denying effective treatment.
After an estrogen-associated event, the responsible preparation is stopped during assessment and alternative contraception or therapy is selected with gynecology. Smoking, hypertension, and migraine with aura are addressed. Chronic anticoagulation is not automatic without a thrombophilia justifying it; estrogen withdrawal reduces a provoking factor. A future pregnancy requires preconception counseling. Prevention must consider both thrombotic risk and individual reproductive needs.

COVID-19-associated infarction receives standard revascularization with staff protection and clinical adaptations. Prolonged therapeutic anticoagulation is not prescribed solely for a high D-dimer or previous infection; documented thrombosis or another indication is required; the infectious phase may require venous prophylaxis according to severity and guidelines, but this does not replace coronary therapy. Antiviral interactions and renal function influence antithrombotics.
Cocaine and stimulants require cessation, benzodiazepines for sympathetic overactivity, and vasodilators when indicated, in addition to thrombosis management. An isolated nonselective beta-blocker is not the first response during acute intoxication. Dependence and relapse require a dedicated pathway; toxicological prevention is part of vascular therapy. Thrombus or stenosis is treated according to anatomy. Abstinence does not remove other cardiovascular factors.

Prognosis depends on ischemic mass, final flow, ventricular function, and persistence of the cause. Stent thrombosis, high-risk APS, MPNs, and active cancer entail risks of recurrence and treatment-related bleeding. Follow-up must integrate cardiology, hematology, and other relevant specialties; competing risk precludes simple formulas. Adherence, blood count, INR when needed, and symptoms are monitored. Cardiac rehabilitation is adapted to systemic disease.

Complications

Persistent occlusion causes transmural infarction, remodeling, and heart failure. Sudden thrombosis in a vessel without previous stenosis may affect a territory lacking collaterals. Damage is the same as for any infarction of equal extent even without causal plaque; ventricular function and regional abnormalities are assessed by echocardiography; cardiac magnetic resonance imaging characterizes and quantifies infarct extent. Heart failure therapy follows function and symptoms. Secondary prevention adds specific etiologic control.
Fragments may migrate into the microcirculation spontaneously or during PCI, causing no-reflow and microvascular obstruction. Persistent ST elevation and reduced blush indicate insufficient tissue perfusion despite epicardial TIMI 3 flow; distal embolization increases infarct size and severity. Vasodilators treat the vasomotor component but do not dissolve every microthrombus. Particularly cautious procedural technique tangibly reduces iatrogenic risk.

Ventricular tachycardia, ventricular fibrillation, block, and arrest result from acute ischemia or scar. Stent thrombosis may present as sudden death before angiographic confirmation, explaining the ARC probable and possible categories. The arrhythmic complication requires reperfusion and advanced protocols. Late risk depends on ventricular function and residual substrate. Thrombotic etiology alone does not determine a defibrillator indication.
Cardiogenic shock may follow proximal occlusion, multivessel thrombosis, or infarction in a heart with reduced baseline function. Pharmacological and mechanical support is selected by hemodynamic phenotype and recovery potential. In catastrophic APS or sepsis, vasoplegia and microthrombosis add extracardiac components; multifactorial shock requires repeated diagnosis. Revascularizing the culprit vessel remains a priority. Support does not correct coagulopathy or the stent defect.

Recurrence may affect the same segment, another vessel, or the newly treated stent. Causes include uncontrolled APS, active clonal disease, interrupted antiplatelet therapy, persistent underexpansion, and cancer progression. A new occlusion must not automatically be called drug resistance; coronary reocclusion requires urgent repeat angiography. Mechanics, adherence, interactions, and diagnosis are reassessed. Recurrence changes follow-up intensity and sometimes long-term strategy.
Antiplatelet drugs and anticoagulants may cause bleeding, particularly in combination. APS with thrombocytopenia, an MPN with acquired von Willebrand disease, mucosal cancer, renal failure, and recent surgery increase risk. Bleeding may force treatment interruption and promote new thrombosis; the thrombosis-bleeding conflict requires the shortest effective combination duration. Gastroprotection and correction of modifiable factors help. Every interruption needs a restart plan.

Mechanical complications of infarction include free-wall rupture, ventricular septal defect, and acute mitral regurgitation from papillary muscle rupture. A new murmur, pulmonary edema, or sudden deterioration requires immediate echocardiography. Treatment is surgical or percutaneous according to anatomy and stability; the mechanical catastrophe does not await thrombophilia definition. Temporary support may permit transfer. Prognosis depends on rapid recognition and repair feasibility.
An incorrect etiologic diagnosis is an important clinical complication. Calling local thrombosis an embolism may miss APS or a stent defect; attributing unseen erosion to thrombophilia may produce unnecessary anticoagulation. Conversely, DAPT alone in arterial APS leaves systemic risk; diagnostic iatrogenesis is reduced by imaging and reassessment. A provisional diagnosis must be declared as such. The discharge plan includes pending tests and responsibility for interpreting them.