Thromboembolism in myocardial infarction: causes, left ventricular thrombus, stroke, pulmonary embolism and prevention

Thromboembolism is a condition in which a blood clot forms in one location, then completely or partially blocks the vessel at the site of formation or breaks off and is carried by the bloodstream to another vessel. In myocardial infarction, thromboembolic complications can affect the coronary arteries, the left ventricular cavity, the cerebral arteries, the vessels of the extremities, the kidneys, the spleen, as well as the venous system and the pulmonary arteries. [1]

It's important not to confuse these different processes. Coronary artery thrombosis is a common cause of a heart attack itself, when a clot forms at the site of a damaged atherosclerotic plaque and blocks blood flow to the heart muscle. Post-heart attack thromboembolism is a complication when a clot forms, for example, in the left ventricle or deep veins of the legs, and can then travel to the brain, limb, or pulmonary artery. [2]

The most common source of post-infarction arterial embolism is a thrombus in the left ventricle. It most often forms after a large anterior infarction, when the apex or anterior wall of the left ventricle contracts poorly, blood stagnates in this area, and the damaged inner surface of the heart promotes clotting. [3]

Another group of complications is venous thromboembolism: deep vein thrombosis and pulmonary embolism. After a heart attack, the risk of venous thromboembolism may increase due to hospitalization, decreased mobility, heart failure, older age, cancer, obesity, infection, and other factors. [4]

The practical point is that thromboembolism after a heart attack does not always present with heart pain. It can manifest as sudden weakness in an arm or leg, speech impairment, vision loss, acute pain and coldness of the limb, severe shortness of breath, chest pain when breathing, hemoptysis, or a sudden drop in blood pressure. [5]

Type of thromboembolic complication	Where does a blood clot form?	Where can it go?
Left ventricular thrombus	Inside the left ventricle after the infarction zone	Brain, kidneys, spleen, limbs
Ischemic stroke after myocardial infarction	Often from the heart or large arteries	Arteries of the brain
Systemic arterial embolism	Heart or large arteries	Limbs and internal organs
Deep vein thrombosis	Veins of the leg, thigh, or pelvis	May cause pulmonary embolism
Pulmonary thromboembolism	Usually a deep vein thrombosis	Pulmonary arteries
Stent thrombosis	Inside the coronary stent	Recurrent coronary artery occlusion

Code according to ICD 10 and ICD 11

In the International Classification of Diseases, 10th revision, acute myocardial infarction is classified under I21, and subsequent infarction under I22. Individual thromboembolic complications are coded according to their location and type: pulmonary embolism is classified under I26, cerebral infarction under I63, arterial embolism and thrombosis under I74, and venous thrombosis and embolism under groups I80-I82 depending on the location. [6]

In the International Classification of Diseases, 11th revision, acute myocardial infarction is classified as BA41, including variants with and without ST-segment elevation. For pulmonary thromboembolism, the International Classification of Diseases, 11th revision uses the group BB00, and for deep vein thrombosis, BD71; in cases of thromboembolic complications after an infarction, both the infarction and the specific complication are usually reflected in the documentation. [7]

System	Code	Formulation	How does it relate to the topic?
ICD 10	I21	Acute myocardial infarction	The main diagnosis of acute myocardial infarction
ICD 10	I22	Subsequent myocardial infarction	Recurrent infarction in the acute period
ICD 10	I26	Pulmonary embolism	A venous thrombus enters the pulmonary arteries
ICD 10	I63	Cerebral infarction	Possible outcome of embolism in a cerebral artery
ICD 10	I74	Arterial embolism and thrombosis	Systemic arterial embolism
ICD 10	I80-I82	Phlebitis, thrombophlebitis, venous embolism and thrombosis	Deep vein thrombosis and other venous thromboses
ICD 11	BA41	Acute myocardial infarction	Modern rubric of infarction
ICD 11	BB00	Pulmonary thromboembolism	Pulmonary artery occlusion
ICD 11	BD71	Deep vein thrombosis	Source of possible pulmonary embolism

Why do blood clots form after a heart attack?

During a heart attack, several factors converge to promote thrombus formation. The damaged heart wall loses its normal inner surface, blood moves more slowly in the poorly contracting area, and inflammation and stress activate the coagulation system. This follows classical logic: thrombi are more likely to form where there is damage to the vascular or cardiac surface, blood stagnation, and increased blood clotting activity. [8]

The left ventricular apex is most vulnerable after anterior infarction. If this region contracts poorly or barely moves at all, blood stagnates there, and a mural thrombus can form. Recent reviews show that the risk of left ventricular thrombus formation is significantly higher in cases of anterior infarction and reduced left ventricular ejection fraction. [9]

The time it takes to restore coronary blood flow is crucial. The sooner the culprit artery is opened, the smaller the area of necrosis, the better the contractility is maintained, and the lower the risk of developing a large congestive area within the ventricle. Therefore, early percutaneous coronary intervention and modern antithrombotic therapy have reduced the incidence of some post-infarction thromboembolic complications compared to the pre-interventional era. [10]

Post-infarction venous thromboembolism develops according to a different logic. Bed rest, decreased mobility, heart failure, dehydration, advanced age, cancer, obesity, infections, central venous catheters, and previous thromboses are all important factors. A study of the risk of venous thromboembolism after a heart attack showed that the 30-day risk is increased compared to the general population, although the absolute risk remains low and varies significantly with comorbidities. [11]

A separate issue is the combination of thrombotic and bleeding risks. After a heart attack, patients often require antiplatelet drugs, sometimes anticoagulants, and, if stenting is performed, protection against stent thrombosis. However, each additional drug that inhibits coagulation increases the risk of bleeding. Therefore, thromboembolism prevention after a heart attack always requires an individualized balance. [12]

Factor	How does it increase the risk of a blood clot?
Anterior infarction	Often damages the apex of the left ventricle
Low ejection fraction	Blood moves more slowly inside the ventricle
Akinesia or dyskinesia of the wall	A zone of blood stagnation is formed
Late revascularization	The area of necrosis and wall weakness increases
Heart failure	Increases congestion and reduces mobility
Bed rest	Increases the risk of deep vein thrombosis
Oncological disease	Enhances blood clotting
Chronic kidney disease	Complicates the balance between thrombosis and bleeding

Left ventricular thrombus after infarction

Left ventricular thrombus is one of the most well-known thromboembolic complications of myocardial infarction. It most often occurs after ST-segment elevation infarction, especially anterior infarction, when the apex of the left ventricle is damaged, creating a zone of weak or absent contraction. [13]

The current incidence of left ventricular thrombus is lower than in the era before the widespread use of primary percutaneous coronary intervention, but the problem has not disappeared. A 2024 meta-analysis of ST-segment elevation myocardial infarction in the modern era found that left ventricular thrombus continues to be detected, especially with more sensitive imaging, including cardiac magnetic resonance imaging. [14]

A particularly high risk is observed with a combination of anterior infarction and reduced ejection fraction. Current data based on cardiac magnetic resonance imaging suggest that thrombus incidence may be significantly increased in patients with anterior infarction and reduced left ventricular systolic function. [15]

The insidious nature of a left ventricular thrombus is that it often produces no distinct symptoms until embolism occurs. A patient may feel relatively stable after stenting, but a mural clot may already be forming within the ventricle. Therefore, echocardiographic evaluation is important after a major infarction, especially if there is a reduced ejection fraction or abnormal apical motion. [16]

The American Heart Association emphasizes that left ventricular thrombus remains a challenging clinical problem despite advances in reperfusion therapy. A 2022 document addresses prevention, diagnosis, imaging choices, duration of anticoagulation, and the role of oral anticoagulants in patients with left ventricular thrombus. [17]

Sign of high risk of left ventricular thrombus	Why is it important?
Anterior myocardial infarction	Often damages the apex and anterior wall
Reduced ejection fraction	Blood is pushed out of the ventricle worse
Apical akinesia	Blood stagnates in a sedentary area
Large ST-segment elevation infarction	More necrosis and inflammation
Late opening of the artery	More myocardial damage
History of thrombus	Increased thrombotic tendency is possible
Poor visualization with conventional echocardiography	A more precise method may be required

Stroke and systemic embolism after infarction

If a thrombus breaks loose from the left ventricle, it enters the aorta and can then travel to the arteries of the brain, kidneys, spleen, intestines, or extremities. The most dangerous and clinically common consequence is ischemic stroke, when the embolus blocks a cerebral artery and causes brain death. [18]

Signs of a stroke after a heart attack require immediate attention: sudden weakness or numbness of the face, arm, or leg, speech impairment, facial asymmetry, sudden vision loss, severe dizziness, loss of coordination, or confusion. In this situation, symptoms should not be attributed to weakness after a heart attack or the effects of medications. [19]

Systemic embolism can present with more than just stroke. An embolism in an artery in a limb can cause sudden pain, coldness, pallor, numbness, weakness, and loss of pulse below the site of the blockage. An embolism in the renal or splenic artery can cause sharp pain in the abdomen or side, while an embolism in the intestinal vessels can cause severe abdominal pain that is out of proportion to the initial scant physical examination findings. [20]

The risk of embolism depends not only on the presence of a thrombus but also on its shape. A mobile thrombus or one protruding into the ventricular cavity is usually more dangerous than a dense mural thrombus, although even a mural thrombus requires careful evaluation. Therefore, in the imaging report, it's not just the words "there is a thrombus" that are important, but also its size, mobility, location, and dynamics. [21]

Stroke prevention in the presence of a left ventricular thrombus typically involves anticoagulation, but this decision is complicated by the fact that after a heart attack and stenting, the patient is often already receiving dual antiplatelet therapy. Current guidelines seek to reduce the duration of triple antithrombotic therapy in patients who require both anticoagulants and antiplatelet agents, as bleeding significantly worsens the prognosis. [22]

Where does the embolus go?	Possible manifestation
Brain artery	Stroke, speech impairment, limb weakness
Retinal artery	Sudden loss of vision in one eye
Artery of the arm or leg	Sharp pain, coldness, no pulse
Renal artery	Pain in the side, blood in the urine, deterioration of kidney function
Splenic artery	Pain in the left hypochondrium
Intestinal arteries	Severe abdominal pain and risk of intestinal ischemia

Post-infarction venous thromboembolism: deep vein thrombosis and pulmonary embolism

Venous thromboembolism differs from arterial embolism following a left ventricular thrombus. Here, the thrombus most often forms in the deep veins of the legs or pelvis and can then break off and travel through the right side of the heart to the pulmonary arteries. This complication is called pulmonary embolism. [23]

Following a heart attack, venous thromboembolism is primarily associated with hospitalization and decreased mobility, especially if the patient is in intensive care, has heart failure, has suffered shock, stroke, infection, or surgery. The American Society of Hematology emphasizes that hospitalization for an acute medical illness is an important time for assessing the risk and preventing venous thromboembolism. [24]

Deep vein thrombosis can present with pain, swelling, distension, redness, or warmth in one leg, but can sometimes be virtually asymptomatic. Pulmonary embolism more often causes sudden shortness of breath, chest pain when breathing, rapid pulse, cough, hemoptysis, a drop in blood pressure, or fainting. [25]

A 2020 study found that the 30-day risk of venous thromboembolism after a heart attack is higher than in the general population, although the absolute risk remains low. The risk is particularly increased by comorbid conditions such as hemiplegia and cancer, so prevention is not needed equally for everyone, but rather for those whose risk of thrombosis outweighs the risk of bleeding. [26]

NICE recommends assessing the risk of venous thromboembolism in hospitalized patients and using pharmacological prophylaxis for at least 7 days in acutely ill medical patients if the risk of thrombosis outweighs the risk of bleeding. This is important after a heart attack, as some patients are already receiving anticoagulants for acute coronary syndrome, while others require separate prophylaxis due to immobility. [27]

State	Where is the clot?	Main symptoms
Deep vein thrombosis of the leg	Deep veins of the leg	Swelling, pain, distension, sometimes asymptomatic
Deep vein thrombosis of the thigh or pelvis	Large deep veins	Severe leg swelling, pain, risk of embolism
Pulmonary thromboembolism	Pulmonary arteries	Sudden shortness of breath, pain when breathing, tachycardia
Massive pulmonary embolism	Large pulmonary arteries	Drop in blood pressure, fainting, shock
Venous thromboembolism in a patient in intensive care	Veins of the legs, pelvis or catheters	Often masked by a severe general condition

Stent thrombosis and recurrent coronary occlusion

Stent thrombosis is the formation of a thrombus within a previously placed coronary stent. It is not a classic "embolism" from another site, but in terms of clinical danger, it is considered one of the most serious thrombotic complications after a heart attack, as it can cause reocclusion of the coronary artery, a new heart attack, cardiogenic shock, or sudden death. [28]

The risk of stent thrombosis is particularly high with premature discontinuation of antiplatelet drugs, insufficient stent deployment, complex arterial lesions, diabetes mellitus, chronic kidney disease, ongoing smoking, and high thrombotic activity during the acute phase of myocardial infarction. Therefore, after stenting, patients are typically prescribed dual antiplatelet therapy, with the drug and duration selected based on the balance of ischemic and bleeding risks. [29]

If a patient suddenly experiences recurring chest pain, cold sweats, shortness of breath, weakness, or syncope after stenting, recurrent ischemia or stent thrombosis should be considered until proven otherwise. In this situation, a scheduled visit should not be delayed: an urgent electrocardiogram, cardiac troponin, and assessment of the need for repeat coronary angiography are required. [30]

Stent thrombosis is particularly challenging when the patient simultaneously has a left ventricular thrombus and requires anticoagulation. Physicians must then combine stent thrombosis protection with cardiac embolism prevention, but excessively prolonged triple therapy dramatically increases the risk of bleeding. The 2025 guidelines indicate that in patients with acute coronary syndrome requiring oral anticoagulation, aspirin is typically discontinued after 1-4 weeks of triple antithrombotic therapy, with continued oral anticoagulation and a platelet P2Y12 receptor inhibitor. [31]

It's important for patients to understand that a stent is not a "permanent plug" that protects the artery on its own. Its safety during the first few months directly depends on properly selected antithrombotic therapy, adherence to treatment, smoking cessation, and control of cholesterol, blood pressure, and diabetes. [32]

Risk factor for stent thrombosis	Why is it dangerous?
Unauthorized discontinuation of antiplatelet therapy	Platelets can quickly form a clot inside the stent
Complex coronary artery disease	Technically, the risk of an incomplete result is higher
Diabetes mellitus	Higher thrombotic and atherosclerotic risk
Chronic kidney disease	There is a higher risk of thrombosis and bleeding at the same time
Smoking	Increases inflammation, spasm and thrombus formation
Recurrent pain after stenting	May be a sign of recurrent coronary occlusion

Diagnosis of thromboembolism after myocardial infarction

The primary method for detecting left ventricular thrombus is echocardiography. It shows ejection fraction, wall motion, apical akinesia or dyskinesia, and can also visualize the thrombus. If the standard image is of poor quality, contrast echocardiography or more accurate imaging techniques are used. [33]

Cardiac magnetic resonance imaging is considered a more sensitive method for detecting left ventricular thrombus, especially when echocardiography is inconclusive. The American Heart Association notes that cardiac magnetic resonance imaging may be particularly useful when echocardiography is inconclusive but clinical suspicion remains high. [34]

If a stroke is suspected, urgent neurological evaluation and brain imaging are needed. The physician must determine whether the cause is ischemic stroke, hemorrhage, transient ischemic attack, or another condition, because treatment and the safety of antithrombotic therapy depend on the type of stroke. [35]

If deep vein thrombosis is suspected, the primary initial investigation is usually an ultrasound examination of the veins with compression testing. If pulmonary embolism is suspected, clinical probability assessment, blood oxygen saturation, laboratory tests, an electrocardiogram, echocardiography in severe cases, and pulmonary artery computed tomography (CT) scanning, if safe and available, are used. [36]

If stent thrombosis is suspected, the key tests are an electrocardiogram, cardiac troponin, and urgent coronary angiography, if indicated. Unlike a left ventricular thrombus, the problem is located within the coronary artery, so imaging of the cardiac cavity does not replace assessment of the coronary bed. [37]

Suspected complication	Basic diagnostic methods
Left ventricular thrombus	Echocardiography, contrast echocardiography, cardiac magnetic resonance imaging
Ischemic stroke	Neurological examination, computed tomography or magnetic resonance imaging of the brain
Systemic embolism of the limb	Examination, pulse, vascular ultrasound, angiography
Deep vein thrombosis	Ultrasound examination of veins
Pulmonary thromboembolism	Clinical assessment, computed tomography of the pulmonary arteries, echocardiography in case of instability
Stent thrombosis	Electrocardiogram, troponin, coronary angiography

Treatment of thromboembolic complications

If a left ventricular thrombus is confirmed after a heart attack, oral anticoagulation therapy is typically considered. The American Heart Association recommends that patients with a left ventricular thrombus after a heart attack typically receive anticoagulation for approximately 3 months, but the duration and choice of drug depend on the thrombus dynamics, bleeding risk, and concomitant antiplatelet therapy. [38]

If a left ventricular thrombus has not yet been identified but the risk is very high, such as a large anterior infarction and severe apical akinesia, the question of prophylactic anticoagulation remains complex. The American Heart Association recommends that prophylactic anticoagulation after an infarction may last for 1-3 months, but the decision should be based on the risk of bleeding and be individualized. [39]

For venous thromboembolism, treatment depends on its severity. Deep vein thrombosis and stable pulmonary embolism are usually treated with anticoagulants, while massive pulmonary embolism with shock may require more aggressive treatments, including thrombolysis or interventional treatment under strict indications. In cases of recent infarction, the decision is particularly difficult because the risk of bleeding can be high. [40]

In cases of stent thrombosis, treatment usually requires urgent coronary angiography and restoration of coronary blood flow. This is not a situation where "reinforcing the pills at home" is sufficient: reocclusion of a coronary artery can quickly lead to a major heart attack, arrhythmia, or shock. [41]

The most difficult part of treatment is the drug combination. After a heart attack, a patient may require dual antiplatelet therapy, and in the case of a left ventricular thrombus or venous thromboembolism, an anticoagulant as well. Such combinations increase the risk of bleeding, so current guidelines aim to reduce unnecessary duration of triple therapy and select the safest regimen. [42]

Situation	Possible tactics
Confirmed left ventricular thrombus	Oral anticoagulation with repeated imaging
Very high risk of left ventricular thrombus without confirmation	Individual discussion of prophylactic anticoagulation
Ischemic stroke after myocardial infarction	Urgent neurological care and search for the source of embolism
Deep vein thrombosis	Anticoagulation in the absence of contraindications
Pulmonary thromboembolism	Anticoagulation; in case of shock, reperfusion tactics are possible
Stent thrombosis	Urgent coronary assessment and restoration of blood flow
High risk of bleeding	Reduction of excessive antithrombotic load

Prevention of thromboembolism after myocardial infarction

The primary prevention of left ventricular thrombus is early restoration of coronary blood flow and reduction of myocardial damage. The better preserved left ventricular contractility, the less blood congestion and the lower the risk of intracardiac thrombus formation. Therefore, timely percutaneous coronary intervention, antithrombotic therapy, and secondary prevention are directly related to embolism prevention. [43]

After a major anterior infarction, re-evaluation of the heart is important. If the initial echocardiogram was performed early and the image quality is limited, and the risk of thrombus remains high, the physician may order a repeat echocardiogram, contrast study, or cardiac magnetic resonance imaging. [44]

Prevention of venous thromboembolism begins with risk assessment for each hospitalized patient. NICE recommends assessing the risk of venous thromboembolism and bleeding in hospitalized patients, and administering pharmacological prophylaxis to acutely ill medical patients if the risk of thrombosis outweighs the risk of bleeding. [45]

Equally important are early mobilization, treatment of heart failure, adequate hydration, infection control, avoidance of unnecessary bed rest, and mechanical prophylaxis in patients at high risk of bleeding. The American Society of Hematology notes that in hospitalized medical patients, prophylaxis should consider both thrombotic and bleeding risks. [46]

Prevention of stent thrombosis requires strict adherence to antiplatelet therapy. Patients should not independently discontinue aspirin, ticagrelor, prasugrel, clopidogrel, or anticoagulants if prescribed, even before dental procedures or minor surgery; any changes should be discussed with a cardiologist and a specialist. [47]

Prevention direction	What does it include?
Early revascularization	Reduction of infarction area and risk of left ventricular thrombus
Echocardiographic monitoring	Search for thrombus, assessment of ejection fraction and akinesia
Antithrombotic therapy	Protection against coronary thrombosis and stent
Anticoagulation as indicated	Prevention of embolism in left ventricular thrombus or venous thromboembolism
Assessing the risk of venous thromboembolism	Decision on inpatient prophylaxis
Early mobilization	Reduction of venous congestion
Bleeding control	Preventing harm from excessive antithrombotic therapy

What a patient should know after discharge

After a heart attack, it's important to understand what medications are prescribed and why. Antiplatelet drugs protect the stent and coronary arteries, an anticoagulant, if prescribed, protects against embolism from a left ventricular thrombus or venous thrombi, and statins, blood pressure medications, and diabetes treatment reduce the risk of recurrent vascular events. [48]

Blood thinners should not be discontinued on your own due to bruising, dental work, or fear of bleeding. However, dangerous signs of blood loss should not be ignored: black stools, blood in the urine, bloody vomiting, severe nosebleeds, rapidly growing hematomas, sudden weakness, or a drop in blood pressure. A doctor should monitor the situation. [49]

Seek immediate medical attention if you experience signs of a stroke: facial asymmetry, arm or leg weakness, speech impairment, sudden vision loss, severe imbalance, or confusion. Following a heart attack, such symptoms may indicate a cardiac embolism or other vascular accident. [50]

Urgent care is also needed for signs of pulmonary embolism: sudden shortness of breath, chest pain when inhaling, hemoptysis, fainting, a marked increase in heart rate, or a drop in blood pressure. The combination of these symptoms with swelling or pain in one leg after a recent hospitalization is especially worrisome. [51]

It is helpful for patients to have a written list of diagnoses, stents, medications, dosages, date of heart attack, echocardiogram results, and information about a left ventricular thrombus, if present. This helps doctors quickly make the right decision in the event of recurrent chest pain, stroke, bleeding, or the need for surgery. [52]

Symptom after a heart attack	Possible cause	What to do
Sudden weakness of an arm or leg	Stroke or systemic embolism	Call for help immediately
Speech impairment	Stroke	Call for help immediately
Sharp pain and coldness in the leg	Arterial embolism	Urgent vascular care
Swelling and pain in one leg	Deep vein thrombosis	Urgent medical assessment
Sudden shortness of breath and pain when inhaling	Pulmonary thromboembolism	Call for help immediately
New pressing pain in the chest	Stent thrombosis or recurrent ischemia	Urgent cardiac evaluation
Black stool or blood in urine	Bleeding during therapy	Notify your doctor immediately

Frequently asked questions

What is thromboembolism in myocardial infarction?
It is a complication in which a clot forms in the heart, veins, or vessel and then blocks blood flow locally or travels to another vessel. Of particular importance after an infarction are left ventricular thrombus, ischemic stroke, systemic arterial embolism, deep vein thrombosis, pulmonary embolism, and stent thrombosis. [53]

Why might a thrombus form in the left ventricle after a heart attack?
After a major heart attack, part of the left ventricular wall contracts poorly, especially in the apex. Blood flows more slowly there, the inner surface of the heart is damaged, and the coagulation system is activated, creating conditions for a mural thrombus. [54]

Which type of infarction is most often complicated by left ventricular thrombus?
Most commonly, it is a large anterior infarction with ST-segment elevation, reduced ejection fraction, and left ventricular apical akinesia. Current data suggest that the risk is particularly increased with the combination of anterior infarction and reduced systolic function. [55]

Can a thrombus in the left ventricle be felt?
Usually not. A thrombus within the ventricle itself often produces no specific symptoms until an embolism occurs. Therefore, after a major anterior infarction, cardiac imaging is important, primarily echocardiography, and if in doubt, cardiac magnetic resonance imaging. [56]

What is the danger of a left ventricular thrombus?
It can become a source of embolism in the cerebral or peripheral arteries. The most dangerous consequence is ischemic stroke, but embolism in the arteries of the extremities, kidneys, spleen, or intestines is also possible. [57]

How is a left ventricular thrombus treated after a heart attack?
Oral anticoagulation therapy for approximately 3 months with repeated imaging is typically considered, but the specific regimen depends on the size and shape of the thrombus, the risk of bleeding, the presence of a stent, and the need for antiplatelet drugs. [58]

Why might a pulmonary embolism occur after a heart attack?
A pulmonary embolism typically occurs when a blood clot forms in the deep veins of the legs or pelvis, then breaks off and travels to the pulmonary arteries. After a heart attack, factors that contribute to this include hospitalization, immobility, heart failure, age, and underlying medical conditions. [59]

What symptoms indicate pulmonary embolism after a heart attack?
The most alarming are sudden shortness of breath, chest pain when breathing, rapid pulse, hemoptysis, fainting, a drop in blood pressure, and a sharp deterioration in health. These symptoms require immediate medical attention. [60]

Is stent thrombosis a thromboembolism?
Strictly speaking, it is a localized thrombosis within a coronary stent, not an embolism from elsewhere. However, clinically, it is the most important thrombotic complication after a heart attack, as it can cause a recurrent heart attack, shock, or sudden death. [61]

Is it possible to completely prevent thromboembolism after a heart attack?
It's impossible to completely guarantee the absence of thromboembolism, but the risk can be significantly reduced by promptly restoring coronary blood flow, taking prescribed antithrombotic medications, monitoring the ejection fraction, identifying left ventricular thrombi, administering venous thromboembolism prophylaxis in the hospital, and not discontinuing medications on your own. [62]

Key points from experts

Glenn N. Levine, MD, is the lead author of the American Heart Association's scientific position statement on left ventricular thrombus. His group's main practical message: left ventricular thrombus after myocardial infarction remains a complex complication that requires consideration of the risk of embolism, the quality of imaging, the need for anticoagulation, and the risk of bleeding when combined with antiplatelet therapy. [63]

Sunil V. Rao, MD, chair of the American College of Cardiology-American Heart Association 2025 Guidelines Task Force on Acute Coronary Syndrome. The key message of the guideline is that a patient with acute coronary syndrome requires a full care pathway—from early diagnosis and revascularization to antithrombotic therapy and secondary prevention—because thrombotic complications remain a major threat. [64]

B. Bikdeli et al. review of key antithrombotic recommendations for 2025. Practical conclusion: If a patient after acute coronary syndrome requires both oral anticoagulation and antiplatelet therapy, the duration of triple therapy should be kept to the minimum necessary because bleeding is a serious risk. [65]

HJ Schünemann and the American Society of Hematology panel on venous thromboembolism prevention in hospitalized medical patients. Their key message: hospitalization for acute illness is an important moment for assessing the risk of venous thromboembolism, and pharmacologic prophylaxis is indicated for patients with an acceptable risk of bleeding. [66]

Robert A. Byrne, Professor of Cardiology, Chair of the 2023 European Society of Cardiology Task Force on Acute Coronary Syndromes. The practical implication of the European guideline is that ST-segment elevation and non-ST-segment elevation infarction should be managed as a single spectrum of acute coronary syndrome, where antithrombotic therapy, invasive strategy, and complication prevention should be tailored to the patient's risk. [67]

Result

Thromboembolism in myocardial infarction includes several different complications: left ventricular thrombus with the risk of stroke and systemic embolism, venous thromboembolism with deep vein thrombosis and pulmonary embolism, and stent thrombosis as a dangerous coronary thrombotic complication. These conditions have different mechanisms, symptoms, diagnostic methods, and treatments. [68]

The most common arterial threat after a major anterior infarction is a left ventricular thrombus. It is identified using echocardiography, followed by cardiac magnetic resonance imaging if necessary, and, if confirmed, anticoagulant therapy with repeat imaging is usually considered. [69]

The primary prevention measures are rapid restoration of coronary blood flow, appropriate antithrombotic therapy, in-hospital assessment of the risk of venous thromboembolism, early mobilization, and strict adherence to medications after discharge. If signs of stroke, pulmonary embolism, acute limb ischemia, bleeding, or recurrent chest pain occur, seek immediate medical attention. [70]