It is the formation of a thrombus within an artery.
In most cases, arterial thrombosis follows the rupture of the atheroma (a fat-rich deposit in the wall of the blood vessel) and is therefore called atherothrombosis.
An arterial embolism occurs when clots migrate downward and can affect any organ.
Alternatively, arterial occlusion results from embolism of blood clots originating in the heart (“cardiogenic” emboli).
The most common cause is atrial fibrillation, which causes blood stasis within the atria with easy thrombus formation, but clots can develop within the heart for other reasons.
A stroke is the rapid deterioration of brain function due to a disturbance in the blood supply to the brain. This can be due to ischemia, thrombus, embolus (a lodged particle), or bleeding.
A thrombus (blood clot) usually forms around the atherosclerotic plaques in a thrombotic stroke.
Since the blockage of the artery is gradual, the onset of symptomatic thrombotic attacks is slower. Thrombotic stroke can be divided into two categories: extensive vessel disease and small vessel disease.
The first affects vessels such as the internal and vertebral carotids and the circle of Willis. The latter can affect smaller ships, such as the branches of the process of Willis.
Myocardial infarction (MI), or heart attack, is caused by ischemia (restriction in the blood supply), often due to the obstruction of a coronary artery by a thrombus.
This restriction provides an insufficient oxygen supply to the heart muscle, resulting in tissue death (infarction).
Then a lesion is formed, which is a heart attack. Myocardial infarction can quickly become fatal if emergency medical treatment is not received immediately. If diagnosed within 12 hours of the initial episode (attack), thrombolytic therapy is started.
Venous and arterial thrombosis: Two aspects of the same disease?
Venous and arterial thrombotic disorders have long been viewed as separate pathophysiological entities, partly as a result of noticeable anatomical differences as well as their different clinical presentations.
In particular, arterial thrombosis has long been largely a phenomenon of platelet activation, whereas venous thrombosis is essentially a matter of activation of the coagulation system.
However, there is evidence that this dichotomy is probably an oversimplification.
Fibrin-rich thrombi form in the left atrial appendage of patients with atrial fibrillation and the coronary artery system of patients with myocardial infarction.
Consequently, anticoagulant drugs are highly effective for preventing arterial embolism related to atrial fibrillation and for the prevention and treatment of coronary artery disease.
Similarly, platelets play an unavoidable role in thrombus formation in the venous system, and antiplatelet agents effectively prevent venous thromboembolic disorders, although to a lesser extent than anticoagulant drugs.
As another example, subjects with retinal vein thrombosis often have associated cardiovascular risk factors, and the causes of mortality in follow-up are often arterial vascular events.
Causes of the condition
In most cases, atrial thrombosis is caused by atherosclerosis, a condition in which plaque builds up around the arterial wall and causes the arteries to narrow or harden.
The arteries are lined by endothelium, which allows blood to flow smoothly. When the endothelium is damaged, plaque primarily made up of cholesterol, calcium, and other substances in the blood, begins to build upon the artery wall.
The condition increases the risk of blood clots. The plaque eventually breaks open in some cases and causes blood cell fragments to collect in the affected area. These fragments can stick together and form blood clots.
The risk of developing atherosclerosis can be increased by an unhealthy and sedentary lifestyle, overweight or obese, diabetes, a family history of the condition, and high blood and cholesterol levels.
Risk factors for arterial thrombosis
Thrombophilia is considered a condition that predisposes to the development of thrombosis.
Arterial thrombosis generally occurs after erosion or rupture of an atherosclerotic plaque and, through platelet-mediated thrombi, can cause ischemic lesions, especially in tissues with a terminal vascular bed.
Cardiac ischemia and stroke are the most severe clinical manifestations of atherothrombosis.
Ischemia can arise slowly from the progression of atherosclerotic disease (stable angina, claudication) or acutely in the case of vascular thromboembolization (rupture of the atherosclerotic plaque) or intracardiac (atrial fibrillation, mechanical valve prosthesis).
There is an exponential increase in the risk of venous and arterial thrombotic events with age, and the rise in life expectancy in the second half of the 20th century is an essential cause of the current epidemic of arterial and venous thrombosis.
Possible mechanisms include the cumulative effects of risk factors on the arterial wall, decreased regular exercise, increased immobility resulting in venous stasis, and increased systemic activation of blood coagulation.
Plasma concentrations of some coagulation factors (factors V, VII, VIII, and IX, fibrinogen) increase progressively.
The same is true for the von Willebrand factor (vWF), an essential protein in platelet vessel wall interactions.
Usually, the clotting process is under the control of various inhibitors that limit the formation of clots near the wall of the damaged vessel, thus preventing the spread of the thrombus.
This delicate balance can be disrupted whenever the procoagulant activity of one of the clotting factors increases or the activity of one of the natural inhibitors decreases, leading to thrombus formation.
This occurs with inherited deficiencies of natural inhibitors and inherited gain-of-function mutations of some clotting factors.
Hereditary deficiencies of antithrombin, protein C, and protein S are rare but vital risk factors for venous thrombosis; they have little or no effect on arterial thrombosis.
Antithrombin directly inhibits several activated clotting factors, particularly thrombin and activated factor X. The inhibitory effect is amplified by its binding to glycosaminoglycans on the endothelial surface with heparin-like activity.
Antithrombin deficiency results in significantly reduced inhibition of thrombin and activated factor X and an increased tendency to clot formation, particularly in the venous system where the clotting pathway (as opposed to platelets) plays a vital role in the shape of thrombi.
Metabolic syndrome and smoking
One of the most widely used definitions of metabolic syndrome is based on at least three of the following diagnostic criteria: elevated waist circumference (abdominal obesity), elevated triglycerides, reduced high-density lipoprotein cholesterol, and elevated blood pressure, high glucose, and high blood pressure.
There is increasing evidence of an association between atherothrombosis and metabolic syndrome. Nine risk factors were identified that accounted for more than 90% of the risk of acute myocardial infarction.
Risk factors included lifestyle factors such as smoking, comorbidities (hypertension, diabetes, abdominal obesity, abnormal lipid profiles), as well as psychosocial factors.
Meta-analysis of randomized controlled trials on blood pressure and cholesterol reduction and studies on smoking cessation confirmed that these three risk factors play a causal role in arterial disease.
Partly through atherogenesis and partly through systemic activation of blood clotting and inflammation.
Despite the unequivocal benefit achieved with lifestyle modification, blood pressure control, statins, active angiotensin II, and antiplatelet agents, the residual risk of recurrent acute events in patients with the established atherothrombotic disease remains significant.
The residual risk is probably related to the progression of atherosclerosis despite the use of statins and active agents with angiotensin II, insufficient platelet activation inhibition by aspirin and thienopyridines, and other factors not yet identified.
Trauma, surgery, and immobilization
These transient conditions are associated with an increased risk of venous thrombosis.
Although venous thromboembolism is the most common thrombotic complication of surgery, iatrogenic surgical injuries can also lead to arterial occlusion.
Furthermore, arterial thrombosis secondary to surgery may represent the first manifestation of heparin-induced thrombocytopenia, an autoimmune disease triggered by exposure to heparin that is commonly administered as antithrombotic prevention of postoperative venous thromboembolism.
Cancer is one of the most essential acquired risk factors for venous thromboembolism.
Some authors estimate an annual incidence of venous thromboembolism of 1 in 200 cancer patients, and 20% of venous thromboembolism cases occur in cancer patients.
Oral contraceptives and hormone therapy
Several clinical studies have investigated the risk of thrombosis with hormone-based oral contraceptives.
However, due to the variety of preparations and the heterogeneity of the study populations, these studies showed different or even contradictory results.
The evidence of venous thromboembolism related to oral contraceptives has been derived primarily from nested case-control studies and attributes a relative risk of venous thromboembolism to oral contraceptives (compared to no help).
With an increase from 2 to 6, the relative risk of venous thromboembolism is observed in oral contraceptive users compared to non-users.
Venous thromboembolism remains the leading cause of maternal mortality worldwide (the rate of maternal deaths from venous thromboembolism is 0.12 per 10,000 live and stillbirths).
From a biological point of view, normal pregnancy is characterized by a hypercoagulable state.
Pregnancy is associated with hemostatic changes that include increased levels of most procoagulant factors, decreased levels of some natural anticoagulants, and reduced fibrinolytic activity.
These changes help maintain placental function during pregnancy and minimize blood loss in childbirth.
The air pollution
Air pollution is made up of gaseous and particulate pollutants. The former include carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3).
The latter include particulate matter (MP) with a cut-off of fewer than ten μm in aerodynamic diameter (PM10), fine particles less than 2.5 μm (PM2.5), and ultrafine particles less than 0.1 μm ( PM0.1).
Compared to aerodynamic diameter and PM2.5, ultrafine particles have a greater total surface area and, therefore, a more significant potential to transport toxic substances, including metals, elemental and organic carbon, among others.
Due to their small size, the ultrafine particles settle deep into the lung alveoli and can reach the bloodstream.
Particulate matter is the type of air pollutant that causes the most severe and numerous effects on human health due to the wide range of different toxic substances it contains.
Over the past decade, a growing body of epidemiological and clinical evidence has led to increased concern about the harmful effects of air pollution on the cardiovascular system.
In recent decades, several studies have investigated the relationship between thrombosis and travel, but it is still debated whether long-distance travel and symptomatic venous thromboembolism are associated.
Since most travelers who develop deep vein thrombosis or pulmonary embolism also have one or more other predisposing risk factors.
Symptoms of arterial thrombosis
Arterial thrombosis is a blood clot that develops in an artery. It is dangerous as it can obstruct or stop blood flow to major organs, such as the heart or brain.
If a blood clot narrows one or more arteries leading to the heart, muscle pain, known as angina, can occur.
If a blood clot blocks the arteries that lead to part of the heart muscle, it will cause a heart attack. If it blocks a street in the brain, it will cause a stroke.
Therefore, the symptoms depend on where the blood clot has formed. Each person’s symptoms can vary. Symptoms can include:
- Pain in one leg (usually the calf or inner thigh).
- Swelling in the leg or arm.
- Chest pain.
- Numbness or weakness on one side of the body.
- Sudden change in your mental state.
The symptoms of thrombosis may resemble other blood disorders or health problems. Always consult your healthcare provider for a diagnosis.
Arterial thrombosis does not cause any noticeable symptoms until an artery is blocked and blood flow to parts of the body is cut off. Depending on the location of the blockage, a patient may suffer from:
Heart attack symptoms include chest pain or discomfort that radiates to other areas of the upper body, shortness of breath, nausea, and dizziness.
The symptoms of stroke include sudden confusion, numbness or weakness on one side of the body, vision problems, and loss of balance, among others.
Pulmonary embolism, the symptoms of which include:
- Chest pain
- Coughing up blood
- The sudden and unexplained onset of shortness of breath
- A rapid pulse
How is thrombosis diagnosed?
Your healthcare provider will take your medical history and do a physical exam. Other tests may include:
Ultrasound: This test uses sound waves to check blood flow in your arteries and veins.
Blood tests: These may include tests to see how well your blood can clot.
Venography: For this test, a dye is injected into your veins. X-rays are then taken to show blood flow and look for clots. The paint makes your veins easier to see on x-rays.
Magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), or computed tomography (CT). The imaging procedure that will be used will depend on the type of blood clot you have and where it is located.
Tips to help you get the most out of a visit to your healthcare provider:
Know the reason for your visit and what you want to happen. Before your visit, write down the questions you want to be answered. Take someone with you to help you ask questions and remember what your provider tells you.
At the visit, write down the name of a new diagnosis and any new drugs, treatments, or tests. Also, write down any further instructions your provider gives you.
Learn why a new drug or treatment is being prescribed and how it will help you. Also, know what the side effects are. Ask if your condition can be treated in other ways.
Learn why a test or procedure is recommended and what the results might mean. Know what to expect if you don’t take medicine or don’t have the test or procedure.
If you have a follow-up appointment, write down the date, time, and purpose of that visit. Learn how you can contact your provider if you have questions.
Treatment of arterial thrombosis
Your healthcare provider will create a treatment plan for you based on:
- Your age, general health, and medical history.
- How sick you are.
- How well do you handle certain medications, treatments, or therapies?
- If your condition is expected to get worse.
There are two main types of treatment for arterial thrombosis.
Medication can help dissolve clots and restore blood flow to the brain or heart.
Since arterial thrombosis does not cause symptoms, it is often diagnosed when the patient has already had a stroke or heart attack.
As a preventive measure, people who are considered high risk, or those who have the risk factors listed above, are given medications to prevent blood clots. These medications include:
Statins: Statins are a class of drugs that block the action of an enzyme in the liver that the body uses to make cholesterol to lower cholesterol levels in the patient’s blood.
Blood thinners: Blood thinners, such as warfarin, are also called blood thinners. They work by slowing down blood clotting.
Antiplatelets: Antiplatelets, such as low-dose aspirin, are commonly used to reduce the risk of a heart attack.
Thrombolytics: Thrombolytics work by dissolving dangerous clots in blood vessels to restore normal blood flow and prevent irreversible damage to tissues and organs.
If non-surgical therapies fail to dissolve the blood clot, a surgical procedure called a thrombectomy or embolectomy may be recommended.
The surgery involves a surgeon accessing the affected artery. To:
- Unlock it.
- Diverting blood flow through another blood vessel.
- “Grafting” the blood vessel to travel around or pass the blocked section.
It can be done using a catheter (minimally invasive method) with a balloon at the tip. For the procedure, the catheter is inserted into a small cut in the body and threaded to the site of the blockage.
The tiny balloon is inflated and deflated to remove the clot. In some cases, open surgery is necessary and is often preferred in emergencies.
It involves making a large incision to open the artery to remove the blood clot.
Although both procedures are highly effective in treating atrial thrombosis, the minimally invasive method is generally preferred because it minimizes the ordinary risks of surgery, including infection, bleeding, and scarring.
It also minimizes recovery time, allowing patients to return to their daily routine in days.
In cases where the artery is damaged beyond repair, surgeons recommend coronary artery bypass graft surgery. A blood vessel taken from another part of the patient’s body is used to bypass the blockage to restore normal blood flow to the heart.
What are the complications of thrombosis?
Thrombosis can block blood flow in both veins and arteries. Complications depend on the location of the thrombosis. More severe problems include stroke, heart attack, and severe breathing problems.
Prevention of arterial thrombosis
If you’ve had a blood clot in an artery, you may need to take medicine to prevent it.
It is also vital that you live a healthy lifestyle. This includes:
- Stop smoking (if you smoke).
- Doing some physical activity.
- Reducing the amount of salt and saturated fat you eat.
- Manage other health problems like diabetes, high blood pressure, and high cholesterol.
- Return to activity as soon as possible after surgery.
- Exercising your legs during long trips.
A large body of evidence in the last 20 years has improved our understanding of the biochemical mechanisms involved in the pathogenesis of thrombus formation, both in arteries and veins.
We are beginning to understand that changes in blood clotting, inflammation, and the immune response are intricately related and interdependent.
Increased generation of thrombin, the last enzyme involved in coagulation, platelet activation, and also cell signaling effector molecules, is crucial not only in the development of venous thromboembolism but also in atherothrombosis.
On the other hand, traditional cardiovascular risk factors may also play a role in venous thromboembolism.
Therefore, the pathogenesis of thrombosis must be considered from a multifaceted perspective, as confirmed by the amount of epidemiological data on genetic and environmental thrombotic risk factors.
However, a significant proportion of arterial and venous thrombotic events occur without a plausible explanation, especially among young individuals.