1.
What is thrombosis
Thrombosis is a group of diseases in which the flowing blood coagulates in the lumen of blood vessels (arteries or veins) or in the heart cavity, forming blood clots and blocking the lumen of blood vessels, causing a significant reduction in blood flow or even complete interruption. If the clot occurs in an artery, it leads to severe ischemia or interruption of blood flow to the organ or tissue supplying blood, such as cerebral insufficiency, unstable angina; or even necrosis, such as acute myocardial infarction, stroke. If the thrombus occurs in the vein, such as deep vein thrombosis of the lower limbs, it can cause impaired blood return to the lower limbs, causing edema and venous insufficiency, etc.
2.
What is embolism
Embolism is a syndrome in which the formed thrombus in the heart or blood vessels is dislodged and blocked by blood flow to other important organs and blood vessels, such as atrial fibrillation often has thrombus formation in the left atrium, once the thrombus is dislodged, it can block the cerebral blood vessels by blood flow, causing brain tissue necrosis (cerebral embolism) or peripheral blood vessels (such as lower limb arteries, renal arteries); deep vein thrombosis in the lower limbs can be dislodged and block the pulmonary arteries (pulmonary embolism), causing acute right heart failure, which may lead to death of the patient.
3.
What is the harm of thromboembolism?
Thromboembolism leads to the reduction or interruption of blood supply to organs or tissues, or the accumulation of blood in an organ or tissue, resulting in organ failure or dysfunction, disability, incapacity, or even death. Thromboembolic disease is very common in clinical practice, which seriously endangers the life and health of the public and affects the happiness of families, and causes large medical expenses and labor waste to individuals, units and the country due to thrombosis and embolism every year.
4.
What is atrial fibrillation?
The heart is like a pump that pumps blood throughout the body with each beat, providing oxygen and nutrients to tissues and organs throughout the body. This mechanical activity of the heart is controlled and governed by electrical activity, which normally originates from the sinus node located in the atria. The sinus node regularly sends out electrical impulses, 60-100 times per minute, to all parts of the heart, causing sequential and regular contractions in all parts of the heart (atria to ventricles).
In atrial fibrillation, the electrical activity of the heart is no longer governed by the sinoatrial node and is replaced by rapid, disorganized electrical activity in the atria, with corresponding rapid and irregular contraction and diastole of the ventricles.
5.
What is the incidence of atrial fibrillation?
According to statistics, atrial fibrillation accounts for about 4% of the adult population, and the occurrence of atrial fibrillation is clearly age-related, with the incidence of atrial fibrillation beginning to increase after the age of 40 and starting to increase significantly after the age of 65, with each 10-year increase in age. The incidence of atrial fibrillation in the elderly is about 7-14%.
6.
What are the high-risk factors for thromboembolism due to atrial fibrillation
Prior transient ischemic attack (TIA), stroke or peripheral vascular embolism, hypoplastic left ventricular function (echocardial insufficiency of moderate or severe, or recent congestive heart failure) or hypertensive patients.
Patients with high-risk factors (mitral stenosis, mitral annular calcification, higher age, hypertension, chronic heart failure, significant coronary artery disease, diabetes mellitus, hyperthyroidism, and ultrasound findings of left ventricular insufficiency, left atrial enlargement, and spontaneous echoes in the left atrium) should be considered for oral anticoagulation.
Secondary risk factors are also diabetes mellitus, coronary artery disease, age between 65 and 75 years and hyperthyroidism.
A low-risk group is defined as patients under 60 years of age without valvular or organic heart disease, hypertension, diabetes mellitus, coronary artery disease, or hyperthyroidism. Such patients have a 15-year cumulative stroke incidence of 1 or 3% and do not need anticoagulation, taking aspirin is sufficient; patients with a history of stroke or transient ischemic attack can have an annual stroke incidence of 12%.
7.
What are the dangers of atrial fibrillation
In atrial fibrillation, the volume of blood discharged from the heart is reduced by more than a quarter or even 50%, especially when there is also impairment of ventricular function. Atrial fibrillation can induce or aggravate heart failure and pulmonary edema, and induce myocardial ischemia. The loss of atrial contractility can lead to intra-atrial thrombus formation, which can cause cerebral embolism or other peripheral vascular embolism. Atrial fibrillation is an independent risk factor for stroke. The average annual incidence of ischemic stroke in patients with atrial fibrillation is 5%, accounting for 10%-15% of cerebral infarction; the risk of cerebral embolism in patients with non-valvular atrial fibrillation is 5-7 times higher than that without atrial fibrillation, and the proportion is even higher when the heart has valvular disease (such as rheumatic heart disease).
The annual risk of cerebral thromboembolism in patients with atrial fibrillation is about 5%, and thrombosis due to atrial fibrillation accounts for 10%-15% of cerebral infarctions, and strokes after atrial fibrillation have a higher rate of death and disability.
A retrospective study showed that 71% of cerebral embolisms died or left severe neurological symptoms within 6 weeks of observation. In prospective studies of both sexes, 63% and 44% of stroke patients with atrial fibrillation died or were disabled, respectively.
8.
How to prevent cerebral embolism in atrial fibrillation?
The most fundamental and effective treatment for patients with atrial fibrillation is to consider pharmacological or electrical resuscitation while treating the primary disease, but if the onset of atrial fibrillation is greater than 48 hours, anticoagulation must be performed before and after resuscitation. If resuscitation is unsuccessful or if sinus rate cannot be maintained after resuscitation, long-term anticoagulation must be considered.
A meta-analysis of several randomized trials showed that in patients with non-valvular atrial fibrillation, the annual stroke rate was 4.5% in patients without antithrombosis compared with 1.4% in patients treated with oral anticoagulation, with a 68% reduction in stroke risk; there was no significant increase in major bleeding in patients treated with anticoagulation; and anticoagulation reduced mortality by 33%
Aspirin was also effective in reducing the overall risk of ischemic stroke by 21%, with an annual stroke incidence of 8.1% in the no-medication group and 6.3% in the aspirin-treated group.
In patients with atrial fibrillation who had already had a cerebral embolism, oral anticoagulation reduced the annual primary cardiovascular event (vascular death, nonfatal stroke, nonfatal myocardial infarction, or peripheral vascular embolism) by 47% and the risk of stroke by 66%, and no patient in the anticoagulation group had a cerebral hemorrhage. Aspirin reduced the primary endpoint event by 17% and stroke by 14%, with no statistical difference compared with the placebo control group.
9.
Are oral anticoagulants safe and do they have a high incidence of bleeding?
The incidence of cerebral hemorrhage with oral anticoagulants is very low, with an overall annual incidence of about 0.5%, similar to that of oral aspirin, and bleeding events are associated with an increased international normalized ratio (INR) and age at the time of monitoring.
The appropriate dose of the drug should be effective in preventing cerebral embolism while ensuring safety.
10.Do I still need antithrombotic after cerebral embolism? When should I start?
The risk of recent recurrence after an embolism is high, and anticoagulation therapy must be started early, but premature anticoagulation may increase the risk of brain tissue turning into hemorrhage after embolism.
It is recommended that anticoagulation be started 24 hours after stroke when CT confirms the absence of hemorrhage in small and medium embolic cerebral infarcts, while anticoagulation should be delayed in large infarcts until 7 days after stroke when CT excludes prolonged hemorrhage.
11.
Why should blood tests be performed to monitor the use of oral anticoagulants?
During the period of taking warfarin, you should go to the hospital for blood test according to the doctor’s prescription, which is called International Normalized Ratio, or INR for short, and the doctor must adjust the patient’s medication dose timely and accurately according to the results of the blood test to ensure the antithrombotic effect and minimize the risk of bleeding.
The doctor decides the dose of warfarin needed according to the patient’s blood test results to achieve individualized treatment.
12.What kind of thrombotic diseases can be treated with oral anticoagulant drugs?
(1)
Primary and secondary prevention of venous thromboembolism (pulmonary embolism and deep vein thrombosis).
(2)
prevention of peripheral vascular embolism in patients with mechanical and bioprosthetic valve replacement, or in patients with atrial fibrillation (including non-valvular atrial fibrillation).
(3)
prevention of acute myocardial infarction in patients with peripheral arterial disease.
(4)
prevention of stroke, recurrent myocardial infarction, and death in patients with acute myocardial infarction
(5)
Prevention of peripheral vascular embolism in certain patients with mitral stenosis
13. Thrombosis Prevention and Control Clinic
Thrombotic disorders span multiple disciplines and are highly specialized in diagnosis, medication, and monitoring, so it is best for patients to visit a well-equipped thrombosis clinic.
Our own preliminary experience is that thrombosis clinic with bedside INR monitoring is a powerful measure to improve the antithrombotic efficacy of warfarin and ensure patient safety, and combined with various ways of patient education, it can also improve patient compliance with medication and enhance psychological tolerance and self-confidence in fighting the disease.
14.Does rheumatic valve disease require antithrombotic therapy?
Theoretically, all valve diseases should receive antithrombotic therapy if there is no risk of bleeding, which shows the importance of antithrombotic therapy. The higher the risk of thrombosis, the greater the benefit of antithrombotic therapy.
Peripheral vascular embolism is significantly more common in rheumatic mitral valve lesions than in other forms of valve disease, with a presumed incidence of at least one in five throughout the disease course. When combined with atrial fibrillation, the incidence is seven times higher than in those with sinus rhythm.
It should be clear that the same bleeding events do not offset the decline in thromboembolic events, which have a more severe outcome.
15. Patients undergoing valve replacement surgery must take oral anticoagulants for a long time or for life.
There is still a high mortality rate after successful valve replacement surgery, and many patients die not from cardiac problems but from cerebral embolism or cerebral hemorrhage.
The reason for this is the failure to manage this group of patients with good monitoring, follow-up, and proper and rational use of oral anticoagulants, resulting in inadequate or excessive antithrombosis, which neither effectively prevents thromboembolism nor detects excessive anticoagulation in time for thromboembolism or severe hemorrhage to occur.
Long-term (permanent) oral antithrombotic therapy is strongly recommended for all mechanical valve patients as a fundamental measure to prevent thromboembolic events after valve replacement.