The formation of coronary thrombosis directly leads to the development of acute coronary syndrome, which is an acute condition of coronary heart disease and is the most critical at the onset, and is the main cause of death from coronary heart disease with a high risk of recurrence. At the 2015 China Heart Congress, Prof. Yi Mao from Fu Wai Hospital gave a presentation on “Mechanisms and management strategies of acute coronary thrombosis”, the highlights of which are as follows: Yi Mao, Department of Cardiovascular Medicine, Fu Wai Hospital, Beijing
Prof. Yi Mao gave a wonderful test report at the conference
I. Three basic conditions for thrombus formation
Both venous thrombosis and coronary thrombosis require the following three conditions: endothelial damage (local trauma to vassel wall), hypercoagulation and stasis.
1. Endothelial injury, failure of the gateway
First of all, endothelial damage, it is worth mentioning that the vascular wall can form coronary atherosclerosis, which can be thinned, but the rupture problem needs to be paid attention to. In conventional coronary arteries plaque grows spontaneously, when the lumen is narrowed to more than 80%, hemodynamic changes occur, which can easily lead to plaque rupture, resulting in exposure of collagen, laminin, microfibers and vW factor, and formation of thrombus.
Even if the endothelium does not rupture, the influence of many factors such as glycated LDL and oxidized LDL can lead to endothelial dysfunction, which is an important cause of acute coronary thrombosis and can cause a very serious and fatal risk in the absence of obvious arterial plaque rupture.
Other factors that contribute to endothelial dysfunction include hyperlipidemia, CO, nicotine, alcohol, mechanical injury, hyperglycemia, and stress. Focusing on smoking, smoking is a new important factor causing endothelial injury. The vascular endothelium itself has a negative charge, and the cells in the blood also have a negative charge. When the vascular endothelium is injured, the vessel wall is directly hit by the blood, plus the secretion of various substances secreted by the endothelium itself, such as ATPase, ADPase and thrombogenic factor (TM), and the secretion of anticoagulant substances is reduced, and the secretion of procoagulant substances is increased and the increase in secretion of endothelin aggravate the blockage of the original blood vessels.
2. Hypercoagulable state and accelerated embolization
The second most influential factor in promoting acute coronary thrombosis is that the blood is in a hypercoagulable state, such as when platelets are in a high speed blood flow state, when there is severe stenosis and blood collision in the blood vessels, or when it is cold, etc., which can easily trigger platelet activation and adhesion after contact with the broken blood vessels, leading to the formation of thrombus.
3.Slow blood flow and thrombus collection
The third point is that the blood flow is in a relatively stationary state, and although platelets accumulate on the vessel wall, they do not necessarily trigger thrombosis. The formation of acute coronary syndrome is due to endothelial rupture and the formation of a thrombus at that place, and there is relatively stationary blood after the thrombus, thus causing the narrowing and blockage of the lumen.
For patients who have stents placed in their vessels, the stent itself, which is an irritation to the vessel wall, and once a thrombus is formed in the stent part, the blood flow is relatively stationary after the thrombus and the blood flow is in a hypercoagulable state, triggering the 3 mechanisms of acute coronary syndrome formation.
Second, the treatment after thrombosis
The clinical principles for the management of acute coronary thrombosis are: small thrombus – direct dilation and stent implantation; large thrombus – mechanical methods are recommended to extract the thrombus directly. In addition to mechanical aspiration and stent placement, it must be combined with pharmacological treatment. Nowadays, more anti-platelet drugs are used, most of which are GP Ⅱb/Ⅲa receptor antagonists, and there is a difference in mortality within 30 minutes with or without the application of GP Ⅱb/Ⅲa receptor antagonists, which can effectively improve the patient’s prognosis, reduce the embolic situation and decrease the mortality of patients within 30 days.
In addition to acute coronary thrombosis, another type of thrombosis is post-stent implantation thrombosis; those within one month are early thrombosis, those within one month to one year are late thrombosis, and those over one year are called late late thrombosis. 2013 meta-analysis showed high mortality of post-stent thrombosis, and the risk of stent thrombosis in DES should not be neglected. Factors affecting thrombosis after stent implantation include discontinuation of antiplatelet therapy, complexity of coronary lesions, length and number of stents, diabetes mellitus, smoking status, and so on. The higher the complexity of the coronary lesion, the higher the risk of stent thrombosis. 2014 latest observational study showed that STEMI is an independent predictor of stent thrombosis risk. In general, the formation of thrombosis is satisfied by the above three basic conditions.
Third, how to reduce the risk of stent thrombosis
So, how to avoid the risk of thrombosis?
Strategy 1: Pre-procedure patient screening to screen for patients likely to adhere to a drug regimen (including those who can afford dual antibiotic therapy).
Strategy 2: Carefully select stents and use stents with a low incidence of stent thrombosis.
Strategy 3: Adhere to dual antiplatelet agents as much as possible during perioperative treatment; dual anti-treatment is key to reducing the incidence of thrombosis.