Introduction
Coronary artery dilatation(coronary artery ectasia, CAE) is a rare coronary artery disease. Dilated coronary arteries can cause slow blood flow and are prone to thrombosis. Angina and myocardial infarction can also occur in patients with CAE without atherosclerotic stenosis. The development of non-invasive imaging techniques in recent years, as well as the use of antiplatelet drugs and vasoactive drugs, has helped to improve the diagnosis, treatment and prognosis of CAE.
Definition, morphology, and incidence of coronary artery dilatation
CAE is defined as a localized or diffuse dilatation of the epicardial coronary artery, at least 1.5 to 2 times greater than the adjacent normal coronary segment, and >2.0 times of localized expansion is called coronary artery aneurism (CAA). The morphology of CAE is diverse, with diffuse dilatation, widening of coronary arteries, and partial localized coronary aneurysms, pseudoaneurysms, plaque ruptures, or coronary dissection. According to the location and extent of CAE, Markis JE et al. suggested that CAE be divided into four types in 1976: type I, diffuse dilatation of 2/3 coronary vessels; type II, diffuse dilatation of one coronary artery plus another crown Localized dilatation of the vascular; type III, diffuse dilatation of a single coronary artery; type IV, single vessel limitation or segmental dilatation. However, some lesions cannot be classified into the above four types, so some researchers have improved the above types, as shown in Table 1. In addition, some scholars classify CAE into two categories according to the anatomy of CAE: fusiform or vesicular. Early studies defined the dispersed cystic type CAE as CAA, ie the transverse diameter of the site of the aneurysm was greater than the longitudinal diameter (longitudinal axis of the vessel), limiting CAE to a fusiform diffuse coronary dilatation, or the length of the aneurysm The diameter is at least 2 times larger than the transverse diameter. True coronary aneurysms account for 27% of CAE, 40% of which are dilated lesions after atherosclerotic stenosis.
The incidence of CAE reported in most literatures fluctuated between 1.4% and 5%. The diagnosis of CAE before 1967 relied mainly on autopsy, and the detection rate was very low (0.22% to 1.4%). The development of coronary angiography and imaging diagnostics has greatly improved the detection rate of CAE. There are reports from India that 10 patients with ischemic heart disease have a CAE incidence of less than 40 years old and the incidence of CAE is higher than 40 years old. Up to 12%. It has recently been reported that the coronary angiography rate of CAE in the Turkish population is 9.9%. Table 2 summarizes the incidence of CAE in coronary angiography reported in recent years, which is generally low, with a high incidence of individual populations, suggesting that there are still some undetermined factors affecting CAE. The incidence of CAE in patients with coronary heart disease is relatively high, and the prevalence of CAE in patients with myocardial infarction is 2.6%. Stajduhar et al reported that 8% of patients treated with abdominal aortic aneurysm complicated with CAE, and the incidence of CAE in patients treated with obstructive peripheral vascular disease was only 2.9%, suggesting that CAE may have the same pathogenesis as abdominal aortic aneurysm. .
CAE can occur in all three vessels of the coronary arteries, but 75% of CAE patients involve only a single vessel16. In patients with coronary heart disease, the most common site of CAE is the proximal and middle segments of the right coronary artery, with an incidence of up to 60%, followed by the left anterior descending and circumflex, but the pathological mechanism of high CAE in the right coronary is unclear.
The etiology and pathogenesis of coronary artery dilatation
At present, the etiology of CAE is not fully understood. Observational studies have found that some diseases are closely related to the occurrence of CAE, which may be the cause of CAE.
2.1 Atherosclerosis 50% of CAE patients can be attributed to atherosclerotic disease. CAE may be a variant of atherosclerotic lesions. Severe atherosclerotic inflammatory reactions can be combined with extracellular matrix degradation, involving the middle and outer layers of the blood vessels, which can cause vascular remodeling and expansion when the blood vessels are maladaptive. But the strange thing is that diabetes does not seem to have this inflammatory effect. In addition, some CAEs are associated with coronary atherosclerotic stenosis, mainly characterized by stenosis and expansion.
2.2 Kawasaki disease is one of the most common causes of acquired heart disease in children, accounting for 15% to 25% of CAE patients. It is a late complication of Kawasaki disease. Delayed diagnosis and treatment can increase the prevalence of CAE. Anti-inflammatory treatment can improve the crown. Pulse expansion. In addition, the regional prevalence of Kawasaki disease also determines the incidence of CAE in Kawasaki disease. For example, the prevalence of children in the United States is much lower than that in Japan.
2.3 Connective tissue disease, arteritis: 10% to 20% of CAE patients are attributed to arteritis or connective tissue disease.
2.4 Congenital coronary artery disease: A small number of patients with CAE have abnormal congenital coronary origin, and coronary-cardiac fistula can cause CAE.
2.5 rare diseases: including infectious diseases, such as fungi, syphilis, borreliosis, EB virus and other infections involving coronary artery, trauma or dissection, simple CAE, intervention-related CAE.
Simple CAE is defined as the exclusion of the above-mentioned causes such as atherosclerosis, connective tissue disease and other heart diseases. The incidence of simple CAE is low, and the detection rate of coronary angiography is 0.1% to 0.32%.
The incidence of intervention-related CAE increased gradually. The incidence of CAA after PTCA and bare metal stents was reported to be 2% to 10%. There was no difference in the incidence of CAA between bare metal stents and PTCA. In the current era of drug stenting, with the routine use of high-pressure balloon dilation after stenting, long-term follow-up has been reported by CAA, which may be related to the pro-inflammatory response and thrombogenic properties of drug-eluting drug coatings. Induces apoptosis of vascular smooth muscle and promotes thinning and expansion of the arterial wall. In addition, the interventional procedure also weakens or destroys the vessel wall structure to varying degrees.
Although the pathogenesis of CAE is not clear, atherosclerosis is clearly the main pathogenesis of CAE. In addition, inflammatory response, extracellular matrix degradation and genetic susceptibility may participate in the development of CAE to varying degrees. Plasma cytokines such as soluble VCAM-1, ICAM-1 and E-selectin were significantly elevated in patients with CAE alone, suggesting that cytokine-induced extensive full-thickness vascular inflammation may lead to arterial remodeling and expansion. The imbalance of matrix metalloproteinase (MMP) and MMP activity by tissue-specific inhibitors (TIMPs) can lead to degradation of matrix components (elastic layers) and vasodilation. Patients with aortic aneurysm often have a susceptibility to CAE suggestive gene susceptibility to simple CAE. RAS system gene and matrix metalloproteinase gene mutation may increase the susceptibility of CAE.
Clinical characteristics and diagnostic assessment
There are more males than females in CAE, and the clinical manifestations are non-specific. Angina is the most common. ST elevation myocardial infarction or non-ST elevation myocardial infarction is relatively rare. Malignant arrhythmia and sudden death can also occur when spontaneous dissection is formed. Hypertension and hyperlipidemia are the most common risk factors for CAE, but contrary to coronary heart disease, most studies have found that CAE is not associated with diabetes.
The symptoms of myocardial ischemia in CAE are mainly related to the following mechanisms:
(1) CAE has a slow blood flow. Studies have shown that expanded coronary blood flow is increased but coronary blood flow reserve is decreased, suggesting that there is microcirculatory dysfunction in CAE patients.
(2) CAE is prone to thrombosis. Blood flow in the vasodilatation site is slow, endothelial dysfunction, easy to form a thrombus or distal microembolism. Another part of CAE is the formation of atherosclerotic plaque ulcer, rupture of plaque into the adventitia to form pseudoaneurysm, easy to form spontaneous dissection, coronary spasm, etc., leading to clinical manifestations of acute myocardial ischemia. Huge CAE may break into the heart chamber or coronary sinus, the most serious is broken into the pericardium causing pericardial tamponade and even death. The volume expansion of CAE tumors is usually slow, but the CAE tumors caused by infection with fungi can rapidly expand in a short period of time.
Coronary angiography is the main means of diagnosing CAE, and can simultaneously understand the shape of the tumor, abnormal blood flow, lesion location and number. However, intravascular ultrasound (IVUS) can identify true hemangiomas and pseudohemangiomas. Non-invasive imaging methods include ultrasound, coronary CT and MRI, and radionuclides. Ultrasound is of great value in the diagnosis and follow-up of CAE caused by Kawasaki disease in adolescents. It can also understand the aortic dilation and cardiac structure, but the evaluation of the overall coronary condition is far less than CT or MRI. Multi-slice CT and enhanced MRI can accurately depict the origin, direction and pathology of coronary arteries. Compared with CT, MRI can avoid the damage of contrast agent and X-ray, and also shows blood flow, thrombus and other conditions, and has more clinical value.
No specific markers have been found that can help improve the diagnosis of CAE. Although 50% of CAE patients have elevated cytokines, TNF, IL-6 and other inflammatory factors, these inflammatory factors are also elevated in coronary atherosclerotic disease, but can not distinguish coronary stenosis or expansion . The CRP and WBC counts in CAE patients also increased significantly, but were also not specific.
treatment
There are currently no best or more recognized CAE treatment options. There is no evidence-based medical evidence for drug therapy, interventional therapy or surgical treatment. Because of the low relative incidence of CAE and the complex etiology, large-scale clinical trials cannot be performed for comparative evaluation.
Medical treatment of CAE: Because the pathological features of CAE are slow blood flow and easy thrombosis, traditional drug therapy emphasizes long-term chronic anticoagulant therapy, but no prospective study has confirmed that anticoagulant therapy can reduce cardiac adverse events in CAE patients. In the classic treatment plan proposed by Sorrell et al in 1996, anticoagulant therapy is recommended to use warfarin (maintain INR 2.0 to 2.5) andaspirinTablets (75-360 mg·d), but new antiplatelet drugs such as the ADP inhibitor clopidogrel were not yet in clinical use. When CAE patients have acute thrombosis, intravenous heparin and thrombolytic therapy are not different from coronary heart disease antithrombotic therapy. However, when CAE is associated with coronary stenosis, antithrombotic therapy is the same as coronary heart disease. Because of the good prognosis of simple CAE, simple antiplatelet is the main treatment. In addition, diltiazem can be applied to prevent vasospasm. Patients with CAE should avoid the use of nitrates to avoid aggravating epicardial vasodilatation and aggravating or aggravating angina. ACEI drugs and statins are also applicable. It is best to conduct an overall evaluation of CAE patients, especially major arterial and venous systems, pay attention to the cause of the disease, and control risk factors.
Interventional therapy: Early studies have found that the use of PTCA in the treatment of stenotic lesions adjacent to the dilatational segment of CAE patients has no improvement in prognosis, so interventional therapy for CAE is not recommended. With the development of interventional instruments and techniques, researchers have attempted to treat bare coronary artery lesions in patients with CAE with metal stents. Because drug stents are prone to thrombosis, drug stents are not recommended for CAE. PCI may also be considered when CAE is present in infarct-related arteries, but this group of patients has severe thrombotic load, high incidence of slow blood flow and distal embolization, slow ST segment regression, and slow collateral formation. The polytetrafluoroethylene (PTFE) stent is a stent graft. Studies have shown that PTFE treatment of CAA with a diameter of 5.8 to 10 mm can reduce or even eliminate the tumor and reduce cardiovascular events. However, the overall flexibility of the PTFE stent is poor, and collateral occlusion can occur. Long-term follow-up found that 20.8% of CAE patients treated with PTFE stents had in-stent restenosis (more common in patients with CAA >10 mm), and cases of late thrombosis were reported. PTFE stent treatment should focus on anticoagulation problems. Some research centers believe that dual antiplatelet therapy can be used, and does not advocate long-term use of warfarin anticoagulant therapy, but there is no uniform standard treatment plan. In recent years, there have been reports of carotid stents and distal thrombus protection devices (tapered).
Self-expanding ACCULIN and autologous vein-coated stents for CAE have good short-term treatment, but their safety and efficacy need further study. For some sacral CAE or CAE complicated with coronary artery spasm, spring ring closure can also be used.
Surgical treatment: Surgical treatment is preferred for left main aneurysms, CAE patients with tumor diameters >10 mm or tumors that are 3 to 4 times larger than the origin of the vessels. Coronary bypass can be used depending on tumor size, collateral distribution and stenosis. The hemangioma is ligated or removed at the same time. Emergency surgical procedures should be considered for concurrent life-threatening adverse events (eg, fistula rupture of the heart or severely diverted fistula formation). Surgical thrombectomy may also be considered when a large tumor is combined with thrombosis. Surgical treatment has a good prognosis.
Prognosis and summary
Early detection of CAE patients with a 2-year mortality rate of about 15%, similar to the three-vessel disease of receiving drug treatment. However, most studies have found that CAE is a variant of coronary heart disease without additional risk, and there is no difference in mortality between patients with non-CAE CAD. Studies have shown that elevated CRP and increased TIMI blood flow frames predict a poor prognosis for CAE, but further confirmation is needed.
In conclusion, CAE is a rare form of coronary artery disease, which may be a manifestation of atherosclerotic disease, seen in 3% to 8% of coronary angiography populations. New non-invasive imaging techniques and new antiplatelet drugs will effectively promote the diagnosis and treatment of CAE, but the selection of optimized treatment strategies is still challenging.
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