Kawasaki disease (KD), first reported by Tomosaki Kawasaki in 1967, is an acute febrile rash disease with inflammatory lesions in small and medium-sized blood vessels throughout the body, especially involving the coronary arteries, and has become one of the most common acquired heart diseases in children. The incidence of coronary artery lesions can be significantly reduced by regular treatment; however, in recent years, the number of patients with severe KD has increased year by year, and the incidence of propecia-resistant KD has also started to increase. The epidemiological survey conducted in Shanghai from 1998 to 2002 found that the incidence of KD ranged from 16.18/100,000 to 36.18/100,000, and 24.3% of KD patients were combined with cardiovascular lesions, of which 68% were coronary artery dilatation and 10% were coronary artery aneurysm, with a mortality rate of 0.26%. The severity of KD depends on the degree of coronary artery damage, and once it develops into a coronary artery aneurysm, it is easy to form hemorrhage. The severity of KD depends on the degree of damage to the coronary arteries. Once coronary aneurysms develop, thrombosis can easily form, which can progress to obstructive dilatation of the coronary arteries, causing myocardial ischemia and even myocardial infarction and sudden death in young adults, so KD is also called “coronary heart disease” in children. In this paper, we discuss the mechanism, development and correlation between KD combined with coronary artery lesions and adult myocardial infarction. I. Morphological changes of coronary arteries in KD Kato et al. 1996 reported the follow-up data of 594 patients with KD for 10-21 years and described the changes of coronary artery lesion (CAL) in KD combined with coronary artery lesion in different time periods, which became the basis for studying the morphological changes of coronary arteries in KD patients. CAL recovery, no change, further deterioration leading to coronary stenosis, and occasionally coronary aneurysm rupture in a very small number of KD patients. It was found that mild CAL (coronary artery I.D. <5 mm) has a relatively low risk of coronary stenosis and is more likely to recover; coronary artery aneurysm (CAA), on the other hand, undergoes a series of different morphologic changes, with typical changes of coronary artery recovery or coronary artery obstruction occurring mostly within 2 years of onset, while coronary artery stenosis often occurs 2 years after onset or more Coronary artery stenosis often occurs 2 years after onset or more distantly, and coronary artery calcification occurs 5 years after onset. Coronary artery rupture occurs during the acute phase of KD when the coronary arteries are rapidly dilating, but it has also been reported 20 years after the onset of KD. Because of the difficulty in obtaining coronary artery tissue in KD, the study of its histopathology is always a difficult task at present. It has been found that the most prominent histological change of coronary arteries in the distant stage of KD is the thickening of the intima, which contains the proliferation of extracellular matrix and smooth muscle cells migrating. Coronary intimal thickening can occur in all forms of CAL, including in patients recovering from KD or in patients with normal coronary arteries as demonstrated by cardiac ultrasound. Most occlusions of coronary arteries are due to thromboembolism and, to a lesser extent, to extracellular matrix proliferation accumulation and intimal thickening. The aneurysmal occlusion and "intra-arterial pattern" often observed in revascularization is the result of the development of a deep intima adjacent to the middle layer, or a thickened layer of smooth muscle cells surrounding numerous microvessels. Pathological examination of acute and subacute fatal cases revealed smooth muscle inflammatory infiltration and intimal edema in the vessel wall, initially dominated by polymorphonuclear cells, but quickly replaced by mononuclear cells, mainly CD4+, T-lymphocytes, macrophages and IgA-rich plasma cells. In severely damaged vessels, inflammation spreads to all 3 layers of the vessel wall and destroys the inner elastic layer, the vessel loses its structural integrity and becomes weak, the elastic fibers of the intima break down, eventually leading to vasodilation or aneurysm formation, and the lumen may be obstructed by fibrinous thrombosis. Over time, the hardening and thickening of the vessel wall narrow the lumen and significantly reduce blood flow through it, leading to myocardial infarction or sudden death. Intravascular Ultrasound (IVUS) provides useful information on the morphology and histology of the coronary arteries. In normal children, the coronary arteries have a thin and smooth intima, forming a smooth inner lumen. With intimal hyperplasia, the acoustic signal shows symmetrical or asymmetrical layers of intimal thickening. Such changes can be found in coronary aneurysms, transthoracic cardiac ultrasound showing normal coronary arteries or coronary stenosis, which is consistent with the coronary histopathological features of KD. further study by Tsuda et al. showed that IVUS is highly sensitive and specific for predicting future coronary intimal thickening in KD combined with CAL in coronary arteries with an internal diameter of more than 4 mm. And for coronary artery calcification, IVUS has even higher sensitivity. Understanding the mechanisms of coronary artery reconstruction, especially local stenosis due to coronary intimal hyperplasia, is particularly important for the long-term treatment of KD combined with CAL and reducing the incidence of cardiovascular sequelae.Suzuki et al [15] found that vascular segments with coronary artery stenosis in KD patients expressed a large number of vascular growth factors including TGF-β, VEGF, FGF, etc. by immunohistochemistry and other methods. growth factors. Both platelet aggregation and intimal thickening are present in coronary artery aneurysms and activate both TGF-β, VEGF, FGF and other factors, leading to extracellular gliosis and smooth muscle cell proliferation, which are completely different from the occurrence of coronary atherosclerosis in adults. Prognosis of KD The prognosis of KD mainly refers to the prognosis of coronary artery lesions, which first lead to coronary arteritis during the course of the disease, followed by the development of coronary artery dilatation and then progress to coronary aneurysm formation, and some children may develop coronary artery stenosis in the distant stage, leading to myocardial ischemia and myocardial infarction. In China, the majority of children with KD have not undergone coronary angiography, so there is no gold standard for long-term prognosis. 191 cases (20.1%) of coronary artery aneurysms were found in 810 children who underwent coronary angiography after the acute phase of KD; among them, 171 cases were reviewed after 1 to 1.5 years, and 99 cases (58%) were found to have regressed coronary artery aneurysms, while the remaining 72 cases (42%) still had abnormal changes. The stenosis formed during the process of coronary artery wall repair can easily lead to coronary embolism and myocardial ischemia. The most severe type of coronary aneurysm is the giant coronary aneurysm (coronary I.D. ≥8 mm), which is unlikely to regress and is more likely to cause embolism, rupture, or stenosis. In the long-term follow-up data of Kato et al, 50% of the giant coronary aneurysms developed coronary stenosis or complete embolization and myocardial infarction leading to death. Tsuda et al reported 12 KD patients who died from coronary artery damage over 25 years, with the time to death ranging from 2 months to 24 years from the acute phase of KD [. A follow-up study of 15 cases of giant coronary artery aneurysms at the Guangzhou Women's and Children's Medical Center in China found that only 2 cases (13.3%) returned to normal, significantly lower than the coronary artery dilatation group and the small and medium-sized coronary artery aneurysm group; ATP-loaded echocardiography showed that the incidence of ventricular wall motion abnormalities was significantly higher in the giant coronary artery aneurysm group than in the coronary artery dilatation group, but the difference was not statistically significant with the small and medium-sized coronary artery aneurysm group; 6/15 The coronary arteriogram was performed in 6/15 cases, 4/6 cases still had coronary artery aneurysm, 1/6 cases regressed to mild coronary artery dilatation, 5/6 cases had coronary artery stenosis or (and) occlusion, one of which was recanalized after occlusion, and one case combined with collateral vessel formation; 2 cases died in the giant coronary artery aneurysm group, the coronary arteries were largely visible at autopsy, the branches of the left and right coronary arteries were bead-like enlarged, and the lumen of the aneurysm-like dilated coronary artery was seen to be filled with The lumen of the aneurysm-like dilated coronary artery was filled with dark red thrombus-like material, and the wall was significantly thickened. Pathological examination of coronary artery branches and anterior descending branches showed intimal thickening and inflammatory cell infiltration. The long-term prognosis of patients with KD combined with mild coronary artery dilatation is not well understood. The incidence of somatic aneurysms in children without intravenous gammaglobulin treatment is 1% to 2%, mostly with coronary artery aneurysms. The long-term effects of remission of coronary aneurysms remain unclear, and intravascular ultrasound shows specific thickening at the site of receding coronary aneurysms. A group of studies showed extensive systemic endothelial cell hypofunction in KD patients and dyslipidemia during and after the acute phase of KD, suggesting that KD may be a high risk factor for coronary artery disease and atherosclerosis in adults. III. Management and treatment of KD patients with coronary artery damage in adults The main risk of KD lies in its cardiovascular system complications, especially coronary artery damage, including coronary aneurysm, coronary stenosis, thrombosis and vascular occlusion. In addition, KD in the acute phase can be associated with other cardiovascular complications such as myocarditis, valve damage, and pericarditis. The National Kawasaki Disease Epidemiological Survey in Japan noted that coronary artery aneurysms occurred in approximately 25% of children with Kawasaki disease who were not treated with intravenous gammaglobulin infusion. Cardiac ultrasound shows that coronary aneurysms occur 1-2 weeks after the onset of the disease, with an average of 11.4 days in the course of the disease. Most aneurysms will regress after the acute phase, and about 30-60% will retract within 1 year; a few aneurysms will further increase in size or even rupture; a few may develop new aneurysms; about 1/3 progress to stenosis after the start of regression or due to thrombosis, eventually leading to vessel occlusion, which can cause myocardial infarction or even sudden death. Since the coronary artery damage that occurs in KD is often a long and progressive process, most patients who have KD in childhood and develop coronary artery damage do not develop symptoms of myocardial ischemia and infarction until adulthood. This also means that patients with KD with coronary artery damage have grown to adulthood because they have been followed by pediatricians for a long time. This group of patients will be managed by adult cardiovascular physicians. Kate et al. were the first to conduct a survey in 1992 on the possible etiology of adult cardiovascular disease as a result of having KD in childhood. Of the 130 adult patients presenting with coronary aneurysms from 354 hospitals, 2 were definitively identified and 19 were highly suspected to have had KD in childhood. the investigators also hypothesized that the remaining 109 patients may have also had KD in childhood, but for various reasons the information could not be verified. burns et al. later summarized 74 cases of cardiovascular disease attributed to KD in childhood in young adults. KD as a cause of cardiovascular disease in young adult patients with a mean age of 27.4 years. The presenting symptoms were mainly chest pain/myocardial infarction (60.8%), arrhythmias (10.8%) and sudden death (16.2%). Circumferential calcified spots were visible on chest radiographs in about 1/3 of these patients. Coronary aneurysms were seen in 93.2% of coronary angiograms, coronary occlusions in 66.1% of patients, and extensive collateral circulation formation in 44.1% of patients. Therefore, in adult patients presenting with myocardial infarction or sudden death, especially young adult patients or those without risk factors for atherosclerosis, attention must be paid to tracing the history of KD in childhood. The introduction of imaging can help identify certain patients who had KD in childhood. Calcification of the coronary artery wall at the site of a pre-existing aneurysm formation and subsequent remodeling is the main imaging feature of KD and is often clearly demonstrated by chest radiographs. A Japanese study of young adult patients 20 years after the acute phase of Kawasaki disease found that 94% of patients had calcification of coronary artery aneurysms ≥6 mm in diameter. Therefore, young patients with calcification in the coronary arteries without risk factors and manifestations of atherosclerosis should be highly suspected of having prior KD. In summary, KD is not only a pediatric disease. It requires the collaboration of pediatricians and physicians, especially cardiovascular physicians, to better and more scientifically manage and treat these patients with KD as minors or adults.