vessel and the heart not receiving enough blood and oxygen. This can eventually lead to heart muscle tissue death, i.e., myocardial infarction (MI). MI caused by thrombotic occlusion in an aneurysmal, stenotic, or both aneurysmal and stenotic coronary artery is the main cause of death from Kawasaki disease. The highest risk of MI occurs in the first year after the onset of the disease. MI in children presents with different symptoms from those in adults. The main symptoms were shock, unrest, vomiting, and abdominal pain; chest pain was most common in older children. Most of these children had the attack occurring during sleep or at rest, and around one-third of attacks were asymptomatic. Valvular insufficiencies, particularly of mitral or tricuspid valves, are often observed in the acute phase of Kawasaki disease due to inflammation of the heart valve or inflammation of the heart muscle-induced myocardial dysfunction, regardless of coronary involvement. These lesions mostly disappear with the resolution of acute illness, but a very small group of the lesions persist and progress. There is also late-onset aortic or mitral insufficiency caused by thickening or deformation of fibrosed valves, with the timing ranging from several months to years after the onset of Kawasaki disease. Some of these lesions require valve replacement. Other Other Kawasaki disease complications have been described, such as aneurysm of other arteries: aortic aneurysm, with a higher number of reported cases involving the abdominal aorta, axillary artery aneurysm, brachiocephalic artery aneurysm, aneurysm of iliac and femoral arteries, and renal artery aneurysm. Other vascular complications can occur such as increased wall thickness and decreased distensibility of carotid arteries, aorta, and brachioradial artery. This change in the vascular tone is secondary to endothelial dysfunction. In addition, children with Kawasaki disease, with or without coronary artery complications, may have a more adverse cardiovascular risk profile, such as high blood pressure, obesity, and abnormal serum lipid profile. Gastrointestinal complications in Kawasaki disease are similar to those observed in Henoch–Schönlein purpura, such as: intestinal obstruction, colon swelling, intestinal ischemia, intestinal pseudo-obstruction, and acute abdomen. Eye changes associated with the disease have been described since the 1980s, being found as uveitis, iridocyclitis, conjunctival hemorrhage, optic neuritis, amaurosis, and ocular artery obstruction. It can also be found as necrotizing vasculitis, progressing into peripheral gangrene. The neurological complications per central nervous system lesions are increasingly reported. The neurological complications found are meningoencephalitis, subdural effusion, cerebral hypoperfusion, cerebral