New progress in the treatment of Cqs disease time: March 09, 2015 Source: original site click: 912 times I want to comment (0) "Font: Big Small"
new progress in treatment of Cqs disease
Giofuyong 蔺婧
Department of Pediatrics, Shaanxi provincial People's Hospital
(Third affiliated Hospital of Xi ' an Jiaotong University medical school)
Cqs disease (Kawasaki DISEASE,KD) is a systemic vascular inflammatory disease, which was first reported in 1967 by Cqs-Fu doctors, formerly known as mucosal cutaneous lymphatic binding (mucocutaneous lymph Node syndrome,mcls), Since 1970, 80% of children under 5 years of age have been reported around the world. The basic pathological changes of the disease are systemic vasculitis, mainly invasion of large and medium blood vessels, coronary artery disease is a serious complication, especially coronary artery aneurysm (CAA) and coronary artery stenosis is the most serious, can lead to ischemic heart disease, myocardial infarction and sudden death. KD has now replaced rheumatic fever as the primary cause of childhood acquired cardiovascular disease, and after nearly 40 years of efforts, there have been many new advances in epidemiology, prevention, diagnosis and treatment.
Progress in Treatment
1 Treatment of acute phase KD
The main objective is to control non-specific vasculitis of the body and prevent the occurrence of coronary artery damage (CAL).
1.1 Intravenous Immunoglobulin (IVIG) 1984 Furusho[1] IVIG was applied to KD for treatment and success. Since then, IVIG has gradually been widely used in the treatment of KD, and finally determined its central position in KD treatment. IVIG prevention of CAA mechanism is unclear, its role may be: ① large doses of ivig to the negative feedback regulation of the immune, so that cd8+ cells increased, the activation of cd4+ cells decreased, thereby reducing the synthesis of IgG; ② feedback inhibits polyclonal activated secretory B cells producing autoantibodies such as anti-endothelial cell antibodies ③, which binds the FC receptors on the walls of monocytes, lymphocytes and other immune active cells, inhibits the overactive activation of the immune cells, inhibits the production of interleukin 1, tumor necrosis factor, and ④ the FC receptors on the surface of the platelet, prevents platelet adhesion, aggregation, prevention of thrombus, and ⑤ the FC receptor of the closed vascular endothelial cells, Inhibition of platelet-derived growth factor and vascular pathway activation caused by vascular endothelial injury, thereby inhibiting the immune damage of blood vessels; ⑥ by some specific antibody to some unknown pathogenic bacteria or toxins exogenous antigen [2,3].
There are three methods of intravenous infusion of IVIG: ①ivig 2.0g/kg, intravenous input in 10~12h, the method is used in the United States and Japan, ② 5-day therapy: IVIG 400mg/kg d-1,2~3h internal vein input, with 5 days; ③ivig 1.0g/kg, Internal venous input in 4~6h. Three kinds of treatment can prevent Cal occurrence, but it is better than 5 days to 2.0g/kg and reduce the symptoms, shorten hospitalization time and so on, and has obvious effect in preventing coronary artery lesions [4]. The occurrence of CAA was negatively correlated with the dose of IVIg, and the decrease in the incidence of coronary anomalies depended on the dose of IVIg [5]. However, there is still controversy over the use of 2.0g/kg or 1.0g/kg, and there are data reports that [6,7],ivig single agent 1g/kg and single agent 2g/kg have no significant difference in the concentration of IG in the plasma after the input of a single agent 1.0g/kg and a single agent 2g/kg respectively 15.56g/ L and 18.10g/l, both reach the level of the lowest effective plasma concentration 15g/l needed to treat KD, and consider the single agent 1g/kg to be the most economical and effective dosage. However, the comparison of the effectiveness of the two to reduce the incidence of CAA, still need a multi-center, large sample of randomized controlled study to demonstrate.
The use of IVIg time should be given within 10 days after onset, if possible, should try to give better curative effect within 7 days, if more than 10 days before the diagnosis of KD, after the onset of 10 days can still consider the application of IVIg. In recent years, there has been widespread concern about whether the use of IVIg in 5 days of KD onset has further reduced CAL efficacy, 2004 Muta et [8] 9000 cases of large sample cohort studies showed that There was no significant difference in the incidence of Cal among patients who received IVIG treatment within 4 days and 5 days after the illness, but the chance of repeated IVIg in the anterior group increased significantly compared with the latter group.
3.1 Different dates effect of intravenous infusion of large doses of immunoglobulin (IVIG)
In 1993, 2652 hospitals with more than 100 beds were surveyed in Japan, and 11221 cases were found, of which 8958 (79.8%) were used IVIg. In these cases, the doses used by most patients were 1000mg/kg (36.3%), followed by 2000mg/kg (16.9%) and 1200mg/kg (16.85%). 53.8% of the patients began to use the drug on the 5th day after onset and 83.7% of the patients began to use the drug on the 7th day after onset. The results suggest that the proportion of patients with cardiac sequelae after the 9th day after the onset of dose >2000mg/kg is significantly higher than those with ① >2000mg/kg, and the ②ivig is ineffective in preventing cardiac sequelae. The study concluded that >2000mg/kg or IVIg in the 9th day of onset could have adverse or even risk factors for the prevention of cardiac sequelae, so Argentina researchers believe that when high doses of IVGV are ineffective and risk factors are present, hormonal shock therapy [2] is used, but the United Kingdom, Italy and the United States adopt 2g/ KG diluted in 10 hours to the hour of slow drip, such as 48 hours ~72 hours again fever or unexplained when the cause can be given again [10,11].
3.2 Aspirin
is the preferred medicine for KD treatment. The drug is an enzyme inhibitor that has anti-inflammatory effects and prevents platelet aggregation and thrombosis. The domestic commonly used dosage is daily 30mg~50mg/kg 3 times to take orally, the United States uses the dosage 20mg/kg times, 4 times daily, even takes 14th, if the echocardiography indicates the coronary artery normal or suspicious when the aspirin changes to the daily 3mg~5mg/kg altogether 2 months to the month [12].
IVIg treatment, although the incidence of coronary tumors to 3%--5%, but the latest foreign articles said, acute vasculitis, myocarditis, valvular heart disease may become sequelae, the damage caused by these sequelae may occur after the child develops to a certain stage.
1.2 Aspirin (ASA) ASA has antipyretic, analgesic, anti-inflammatory, anti-platelet aggregation role, and KD has systemic vascular inflammation, high fever, platelet rise and other manifestations, so ASA to KD treatment effective, ASA has become the first choice of KD basic treatment of drugs. Its role is mainly by inhibiting the activity of the platelet cyclooxygenase (COX), reducing the formation of prostaglandin (PG) and thrombus, while alleviating the inflammatory response, inhibiting platelet aggregation and thrombosis. Since the ASA itself has no anti-Cal effect, it needs to be combined with IVIG. However, there is still controversy over the dosage and maintenance time of the ASA. The United States usually give 80~100mg/kg d-1, divided 4 times to take, because the large doses of ASA to gastrointestinal stimulation, Japan and other Asian countries to give 30~50 mg/kg d-1, through the Multi-center study is equally effective [9]. The time limit for using medium to large doses of ASA was also different, and many centres reduced the ASA dose after a child's fever 48~72h, instead of a small dose of 3~5mg/kg d-1, but some experts did not change to a small dose until the 14th day of the disease and the Fever 48~72h.
After the ASA is reduced according to the condition need to determine the use of time: ① no coronary abnormalities or acute coronary artery only a single-sex expansion, 6-8 weeks later can be discontinued; ② concurrent small to moderate CAA, should be taken orally in small doses until CAA disappears ③ if one or more large CAA or multiple small to moderate CAA but no coronary artery occlusion, long-term use of small doses of ASA combined with warfarin anticoagulation treatment; ④ concurrent coronary artery occlusion, in addition to long-term use of small doses of ASA combined warfarin, plus taking calcium channel blockers to reduce myocardial oxygen consumption [10].
3.3 Corticosteroid Shock Therapy
Recent studies have suggested that the disease is associated with high antigen levels (Argentina), so the researchers reported that patients with large doses of ivig that were ineffective were able to use corticosteroid shock therapy [1]. TOKYO, Japan A randomized controlled study of 100 cases of Kawasaki disease using a strong pine dragon daily 20mg/kg continuous drip 5th, and then reduced to daily 2mg/kg oral, until CRP normal, or the daily 400mg/kg intravenous immunoglobulin with the 3rd, while giving aspirin daily 50mg/kg, Dipyridamole Daily 5mg/kg, the study suggests that early intravenous infusion of prednisone is a safe and effective way to prevent coronary artery damage.
1.3 Unlike other vascular inflammatory diseases, corticosteroids remain a controversial issue in the treatment of KD. Early studies suggested that the initial treatment of the hormone as KD would increase the incidence of coronary artery abnormalities, but in recent years it has been suggested that [11] hormone therapy can shorten the period of fever and hospitalization, decrease the erythrocyte sedimentation rate and C-reactive protein (CRP), and have no significant effect on coronary prognosis. Therefore, the role of corticosteroids in the acute phase and the impact on the coronary arteries still need to be a multi-center large sample randomized controlled trial study to verify. Because corticosteroids have the potential to promote the formation of CAA, and in recent years IVIg treatment KD effect is obvious, the early course of the disease is not advocated the use of corticosteroids [12].
2.2 Recent studies of corticosteroids suggest that KD is associated with high antigen (highly antigenicity) and that the use of glucocorticoid therapy for large doses of IVIG is not possible, and most scholars suggest that hormonal therapy should be limited to patients with more than two doses of ivig that do not relieve fever, and can achieve better results [11,17]. Because hormone therapy can aggravate the state of blood coagulation, it must be associated with the ASA. Common treatment methods: intravenous injection of methylprednisolone 20~30mg/kg d-1 Impact Therapy, given in 2~3h, 1 times a day, with 1-3 days, hot back to prednisone 2mg/kg d-1, sub-oral, until the serum CRP normal, reduced to 1mg/kg d-1, 1 times a day, Gradually reduce the amount, a total of 4-6 weeks to stop the drug.
Treatment of KD in 2 IVIg non-sensitive children
Data statistics show that the risk of coronary dilatation in IVIg-insensitive children is greater than that of IVIg-sensitive children. Data analysis showed that, compared with sensitive children, the following biochemical indexes were higher in children with insensitivity: neutrophil count, C-reactive protein, total bilirubin, aspartic acid transaminase, alanine aminotransferase, lactate dehydrogenase. Children have a two to three increase in biochemical levels (crp≥7.0mg, tb≥0.9mg, or ast≥200iu/l), most likely ivig insensitive patients.
There was a greater rate of coronary injury in IVIg-insensitive children.
2.1 IVIg is a non-sensitive person refers to the initial high dose of IVIG treatment after the completion of 36h continued fever or fever again. About 10% of KD patients did not respond to single dose 2g/kg. The overwhelming majority of experts in resistant IVIg recommended the IVIG (2g/kg) treatment again, and most patients reacted well to the second dose of IVIg [13,14].
3.4-fluoro-propionic acid and prostatic annulus
The two drugs with aspirin can achieve better results. The daily 4mg/kg of fluoride, the heat back reduced to daily 2mg/kg, Prostaglandin 2mg/kg daily, after 2 weeks of medication gradually reduced the amount of drug withdrawal [13].
3.5 Anticoagulant Therapy
Recovery and chronic period for the prevention of myocardial infarction and the relief of coronary artery stenosis or occlusion, the use of small doses of aspirin daily 3mg~5mg/kg, once a day, such as the non-concurrent coronary artery abnormalities, the medication time is not less than 1 years.
3.1 Anticoagulant therapy KD appeared CAA when the blood retention in the tumor, prone to thrombosis embolism, especially when the CAA rapidly expanded, the risk of embolism formation is greater, in order to prevent the formation of CAA, the need for long-term anticoagulant therapy. For such children should take a small dose of ASA for a long time, the patients with severe coronary artery abnormalities, the use of small doses of ASA on the basis of warfarin and clopidogrel and other possible anticoagulant effect is better, but also some people advocate the use of ASA and Heparin [21].
Heparin is mainly used in the higher platelet (>600x109/l), Plasma fibrinogen (FIB) >4g/l, coronary artery thrombosis. Because low molecular weight heparin has better anticoagulant activity, relatively weak antithrombin effect, good anticoagulant reaction and high bioavailability, so the use of low molecular weight heparin has better curative effect. Each dose was 50~100iu/kg, subcutaneous administration, 1 times a day, 7-10 days, with the ⅹa level of coagulation factor 0.5~1.0u/ml adjusted dose [22].
Some new antiplatelet agents are used in the treatment of KD combined with CAA's anticoagulant therapy, such as Ticlopidine and clopidogrel. In addition to anti-platelet activity, there are fibrinolytic and thrombolytic effects, clopidogrel relative small side effects, can be used in combination with ASA, but there is no best dose of the report.
3.6 Pan Sheng Ding
In Japan, 100 cases of 1.5-year-old KD children with IVIg (400mg/kg with 3rd) when oral dipyridamole 5mg/kg to CRP normal after discontinuation. The study confirmed that the joint use of dipyridamole is a complementary
A better way to treat KD [1].
2.4 rituximab (Infliximab) is a monoclonal antibody to tnf-a, may have a role in the treatment of refractory KD, has been tested for the treatment of non-antipyretic children after initial IVIG treatment, and its effectiveness in reducing CAA incidence still needs further proof. Rituximab can be used to treat IVIG in patients with non-sensitive treatment. And in the post-observation, no coronary changes were found. (Usage: 5mg/kg, infusion within two hours)
Acyclovir is a platelet glycoprotein ⅱb/ⅲa receptor inhibitor that reduces the formation of thrombosis in the tumor and facilitates vascular remodeling, and reports [23] patients who received a combined standard treatment for rituximab, and in contrast to standard-treated cases, retracted more in the maximum diameter of CAA, However, more prospective control trials are still needed to treat the patients with large CAA in the acute or subacute period, and may be considered for the treatment of acyclovir.
3.7 Tissue fibrin dissolving activator (TPA)
The study of Kagoshima Hospital in Japan found that TPA was not only effective for acute myocardial infarction, but also effective for asymptomatic thrombosis and coronary artery tumors, because asymptomatic thrombosis can cause sudden death, and it is believed that intravenous infusion of TPA is more effective than intravenously. Dose 14.4 million IU. The heparin and warfarin can be used [13].
3.2 thrombolytic therapy is the primary cause of death in patients with KD coronary artery disease, therefore, thrombolytic therapy is required for the treatment of acute myocardial infarction, thrombolytic therapy is suitable for the treatment of myocardial infarction within 6h of the disease, after 6h thrombolytic effect is poor. urokinase, tissue fibrin dissolving activity (T-PA), and the intravenous thrombolysis therapy (abciximab) were reported, and the coagulation condition should be detected in time of thrombolytic therapy.
3.8 urine kinase
Dissolve in the injection water 2ml~3ml, and then add glucose liquid in 1 hours to input, maintain the amount of 3000u~4000u/kg per hour, lasting 3 hours ~ hours. Dosage 200,000 iu~48 million iu/every 24 hours, given under heparin.
Urokinase is suitable for coronary artery thrombosis or when myocardial infarction occurs. Usage: ①5000u/kg 1h vein input, 3 times daily, when combined with heparin, the dose is 400u/kg d-1;②2 million u/kg, total 96~120 u/kg 1h input, 3000~4000u/kg maintenance 3~10h, Attention should be paid to increase the coagulation time by 1 time times or fib<1g/l (normal value of 3 G/L) has the risk of bleeding, ③ each 5000u/kg,10min within the intra-coronary injection, up to a maximum of three times.
T-PA is suitable for acute myocardial infarction, for asymptomatic thrombosis and CAA is also effective, the administration of T-PA from the coronary vein injection of better effect, dose 14.4 million iu/times.
[19] 2.5 plasma exchange (PE) patients with ineffective IVIG and hormone therapy can use PE,PE to remove too many cytokines in the body and to treat the patient with IVIG resistance. However, because of its own risk, the treatment is generally not recommended.
3.9 Coronary artery bypass grafting surgery
[14] Although many patients were treated with aspirin + dipyridamole + pyridine (ticlopidine), repeated myocardial infarction was not advisable for long-term use of warfarin, and coronary artery bypass grafting was used for such patients.
Treatment of 3 kd coronary artery lesions
Coronary artery disease is the most serious complication of KD, the incidence rate is 20%~25%, the incidence of CAA after using IVIg has been reduced to 5%, the great CAA incidence rate drops to about 1% [20]. There are three main forms of Cal: ① coronary openings, ②caa;③ coronary stenosis. Because of the CAA Intimal hyperplasia and thrombosis, resulting in stenosis of the coronary artery, combined with blood retention in the tumor, the formation of thrombus embolism and lead to myocardial infarction or sudden death, so the coronary lesions should be treated in a timely manner. The treatment of lesions depends on the severity and extent of coronary involvement, usually including anticoagulation, thrombolysis, interventional therapy and surgical treatment.
The filling artery expands above 5mm, must have the late close follow-up, may choose the electrocardiogram, the coronary artery MRI and so on. Depending on the situation of different patients, choose different treatment methods.
Multi-Slice Spiral ct angiography can show the pathological changes of aneurysm more accurately.
The American Heart Association (AHA) does not accurately classify the coronary lesion after Kawasaki disease, and the AHA classification underestimates patients with 19%--32% with minor coronary lesions, as well as patients with moderate coronary lesions in the 35%--78%. We need a standard that considers only the size of the coronary artery, which is the z-fraction of the coronary lumen to the adjusted body surface area. The results of the study showed that the 5.0>z fraction was ≥2.5 as a small coronary artery abnormality. If the 10.0>z fraction is ≥5.0, it is considered a large coronary anomaly, if the Z-score ≥10.0 is considered to be a huge coronary anomaly.
3.3 Interventional therapy with the development of cardiovascular interventional therapy, interventional therapy has also been applied to the treatment of KD coronary artery stenosis and myocardial infarction. Interventional therapy mainly includes percutaneous transluminal coronary angioplasty (PTCA), Intracoronary stent implantation (stent implantation), percutaneous transluminal coronary angioplasty (PTCRA), percutaneous transluminal coronary revascularization (PTCR), and so on.
PTCA is suitable for a single arterial stenosis more than 75%, no wall calcification and myocardial infarction, the coronary artery is too narrow, the degree of more than 90%, the PTCA catheter is not easy to enter the narrow area, and the intima thickening with calcification, the blood vessel wall hardens, the effect of PTCA balloon dilation is poor, When balloon dilatation was insufficient or dilated, the intimal hyperplasia of the coronary arteries resulted in a high recurrence rate [22].
PTCR is suitable for the new thrombosis in the giant CAA 6h, the method is first inserted into the coronary artery by the catheter through the artery directly into the T-PA, so that the coronary artery thrombolysis, postoperative heparin intravenous drip, small doses of ASA and warfarin oral to prevent thrombosis.
3.10 Heart transplant
A total of 8 children with Kawasaki disease in the world were undergoing heart transplants due to severe coronary stenosis, coronary artery tumors, and severe irreversible cardiac insufficiency, including 3 in the United Kingdom and 5 in the US, according to the UK and US state transplant registries. 6 cases survived and 2 died. It is believed that heart transplantation is an effective method for treating severe ischemic heart disease caused by Kawasaki diseases. The transplant indications were: severe cardiac insufficiency, multiple severe coronary artery stenosis, and failure of bypass surgery [1].
3.4 KD Large CAA treatment of KD large CAA (coronary diameter ≥8mm) treatment, the domestic still with drug thrombolysis and anticoagulant therapy. However, for patients with severe left ventricular insufficiency, coronary artery bypass grafting (CABG) should be considered. The long-term curative effect of CABG is related to the age of the children and the material of Vascular bridge, and the long-term patency rate is better for the older children, but the rate of restenosis is very high for the young children, especially the <8-year-old children. A group of data showed [1]: 100 cases of CABG postoperative child follow-up, of whom 9 years of age under the CABG 10 years after the operation of the venous bridge patency rate of (22.2±12.8), arterial bridge (70.5±6.9)%, and >10-year-old children's venous bridge patency rate is (48.8±17.9)% , the arterial bridge is (86.9±6.0)%. Therefore, unless KD coronary stenosis is too severe or acute myocardial infarction occurs, CABG surgery should be delayed to about 13 years of age [24].
Japan reported that although children under 3 years of age are less likely to see Kawasaki disease, they are prone to coronary artery damage and death. [1] It is believed that early detection (4th to 5th day after the disease), aspirin daily 30mg/kg+ large doses of 2000mg/kg (1 times) of intravenous drip can effectively prevent coronary artery damage.
3.11 Udayana (UTI)
UTI is a kind of multi-enzyme inhibitor which acts on a variety of enzymes, such as trypsin, protease and elastase. Clinical studies suggest that UTI is an endogenous anti-stress substance and is also a multi-nucleation leukocyte (PMN) inhibitor and free radical scavenger and a drug that is resistant to endogenous shock. According to the pharmacological action of UTI, the early application of UTI in Cqs disease can block the pathogenic pathway of PMN, inhibit the damage of PMN to fibrin and elastin, prevent the formation of aneurysm and coronary artery stenosis, and reduce the dose of immunoglobulin (1).
2.3 Statin (Ulinastatin,uti) is a trypsin inhibitor. Clinical studies suggest that UTI is a multi-nucleation leukocyte (PMN) inhibitor and free radical scavenger and a drug that resists endogenous shock. The early application of UTI in KD can block the pathogenic pathway of PMN, inhibit the damage of PMN to fibrin and elastin, prevent the formation of CAA and coronary artery stenosis, dose 3000~5000u/kg d-1, divide two times slowly intravenous drip, use 5-9 days, is considered effective in patients with IVIG resistance [18], but the clinical experience is still few, and its effectiveness and safety need to be further studied.
3.12 Ketone Cocoa Base (PTX) +ivig
Ptx+ivig, a multi-center, prospective, randomized clinical trial of 43 children with Kawasaki disease was conducted at Yamaguchi University in Japan. Group A patients were treated with only ivig200mg/kg+ aspirin daily 30mg/kg with 5th, Group B for ivig+ aspirin (dosage same as Group A) +PTX daily 20mg/kg orally, 30th. Results there were no coronary lesions in Group B, and coronary lesions occurred in Group A 14% patients, suggesting that PTX could reduce the TNFA level rapidly and reduce the damage to coronary artery [1].
3.10 Heart transplant
A total of 8 children with Kawasaki disease in the world were undergoing heart transplants due to severe coronary stenosis, coronary artery tumors, and severe irreversible cardiac insufficiency, including 3 in the United Kingdom and 5 in the US, according to the UK and US state transplant registries. 6 cases survived and 2 died. It is believed that heart transplantation is an effective method for treating severe ischemic heart disease caused by Kawasaki diseases. The transplant indications were: severe cardiac insufficiency, multiple severe coronary artery stenosis, and failure of bypass surgery [1].
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[+] Ja-young Hwang1, Kyung-yil Lee1, Jung-woo Rhim1, et al. Arch Dis child 2011;96:1088-1090. Assessment of intravenous immunoglobulin Non-responders in Kawasaki disease
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Fuyong Jiao
Prof. and Head
Children ' s Hospital
Shaanxi provincial People ' s Hospital of Xi,an Jiaotong Univeristy
President of China Society for Prevention of the Child abuse and neglect
Executive Councilor of International Society for Prevention of Child abuse and neglect (Ispcan)
Phone: (029-85368194), 85521331ext2361 (O)
Mail add:no.256 Youyi West rd.xi,an 710068 China
website:http://www.cnspcan.org
E-Mail:[email protected]//[email protected]
New progress in treatment of Cqs disease
