ABSTRACT
Objective: To study the relationship between ABO blood type and spontaneous re-canalization (SR) in patients with acute myocardial infarction (AMI). Methods: A total of 1209 consecutive AMI patients were enrolled. Based on TIMI grade, the patients were divided into 2 groups: Non-SR group, the patients with TIMI grade 0-1,n=442 and SR group, the patients with TIMI grade 2-3,n=767. The relationship between ABO blood type and SR was investigated. Results: Compared with Non-SR group, SR group had more patients with blood type O (32.3% vs 24.7%) and less blood type A (31.7% vs 24.9%). Meanwhile, we found that a lower cholesterol level was related to patients with O blood type and SR occurrence, bothP<0.05. Multi regression analysis indicated that with adjusted age, gender, BMI, hypertension, diabetes, smoking, LDL-C and C-reactive protein, ESR, fibrinogen, D-dimmer, endothelial cardiac function, blood type O may independently predict SR occurrence in AMI patients (OR=1.49, 95% CI 1.10-2.05), while blood type A may have disadvantage for SR (OR=0.65, 95% CI 0.48-0.80). Conclusion: ABO blood type has been related to SR in AMI patients, blood type O is in favor of SR, while blood type A has disadvantage for SR occurrence.
ABSTRACT
Objective To investigate the expression of insulin-like growth factor 2 receptor(IGF-2R)induced by hypoxia and serum deprivation(H/SD)in cultured neonatal rat cardiomyocytes in vitro.Methods Cultured neonatal rat cardiomyocytes were randomly divided into control group and H/SD group.Expression of IGF-2R mRNA was measured by RT-PCR and real time RT-PCR.Level of IGF-2R protein was measured by enzyme-linked immunosorbent assay(ELISA).Results Compared with control group,the expression of IGF-2R mRNA increased significantly (P ＜0.01)in cardiomyocytes cultured in H/SD condition for 12 h and 24 h,and IGF-2R protein was upregulated in cardiomyocytes cultured in H/SD condition for 24 h(P ＜0.05).Conclusion H/SD may induce IGF-2R expression,and IGF-2R may potentially explain the mechanism of cardiomyocyte damage induced by ischemia.