Prognostic significance of QRS fragmentation and correlation with infarct size in patients with anterior ST-segment elevation myocardial infarction treated with percutaneous coronary intervention: Insights from the INFUSE-AMI trial.

BACKGROUND: QRS fragmentation (fQRS) is believed to reflect myocardial scar formation in patients with coronary disease. Whether early formation of fQRS in patients with ST-segment elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI) is correlated with infarct size and prognosis is unknown. We assessed the prognostic value of fQRS at 60min post-PCI and its correlation with infarct size in patients with anterior STEMI managed with primary PCI. METHODS: The INFUSE-AMI trial enrolled 452 patients with anterior STEMI undergoing primary PCI. Electrocardiograms (ECGs) were performed at baseline and 60min post-PCI. Infarct size was evaluated using cardiac magnetic resonance imaging at 30days post-PCI. Target vessel failure (TVF) was defined as the composite of cardiac death, target vessel myocardial infarction, or ischemia-driven target vessel revascularization. Study groups were defined as patients with versus without fQRS at 60min post-PCI. RESULTS: Out of 421 patients with ECG data 60min post-PCI, 68 patients (16.2%) had fQRS. Patients with versus without fQRS had similar baseline characteristics and infarct size (16.9%±8.7% vs. 16.1%±10.5%, p=0.62), but patients with fQRS had higher adjusted risk of 1-year TVF (adjusted HR 2.27, 95% CI 1.06-4.89, p=0.036) and a trend toward a higher risk of the composite cardiac death or target vessel myocardial infarction (9.0% vs. 4.1%, p=0.08) at 1year. CONCLUSION: fQRS in patients with STEMI is associated with TVF but does not correlate with infarct size.

Insulin Sensitivity and Inflammation Mediate the Impact of Fitness on Cerebrovascular Health in Adolescents.

BACKGROUND/OBJECTIVES: To investigate in adolescents the relationships between retinal vessel diameter, physical fitness, insulin sensitivity, and systemic inflammation. METHODS: We evaluated 157 adolescents, 112 with excessive weight and 45 lean, all without type 2 diabetes mellitus. All received detailed evaluations, including measurements of retinal vessel diameter, insulin sensitivity, levels of inflammation, and physical fitness. RESULTS: Overweight/obese adolescents had significantly narrower retinal arteriolar and wider venular diameters, significantly lower insulin sensitivity, and physical fitness. They also had decreased levels of anti-inflammatory and increased levels of proinflammatory markers as well as an overall higher inflammation balance score. Fitness was associated with larger retinal arteriolar and narrower venular diameters and these relationships were mediated by insulin sensitivity. We demonstrate that inflammation also mediates the relationship between fitness and retinal venular, but not arterial diameter; insulin sensitivity and inflammation balance score jointly mediate this relationship with little overlap in their effects. CONCLUSIONS: Increasing fitness and insulin sensitivity and reducing inflammation among adolescents carrying excess weight may improve microvascular integrity. Interventions to improve physical fitness and insulin function and reduce inflammation in adolescents, a group likely to benefit from such interventions, may reduce not only cardiovascular disease in middle age, but also improve cerebrovascular function later in life.

Role of EC-SOD overexpression in preserving pulmonary angiogenesis inhibited by oxidative stress.

UNLABELLED: Angiogenesis is one of the most important processes for normal lung development. Oxidative stress can impair the pulmonary angiogenesis, leading to chronic lung disease or Bronchopulmonary dysplasia (BPD). OBJECTIVE: To investigate the protective effects of EC-SOD overexpression on pulmonary angiogenesis on neonates following exposure to acute hyperoxia. DESIGN/METHODS: Transgenic (TG) and wild-type (WT) neonatal mice (10 mice per group) were exposed either to air (control group) or 95% O(2) for 7 days starting at birth. After exposure, all animals were sacrificed. ROS concentration was measured in lung homogenates using OxiSelect ROS assay kit. Mean vascular density (MVD) was measured using anti CD34 staining. RNA was extracted and the angiogenesis markers, VEGF, VEGFR1 and VEGFR2 and PECAM-1 were analyzed by RT-q PCR. VGEF protein was measured using Western blots. Endothelial progenitor cells (EPCs) was assayed by flow cytometer. RESULTS: There was a significant reduction of ROS in TG hyperoxic neonate group (156±14.2) compared to WT hyperoxic animals (255±35.1). Evaluation of MVD, using anti-CD34, showed marked significant increase of MVD in the TG group following hyperoxic exposure (85±12) in comparison to the WT hyperoxic group (62±8.4), (P<0.05). Among the hyperoxic groups, both RNA and protein of VEGF expression were significantly reduced in the WT animals compared to the TG group (P<0.05). The same trend was found in VEGFR 1 and 2 which were significantly reduced in WT group compared to the TG group (P<0.05). There was no significant difference between hyperoxia TG and control group (P>0.05). PECAM expression was significantly reduced in both hyperoxic compared to normoxic groups (P<0.05). EPC's showed significant reduction in WT hyperoxic group compared to others (P>0.05). CONCLUSIONS: EC-SOD plays a key role in preserving angiogenesis by scavenging free radicals which has an inhibitory effect on angiogenesis process in neonatal mice lung following exposure to hyperoxia.