An emergency ECG sign of ST elevation myocardial infarction.

BACKGROUND: The occlusion of the left anterior descending coronary artery (LAD) is usually characterized by the ST-segment elevation associated with a tall and peaked T wave in precordial leads. CASE PRESENTATION: We reported a case who suffered from typical chest pain and tall and positively symmetrical T waves in leads V2-6, J point depression with upsloping ST-segment depression. However, the coronary angiogram demonstrated a 100% occlusion of midshaft LAD artery. CONCLUSIONS: Recognition of this atypical electrocardiogram (ECG) pattern can ensure immediate reperfusion therapy regarding acute myocardial infarction.

Association of peroxisome proliferator-activated receptor delta and additional gene-smoking interaction on cardiovascular disease.

AIMS: To investigate the impact of peroxisome proliferator-activator receptor delta (PPARD) gene polymorphism and additional gene-smoking interaction on cardiovascular disease (CVD) risk based on this Chinese population. METHODS: A total of 1048 subjects (617 males, 431 females) with a mean age of 52.9 ± 14.1 years old were selected, including 520 CVD patients and 528 normal control subjects. The logistic regression model was used to examine the association between three SNPs and CVD risk, odds ratio (OR), and 95% confident interval (95%CI) were calculated. Generalized multifactor dimensionality reduction (GMDR) was employed to investigate the gene-smoking interaction. RESULTS: Genotypes of variants in rs2016520 and rs9794 were associated with decreased CVD risk, and CVD risk was significantly lower in carriers of C allele of the rs2016520 polymorphism than those with the TT genotype (TC+CC versus TT), adjusted OR (95%CI) = 0.71 (0.56-0.86). In addition, we also found that CVD risk was also significantly lower in carriers of the G allele of the rs9794 polymorphism than those with the CC genotype (CG+ GG versus CC), adjusted OR (95%CI) = 0.69 (0.53-0.86). GMDR analysis suggested a potential gene-environment interaction between rs2016520 and smoking. Overall, the two-locus models had a cross-validation consistency of 10 of 10, and had the testing accuracy of 62.17%, and never smokers with TC or CC of the rs2016520 genotype have the lowest CVD risk, compared to smokers with TT of rs2016520, OR (95%CI) was 0.42 (0.23-0.66). CONCLUSIONS: The minor allele of rs2016520 and rs9794 in PPAR-δ and interaction between rs2016520 and non-smoking were associated with decreased risk of CVD.

Apelin-13 upregulates Egr-1 expression in rat vascular smooth muscle cells through the PI3K/Akt and PKC signaling pathways.

Previous studies have shown that Apelin-13 upregulates early growth response factor-1 (Egr-1) via the extracellular signal-regulated protein kinase (ERK) signaling pathway. Apelin-13 induces proliferation and migration of vascular smooth muscle cells (VSMCs) as well as the upregulation of osteopontin (OPN) via the upregulation of Egr-1. This study was designed to further explore the activity of Apelin-13 in VSMCs by investigating members of the mitogen-activated protein kinase (MAPK) family, in particular Jun kinase (JNK) and p38 mitogen-activated protein kinase (P38). We also examined whether the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) and protein kinase C (PKC) signaling pathways were involved in the regulation of Egr-1 by Apelin-13. We treated rat aortic VSMCs with Apelin-13 and examined the expression of JNK, p-JNK, P38, and p-P38 to investigate whether Apelin-13-mediated increases in Egr-1 occurred through the JNK and P38 signaling pathways. We then pretreated VSMCs with the Gi protein inhibitor pertussis toxin (PTX) and the Gq inhibitor YM254890, added Apelin-13 and looked for changes in Egr-1 expression. Finally, we pretreated with the PI3K inhibitor LY294002 and the PKC inhibitor GF109203X, and treated with Apelin-13. Our results showed that JNK and P38 did not participate in Apelin-13-mediated increase in Egr-1. Instead, Apelin-13 upregulation of Egr-1 was mediated by a PTX-sensitive Gi protein. Apelin-13 did increase ERK phosphorylation through the PI3K/Akt and PKC signaling pathways, resulting in changes in Egr-1 expression. These data provide important targets for future studies to modulate vascular remodeling.

Systematic Review of Association Between Low Ankle-Brachial Index and All-Cause Cardiovascular, or Non-cardiovascular Mortality.

The ankle-brachial index (ABI) is the ratio of the ankle versus brachial systolic blood pressure. ABI of <0.90 indicates the presence of peripheral arterial disease. Some studies indicated that ABI may correlate with the all-cause mortality. The aim of this study was to assess the prognostic significance of ABI of <0.90 as such predictor of all-cause mortality. In addition, we wished to test the association between ABI and cardiovascular or non-cardiovascular mortality. To this end, we carried out a systematic review of the studies published in MEDLINE that reported both ABI and all-cause mortality. The endpoint of interest was the all-cause mortality, including death from coronary disease, stroke, or other causes. Ten studies, with a total of 22,705 patients, were included in this review. ABI of <0.90 was proved to be associated with an increased risk of all-cause mortality [odds ratio 2.74 (95 % confidence interval 2.03-3.68) and number needed to harm 1.66], as well as with cardiovascular [i.e., death from coronary disease or stroke; respectively, 3.23 (1.98-5.29) and 1.26] and non-cardiovascular mortality [respectively, 2.23 (1.40-3.55) and 1.29]. In conclusion, ABI of <0.9 is useful as a prognostic factor for all-cause mortality.