RESUMO
BACKGROUND: Door to balloon time is a crucial factor of mortality in patients with ST-segment elevation myocardial infarction. However, the factors that contribute to failure of achieving door to balloon time ≤ 90 min in an electrocardiogram triage system remain unknown. METHODS: This single-center retrospective observational study collected data from consecutive patients with ST-segment elevation myocardial infarction from April 2016 to March 2021. The primary outcome was the failure to achieve door to balloon time ≤ 90 min. A multivariate logistic regression model was performed to predict factors associated with failure to achieve door to balloon time ≤ 90 min. RESULTS: In total, 190 eligible patients were included. Of these, the 139 (73.2%) patients with door to balloon time ≤ 90 min were significantly younger compared to those with door to balloon time > 90 min (p = 0.02). However, there was no significant difference in sex and timing of hospital arrival between the door to balloon time ≤ 90 and > 90 min groups. Presence of chest pain and ambulance usage were significantly more frequent in patients with door to balloon time ≤ 90 min (p ≤ 0.01, p = 0.02, respectively). Multivariate analysis showed that absence of chest pain (adjusted odds ratio 4.76; 95% confidence interval, 2.04-11.1; p < 0.01) and non-ambulance usage (adjusted odds ratio 3.53; 95% confidence interval, 1.57-7.94; p < 0.01) are predictive factors of failure to achieve door to balloon time ≤ 90 min. CONCLUSION: Patients without chest pain as the chief complaint or non-ambulance usage were significantly associated with the failure to achieve door to balloon time ≤ 90 min.
RESUMO
The mechanism of cellular entry of cadmium remains unclear. We have previously established cadmium-resistant cells from mouse embryonic cells of metallothionein (MT)-null mice, and demonstrated that the down-regulation of a zinc transporter, Zrt/Irt-related protein (ZIP) 8, was responsible for the reduced cadmium incorporation into cells. In the present study, we developed cadmium-resistant cells (A+70 and B+70) from mouse embryonic cells of MT-expressing wild-type mice. The LC50 values of CdCl2 for A+70 and B+70 cells were about 200 µM while that of the parental cells was 30 µM. We found that the cadmium resistance of these cells was conferred not only by enhanced expression of MT, but also by a decrease in cadmium accumulation. Since the uptake rates of cadmium into A+70 and B+70 cells were lowered, we determined the expression levels of the metal transporters and channels potentially involved in the cellular uptake of cadmium. We found a down-regulation of multiple transport systems, including ZIP8, divalent metal transporter 1 (DMT1), and α1 subunits of L-type (Ca(V)1.2) and T-type (Ca(V)3.1) voltage-dependent calcium channels, in A+70 and B+70 cells. Furthermore, A+70 and B+70 cells exhibited cross-resistance to cytotoxicity of MnCl2, probably due to a marked decrease in manganese uptake in these cells. These results suggest that the suppressed expression of ZIP8 and DMT1, which are known to have affinities for both cadmium and manganese, may be responsible for the reduction in the uptake, and consequently the cytotoxicity, of cadmium and manganese in A+70 and B+70 cells.