Impact of admitting department on the management of acute coronary syndrome after an out of hospital cardiac arrest.

AIM: This study aimed to analyze the influence of the hospital admitting department on adherence to the Guidelines of European Society of Cardiology for management of acute coronary syndromes in patients after out-of-hospital cardiac arrest (OHCA) of coronary etiology. METHODS: We studied retrospective-prospective register of 102 consecutive patients with OHCA as a manifestation of acute coronary syndrome (ACS). Patients were admitted to the coronary care unit (CCU) 52, general intensive care unit (GICU) 21, or GICU after initial Cath lab treatment (CAG-GICU) 29. This study compared the differences in the management of ACS in patients with OHCA of coronary etiology based on the admitting department in a tertiary care institution. RESULTS: Twelve of the 21 (57.1%) patients admitted to the GICU were evaluated as having ACS on-site where they experienced OHCA. In the CCU group, 50 out of 52 (96.2%) and 28 of 29 (100%) patients in the CAG-GICU group (P<0.001). Coronary angiography was performed in 10 of 21 patients (48%) admitted to the GICU. It was performed in 49 out of 52 (94%) CCU patients and, in the CAG-GICU group, 28 out of 29 patients. The mean time to CAG differed significantly across groups (that is, GICU 200.7 min., CCU 71.2 min., and CAG-GICU 7.5 min. (P<0.001)). Aspirin was used in 48% of GICU, 96% of CCU, and 79% of CAG-GICU patients (P<0.001), while in the pre-hospital phase, aspirin was used in 9.5% of GICU, 71.2% of CCU, and 50% of CAG-GICU patients (P<0.001). P2Y12 inhibitor prescriptions were lower in patients admitted to the GICU (33% vs. 89% CCU and 57% CAG-GICU, P<0.001). The department's choice significantly affected the time to initiation of antithrombotics, which was the longest in the GICU. CONCLUSION: The choice of admission department for patients with OHCA caused by ACS was found to affect the extent to which the recommended treatments were used. An examination of OHCA patients by a cardiologist upon admission to the hospital increased the likelihood of an early diagnosis of ACS as the cause of OHCA.

Pregestational diabetes increases fetoplacental vascular resistance in rats.

INTRODUCTION: Diabetes is a well-known risk factor in pregnancy. Because maternal diabetes involves oxidative stress that is also induced by chronic hypoxia and can alter vascular function, we sought to determine the effects of chronic maternal hyperglycemia on the fetoplacental vasculature in rats and to compare it with the effects of chronic hypoxia. METHODS: Diabetes was induced in female rats by a streptozotocin injection at a neonatal age. When these animals reached adulthood, their hyperglycemia was confirmed and they were inseminated. Half of them were exposed to hypoxia (10% O2) for the last week before the delivery. One day before the expected date of delivery, one of their placentae was isolated and perfused. RESULTS: Fetoplacental vascular resistance was increased equally by experimental diabetes, chronic hypoxia, and their combination. Fetoplacental perfusion pressure-flow analysis suggested increased resistance in the small vessels in chronic hypoxia and in larger vessels in diabetes. Fetal plasma nitrotyrosine levels, measured as a marker of peroxynitrite (reaction product of superoxide and nitric oxide), mirrored the differences in fetoplacental resistance, suggesting a causative role. Fetoplacental vasoconstrictor reactivity to acute hypoxic stimuli was reduced similarly in all groups. Fasudil, a strong vasodilator agent, reduced fetoplacental vascular resistance similarly in all groups, suggesting that for the observed differences among the groups, the changes in vascular morphology were more important than variances in vascular tone. DISCUSSION: Maternal diabetes increases fetoplacental vascular resistance to a similar extent as chronic hypoxia. These stimuli are not additive. Changes in vascular tone are not responsible for these effects.