Acute hyperglycemia causes microvascular damage, leading to poor functional recovery and remodeling in patients with reperfused ST-segment elevation myocardial infarction.

BACKGROUND: Although acute hyperglycemia (AHG) is associated with poor outcomes in ST-segment elevation myocardial infarction (STEMI) patients, underlying mechanisms have not been fully elucidated. We investigated the influence of AHG on myocardial microcirculation in reperfused STEMI patients. METHODS AND RESULTS: Thirty-four STEMI patients were divided into 2 groups according to the presence (Group H, n 5 11) or the absence (Group L, n 5 23) of AHG. Myocardial blood flow (MBF) and myocardial flow reserve (MFR) in the infarct-related area were compared between 2 groups, using ¹³N-ammonia positron emission tomography. Wall motion abnormality scores (WMASs) and end-diastolic volume indices (EDVI) were also assessed at 1 and 6 months after the onset. Although resting MBF was similar, MFR was lower in Group H than in Group L (1.69 ± 0.37 vs 2.39 ± 0.56, P = .001). WMAS was greater in Group H than in Group L at both 1 month (7.4 ± 3.7 vs 3.7 ± 3.0, P = .011) and 6 months (7.3 ± 3.9 vs 3.1 ± 3.4, P = .015). EDVI tended to be greater in Group H than in Group L at 6 months (103.8 ± 42.9 vs 73.9 ± 16.0 mL/m2, P = .071). Multivariate analysis showed AHG to be independently associated with low MFR. CONCLUSIONS: In STEMI patients, AHG impaired myocardial microcirculation, leading to poor functional recovery and remodeling despite successful reperfusion.

Coronavirus Disease 2019 Complicated by Multiple Simultaneous Intracerebral Hemorrhages.

The relationship between coronavirus disease 2019 (COVID-19) and intracerebral hemorrhage remains unclear. We herein report a case of severe COVID-19 pneumonia complicated by multiple simultaneous intracerebral hemorrhages (MSICH). The patient died eight days after the episode of MSICH. No apparent coagulopathy was observed; however, extracorporeal membrane oxygenation and anticoagulation might have caused the occurrence of MSICH. Laboratory findings showed hypercoagulability, suggesting that thrombotic etiologies, such as sinus thrombosis or cerebral infarction, might also have caused MSICH. MSICH can occur as a fatal complication of COVID-19, and this should be considered when providing treatment.

Acarbose treatments improve arterial stiffness in patients with type 2 diabetes mellitus.

UNLABELLED: Aims/Introduction: Although the improvement of postprandial hyperglycemia by an alpha-glucosidase inhibitor (α-GI) has been associated with a risk reduction of cardiovascular events, the relationship between postprandial hyperglycemia and arterial stiffness has not been well understood. We therefore examined whether ameliorating the postprandial state by α-GI leads to an improvement in arterial stiffness. MATERIALS AND METHODS: A total of 22 patients with type 2 diabetes mellitus were treated with acarbose. Cardio-ankle vascular index (CAVI) as the arterial stiffness was measured by using a VaSera CAVI instrument before and 12 months after acarbose treatment. Serum high-sensitivity C-reactive protein (hs-CRP), pentraxin-3 (PTX3) and matrix metalloproteinase (MMP) -2, -9 were measured at the same time points. Furthermore, circulating peripheral blood mononuclear cells were examined for the frequencies of CD14 positive cells expressing membrane type-1 MMP (MT1-MMP) at the single cell level using flow cytometry. RESULTS: After acarbose treatment, postprandial glucose and glycosylated hemoglobin (HbA1c) were significantly decreased. Serum levels of hs-CRP, PTX3, MMP-2 and MMP-9 were significantly decreased. CAVI showed a significant reduction, although the changes were not significant in blood pressure and heart rate. MT1-MMP expression was significantly decreased by acarbose treatment. In multivariate analysis, improvement of blood glucose, decrease of PTX3 levels and MT1-MMP expression were independent predictors of beneficial change in CAVI. CONCLUSIONS: The present study showed that the beneficial effects of acarbose on arterial stiffness are mediated by an improvement of postprandial hyperglycemia and vascular remodeling markers. In conclusion, acarbose treatment might reduce the risk of cardiovascular diseases by altering the arterial stiffness in postprandial hyperglycemic status. (J Diabetes Invest, doi:10.1111/j.2040-1124.2010.00079.x, 2010).