ABSTRACT
Objective To evaluate the efficacy and safety of combined use of ticagrelor and cilostazol for patients with acute coronary syndrome (ACS) complicated with upper digestive tract diseases following percutaneous coronary intervention ( PCI).Methods A total of 262 consecutive ACS patients complicated with upper digestive tract diseases followed-up for one-year after PCI were included in this study.The patients were allocated into control group (combined use of ticagrelor and aspirin , n＝184) and cilostazol group ( combined use of ticagrelor and cilostazol , n ＝78) for antiplatelet treatment.The basic characteristics of the patients , change of the treatment regimens , cardiovascular events and hemorrhagic events were compared between two groups .Results After one year of follow-up, 16.8%(31/184)patients in control group and 3.8%(3/78)in cilostazol group changed antiplatelet regimens (χ2＝8.200,P＝0.004).There was no statistical difference in use of statins and ACEI/ARB between two groups(P＞0.05).The rate of proton pump inhibitor use in control group was significantly higher than that in cilostazol group [82.1%(151/184) vs.52.6%(41/78), χ2＝24.35, P＝0.000].However, the dosage of β-blockers in cilostazol group was significantly higher than that in control group [(39.1 ±12.4) mg vs.(28.6 ±10.1) mg, t ＝7.174,P＝0.000].No statistical difference was found in total cardiovascular events between two groups [21.7%(40/184) vs.12.8%(10/78),χ2＝2.822,P＝0.121].The incidence of gastrointestinal hemorrhage in control group was significantly increased compared with cilostazol group [12.0%(22/184) vs.2.6%(2/78),χ2＝5.807,P ＝0.018], however, there was no significant difference in hemorrhagic events concerning the thrombolysis for myocardial infarction between two groups [17.4%(32/184) vs.9.0%(7/78), χ2＝3.063,P＝0.089].Conclusion Combined use of cilostazol and ticagrelor is effective and safe for ACS patients with gastrointestinal hemorrhage or a higher risk of hemorrhage .
ABSTRACT
Microcirculation dysfunction is involved in the onset of diabetes and its complications.The pathophysiological mechanisms behind the relationship between microcirculation and diabetes are multifactorial.Islet microcirculation dysfunction affects function of islet β cells.Impairment of microvascular vasomotion might be associated with insulin resistance.Microcirculation dysfunction of target organs mediates diabetic complications.
ABSTRACT
<p><b>BACKGROUND</b>Pericytes, located on microvessels, help to maintain vascular stability and blood-brain barrier integrity. The influence of pericytes on microvessels after spinal cord injury (SCI) is less clear. Therefore, the aim of this study was to investigate whether pericytes took a protective effect on microvessels in melatonin-treated SCI.</p><p><b>METHODS</b>C57BL/6 mice were randomly divided into three groups: sham group, SCI group, and melatonin group (n = 27 per group). Functional recovery was evaluated using the Basso Mouse Scale. Motor neurons were observed using hematoxylin and eosin staining. Pericyte coverage was analyzed using immunofluorescence. Permeability of blood-spinal cord barrier (BSCB) was assessed by administration of Evan's Blue. Protein levels of occludin, aquaporin-4 (AQP4), angiopoietin-1 (Ang1), intercellular cell adhesion molecule-1 (ICAM-1), Bcl-2, and Bax were determined using Western blotting. Mimicking the pathological conditions of SCI, melatonin-treated primary pericytes were subjected to oxygen-glucose deprivation/reperfusion (OGD/R). Secretion of Ang1 was analyzed using an enzyme-linked immunosorbent assay, and the expression of ICAM-1 was detected by immunofluorescence.</p><p><b>RESULTS</b>Melatonin treatment improved locomotor functional outcome and rescued motor neurons. Pericyte coverage was significantly reduced after SCI; melatonin treatment alleviated the loss of pericyte coverage and rescued perfused microvessels 7 days after injury. The permeability of BSCB and loss of occludin were attenuated, and edema formation and upregulation of AQP4 were inhibited, after melatonin treatment. The expression of Ang1 and Bcl-2 was improved, while the expression of ICAM-1 and Bax was inhibited, in melatonin-treated SCI mice. Furthermore, the secretion of Ang1 was increased and the expression of ICAM-1 was inhibited in melatonin-treated pericytes after OGD/R.</p><p><b>CONCLUSIONS</b>Melatonin ameliorated the loss of blood vessels and disruption of BSCB to exert a protective effect on SCI, which might be mediated by increased pericyte coverage. The upregulation of Ang1 in pericytes could inhibit inflammation and apoptosis to protect the microvessels.</p>