Marta Wysocka-Mincewicz, Joanna Gołębiewska, Marta Baszyńska-Wilk, Andrzej Olechowski, Aleksandra Byczyńska, Mieczysław Szalecki
{"title":"Influence of puberty on retinal microcirculation in children with type 1 diabetes without retinopathy using optical coherence tomography angiography.","authors":"Marta Wysocka-Mincewicz, Joanna Gołębiewska, Marta Baszyńska-Wilk, Andrzej Olechowski, Aleksandra Byczyńska, Mieczysław Szalecki","doi":"10.1177/14791641211004427","DOIUrl":"https://doi.org/10.1177/14791641211004427","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to assess the influence of pubertal status on the results of optical coherence tomography angiography (OCTA) in children with type 1 diabetes (T1D).</p><p><strong>Methods: </strong>We enrolled 167 consecutive children with T1D. Retinal superficial capillary plexus (SCP) and deep capillary plexus (DCP) vessel density data underwent analysis. We divided the study population into three subgroups depending on the pubertal status.</p><p><strong>Results: </strong>Analysis of the prepubertal and pubertal subgroups revealed statistically significant differences in foveal thickness (FT) (p < 0.05) and foveal SCP (p < 0.02). Analyzing subgroups of the prepubertal and postpubertal children, we observed statistically significant differences in FT (p < 0.03), whole SCP (p < 0.02), and foveal SCP (p < 0.02). Comparison of the pubertal and postpubertal subjects revealed differences in parafoveal DCP (p < 0.003). In the groups matched depending on diabetes duration, we observed differences between prepubertal, pubertal, and postpubertal children in FT, PFT, and parafoveal SCP and DCP.</p><p><strong>Conclusion: </strong>Our data suggest that in a cohort of pubertal children with a short duration of diabetes, alterations in retinal vessel density occur early and progress during puberty.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 2","pages":"14791641211004427"},"PeriodicalIF":2.4,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/14791641211004427","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25544402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mei Qiu, Liang-Liang Ding, Miao Zhang, Hai-Rong Zhou
{"title":"Safety of four SGLT2 inhibitors in three chronic diseases: A meta-analysis of large randomized trials of SGLT2 inhibitors.","authors":"Mei Qiu, Liang-Liang Ding, Miao Zhang, Hai-Rong Zhou","doi":"10.1177/14791641211011016","DOIUrl":"https://doi.org/10.1177/14791641211011016","url":null,"abstract":"<p><p>There are no relevant meta-analyses that have assessed the safety of the sodium-glucose transporter 2 (SGLT2) inhibitors in different chronic diseases. We aimed at evaluating the safety of four SGLT2 inhibitors in three chronic diseases by meta-analysis of the large randomized trials of SGLT2 inhibitors. We performed random-effects meta-analysis and carried out subgroup analysis according to type of underlying diseases and type of SGLT2 inhibitors. SGLT2 inhibitors versus placebo significantly reduced the risk of acute kidney injury (RR 0.75, 95% CI 0.66-0.85), and showed the reduced trend in the risk of severe hypoglycemia (RR 0.86, 95% CI 0.71-1.03). SGLT2 inhibitors significantly increased the risks of diabetic ketoacidosis (RR 2.57), genital infection (RR 3.75), and volume depletion (RR 1.14); and showed the increased trends in the risks of fracture (RR 1.07), amputation (RR 1.21), and urinary tract infection (RR 1.07). These effects exhibited by SGLT2 inhibitors were consistent across three chronic diseases (i.e. type 2 diabetes, chronic heart failure, and chronic kidney disease) and four SGLT2 inhibitors (i.e. dapagliflozin, empagliflozin, ertugliflozin, and canagliflozin) (all <i>P</i><sub>subgroup</sub> > 0.05). These findings will guide that specific adverse events are monitored when SGLT2 inhibitors are used in clinical practice.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 2","pages":"14791641211011016"},"PeriodicalIF":2.4,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/14791641211011016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38820706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lawrence Fordjour, Charles Cai, Vadim Bronshtein, Mayan Bronshtein, Jacob V Aranda, Kay D Beharry
{"title":"Growth factors in the fetus and pre-adolescent offspring of hyperglycemic rats.","authors":"Lawrence Fordjour, Charles Cai, Vadim Bronshtein, Mayan Bronshtein, Jacob V Aranda, Kay D Beharry","doi":"10.1177/14791641211011025","DOIUrl":"10.1177/14791641211011025","url":null,"abstract":"<p><strong>Background: </strong>Maternal hyperglycemia influences childhood metabolic syndrome, including obesity and hyperglycemia. We tested the hypothesis that the maternal hyperglycemia influences growth factors in the fetal and pre-adolescent offspring.</p><p><strong>Methods: </strong>Hyperglycemia was induced in pregnant rats on embryonic day (E)16 using streptozocin followed by implantation with insulin or placebo pellets at embryonic day 18 (E18). Fetuses at E20 and pre-adolescent pups at postnatal day 14 (P14) were studied: (1) normal untreated controls (CTL) at E20; (2) hyperglycemic placebo-treated (HPT) at E20; (3) hyperglycemic insulin-treated (HIT) at E20; (4) CTL at P14; and (5) HIT at P14. Fetal and pre-adolescent growth factors were determined.</p><p><strong>Results: </strong>Biomarkers of hypoxia were elevated in the HPT group at E20. This group did not survive to term. Maternal insulin improved fetal survival despite lower fetal body weight at E20, however, at normal birth (postnatal day 0 (P0)) and at P14, body weights and blood glucose were higher than CTL. These high levels correlated with aberrant growth factors. Maternal hyperglycemia influenced glucose-6-phosphate dehydrogenase, glucagon, insulin, interleukin-10, and leptin genes.</p><p><strong>Conclusions: </strong>The impact of maternal hyperglycemia on pre-adolescent glucose and body weight was not a consequence of maternal overnutrition. This suggests an independent link which may affect offspring metabolic health in later life.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 2","pages":"14791641211011025"},"PeriodicalIF":2.4,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/28/1a/10.1177_14791641211011025.PMC8482349.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38840363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Age-associated decline of monocyte insulin sensitivity in diabetic and healthy individuals.","authors":"Suguru Nakamura, Kentaro Mori, Hideyuki Okuma, Tetsuo Sekine, Asako Miyazaki, Kyoichiro Tsuchiya","doi":"10.1177/1479164121989281","DOIUrl":"https://doi.org/10.1177/1479164121989281","url":null,"abstract":"<p><strong>Objective: </strong>It is unclear whether monocyte/macrophage insulin signaling in humans is affected by type 2 diabetes (T2DM), systemic insulin sensitivity, and other unknown factors.</p><p><strong>Research design and methods: </strong>Fifty-three adult volunteers (control group) not taking any medication and without cardiovascular risk factors, and 59 patients with T2DM (T2DM group) were included. Monocytes were isolated and cultured from all participants.</p><p><strong>Results: </strong>In cultured monocytes, insulin-stimulated AKT and FOXO3 phosphorylation was significantly suppressed in T2DM compared with that in the control group. Insulin-stimulated phosphorylation of AKT was significantly correlated with body mass index and serum insulin level only in the control group. In both groups, significant negative correlation between age and insulin-stimulated phosphorylation of AKT and FOXO3 was commonly observed. In the control group, lipopolysaccharide (LPS)-stimulated induction of <i>TNFA</i>, and <i>NOS2</i> was significantly and negatively correlated with insulin-stimulated AKT phosphorylation. Age was also significantly correlated with LPS-stimulated induction of <i>TNFA</i>.</p><p><strong>Discussion: </strong>Aging plays an important role in the development of monocyte insulin resistance, not only in patients with T2DM but also in healthy participants. Monocyte insulin sensitivity is negatively correlated with inflammatory responses and may be helpful for subclinical risk assessment of CVDs and/or insulin resistance in participants without risk factors.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 1","pages":"1479164121989281"},"PeriodicalIF":2.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1479164121989281","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25388515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Helena W Rodbard, Andrea Giaccari, Bertrand Cariou, Satish Garg, Michael J Davies, Kiernan Seth, Sangeeta Sawhney
{"title":"Effect of sotagliflozin as an adjunct to insulin therapy on blood pressure and arterial stiffness in adults with type 1 diabetes: A post hoc pooled analysis of inTandem1 and inTandem2.","authors":"Helena W Rodbard, Andrea Giaccari, Bertrand Cariou, Satish Garg, Michael J Davies, Kiernan Seth, Sangeeta Sawhney","doi":"10.1177/1479164121995928","DOIUrl":"https://doi.org/10.1177/1479164121995928","url":null,"abstract":"<p><strong>Objective: </strong>Evaluate the effect of sotagliflozin, a dual inhibitor of sodium glucose cotransporter (SGLT) 1 and 2, on arterial stiffness in patients with type 1 diabetes (T1D) treated with sotagliflozin as adjunct to optimized insulin therapy.</p><p><strong>Methods: </strong>In this post hoc analysis, indirect markers of arterial stiffness, including pulse pressure, mean arterial pressure (MAP), and double product, were calculated using observed systolic blood pressure (SBP), diastolic blood pressure (DBP), or pulse rate at 24 weeks using data from a pooled patient population from the inTandem1 and inTandem2 randomized controlled trials (<i>n</i> = 1575).</p><p><strong>Results: </strong>Baseline characteristics were similar among groups. Relative to placebo at Week 24, sotagliflozin 200 mg and 400 mg reduced SBP by 2.03 mm Hg (95% CI -3.30 to -0.75; <i>p</i> = 0.0019) and 2.85 mm Hg (-4.12 to -1.57; <i>p</i> < 0.0001), respectively. DBP decreased by 1.1 and 0.9 mm Hg, MAP by 1.4 and 1.6 mm Hg, and double product by 202.5 and 221.1 bpm × mm Hg, respectively (<i>p</i> < 0.05 for all). No increases in heart rate were observed.</p><p><strong>Conclusion: </strong>In adults with T1D, adding sotagliflozin to insulin significantly reduced blood pressure and other markers of arterial stiffness and vascular resistance.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 1","pages":"1479164121995928"},"PeriodicalIF":2.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1479164121995928","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25388100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Vascular inflammation, atherosclerosis, and lipid metabolism and the occurrence of non-high albuminuria diabetic kidney disease: A cross-sectional study.","authors":"Yuwei Yang, Peng Xu, Yan Liu, Xiaohong Chen, Yiyang He, Jiafu Feng","doi":"10.1177/1479164121992524","DOIUrl":"10.1177/1479164121992524","url":null,"abstract":"<p><strong>Aim: </strong>Atherosclerosis involves vascular endothelial damage and lipid metabolism disorder, which is closely related to the occurrence and development of diabetic kidney disease (DKD). However, studies on non-high albuminuria DKD (NHADKD) with an albumin to creatinine ratio (ACR) <30 mg/g are rare. This study is to investigate the relationship between atherogenic factors and the occurrence of NHADKD.</p><p><strong>Methods: </strong>Serum lipid indicators, lipoprotein-associated phospholipase A2 (Lip-PLA2) and homocysteine levels were measured in 1116 subjects to analyze their relationship with NHADKD.</p><p><strong>Results: </strong>Among all subjects, Lip-PLA2 had the closest but relatively weak correlation with ACR (<i>r</i> = 0.297, <i>p</i> < 0.001) and only homocysteine was moderately correlated with eGFR (<i>r</i> = -0.465, <i>p</i> < 0.001). However, in patients with NHADKD, these atherosclerotic factors were weakly correlated or uncorrelated with eGFR (max. |<i>r</i>| = 0.247). Stratified risk analysis showed that when ACR was <10 mg/g, homocysteine [OR = 6.97(4.07-11.95)], total cholesterol (total-Chol) [OR = 6.04(3.03-12.04)], and high-density lipoprotein cholesterol (HDL-Chol) [OR = 5.09(2.99-8.64)] were risk factors for NHADKD. There was no significant difference of OR between these three factors (<i>Z</i> = 0.430-1.044, all <i>p</i> > 0.05). When ACR was ⩾10mg/g, homocysteine [OR = 17.26(9.67-30.82)] and total-Chol [OR = 5.63(2.95-10.76)] were risk factors for NHADKD, and OR<sub>homocysteine</sub> was significantly higher than OR<sub>total-Chol</sub> (<i>Z</i> = 3.023, <i>p</i> < 0.05).</p><p><strong>Conclusions: </strong>The occurrence of NHADKD may be related to the levels of homocysteine, total-Chol, HDL-Chol, and Lip-PLA2 in blood. Among them, homocysteine may be most closely related to NHADKD.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 1","pages":"1479164121992524"},"PeriodicalIF":2.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/09/fa/10.1177_1479164121992524.PMC8482348.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25357205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"DNA aptamer raised against receptor for advanced glycation end products suppresses renal tubular damage and improves insulin resistance in diabetic mice.","authors":"Ami Sotokawauchi, Takanori Matsui, Yuichiro Higashimoto, Yuri Nishino, Yoshinori Koga, Minoru Yagi, Sho-Ichi Yamagishi","doi":"10.1177/1479164121990533","DOIUrl":"https://doi.org/10.1177/1479164121990533","url":null,"abstract":"<p><strong>Objective: </strong>Interaction of advanced glycation end products (AGEs) with the receptor RAGE plays a role in diabetic nephropathy. However, effects of RAGE-aptamer on tubular damage remain unknown. We examined whether RAGE-aptamer inhibited tubular damage in KKAy/Ta mice, obese type 2 diabetic mice with insulin resistance.</p><p><strong>Materials and methods: </strong>Male 8-week-old KKAy/Ta mice received continuous intraperitoneal infusion of either control-aptamer or RAGE-aptamer for 8 weeks. Blood biochemistry and blood pressure, and urinary N-acetyl-β-D-glucosaminidase (NAG) activity and albumin excretion levels were monitored. Kidney and adipose tissue samples were obtained for immunohistochemical analyses.</p><p><strong>Results: </strong>Although RAGE-aptamer did not affect blood glucose, blood pressure, body weight, or serum creatinine values, it significantly inhibited the increase in urinary NAG activity and HOMA-IR in diabetic mice at 12 and 16 and at 16 weeks old, respectively. Furthermore, compared with control-aptamer-treated mice, renal carboxymethyllysine, RAGE, and NADPH oxidase-driven superoxide generation were significantly decreased in RAGE-aptamer-treated mice at 12 weeks old with subsequent amelioration of histological alterations in glomerular and interstitial area, while adipose tissue adiponectin expression was increased.</p><p><strong>Conclusion: </strong>Our present results suggest that RAGE-aptamer could inhibit tubular injury in obese type 2 diabetic mice partly by suppressing the AGE-RAGE-oxidative stress axis and improving insulin resistance.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 1","pages":"1479164121990533"},"PeriodicalIF":2.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1479164121990533","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25327682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hao-Kuang Wang, Chih-Yuan Huang, Yun-Wen Chen, Yuan-Ting Sun
{"title":"Hyperglycemia compromises the ischemia-provoked dedifferentiation of cerebral pericytes through p21-SOX2 signaling in high-fat diet-induced murine model.","authors":"Hao-Kuang Wang, Chih-Yuan Huang, Yun-Wen Chen, Yuan-Ting Sun","doi":"10.1177/1479164121990641","DOIUrl":"10.1177/1479164121990641","url":null,"abstract":"<p><strong>Aim: </strong>Diabetes-related cerebral small vessel disease (CSVD) causes neurological deficits. Patients with diabetes showed pericyte loss as a hallmark of retinopathy. Cerebral pericytes, which densely localize around brain capillaries, are quiescent stem cells regulating regeneration of brain and may have a role in CSVD development. This study investigated whether diabetes impairs ischemia-provoked dedifferentiation of pericytes.</p><p><strong>Methods: </strong>A murine high-fat diet (HFD)-induced diabetes model was used. After cerebral ischemia induction in the mice, pericytes were isolated and grown for a sphere formation assay.</p><p><strong>Results: </strong>The sphere counts from the HFD group were lower than those in the chow group. As the spheres formed, pericyte marker levels decreased and SOX2 levels increased gradually in the chow group, but not in the HFD group. Before sphere formation, pericytes from the HFD group showed high p21 levels. The use of a p21 inhibitor rescued the reduction of sphere counts in the HFD group. At cellular level, hyperglycemia-induced ROS increased the level of p21 in cerebral pericytes. The p21-SOX2 signaling was then activated after oxygen-glucose deprivation.</p><p><strong>Conclusion: </strong>HFD-induced diabetes compromises the stemness of cerebral pericytes by altering p21-SOX2 signaling. These results provide evidence supporting the role of pericytes in diabetes-related CSVD and subsequent cerebral dysfunction.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 1","pages":"1479164121990641"},"PeriodicalIF":2.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8d/eb/10.1177_1479164121990641.PMC8482726.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25348172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yong Hoon Kim, Ae-Young Her, Myung Ho Jeong, Byeong-Keuk Kim, Sung-Jin Hong, Seunghwan Kim, Chul-Min Ahn, Jung-Sun Kim, Young-Guk Ko, Donghoon Choi, Myeong-Ki Hong, Yangsoo Jang
{"title":"Prediabetes versus type 2 diabetes mellitus based on pre-percutaneous coronary intervention thrombolysis in myocardial infarction flow grade in patients with ST-segment elevation myocardial infarction after successful newer-generation drug-eluting stent implantation.","authors":"Yong Hoon Kim, Ae-Young Her, Myung Ho Jeong, Byeong-Keuk Kim, Sung-Jin Hong, Seunghwan Kim, Chul-Min Ahn, Jung-Sun Kim, Young-Guk Ko, Donghoon Choi, Myeong-Ki Hong, Yangsoo Jang","doi":"10.1177/1479164121991505","DOIUrl":"https://doi.org/10.1177/1479164121991505","url":null,"abstract":"<p><strong>Background: </strong>We compared the 2-year clinical outcomes between prediabetes and type 2 diabetes mellitus (T2DM) according to the pre-percutaneous coronary intervention (PCI) thrombolysis in myocardial infarction (TIMI) flow grade in patients with ST-segment elevation myocardial infarction.</p><p><strong>Methods: </strong>Overall, 6448 STEMI patients were divided into two groups: pre-PCI TIMI 0/1 group (<i>n</i> = 4854) and pre-PCI TIMI 2/3 group (<i>n</i> = 1594). They were further divided into patients with normoglycemia, prediabetes, and T2DM. The major endpoint was major adverse cardiac events (MACEs), defined as all-cause death, recurrent myocardial infarction, or any repeat revascularization.</p><p><strong>Results: </strong>In the pre-PCI TIMI 0/1 group, all-cause death rate was higher in both prediabetes (adjusted hazard ratio [aHR]: 1.633, <i>p</i> = 0.045) and T2DM (aHR: 2.064, <i>p</i> = 0.002) groups than in the normoglycemia group. In the pre-PCI TIMI 2/3 group, any repeat revascularization rate was also higher in both prediabetes (aHR: 2.511, <i>p</i> = 0.039) and T2DM (aHR: 3.156, <i>p</i> = 0.009) than normoglycemia. In each group (pre-PCI TIMI 0/1 or 2/3), the MACEs and all other clinical outcomes rates were similar between the prediabetes and T2DM groups.</p><p><strong>Conclusions: </strong>Prediabetes showed comparable worse clinical outcomes to those of T2DM regardless of the pre-PCI TIMI flow grade.</p>","PeriodicalId":11092,"journal":{"name":"Diabetes & Vascular Disease Research","volume":"18 1","pages":"1479164121991505"},"PeriodicalIF":2.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1479164121991505","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25328834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}