bluuebunny/crossref_metadata_2025_split huggingface dataset:
713-P: Is There a Correct Time to Measure Fasting Blood Sugar in Persons with Type 2 Diabetes Melitus?
Authors: SABOO BANSHI D. , VYAS TARJANI C. , CHENNAMSETTI KAUMUDI , PAREKH MALAY N. , PATEL VIDISHA , PRAJAPATI AAKASH M. 
Published: May 2022

Aim: To decide most appropriate time to measure fasting blood sugar (FBS) using continuous glucose monitoring (CGM) .
Methodology: All persons who came to our clinic between 1st March to 30th August’21 were screened. Out of 60 persons with A1c &lt;7.5, with FBS &gt;130mg/dl who were measuring after 7.30am (using glucose meter) and having dinner before 9:30 pm, 28 persons who consented for CGM (Libre Pro) were included. Persons who were on SU/insulin or had nocturnal hypoglycaemia, T1DM, CRF, CLD, steroids or malignancy were excluded. The enrolled persons were told to measure their blood sugar between 5.30am to 6.30 am ; 6.30 am to 7.30am ; 7.30am to 8.30am on alternate days for 14 days by glucose meter along with CGM.
Results: Observed glucose values on different times were106±10mg/dl between 5.30 to 6.30am ;114±12mg/dl between 6.30 to 7.30am and 130±16mg/dl between 7.30 to 8.30am. These sugar values of all persons were correlated with CGM Libre pro data. AGP data of 2 out of the 28 persons have been shown in the graphs attached.
Discussion: It is a routine clinical practice to ask PWD to measure FBS but there is ambiguity in timings as no specification of timing is advised. It is important that patients measure fasting sugar around 6.30 am ± 1 hour as it correlates best with sunrise and has less effect of Dawn phenomenon.
Conclusion: To optimise treatment, persons with diabetes should be advised to measure their FBS before 7.30 am.

Disclosure
B.D.Saboo: None. T.C.Vyas: None. K.Chennamsetti: None. M.N.Parekh: None. V.Patel: None. A.M.Prajapati: None.
722-P: Tirzepatide Improves Multiple Aspects of Beta-Cell Function
Authors: MARI ANDREA , LI JING , URVA SHWETA , HEISE TIM , DE VRIES J. HANS , PRATT EDWARD J. , HEINE ROBERT J. , THOMAS MELISSA K. , MILICEVIC ZVONKO , MATHER KIEREN J. 
Published: May 2022

We investigated the effect of tirzepatide (TZP) 15 mg (novel GIP-GLP-1 dual receptor agonist) , placebo and semaglutide 1 mg (SEMA) on beta-cell function using euglycaemic and hyperglycemic glucose clamps (EGC, HGC) and Mixed Meal Tolerance Tests (MMTT) in a 28-week double-blind randomized controlled trial of people with type 2 diabetes. During EGC and HGC, TZP improved insulin sensitivity (M-value) , first and second phase insulin secretion (ISR) and beta-cell glucose sensitivity (ratio of ISR and glucose increments) more than SEMA and placebo (Table; EASD symposium 2021) . During MMTT, both fasting and AUC glucose were reduced more with TZP than with SEMA or placebo, while incremental glucose AUC was reduced with TZP and SEMA vs. placebo similarly. Despite similarly reduced incremental glucose AUC, insulin AUC and incremental insulin AUC were reduced by TZP but not by SEMA. Model-derived beta-cell glucose sensitivity was increased with TZP and SEMA from baseline similarly. In contrast, ISR at 7.2 mmol/L glucose increased more with TZP than with placebo and SEMA (Table) . The glucose-lowering effect of TZP is mediated through improvements in multiple aspects of beta-cell function, including beta-cell glucose sensitivity and ISR, and in insulin sensitivity, resulting in pronounced lowering of fasting and postprandial glucose. These effects help explain the superior improvement in glucose control seen with TZP vs. comparators in clinical trials.

Disclosure
A. Mari: Consultant; Lilly. Research Support; Lilly. J. Li: Employee; Eli Lilly and Company. Stock/Shareholder; Eli Lilly and Company. S. Urva: Employee; Eli Lilly and Company. T. Heise: Advisory Panel; Novo Nordisk A/S. Research Support; ADOCIA, AstraZeneca, Biocon, Boehringer Ingelheim International GmbH, Crinetics Pharmaceuticals, Inc., Eli Lilly and Company, Gan & Lee Pharmaceuticals, Genova, Nestlé, Neuraly Inc., Novo Nordisk A/S, Sanofi, Zealand Pharma A/S. Speaker's Bureau; Eli Lilly and Company, Gan & Lee Pharmaceuticals, Novo Nordisk A/S. J. De Vries: Advisory Panel; ADOCIA, Novo Nordisk A/S, Zealand Pharma A/S. Speaker's Bureau; Novo Nordisk A/S. E.J. Pratt: Employee; Eli Lilly and Company. R.J. Heine: Employee; Eli Lilly and Company. M.K. Thomas: Employee; Eli Lilly and Company. Stock/Shareholder; Eli Lilly and Company. Z. Milicevic: Employee; Eli Lilly and Company. K.J. Mather: Employee; Eli Lilly and Company. Stock/Shareholder; Eli Lilly and Company.

Funding
Eli Lilly and Company
725-P: Protein Biomarkers Associated with Dulaglutide and Cardiovascular Events in REWIND
Authors: WILSON JONATHAN M. , PARE GUILLAUME , LEE SHUN FU , COLHOUN HELEN M. , QIAN HUI-RONG , PIRRO VALENTINA , HOOVER ANASTASIA , LAKSHMANAN MARK , RUOTOLO GIACOMO , DUFFIN KEVIN L. , GERSTEIN HERTZEL C. 
Published: May 2022

In the REWIND trial, dulaglutide (DU) reduced the risk of CV outcomes compared with placebo (PL) (Major Adverse Cardiovascular Event [MACE]-3 hazard ratio 0.88) . This post hoc analysis studied circulating protein biomarkers associated with CV events to better understand how DU reduces CV risk.
Patients ≥50 years of age with T2D, A1C ≤9.5%, BMI ≥23 kg/m2, and CV risk were treated DU (1.5 mg weekly) or PL. This case/control study matched 9 cases with MACE with 9 non-MACE controls. A total of protein biomarkers were measured by immunoassay in plasma and serum. Biomarkers associated with DU were first identified by fitting the natural log (ln) of biomarker changes from baseline to 2 years of treatment to an ANCOVA model; the p value cutoff was 0.0026 after Bonferroni correction. Then, the identified biomarkers were fit to a logistic regression model for MACE case/control to test possible impact on CV outcome.
Four biomarkers were associated with DU: C-reactive protein (hsCRP) , N-terminal prohormone of brain natriuretic peptide (NT-proBNP) , and Growth/Differentiation Factor-15 (GDF-15) had attenuated increases over 2 years for DU vs. PL, and C-peptide had a greater increase over 2 years for DU vs. PL. Logistic regression analyses showed that patients with smaller increases in hsCRP, NT-proBNP, and GDF-15 were less likely to have MACE. C-peptide levels did not significantly impact MACE occurrence.

Disclosure
J.M.Wilson: Employee; Eli Lilly and Company. K.L.Duffin: Employee; Eli Lilly and Company, Stock/Shareholder; Eli Lilly and Company, Pfizer Inc. H.C.Gerstein: Advisory Panel; Abbott, Eli Lilly and Company, Hanmi Pharm. Co., Ltd., Novo Nordisk, Pfizer Inc., Sanofi, Viatris Inc., Consultant; Kowa Company, Ltd., Other Relationship; DKSH, Eli Lilly and Company, Sanofi, Zuellig Pharma Holdings Pte. Ltd., Research Support; AstraZeneca, Eli Lilly and Company, Merck & Co., Inc., Novo Nordisk, Sanofi. G.Pare: Advisory Panel; Amgen Inc., Bayer AG, Sanofi, Research Support; Bayer AG. S.Lee: None. H.M.Colhoun: Advisory Panel; Bayer AG, Eli Lilly and Company, Novo Nordisk, Consultant; AstraZeneca, Research Support; AstraZeneca, Stock/Shareholder; Bayer AG, Roche Pharmaceuticals. H.Qian: Employee; Eli Lilly and Company, Stock/Shareholder; Apple, Eli Lilly and Company. V.Pirro: Employee; Eli Lilly and Company, Stock/Shareholder; Eli Lilly and Company. A.Hoover: Employee; Eli Lilly and Company. M.Lakshmanan: Employee; Eli Lilly and Company, Stock/Shareholder; Eli Lilly and Company. G.Ruotolo: None.

Funding
Eli Lilly and Company
73-OR: Loss of NADPH Oxidase–Derived Superoxide Impairs Autoreactive T Cell Trafficking into Islets to Delay Type 1 Diabetes Development
Authors: BLUM SAMUEL I. , BARRA JESSIE , BAKER ROCKY L. , TSE HUBERT M. 
Published: May 2022

Type 1 diabetes (T1D) and β-cell destruction is mediated by proinflammatory cytokines, reactive oxygen species (ROS) , and immune cells. NADPH oxidase (NOX) -derived superoxide, a precursor for many ROS, regulate cell signaling, cellular differentiation, survival, and autoimmune responses in T1D. We previously discovered that NOX-derived superoxide promote chemokine synthesis and skew macrophages and T cells towards a proinflammatory response in T1D. Yet, it remains unknown if NOX is necessary for diabetogenic T cell trafficking into islets. Using non-obese diabetic (NOD) mice lacking NOX-derived superoxide (NOD.Ncf1m1J ) , we tested the hypothesis that loss of NOX-derived superoxide delays T1D by impairing autoreactive T infiltration into islets. Female NOD.Ncf1m1J mice (n=20) had a significant delay in spontaneous T1D development, as only 20% became diabetic by 40-weeks of age compared to 90% NOD mice (n=23) . Flow cytometry analysis of 12-week-old NOD.Ncf1m1J mice revealed a significant reduction in pancreatic CD4 T cells expressing CD69+ (5.5-fold) , CCR2+ (1.9-fold) and CCR5+ (2.1-fold) compared to NOD. NOD.Ncf1m1J islets also had significantly fewer total CD4+ T cells (1.8-fold) , CD25+ CD4+ T cells (2.0-fold) , naïve CD4+ T cells (2.0-fold) , and effector CD4+ T cells (2.2-fold) compared to NOD. Utilizing tetramer staining to identify autoreactive T cells, we observed a significant reduction in NOD.Ncf1m1J islet-infiltrating CD4+ T cells specific for insulin (Ins) (2.6-fold) , Ins-chromogranin A hybrid peptide (HIP) (3.0-fold) , and Ins-islet amyloid polypeptide HIP (2.6-fold) compared to NOD. Our findings provide evidence that loss of NOX-derived superoxide can impair autoreactive T cell activation and islet-infiltration as a possible mechanism to delay T1D development. Future studies will determine if NOX regulates islet chemokine synthesis to mediate autoreactive T infiltration into islets.

Disclosure
S.I.Blum: None. J.Barra: None. R.L.Baker: None. H.M.Tse: None.

Funding
Translational and Molecular Sciences T32 (GM109780) , Immunologic Diseases and Basic Immunology T32 (AI007051) , National Institutes of Health NIDDK F31 (DK130551) , National Institutes of Health NIDDK R (DK126456) , National Institutes of Health NIDDK RO1 (DK127497) .
733-P: Initiation of iGlarLixi vs. Basal-Bolus Insulin (BB) in Adults with Type 2 Diabetes (T2D) Advancing from Basal Insulin (BI) Therapy: The SoliComplex Real-World Study
Authors: PANTALONE KEVIN M. , HELLER CAROLINE , LAJARA ROSEMARIE , LEW ELISHEVA , LI XUAN , DEX TERRY A. , KILPATRICK RACHEL 
Published: May 2022

Aim: When T2D is suboptimally controlled with BI, 1-3 daily injections of prandial insulin are commonly added (BB regimen) . Once daily iGlarLixi is an alternative treatment. This analysis evaluated the use of iGlarLixi vs. BB on T2D outcomes.
Methods: This retrospective analysis of the US Optum Clinformatics database compared outcomes in adults (≥18 y) with T2D who previously received BI and newly initiated iGlarLixi or BB between Jan 1, 2017, and Jun 30, 2020. Persistence (primary endpoint) , adherence, healthcare resource utilization (HRU) , costs, any hypoglycemia, and HbA1c change were assessed at 12 months.
Results: Propensity score matching generated cohorts (n=1070 each) that were well balanced with similar mean ± SD age (iGlarLixi: 63.9 ± 11.0 y; BB: 64.5 ± 11.3 y) , HbA1c (iGlarLixi: 9.2 ± 1.7%; BB: 9.2 ± 1.8%) , oral agent use, BI use, and HRU. The primary endpoint was met with treatment persistence being statistically significantly higher for iGlarLixi vs. BB at 12 months. Adherence was numerically higher for iGlarLixi, and hypoglycemia rates, HRU and costs, numerically lower. HbA1c reduction was similar between groups (Table) .
Conclusions: In this observational study, initiation of once daily iGlarLixi vs. BB insulin was associated with higher persistence and similar HbA1c reduction without increasing HRU or costs.

Disclosure
K.M. Pantalone: Consultant; AstraZeneca, Bayer AG, Corcept Therapeutics, Diasome, Eli Lilly and Company, Merck & Co., Inc., Novo Nordisk, Sanofi. Research Support; Bayer AG, Merck & Co., Inc., Novo Nordisk. Speaker's Bureau; AstraZeneca, Corcept Therapeutics, Merck & Co., Inc., Novo Nordisk. C. Heller: Consultant; Sanofi. Employee; Aetion. R. Lajara: None. E. Lew: Employee; Sanofi. X. Li: Employee; Eisai Co., Ltd., Sanofi. T.A. Dex: Employee; Sanofi. Stock/Shareholder; Pfizer Inc., Teva Pharmaceutical Industries Ltd., Viatris Inc. R. Kilpatrick: Speaker's Bureau; Abbott Diabetes, Amgen Inc., Novo Nordisk, Sanofi.

Funding
Sanofi
734-P: The Effect of Adjunctive Therapy with Liraglutide on Insulin Sensitivity in Overweight Persons with Type 1 Diabetes
Authors: DEJGAARD THOMAS F. , FRANDSEN CHRISTIAN S. , JOHANSEN NICKLAS , MADSBAD STEN , KNOP FILIP K. , ANDERSEN HENRIK U. 
Published: May 2022

Type 1 diabetes is associated with an almost threefold higher mortality rate than the general population, primarily driven by excess mortality from cardiovascular disease. Insulin sensitivity evaluated by the estimated glucose disposal rate (eGDR) is a recognized predictor of cardiovascular disease. Here, we evaluated the effect of adjunctive therapy with the glucagon-like peptide 1 receptor agonist (GLP-1RA) liraglutide on eGDR in patients with type 1 diabetes. We calculated eGDR post-hoc in a randomized (1:1) , placebo-controlled, double-blind, clinical trial (NCT01612468) that evaluated the effect of liraglutide 1.8 mg once daily (uptitrated via 0.6 mg and 1.2 mg over 2 weeks) as add-on to insulin treatment compared with placebo in 100 overweight persons with type 1 diabetes (35/65 women/men, age 48 (12) years (mean (standard deviation)) , diabetes duration 23 (12) years, BMI 30 (3) kg/m2, glycated hemoglobin A1c 8.7 (0.7) % / 72 (8) mmol/mol) . After 12 weeks of treatment, liraglutide significantly increased eGDR compared with placebo. However, at end of treatment at week 26, the between-group difference was not statistically significant (Table 1) . These data indicate that liraglutide may improve eGDR, a recognized predictor of cardiovascular disease, in overweight persons with long-standing type 1 diabetes and inadequate glycemic control.

Disclosure
T.F.Dejgaard: Advisory Panel; Novo Nordisk, Research Support; Novo Nordisk, Speaker's Bureau; AstraZeneca, Boehringer Ingelheim International GmbH, Novo Nordisk. C.S.Frandsen: None. N.Johansen: Employee; Novo Nordisk A/S. S.Madsbad: None. F.K.Knop: Advisory Panel; Boehringer Ingelheim International GmbH, Eli Lilly and Company, Merck Sharp & Dohme Corp., Novo Nordisk, Sanofi, ShouTi, Zucara Therapeutics, Consultant; AstraZeneca, Eli Lilly and Company, Novo Nordisk, Pharmacosmos A/S, Sanofi, ShouTi, Zealand Pharma A/S, Zucara Therapeutics, Research Support; AstraZeneca, Novo Nordisk, Sanofi, Zealand Pharma A/S, Speaker's Bureau; AstraZeneca, Bayer AG, Boehringer Ingelheim International GmbH, Eli Lilly and Company, Novo Nordisk, Sanofi, Stock/Shareholder; Antag Therapeutics. H.U.Andersen: Advisory Panel; Abbott Diabetes, Stock/Shareholder; Novo Nordisk A/S.

Funding
Supported by an unrestricted grant by Novo Nordisk
735-P: Direct Anti-Inflammatory and Antifibrotic Effects of a Novel Long-Acting Glucagon/GIP/GLP-1 Triple Agonist, HM15211, in Thioacetamide-Induced Mouse Model of Liver Injury and Fibrosis
Authors: KIM JUNG KUK , LEE JONG SUK , KIM YOHAN , LEE SEON MYEONG , KWON HYUNJOO , PARK EUNJIN , CHOI JAEHYUK , BAE SUNGMIN , KIM DAEJIN , LEE SANG HYUN , CHOI IN YOUNG 
Published: May 2022

HM152 is a novel long-acting triple agonist consisting of Glucagon/GIP/GLP-1 triple agonist conjugated to human IgG FC fragment via short PEG linker. Previously, therapeutic benefits of HM152 were demonstrated in diet-induced animal models of NASH and fibrosis. Here, direct anti-inflammatory and -fibrotic effects of HM152 were further evaluated in TAA (thioacetamide) -induced liver injury and fibrosis mouse, and investigate underlying mechanism. To induce liver injury and fibrosis, gradually increased dose of TAA was injected to mouse for 12 weeks, and HM152 was administered during last weeks. Interestingly, HM152 treatment significantly reduced hepatic hydroxyproline (-51% vs. Veh, p&lt;0.01) , Sirius red positive area (-65% vs. Veh, p&lt;0.001) , and fibrosis score (0.7 for HM152 vs. 3.0 for Veh, p&lt;0.001) . Considering baseline fibrosis score at week 2 (1.0) , HM152 could confer both potential reversal effect on pre-existing fibrosis and prevention effect on fibrogenesis. Consistently, expression of hepatic marker genes for fibrosis (i.e. collagen-1α1) and inflammation (i.e. F4/80, TNF-α) were significantly reduced in HM152 group. Furthermore, multiplex cytokine analysis revealed that HM152 treatment was associated with robust reduction across pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6. Significant reduction in blood level of liver enzymes was also confirmed. Mechanistically, PMA/LPS-induced pro-inflammatory cytokine secretion of THP-1 cell was significantly attenuated by HM15211. TGF-β-induced collagen production was also reduced in LX2 cell.
In conclusion, HM152 markedly improved liver inflammation and fibrosis in TAA mice, and related mechanism was elaborated by in vitro studies. Thus, HM152 could be a novel therapeutic option for fibrosis due to NASH. Human study is ongoing to assess the clinical relevance of these findings.

Disclosure
J.Kim: None. S.Lee: n/a. I.Choi: None. J.Lee: None. Y.Kim: None. S.Lee: None. H.Kwon: Employee; Hanmi Pharm. Co., Ltd. E.Park: Employee; Hanmi Pharm. Co., Ltd. J.Choi: Employee; Hanmi Pharm. Co., Ltd. S.Bae: None. D.Kim: None.
74-OR: Adoptively Transferred T Lymphocytes with Reduced iPLA2b Expression Delays Type 1 Diabetes Development in NOD Mice
Authors: WHITE TAYLEUR , CHALFANT CHARLES , DILORENZO TERESA P. , RAMANADHAM SASANKA , STEPHENSON DANIEL 
Published: May 2022

Type 1 diabetes (T1D) is a T-cell mediated autoimmune disease characterized by the destruction of insulin-producing pancreatic islet β-cells. An understudied area is the role lipid signaling plays in this process. We find that the Ca2+-independent phospholipase A2β (iPLA2β) is induced under a diabetic milieu and mitigation of iPLA2β activity attenuates β-cell death. iPLA2β, a member of the PLA2 family, hydrolyzes the sn-2 substituent from glycerophospholipid substrates to yield a free fatty acid. When the fatty acid is arachidonic acid, it can be metabolized to eicosanoids, many of which are pro-inflammatory. To address our overarching hypothesis that iPLA2β-derived lipids (iDLs) contribute to T1D development, we investigated the role of immune cell-iDLs by utilizing a T-cell adoptive transfer. We isolated CD4+/8+ T-cells from splenocytes prepared from 11-week-old donor female NOD and NOD.iPLA2 β +/- (HET) . These were transferred i.p. to 4-week-old NOD.scid recipient mice. We find that NOD4/8-recipient mice develop T1D between 14-16 weeks of age. In contrast, T1D onset in HET4/8-recipient mice is delayed by 12 weeks and this was associated with better glucose tolerance, compared to NOD4/8 T-cell recipients. This finding is also supported by histology analysis of the pancreatic islet, which revealed less islet infiltration, more islet abundance, and the frequency of CD4 T cells were increased in the pancreas of HET4/8-recipient mice compared to NOD4/8 recipients. Further, lipidomics analyses revealed that HET donor T-cell production of proinflammatory lipids (i.e., PGE2 and DHETs) is decreased, relative to NOD T-cells. These findings suggest that pro-inflammatory iDLs generated by CD4 T-cells are critical contributors T1D development and can be targeted to counter T1D onset.

Disclosure
T.White: None. C.Chalfant: None. T.P.Dilorenzo: None. S.Ramanadham: None. D.Stephenson: None.

Funding
Training Program in Cell, Molecular, and Developmental Biology (5T32GM008111-34) NIH/NIDDK (R01DK110292) NIH/NIAID R21 (AI 146743) Cell, Developmental, & Integrative Biology (CDIB) , the University of Alabama at Birmingham
741-P: Real-World Weight-Loss Effectiveness of GLP-1 Agonists among Patients with Type 2 Diabetes: A Retrospective Cohort Study
Authors: LUO JING , SHU INGRID , KORYTKOWSKI MARY T. , ROMETO DAVID A. , ARNOLD JONATHAN , WHITE GRETCHEN E. 
Published: May 2022

The real-world weight loss effectiveness of GLP-1RAs have not been well described. We conducted a cohort study using EHR data from an integrated healthcare system based in PA. Non-pregnant adults first dispensed a GLP-1RA between 20 and 2018 were eligible. We excluded those without: 1) at least 72 weeks of continuous enrollment after the first dispense date,2) at least 1 year of baseline enrollment data, and3) at least one valid weight measurement within the 8 wks before the dispense date and at least one weight measure during follow-up. We used descriptive statistics to report percent change in body weight from baseline in each 8 wk follow-up interval ending in +72 wks. We used linear mixed models with a person-level random intercept controlling for variables associated with missing weight data to estimate percent body weight change during follow-up. Our cohort included 2,398 patients (mean[SD] age 48.4[10.3], 53% female) , with a BMI[SD] of 37[7.5] and a mean baseline weight of 238[54] lbs. In the final 8 wk interval of follow-up (64-72 wks) , the modeled mean percent weight change was -2.5% (95% CI: -2.8 to -2.1) . An estimated 29.9% (95% CI: 27.2 to 32.6) of patients lost at least 5% body weight at this time. In this real-world study using data from ∼2,400 patients with overweight or obese and type 2 diabetes, starting a GLP-1RA was associated with a modest amount of weight loss through 72 weeks.

Disclosure
J.Luo: None. I.Shu: None. M.T.Korytkowski: None. D.A.Rometo: Advisory Panel; Nestlé Health Science. J.Arnold: None. G.E.White: None.

Funding
NIDDK (K23ADK120956)
748-P: Clinically Relevant Predictors of Cardiovascular Events in Patients with Type 2 Diabetes Mellitus: A Pooled Analysis from Clinical Studies
Authors: MALHOTRA ANKUR , BADER GIOVANNI 
Published: May 2022

Patients with type 2 diabetes mellitus (T2DM) are at greater risk of developing cardiovascular disease (CVD) . We aimed to explore the association between several baseline parameters and risk of cardiovascular (CV) events in patients with T2DM and whether evidence from clinical data at T2DM onset could be useful in identifying patients at risk of subsequent CV events. Data for baseline visits were extracted from 34 globally conducted clinical studies. Framingham risk equation was used to assess the CV risk at baseline. In the overall pooled population (n=18,076) , 2130 (13.6%) patients had CVD history at baseline. The mean (SD) age of the patients was 56.8 (10.7) years, total cholesterol was 196.4 (41.0) mg/dL, low-density lipoprotein (LDL) was 115.4 (36.8) mg/dL, systolic blood pressure (SBP) was 132.7 (14.6) mmHg with disease duration of 5. (5.10) years and Framingham risk score (FRS) of 20.71 (12.68) . An incremental risk for subsequent CV events was observed in patients having none or multiple risk factors. Patients having CVD history and FRS ≥20% were significantly associated with a higher risk of CV events (HR [95% CI]: 7.8 [5.0, 12.3]; p&lt;0.001; Figure) . Overall, these analyses suggests that clinical data collected at the onset and follow-up of T2DM such as CVD history, high LDL and SBP may help in identifying patients who are at high risk of subsequent CV events.

Disclosure
A.Malhotra:Employee; Novartis India . G.Bader:Employee; Novartis AG.

Funding
Novartis Pharma AG