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controversy regarding the clinical signi fi-\ncance of racial differences in A1C (9 –12).\nThere is an emerging understanding ofgenetic determinants that may modifythe association between A1C and glu-cose levels (13). However, race is not a\ngood proxy for these genetic differences | [
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good proxy for these genetic differences\nthat are likely present in a small minorityof individuals of all racial groups. There-fore, race should not be a considerationfor how A1C is used clinically for glyce-mic monitoring. Limitations of laboratorytests and within-person variability in glu-\ncose and A1C underscore t... | [
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cose and A1C underscore the importance\nof using multiple approaches to glycemicmonitoring and further evaluation ofdiscordant results in all racial or ethnicgroups.\nSerum Glycated Protein Assays as\nAlternatives to A1C\nFructosamine and glycated albumin are | [
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Alternatives to A1C\nFructosamine and glycated albumin are\nalternative measures of glycemia that areapproved for clinical use for monitoringglycemic status in people with diabetes.Fructosamine re flects total glycated se-\nrum proteins (mostly albumin). Glycated\nalbumin assays re flect the proportion of\ntotal albumin ... | [
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total albumin that is glycated. Due to the\nturnover rate of serum protein, fructos-amine and glycated albumin refl ect glyce-\nmia over the past 2 –4w e e k s ,as h o r t e r -\nterm time frame than that of A1C. Fruc-tosamine and glycated albumin are highly\ncorrelated in people with diabetes, and | [
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correlated in people with diabetes, and\nthe performance of modern assays is typi-cally excellent. Fructosamine and glycatedalbumin have been linked to long-termcomplications in epidemiologic cohortstudies (14 –18). However, there have\nbeen few clinical trials, and the evidence\nbase supporting the use of these bio- | [
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base supporting the use of these bio-\nmarkers to monitor glycemic status ismuch weaker than that for A1C. In peo-ple with diabetes who have conditionswhere the interpretation of A1C may beproblematic or when A1C cannot be mea-\nsured (e.g., homozygous hemoglobin var- | [
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sured (e.g., homozygous hemoglobin var-\niants), fructosamine or glycated albuminmay be useful alternatives to monitor gly-cemic status (8).Correlation Between A1C and Blood\nGlucose Monitoring and Continuous\nGlucose Monitoring\nTable 6.1 provides rough equivalents of\nA1C and mean glucose levels based on data | [
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A1C and mean glucose levels based on data\nfrom the international A1C-Derived Average\nGlucose (ADAG) study. The ADAG study as-\nsessed the correlation between A1C andfrequent BGM and CGM in 507 adults(83% non-Hispanic White) with type 1,type 2, and no diabetes (19,20). TheAmerican Diabetes Association (ADA)\nand the A... | [
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and the American Association for Clinical\nChemistry have determined that the cor-relation ( r= 0.92) in the ADAG trial is\nstrong enough to justify reporting boththe A1C result and the estimated aver-\nage glucose (eAG) result when a clinician | [
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age glucose (eAG) result when a clinician\norders the A1C test. Clinicians shouldnote that the mean plasma glucose num-bers in Table 6.1 are based on /C242,700\nreadings per A1C measurement in theADAG trial.\nGlycemic Assessment by Blood\nGlucose Monitoring\nFor many people with diabetes, glucose\nmonitoring, either us... | [
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monitoring, either using BGM by capil-\nlary ( finger-stick) devices or CGM in addi-\ntion to regular A1C testing, is key for\nachieving glycemic goals. Major clinicaltrials of insulin-treated individuals haveincluded BGM as part of multifactorialinterventions to demonstrate the benefi t\nof intensive glycemic control on... | [
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of intensive glycemic control on diabetes\nTable 6.1 —Equivalent A1C levels and\nestimated average glucose (eAG)\nA1C (%) mg/dL* mmol/L\n5 97 (76 –120) 5.4 (4.2 –6.7)\n6 126 (100–152) 7.0 (5.5 –8.5)\n7 154 (123–185) 8.6 (6.8 –10.3)\n8 183 (147–217) 10.2 (8.1 –12.1)\n9 212 (170–249) 11.8 (9.4 –13.9)\n10 240 (193–282) 13... | [
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9 212 (170–249) 11.8 (9.4 –13.9)\n10 240 (193–282) 13.4 (10.7 –15.7)\n11 269 (217–314) 14.9 (12.0 –17.5)\n12 298 (240–347) 16.5 (13.3 –19.3)\nData in parentheses are 95% CI. A calcula-\ntor for converting A1C results into eAG, in\neither mg/dL or mmol/L, is available at | [
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either mg/dL or mmol/L, is available at\nprofessional.diabetes.org/eAG. *These esti-m a t e sa r eb a s e do nA D A Gd a t ao f/C24 2,700\nglucose measurements over 3 months per\nA1C measurement in 507 adults with type 1,\ntype 2, or no diabetes. The correlation be-tween A1C and average glucose was 0.92 | [
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(19,20). Adapted from Nathan et al. (19).S112 Glycemic Goals and Hypoglycemia Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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complications (21). BGM is thus an integral\ncomponent of effective therapy for individ-\nuals taking insulin. In recent years, CGM\nhas become a standard method for glucose\nmonitoring for most people with type 1\ndiabetes. Both approaches to glucose mon-\nitoring allow people with diabetes to evalu-ate individual res... | [
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assess whether glycemic goals are being\nsafely achieved. The speci ficn e e d sa n d\ngoals of individuals with diabetes shoulddictate BGM frequency and timing. Please\nrefer to Section 7, “Diabetes Technology, ”\nfor a more complete discussion of the use\nof BGM and CGM.\nGlycemic Assessment by Continuous\nGlucose Mon... | [
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Glycemic Assessment by Continuous\nGlucose Monitoring\nRecommendations\n6.3 Standardized, single-page glucose\nreports from CGM devices with visual\ncues, such as the ambulatory glucose\nprofile, should be considered as a stan-\ndard summary for all CGM devices. E\n6.4Time in range (TIR) is associated | [
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6.4Time in range (TIR) is associated\nwith the risk of microvascular compli-cations and can be used for assess-\nment of glycemic status. Additionally, | [
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ment of glycemic status. Additionally,\ntime below range and time aboverange are useful parameters for theevaluation of the treatment plan(Table 6.2 ).CCGM is particularly useful in people with dia-betes who are at risk for hypoglycemia and iscommonly used in people with type 1 diabe-\ntes (21). Use of CGM in type 2 di... | [
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tes (21). Use of CGM in type 2 diabetes (as\nwell as in several other forms of diabetes) isgrowing, especially in people who are taking\ninsulin. TIR is a useful metric of glycemic sta-\ntus. A 10- to 14-day CGM assessment of TIR,\nwith CGM wear of 70% or higher, and other | [
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with CGM wear of 70% or higher, and other\nCGM metrics can be used to assess glycemicstatus and are useful in clinical management\n(22–26). TIR, especially mean CGM glucose,\ncorrelates with A1C (27 –31). Time below\nrange ( <70 and <54 mg/dL [ <3.9 and\n<3.0 mmol/L]) and time above range\n(>180 mg/dL [ >10.0 mmol/L]) ... | [
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(>180 mg/dL [ >10.0 mmol/L]) are useful\nparameters for insulin dose adjustments\nand reevaluation of the treatment plan.\nThe international consensus on CGM\nprovides guidance on standardized CGMmetrics ( Table 6.2 ) and their clinical inter-\npretation (32). To make these metrics ac-\ntionable, standardized reports w... | [
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tionable, standardized reports with visual\nsummaries, such as the ambulatory glucoseprofile (Fig. 6.1), are recommended (32)\nand can help individuals with diabetes andhealth care professionals interpret the data\nto guide treatment decisions (27,30). BGM\nand CGM can be useful to guide medicalnutrition therapy and phy... | [
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vent hypoglycemia, and aid medication\nmanagement. CGM metrics, including TIR\n(with time below range and time aboverange), can provide helpful insights to in-\nform a personalized diabetes managementplan. Remote access to glucose data isgrowing and may help improve diabetesmanagement (33 –35).\nCGM systems have evolve... | [
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CGM systems have evolved rapidly in\nboth accuracy and affordability. As such,many individuals with diabetes havethese data available to assist with self-management and their health care profes-sionals’ assessment of glycemic status. Re- | [
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ports can be generated from CGM thatwill allow the health care professional andperson with diabetes to view TIR, a calcu-lated glucose management indicator, andassess hypoglycemia, hyperglycemia, andglycemic variability. As discussed in a 2019consensus report, a report formatted asshown in Fig. 6.1 can be generated (32... | [
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Published data from two retrospectivestudies suggest a strong correlation be-t w e e nT I Ra n dA 1 C ,w i t hag o a lo f7 0 %T I R\naligning with an A1C of /C247% (25,28). Note\nthe goals of therapy next to each metric in\nFig. 6.1 (e.g., low, <4%; very low, <1%) as\nvalues to guide changes in therapy.\nGLYCEMIC GOALS... | [
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values to guide changes in therapy.\nGLYCEMIC GOALS\nRecommendations\n6.5a An A1C goal for many nonpreg-\nnant adults of <7% (<53 mmol/mol)\nTable 6.2 —Standardized CGM metrics for clinical care in nonpregnant individuals with type 1 or type 2 diabetes\nMetric Interpretation Goals\n1. Number of days CGM device is worn ... | [
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-0.0240... |
management\n2. Percentage of time CGM device is active 70% of data from 14 days\n3. Mean glucose Simple average of glucose values *\n4. Glucose management indicator Calculated value approximating A1C\n(not always equivalent)*\n5. Glycemic variability (%CV) target Spread of glucose values #36%† | [
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-0.019924409687519073,
-0.0120... |
5. Glycemic variability (%CV) target Spread of glucose values #36%†\n6. TAR: % of readings and time >250 mg/dL ( >13.9 mmol/L) Level 2 hyperglycemia <5% (most adults);\n<10% (older adults)\n7. TAR: % of readings and time 181 –250 mg/dL (10.1 –13.9 mmol/L) Level 1 hyperglycemia <25% (most adults);\n<50% (older adults) ‡ | [
-0.006075143814086914,
0.032391417771577835,
-0.034301966428756714,
0.04095502942800522,
0.015410901978611946,
0.0011291509727016091,
-0.017800360918045044,
0.11592245101928711,
-0.04888920858502388,
-0.023642634972929955,
-0.023327365517616272,
0.009724598377943039,
-0.07715131342411041,
... |
<50% (older adults) ‡\n8. TIR: % of readings and time 70 –180 mg/dL (3.9 –10.0 mmol/L) In range >70% (most adults);\n>50% (older adults)\n9. TBR: % of readings and time 54 –69 mg/dL (3.0 –3.8 mmol/L) Level 1 hypoglycemia <4% (most adults);\n<1% (older adults) §\n10. TBR: % of readings and time <54 mg/dL ( <3.0 mmol/L) ... | [
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0.06295789778232574,
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-0.00815896037966013,
-0.02299404889345169,
0.1068279892206192,
-0.05472780391573906,
-0.018477147445082664,
0.004049548413604498,
-0.024935845285654068,
0.013563473708927631,
0.027... |
CGM, continuous glucose monitoring; CV, coef ficient of variation; TAR, time above range; TBR, time below range; TIR, time in range. *Goals\nfor these values are not standardized. †Some studies suggest that lower %CV targets ( <33%) provide additional protection against hypoglyce- | [
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0.02942756749689579,
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-0.019010260701179504,
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-0.08923767507076263,
-0.050428129732608795,
0.... |
mia for those receiving insulin or sulfonylureas. ‡Goals are for level 1 and level 2 hyperglycemia combined. §Goals are for level 1 and level 2\nhypoglycemia combined. Adapted from Battelino et al. (32).diabetesjournals.org/care Glycemic Goals and Hypoglycemia S113\n©AmericanDiabetesAssociation | [
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0.006641346029937267,
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0.04206458851695061,
0.04361521452665329,
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0.017361104488372803,
-0.06462762504816055,
-0.018419452011585236,
-0.008... |
AGP Report: Continuous Glucose Monitoring\nTest Patient DOB: Jan 1, 1970\n14 Days: August 8–August 21, 2021 \nTime CGM Active: 100%\nGlucose Metrics \nAverage Glucose ........................................... 175 mg/dL\nGoal: <154 mg/dL\nGlucose Management Indicator (GMI) ............... 7.5%\nGoal: <7% | [
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0.020460927858948708,
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-0.06537359952926636,
0.0297... |
Glucose Management Indicator (GMI) ............... 7.5%\nGoal: <7%\nGlucose Variability ............................................ 45.5%\nGoal: < 36%\nAGP is a summary of glucose values from the report period, with median (50%) and other percentiles shown as if they occurred in a single day.Time in Ranges Goals f... | [
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0.0484464131295681,
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Very High 20%\nHigh 24%\nTarget\nLow 5%\nVery Low 5%46% Goal: >70%Goal: <5%\nGoal: <1%44% Goal: <25%\n10% Goal: <4%\nEach 1% time in range = ~15 minutesmg/dL250\n180\n70\n54\nTarget\nRange\n12am 3am 6am 9am 12pm 3pm 6pm 9pm 12am350\nmg/dL\n250\n 180\n 70\n54\n095%\n75%\n50%\n25%\n5% | [
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0.005080144386738539,
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0.002812175080180168,
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0.04779401794075966,
-0.06606215238571167,
-0.062379926443099976,
-0.020092761144042015,
0.0535... |
mg/dL\n250\n 180\n 70\n54\n095%\n75%\n50%\n25%\n5%\n12pm 12pm 12pm 12pm 12pm 12pm 12pm Sunday Monday T uesday Wednesday Thursday Friday Saturday\n180\n708 9 10 11 12 13 14\n180\n7015 16 17 18 19 20 21mg/dL mg/dL1313 | [
-0.01995561271905899,
-0.0011897834483534098,
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-0.020414844155311584,
-0.06217243894934654,
-0.02490968070924282,
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0.0033334451727569103,
-0.0679403692483902,
0.006581494584679604,
0... |
180\n708 9 10 11 12 13 14\n180\n7015 16 17 18 19 20 21mg/dL mg/dL1313\nFigure 6.1 —Key points included in a standard ambulatory glucose pro file (AGP) report. Reprinted from Holt et al. (21).S114 Glycemic Goals and Hypoglycemia Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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0.0014816380571573973,
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0.14854608476161957,
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-0.03894888609647751,
-0.019103895872831345,
-0.06354161351919174,
-0.... |
without signifi cant hypoglycemia is\nappropriate. A\n6.5b If using an ambulatory glucose\nprofile/glucose management indicator\nto assess glycemia, a parallel goal for\nmany nonpregnant adults is TIR >70%\nwith time below range <4% and time\n<54 mg/dL ( <3 mmol/L) <1%. For\nthose with frailty or at high risk of hy-pogly... | [
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0.021680524572730064,
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0.057940125465393066,
0.10449568927288055,
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-0.009157232940196991,
0.00447930209338665,
-0.0408969484269619,
-0.031220464035868645,
-0.0018... |
<1% time below range is recom-\nmended (Fig. 6.1 and Table 6.2 ).B\n6.6On the basis of health care profes-\nsional judgment and the preference of\nthe person with diabetes, achievement\nof lower A1C levels than the goal of7% (53 mmol/mol) may be acceptablea n de v e nb e n e ficial if it can be achieved\nsafely without ... | [
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safely without signifi cant hypoglycemia\nor other adverse effects of treatment. B\n6.7Less stringent glycemic goals may\nbe appropriate for individuals with lim-\nited life expectancy or where the harms\nof treatment are greater than the ben-efits.B\n6.8a Deintensify hypoglycemia-causing | [
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0.01167661... |
6.8a Deintensify hypoglycemia-causing\nmedications (insulin, sulfonylureas, ormeglitinides), or switch to a medica-tion class with lower hypoglycemiarisk, for individuals who are at high\nrisk for hypoglycemia, within individu-\nalized glycemic goals. B\n6.8b Deintensify diabetes medications | [
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-0.... |
alized glycemic goals. B\n6.8b Deintensify diabetes medications\nfor individuals for whom the harmsand/or burdens of treatment may begreater than the bene fits, within indi-\nvidualized glycemic goals. B\n6.9Reassess glycemic goals based\non the individualized criteria showninFig. 6.2 .E\n6.10 Setting a glycemic goal du... | [
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-0.03010287508368492,
-0.04175615310668945,
-0.05... |
6.10 Setting a glycemic goal during\nconsultations is likely to improvepatient outcomes. E\nFor all populations, it is critical that the\nglycemic goals be woven into the overall\nperson-centered strategy ( Fig. 6.2)( 3 6 ) .\nFor example, less stringent A1C goals are\nappropriate for individuals with limited\nlife exp... | [
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0.03460628539323807,
-0.01898784562945366,
-0.0657... |
life expectancy and/or signi ficant func-\ntional and cognitive impairments. In a\nvery young child, safety and simplicitymay outweigh the need for glycemic\nstability in the short run. Recommended\nglycemic goals for many nonpregnantadults are shown in Table 6.3 .T h e | [
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0.013602267019450665,
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0.0159599... |
recommendations include blood glu-cose levels that appear to correlatewith an A1C of <7% (<53 mmol/mol). For\nglycemic goals in older adults, please refer\nto Section 13, “Older Adults. ”For glyce-\nmic goals in children, please refer toSection 14, “Children and Adolescents. ” | [
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0... |
For glycemic goals during pregnancy,please refer to Section 15, “Management\nof Diabetes in Pregnancy. ”\nThe health care professional needs to\nwork with the individual (as well as with\nfamily members and caregivers) and should\nconsider adjusting goals for simplifying the\ntreatment plan if this change is needed to | [
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treatment plan if this change is needed to\nimprove safety and medication-taking be-\nhavior. Setting speci fic glycemic (and other)\ngoals during consultations is likely to improve\noutcomes for individuals with diabetes (37).Glucose Lowering and Microvascular\nComplications\nHyperglycemia de fines diabetes, and\nachiev... | [
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achieving glycemic goals is fundamental to\ndiabetes management. The level of chronic\nhyperglycemia is the best-established con-comitant risk factor associated with microvas-\ncular complications (i.e., diabetic retinopathy,\nnephropathy, and neuropathy). This is best\nunderstood by the fact that nerve, retinal, | [
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0.0107590... |
understood by the fact that nerve, retinal,\nand kidney cells do not require insulin for in-\ntracellular glucose entry. Consequently, these\ncells, when exposed to elevated ambient glu-\ncose levels even in the presence of insulin\ndeficiency (absolute or relative), will result in\nintracellular metabolic dysfunction a... | [
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intracellular metabolic dysfunction and in-\ncreased risk of microvascular complications.lowPerson / Disease Features\nRisks potentially associated\nwith hypoglycemia andother drug adverse effects\nDisease duration\nLife expectancy\nImportant comorbidities\nEstablished vascular\ncomplications\nIndividual needs and pref... | [
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0.0... |
complications\nIndividual needs and preferences\nResources and support\nsystemMore stringentApproach to Individualization of Glycemic Targets\nLess stringent A1C 7%\nhigh\nlong-standing\nshort\nsevere\nsevere\npreference for less\nburdensome therapy\nlimitedPotentially modifiable Usually not modifiable\nnewly diagnosed... | [
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0.024300426244735718,
-0.066483274102211,
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newly diagnosed\nlong\nabsent\nabsent\nhighly motivated, excellent\nself-care capabilities\nreadily availablefew / mildfew / mild\nFigure 6.2 —Person and disease factors used to determine optimal glycemic targets. Characteristics and\npredicaments toward the left justify more stringent efforts to lower A1C; those towar... | [
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less stringent efforts. A1C 7% = 53 mmol/mol. Adapted with permission from Inzucchi et al. (36).\nTable 6.3 —Summary of glycemic recommendations for many nonpregnant\nadults with diabetes\nA1C <7.0% (<53 mmol/mol)* †\nPreprandial capillary plasma glucose 80–130 mg/dL* (4.4 –7.2 mmol/L) | [
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0.016... |
Preprandial capillary plasma glucose 80–130 mg/dL* (4.4 –7.2 mmol/L)\nPeak postprandial capillary plasma glucose ‡ <180 mg/dL* ( <10.0 mmol/L)\n*More or less stringent glycemic goals may be appropriate for individuals. †CGM may be\nused to assess glycemic status as noted in Recommendation 6.5b and Fig. 6.1 . Goals shou... | [
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be individualized based on duration of diabetes, age/life expectancy, comorbid conditions,\nknown CVD or advanced microvascular complications, hypoglycemia unawareness, and indi-vidual patient considerations (per Fig. 6.2 ).‡Postprandial glucose may be targeted if A1C goals | [
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-0.01... |
are not met despite reaching preprandial glucose goals. Postprandial glucose measurements shouldbe made 1 –2 h after the beginning of the meal, generally peak levels in people with diabetes.diabetesjournals.org/care Glycemic Goals and Hypoglycemia S115\n©AmericanDiabetesAssociation | [
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-0.06859500706195831,
-... |
The Diabetes Control and Complications\nTrial (DCCT) (38), a prospective randomized\ncontrolled trial of intensive (mean A1C/C247% [53 mmol/mol]) versus standard\n(mean A1C /C249% [75 mmol/mol]) glycemic\ncontrol in people with type 1 diabetes,showed de finitively that better glycemic\nstatus is associated with 50 –76% ... | [
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0.059399064630270004,
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status is associated with 50 –76% reduc-\ntions in rates of development and pro-\ngression of microvascular complications\n(retinopathy, neuropathy, and diabetickidney disease). Follow-up of the DCCTcohorts in the Epidemiology of Diabetes\nInterventions and Complications (EDIC) | [
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0.0003092869301326573,
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0.0178... |
Interventions and Complications (EDIC)\nstudy (39,40) demonstrated persistenceof these microvascular bene fits over two\ndecades even though the glycemic sepa-ration between the treatment groups\ndiminished and disappeared during\nfollow-up.\nThe Kumamoto Study (41) and UK Pro- | [
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follow-up.\nThe Kumamoto Study (41) and UK Pro-\nspective Diabetes Study (UKPDS) (42,43)examined the effects of “intensive glyce-\nmic control ”among people with short-\nduration type 2 diabetes, although glyce-mic lowering in these studies was notintensive by current standards (mean A1C\nwas 7.1% vs. 9.4% in the Kumam... | [
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was 7.1% vs. 9.4% in the Kumamoto\nStudy and 7.0% vs. 7.9% in UKPDS). Thesetrials found lower rates of microvascularcomplications in the intervention arms,\nwith long-term follow-up of the UKPDS\ncohorts showing enduring effects on mostmicrovascular complications (44). Thesestudies highlight the long-term bene fits of | [
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early glycemic lowering in type 2 diabetes.\nTherefore, improved glycemia has been\nshown to reduce microvascular complica-tions of type 1 and type 2 diabetes wheninstituted early in the course of disease(2,45). The DCCT (38) and UKPDS (46)\nstudies demonstrated a curvilinear rela- | [
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studies demonstrated a curvilinear rela-\ntionship between A1C and microvascularcomplications. Such results suggest that,on a population level, the greatest num-\nber of complications will be averted by\ntaking individuals with diabetes from veryhigh to moderate glycemic levels. Theseanalyses also suggest that further ... | [
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ing of A1C from 7% to 6% (53 mmol/mol\nto 42 mmol/mol) is associated with fur-ther reduction in the risk of microvascularcomplications, although the absolute riskreductions become much smaller. The im-\nplication of these findings is that there is\nno need to deintensify therapy for an in- | [
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no need to deintensify therapy for an in-\ndividual with an A1C between 6% and 7%in the setting of low hypoglycemia risk with\na long life expectancy. There are newer\nagents that do not cause hypoglycemia,making it possible to maintain glycemic sta-tus without the risk of hypoglycemia (seeSection 9, “Pharmacologic App... | [
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Glycemic Treatment ”). Moreover, CGM use\nwas not as common when these trials were\nconducted and automated insulin delivery\nsystems were not available, which havebeen shown to improve glucose levels with-\nout increasing hypoglycemia.\nAmong individuals with type 2 diabetes, | [
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out increasing hypoglycemia.\nAmong individuals with type 2 diabetes,\nthree landmark trials (Action to ControlCardiovascular Risk in Diabetes [ACCORD],\nAction in Diabetes and Vascular Disease:Preterax and Diamicron MR Controlled\nEvaluation [ADVANCE], and Veterans Af-\nfairs Diabetes Trial [VADT]) were conducted | [
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fairs Diabetes Trial [VADT]) were conducted\nto test the effects of near normalization of\nblood glucose on cardiovascular outcomes.The ADVANCE and VADT trials found mod-\nest reduction in nephropathy with intensive\nglycemic control; ACCORD was stopped af-\nter a median of 3.5 years due to higher\nmortality in the int... | [
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mortality in the intervention arm (47 –51).\nImportantly, these landmark studies were\nconducted prior to the approval of glucagon-\nlike peptide 1 (GLP-1) receptor agonists and\nsodium –glucose cotransporter 2 (SGLT2)\ninhibitors, and intensive glycemic control\nwas achieved predominantly through greater\nuse of insul... | [
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use of insulin. Findings from these studies,\nincluding the concerning increase in mor-\ntality in the intensive treatment arm of\nACCORD, suggest caution is needed intreating diabetes to near-normal A1C\ngoals in people with long-standing type 2\ndiabetes using medications with a high\nrisk for hypoglycemia.\nGlucose ... | [
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risk for hypoglycemia.\nGlucose Lowering and\nCardiovascular Disease Outcomes\nCardiovascular disease (CVD) is a more\ncommon cause of death than microvas-cular complications in populations with\ndiabetes. The modern multifaceted man-\nagement of diabetes, with a focus on the\ntreatment of hypertension and the use | [
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treatment of hypertension and the use\nof statins, has reduced the prevalence ofatherosclerotic CVD to around double\ncompared with that of people without di-\nabetes (52).\nThe DCCT in individuals with type 1 dia-\nbetes and the UKPDS, ACCORD, ADVANCE,and VADT studies in type 2 diabetes all at-tempted to address wheth... | [
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cemic control reduced CVD events (38,47,\n48,50). ACCORD, ADVANCE, and VADT were\nconducted in relatively older participants\nwith a longer duration of diabetes (mean du-ration 8 –11 years) and either CVD or multi-\nple cardiovascular risk factors. Details ofthese studies are reviewed extensively inthe joint ADA positi... | [
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Glycemic Control and the Prevention ofCardiovascular Events: Implications of theACCORD, ADVANCE, and VA Diabetes\nTrials” (53).\nNo signi ficant reduction in composite\nCVD events was demonstrated at the end\nof the intervention in any of these studies,\nand ACCORD was stopped prematurely at | [
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and ACCORD was stopped prematurely at\n3.5 years because of an increase in totalmortality, particularly sudden CVD deaths.Serious concerns with the intensive glyce-mic treatment plan used in ACCORD in-\ncluded the rapid escalation of therapies, | [
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cluded the rapid escalation of therapies,\nt h ee a r l yu s eo fl a r g ed o s e so fi n s u l i n ,m a s -sive weight gain, and frequent hypoglyce-mia. These overall negative results were\nnot unexpected, as blood glucose has sub- | [
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not unexpected, as blood glucose has sub-\nsequently been shown to be a relativelyweak CVD risk factor in isolation comparedwith other CVD risk factors, such as hyper-\ntension or hypercholesterolemia. Conse-\nquently, even if a wide separation in A1Ccould be safely obtained, it would take along time for the CVD bene fi... | [
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However, meta-analysis of individualparticipant data from UKPDS, ACCORD,ADVANCE, and VADT demonstrated asignificant reduction in myocardial in-\nfarctions and major CVD events but no\ndifference in stroke, heart failure, or\nmortality between intensive and less in-tensive glycemic control (54).\nLonger-term epidemiologi... | [
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Longer-term epidemiological follow-up\nhas been performed in these studies, and a\nclear pattern of CVD benefi t has emerged\n(55–57). In the post-DCCT follow-up of\nthe EDIC cohort, participants previ-\nously randomized to the intensive arm\nhad a signi ficant 57% reduction in the\nrisk of nonfatal myocardial infarction... | [
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risk of nonfatal myocardial infarction,\nstroke, or cardiovascular death com-pared with those previously random-\nized to the standard arm (55). The\nbene fit of intensive glycemic control in\nthis cohort with type 1 diabetes hasbeen shown to persist for several deca-\ndes (56) and to be associated with a\nmodest reduct... | [
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modest reduction in all-cause mortal-ity (58).\nUKPDS post-trial monitoring, with 20 years\nof total follow-up, has shown reductions\nin myocardial infarctions and total mortal- | [
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in myocardial infarctions and total mortal-\ni t yb o t hi nt h eg r o u po fo v e r w e i g h ti n d i -viduals treated with metformin and in thegroup previously treated intensively withsulfonylureas or insulin (44). Shorter over-\nall follow-up of the VADT (10 years) has | [
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all follow-up of the VADT (10 years) has\nshown a signifi cant reduction in the primaryS116 Glycemic Goals and Hypoglycemia Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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outcome of major CVD events, with myocar-\ndial infarctions and heart failure being thecommonest outcomes (57). In contrast,shorter follow-up of the ADVANCE studyi nt h eA c t i o ni nD i a b e t e sa n dV a s c u l a rD i s -\nease Preterax and Diamicron MR Con- | [
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ease Preterax and Diamicron MR Con-\ntrolled Evaluation Post Trial ObservationalStudy (ADVANCE-ON) demonstrated no sig-nificant effect on CVD events (59). Even in\nthe epidemiological follow-up of ACCORDin the Action to Control Cardiovascular Riskin Diabetes Follow-On Study (ACCORDION),the excess increase in total morta... | [
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was seen during 3.5 years of intensive\ntreatment was reduced by returning toconventional control, so that there was nodifference in total mortality after a total of9 years of follow-up and the increase in\nCVD deaths was obtunded (60). Collec-\ntively, the results of these studies con firm | [
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tively, the results of these studies con firm\nthat long-term intensive glycemic controlreduces CVD events, particularly myocar-\ndial infarctions.\nAs discussed above, these landmark\nstudies in individuals with type 2 diabetes\nneed to be considered with the importantcaveat that GLP-1 receptor agonists\nand SGLT2 inhi... | [
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and SGLT2 inhibitors were not yet in\nclinical use. These agents with estab-lished cardiovascular and renal benefi ts\nappear to be safe and benefi cial in this | [
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0.031... |
appear to be safe and benefi cial in this\ngroup of individuals at high risk for cardi-orenal complications. Randomized clinicaltrials examining these agents for cardio-vascular safety were not designed to testhigher versus lower A1C; therefore, be-\nyond post hoc analysis of these trials, we | [
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yond post hoc analysis of these trials, we\ndo not have evidence that it is the glucoselowering per se by these agents that con-fers the CVD and renal benefi t( 6 1 ) .A d d i -\ntional bene ficial pleotropic effects of these\nagents may include weight loss, hemody-namic effects, blood pressure lowering,and anti-in flamma... | [
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... |
As discussed further below, severe hy-\npoglycemia is a potent marker of high ab-solute risk of cardiovascular events andmortality (62). Therefore, health care pro-fessionals should be vigilant in preventing\nhypoglycemia and should not aggressively | [
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hypoglycemia and should not aggressively\nattempt to achieve near-normal A1C levelsin people in whom such targets cannotbe safely and reasonably achieved. Asdiscussed in Section 9, “Pharmacologic\nApproaches to Glycemic Treatment, ”addi-\ntion of speci fic SGLT2 inhibitors or GLP-1 | [
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tion of speci fic SGLT2 inhibitors or GLP-1\nreceptor agonists that have demonstratedCVD bene fit is recommended in individu-\nals with established CVD, chronic kidneydisease, and heart failure. As outlined inmore detail in Section 9, “Pharmacologic\nApproaches to Glycemic Treatment, ”and\nSection 10, “Cardiovascular Dis... | [
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Section 10, “Cardiovascular Disease and\nRisk Management,” the cardiovascular ben-\nefits of SGLT2 inhibitors or GLP-1 receptor\nagonists are not contingent upon A1C low-ering; therefore, initiation can be consid-ered in people with type 2 diabetes and\nCVD independent of the current A1C or | [
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CVD independent of the current A1C or\nA1C goal or metformin therapy. Based onthese considerations, the following twostrategies are offered (63):\n1. If already on dual therapy or multiple\nglucose-lowering therapies and not onan SGLT2 inhibitor or a GLP-1 receptoragonist, consider switching to one ofthese agents with ... | [
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benefit.\n2. Introduce SGLT2 inhibitors or GLP-1\nreceptor agonists in people with CVD\nat A1C goal (independent of metformin)for cardiovascular bene fit, independent\nof baseline A1C or individualized A1Cgoal.\nSetting and Modifying Glycemic\nGoals\nGlycemic goals and management should\nbe individualized and not one siz... | [
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be individualized and not one size fits all.\nTo prevent both microvascular and mac-rovascular complications of diabetes,\nthere is a major call to overcome thera-\npeutic inertia and treat to individualizedgoals (53,64).\nNumerous factors must be consid-\nered when setting a glycemic goal. The\nADA proposes general goa... | [
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-0.03431... |
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