TY - JOUR
T1 - Association of obesity with cardiovascular outcomes in patients with type 2 diabetes and cardiovascular disease
T2 - Insights from TECOS
AU - TECOS Study Group
AU - Pagidipati, Neha J.
AU - Zheng, Yinggan
AU - Green, Jennifer B.
AU - McGuire, Darren K.
AU - Mentz, Robert J.
AU - Shah, Svati
AU - Aschner, Pablo
AU - Delibasi, Tuncay
AU - Rodbard, Helena W.
AU - Westerhout, Cynthia M.
AU - Holman, Rury R.
AU - Peterson, Eric D.
N1 - Funding Information:
NJ Pagidipati has received research grants from Amgen, Regeneron Pharmaceuticals, Sanofi-Aventis, and Verily Life Sciences. Y Zheng has no disclosures. JB Green has received grants from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and Sanofi, and personal fees from AstraZeneca, Merck, Boehringer-Ingelheim, and NovoNordisk. DK McGuire has provided clinical trial leadership for AstraZeneca, Sanofi Aventis, Janssen, Boehringer Ingelheim, Merck & Co, Novo Nordisk, Lexicon, Eisai, GlaxoSmithKline, and Esperion, and consultancy for AstraZeneca, Sanofi Aventis, Lilly US, Boehringer Ingelheim, Merck & Co, Pfizer, Novo Nordisk, Applied Therapeutics, and Metavant. RJ Mentz has received grants from Merck, AstraZeneca and GlaxoSmithKline and personal fees from Merck, Astra-Zeneca and Boehringer-Ingelheim. SH Shah has received funding from the NIH (5R01-HL127009-03) and an American Heart Association Strategically Focused Research Network grant (17SFRN33700155). P Aschner has served on advisory boards for AstraZeneca, Boehringer Ingelheim, Janssen, MSD, Novartis, and Sanofi and on the speaker bureau for AstraZeneca, Lilly, Boehringer Ingelheim, MSD, Novartis, Novo Nordisk, and Sanofi. T Delibasi has no disclosures. HW Rodbard has received consulting and speaker fees from Astra-Zeneca, Bayer, BI/Lilly, Janssen, Merck, Novo Nordisk, Sanofi, Regeneron, and research support from Astra-Zeneca, BI/ Lilly, Janssen, Lexicon, Merck, Novo Nordisk, Sanofi, Regeneron. CM Westerhout has no disclosures. RR Holman has received grants from Boehringer Ingelheim, Merck, Bayer, and AstraZeneca and personal fees from Bayer, Novartis, and Novo Nordisk. ED Peterson has received grants from Janssen, Merck, Sanofi, AstraZeneca, Genentech, and Amgen, and has consulting associations with Janssen, Bayer, Merck, and Sanofi. The following is the supplementary data related to this article. Supplemental Figure S1 HbA 1c during study follow-up according to baseline obesity status. Supplemental Figure S1 Supplementary data to this article can be found online at https://doi.org/10.1016/j.ahj.2019.09.016 .
PY - 2020/1
Y1 - 2020/1
N2 - Background: Obesity is a risk factor for type 2 diabetes (T2D) and cardiovascular disease (CVD). Whether obesity affects outcomes among those with T2D and atherosclerotic CVD (ASCVD) remains uncertain. Our objective was to investigate the relationship between body mass index (BMI) and ASCVD outcomes among TECOS participants with T2D and ASCVD. Methods: BMI categories were defined as underweight/normal weight (BMI <25 kg/m2), overweight (25-29.9 kg/m2), obese class I (30-34.9 kg/m2), obese class II (35-39.9 kg/m2), and obese class III (≥ 40 kg/m2). Asian-specific BMI categories were applied to Asian participants. Kaplan-Meier survival analysis and Cox proportional hazards models were used to examine associations between baseline BMI and a composite CV outcome (CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina). Results: For 14,534 TECOS patients with available BMI, mean age was 65.5 years; 29.3% were female, 32.0% non-White, and 23.1% insulin-treated, with median 3 years' follow-up. At baseline, 11.6% (n = 1686) were underweight/normal weight, 38.1% (n = 5532) overweight, 32.2% (n = 4683) obese class I, 12.4% (n = 1806) obese class II, and 5.7% (n = 827) obese class III. The composite CV outcome occurred in 11.4% (n = 1663) of participants; the outcome risk was lower, compared with under/normal weight, in overweight (HR 0.83, 95% CI 0.71-0.98) and obese class I (HR 0.79, 95% CI 0.67-0.93) individuals. Obesity was not associated with worse glycemic control. Conclusions: The majority of TECOS participants with ASCVD and T2D were overweight or obese, yet overweight or obese class I individuals had lower CV risk than those who were under/normal weight. These results suggest the presence of an obesity paradox, but this paradox may reflect an epidemiological artifact rather than a true negative association between normal weight and clinical outcomes.
AB - Background: Obesity is a risk factor for type 2 diabetes (T2D) and cardiovascular disease (CVD). Whether obesity affects outcomes among those with T2D and atherosclerotic CVD (ASCVD) remains uncertain. Our objective was to investigate the relationship between body mass index (BMI) and ASCVD outcomes among TECOS participants with T2D and ASCVD. Methods: BMI categories were defined as underweight/normal weight (BMI <25 kg/m2), overweight (25-29.9 kg/m2), obese class I (30-34.9 kg/m2), obese class II (35-39.9 kg/m2), and obese class III (≥ 40 kg/m2). Asian-specific BMI categories were applied to Asian participants. Kaplan-Meier survival analysis and Cox proportional hazards models were used to examine associations between baseline BMI and a composite CV outcome (CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina). Results: For 14,534 TECOS patients with available BMI, mean age was 65.5 years; 29.3% were female, 32.0% non-White, and 23.1% insulin-treated, with median 3 years' follow-up. At baseline, 11.6% (n = 1686) were underweight/normal weight, 38.1% (n = 5532) overweight, 32.2% (n = 4683) obese class I, 12.4% (n = 1806) obese class II, and 5.7% (n = 827) obese class III. The composite CV outcome occurred in 11.4% (n = 1663) of participants; the outcome risk was lower, compared with under/normal weight, in overweight (HR 0.83, 95% CI 0.71-0.98) and obese class I (HR 0.79, 95% CI 0.67-0.93) individuals. Obesity was not associated with worse glycemic control. Conclusions: The majority of TECOS participants with ASCVD and T2D were overweight or obese, yet overweight or obese class I individuals had lower CV risk than those who were under/normal weight. These results suggest the presence of an obesity paradox, but this paradox may reflect an epidemiological artifact rather than a true negative association between normal weight and clinical outcomes.
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U2 - 10.1016/j.ahj.2019.09.016
DO - 10.1016/j.ahj.2019.09.016
M3 - Article
C2 - 31707324
AN - SCOPUS:85074587762
VL - 219
SP - 47
EP - 57
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
ER -