Carmine Gazzaruso, Pietro Gallotti, Colomba Falcone, Livio Luzi, Adriana Coppola
In newly diagnosed type 2 diabetes without overt complications, higher fasting C-peptide and lower TcPO2 were associated with increased cardiovascular risk. These findings are hypothesis-generating and warrant external validation.
AIMS: Cardiovascular risk stratification at the time of type 2 diabetes diagnosis remains challenging. We evaluated the incidence and baseline predictors of first-ever major adverse cardiovascular events (MACE) in patients with newly diagnosed type 2 diabetes without overt complications.
METHODS: We conducted a prospective cohort study of 937 consecutive adults with newly diagnosed type 2 diabetes, free of overt diabetic complications and pre-existing cardiovascular disease at baseline, followed for a mean of 62.7 ± 21.5 months. Baseline assessment included fasting C-peptide, transcutaneous oxygen tension (TcPO2), structured therapeutic patient education (TPE), and conventional metabolic and cardiovascular variables. Incident MACE was analyzed using Cox proportional hazards regression, and receiver operating characteristic analysis was used to derive an exploratory C-peptide cut-off.
RESULTS: During follow-up, 42 participants (4.5%) experienced a first MACE (0.86 per 100 person-years). In multivariable Cox analysis, higher fasting C-peptide (HR:4.70, 95%CI: 2.47-8.93, p < 0.001), lower TcPO2 (HR:15.15, 95%CI: 7.00-32.80, p < 0.001) were independently associated with MACE; non-participation in structured TPE was also associated with MACE (HR:0.26, 95%CI: 0.14-0.49, p < 0.001), but this finding should be interpreted cautiously given the observational design. The optimal C-peptide cut-off was 3.1 ng/mL (AUC 0.73). As a secondary endpoint, all-cause mortality occurred in 99 of 937 participants (10.6%; 2.02 per 100 person-years) and was independently associated with older age and lower TcPO2.
CONCLUSIONS: In newly diagnosed type 2 diabetes without overt complications, higher fasting C-peptide and lower TcPO2 were associated with increased cardiovascular risk. These findings are hypothesis-generating and warrant external validation.