BackgroundInsomnia with objective short sleep duration (ISSD) but not insomnia with normal sleep duration (INSD) is associated with cardiometabolic morbidity. It has been reported that sleep apnea comorbid with insomnia (COMISA) confers higher cardiovascular risk than each condition alone. We hypothesize that the association of COMISA with clinical (hypertension) and preclinical (inflammatory and metabolic) biomarkers is driven by the ISSD phenotype. MethodsA clinical sample of 101 adults with mild-to-moderate OSA (mmOSA) (5 ≤ AHI <30) and insomnia symptoms underwent polysomnography or home sleep apnea testing, blood pressure measures (BP), fasting blood glucose, insulin, CRP and IL-6 plasma levels. Insomnia was based on PSQI. Objective short sleep duration was based on the median total sleep time of the sample. Participants were classified into 2 groups based on objective sleep duration: mmOSA with ISSD vs. mmOSA with INSD. Analysis of covariance and logistic regression analysis were conducted controlling for confounders. ResultsSystolic and diastolic BP were elevated in the ISSD group compared to INSD group (p = 0.039 and p = 0.004, respectively). Also, the risk of hypertension was significantly higher in the ISSD (OR = 3.88, 95%CI = 1.26–11.95, p < 0.05) compared to INSD group. Plasma IL-6 concentrations and insulin resistance as indexed by glucose/insulin ratio were significantly higher in the ISSD group compared to INSD group (both p < 0.05). CRP levels were not different between the two groups. ConclusionIt appears that the additive adverse effects of COMISA on cardiometabolic risks are driven by the ISSD phenotype, a finding with potential implications for further phenotyping COMISA.