Abstract
BackgroundRecent analyses in a registry of hypertensive patients suggested that preceding left ventricular (LV) hypertrophy (LVH) and/or carotid atherosclerosis are associated with incident type 2 diabetes, independent of confounders. We assess the relation between prevalent cardio-renal target organ damage (TOD) and subsequent incident type 2 diabetes in a population-based study with high prevalence of obesity.MethodsWe selected 2887 non-diabetic participants from two cohorts of the Strong Heart Study (SHS). Clinical exam, laboratory tests and echocardiograms were performed. Adjudicated TODs were LVH, left atrium (LA) dilatation, and high urine albumin/creatinine ratio (UACR). Multivariable logistic regression models were used to identify variables responsible for the association between initial TODs and incident diabetes at 4-year follow-up (FU).ResultsAfter 4 years, 297 new cases of diabetes (10%) were identified, 216 of whom exhibited baseline impaired fasting glucose (IFG, 73%, p < 0.0001). Participants developing type 2 diabetes exhibited higher inflammatory markers, fat-free mass and adipose mass and higher prevalence of initial LVH and LA dilatation than those without (both p < 0.04). In multivariable logistic regression, controlling for age, sex, family relatedness, presence of arterial hypertension and IFG, all three indicators of TOD predicted incident diabetes (all p < 0.01). However, the effects of TOD was offset when body fat and inflammatory markers were introduced into the model.ConclusionsIn this population-based study with high prevalence of obesity, TOD precedes clinical appearance of type 2 diabetes and is related to the preceding metabolic status, body composition and inflammatory status.Trial registration Trial registration number: NCT00005134, Name of registry: Strong Heart Study, URL of registry: https://clinicaltrials.gov/ct2/show/NCT00005134, Date of registration: May 25, 2000, Date of enrolment of the first participant to the trial: September 1988
Highlights
Recent analyses in a registry of hypertensive patients suggested that preceding left ventricular (LV) hypertrophy (LVH) and/or carotid atherosclerosis are associated with incident type 2 diabetes, independent of confounders
Analyses performed in the hypertensive population of the Campania Salute Network (CSN) registry demonstrated that LV hypertrophy and/or carotid atherosclerosis are predictors of incident type 2 diabetes [6], independent of a number of confounders, including age, metabolic syndrome, family history of diabetes, duration of hypertension, and number and type of antihypertensive medications
The generalizability of the findings of the Campagna Salute Network hypertensive registry to unselected populations cohorts has not been evaluated. This analysis has been designed to evaluate the relation between prevalent target organ damage (TOD) and subsequent incident type 2 diabetes in the population of the Strong Heart Study (SHS), and to verify whether conditions associated to pre-diabetes help explain the association
Summary
Recent analyses in a registry of hypertensive patients suggested that preceding left ventricular (LV) hypertrophy (LVH) and/or carotid atherosclerosis are associated with incident type 2 diabetes, independent of confounders. Analyses performed in the hypertensive population of the Campania Salute Network (CSN) registry demonstrated that LV hypertrophy and/or carotid atherosclerosis are predictors of incident type 2 diabetes [6], independent of a number of confounders, including age, metabolic syndrome, family history of diabetes, duration of hypertension, and number and type of antihypertensive medications. The generalizability of the findings of the Campagna Salute Network hypertensive registry to unselected populations cohorts has not been evaluated This analysis has been designed to evaluate the relation between prevalent TOD and subsequent incident type 2 diabetes in the population of the Strong Heart Study (SHS), and to verify whether conditions associated to pre-diabetes help explain the association
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