N-Terminal Prosomatostatin as a Risk Marker for Cardiovascular Disease and Diabetes in a General Population

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Abstract

Context:

Somatostatin inhibits a range of hormones, including GH, insulin, and glucagon, but little is known about its role in the development of cardiometabolic disease.

Objective:

The objective of the study was to investigate whether fasting plasma concentration of N-terminal prosomatostatin (NT-proSST) is associated with the development of diabetes, coronary artery disease (CAD), and mortality.

Design, Setting, and Participants:

NT-proSST was measured in plasma from 5389 fasting participants of the population-based study Malmö Preventive Project, with a mean baseline age of 69.4 ± 6.2 years. Cox proportional hazards models adjusted for traditional cardiovascular risk factors were used to investigate the relationships between baseline NT-proSST and end points, with a mean follow-up of 5.6 ± 1.4 years.

Main Outcome Measures:

CAD, diabetes, and mortality were measured.

Results:

Overall, NT-proSST (hazard ratio [HR] per SD increment of log transformed NT-proSST) was unrelated to the risk of incident diabetes (220 events; HR 1.05; 95% confidence interval [CI] 0.91–1.20; P = .531) but was related to the risk of incident CAD (370 events; HR 1.17; 95% CI 1.06–1.30; P = .003), all-cause mortality (756 events; HR 1.24; 95% CI 1.15–1.33; P < .001), and cardiovascular mortality (283 events; HR 1.33; 95% CI 1.19–1.43; P < .001). The relationships were not linear, with most of the excess risk observed in subjects with high values of NT-proSST. Subjects in the top vs bottom decile had a severely increased risk of incident CAD (HR 2.41; 95% CI 1.45–4.01; P < .001), all-cause mortality (HR 1.84; 95% CI 1.33–2.53; P < .001), and cardiovascular mortality (HR 2.44; 95% CI 1.39–4.27; P < .001).

Conclusion:

NT-proSST was significantly and independently associated with the development of CAD, all-cause mortality, and cardiovascular mortality.

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