⁶⁸Ga-DOTATATE Measurements Predict Progression of Aortic Valve Calcification in Humans

Inflammation potentiates aortic valve calcification (AVC). ⁶⁸Ga-DOTATATE (gallium-68 DOTA-(Tyr³)-octreotate), a positron emission tomography tracer that binds to somatostatin receptors, provides a measure of tissue inflammation. However, the diagnostic and prognostic values of aortic valve (AV) ⁶⁸Ga-DOTATATE uptake in AVC remain unexplored. Here, we tested whether AV ⁶⁸Ga-DOTATATE uptake predicts the progression of AVC.

A total of 683 individuals (median age, 63 years; 46% male) underwent clinical ⁶⁸Ga-DOTATATE positron emission tomography/computed tomography imaging from 2017 to 2023; 209 had follow-up imaging (median, 1.3 years interval). AV inflammation was measured as the maximum standardized uptake value of ⁶⁸Ga-DOTATATE uptake within the AV on baseline positron emission tomography/computed tomography. AVC was quantified on baseline and follow-up computed tomography scans (Hounsfield units >130). AVC progression was assessed as the difference between baseline and follow-up AVC. Individuals with a square root difference of annualized AVC change ≥2.5 were characterized as progressors and <2.5 as nonprogressors. Demographic and clinical data were collected from medical records.

Baseline AV ⁶⁸Ga-DOTATATE uptake correlated with baseline AVC (standardized ρ=0.12; P=0.002). Furthermore, baseline AV ⁶⁸Ga-DOTATATE uptake associated with AVC progression (odds ratio [OR], 3.0 [95% CI, 1.4-6.4]; P=0.004) and remained significant after separately adjusting for baseline AVC (OR, 3.1 [95% CI, 1.5-6.6]), sex (OR, 4.0 [95% CI, 1.7-9.0]), hypertension (OR, 2.8 [95% CI, 1.3-6.2]), diabetes (OR, 3.0 [95% CI, 1.4-6.4]), hyperlipidemia (OR, 2.4 [95% CI, 1.1-5.3]), smoking (OR, 3.1 [95% CI, 1.5-6.7]), chronic kidney disease (OR, 2.9 [95% CI, 1.4-6.3]), and body mass index (OR, 3.0 [95% CI, 1.4-6.3]), became insignificant when adjusting to age (OR, 1.9 [95% CI, 0.8-4.3]).

Our study highlights the use of ⁶⁸Ga-DOTATATE for assessing AV inflammation and predicting AVC progression. These findings underscore the role of inflammation in AVC progression and have potential implications for risk assessment and evaluating therapies in AV disease.