Abstract
Purpose
Emerging data demonstrate that type 2 diabetes mellitus (T2DM) is associated with right ventricular (RV) dysfunction. A cutoff point of 155 mg/dL for the 1-hour (h) post-load plasma glucose, during oral glucose tolerance test (OGTT), identifies patients with normal glucose tolerance (NGT) at high risk to develop T2DM and cardiovascular (CV) disease. We investigated if 1-h post-load glucose may affect RV geometry and function in a group of never-treated hypertensive individuals.
Methods
We enrolled 446 Caucasian newly diagnosed hypertensive outpatients. All patients underwent an OGTT and a standard echocardiography. The tricuspid annular plane systolic excursion (TAPSE) and the RV fractional area change (RVFAC) were measured together with systolic pulmonary arterial pressure (s-PAP) and pulmonary vascular resistances (PVR). Insulin sensitivity was evaluated using the Matsuda index.
Results
Among all partecipants, 296 had NGT, 100 impaired glucose tolerance (IGT), and 50 T2DM. Considering the cutoff point of 155 mg/dl for 1-h glucose, NGT subjects were stratified into two groups: NGT < 155 (n = 207), NGT ≥ 155 (n = 89). Subjects NGT ≥ 155 presented a worse metabolic and inflammatory profile than NGT < 155. RV functional parameters (TAPSE, RVFAC, TAPSE/s-PAP, and TAPSE/PVR) were significantly reduced in NGT ≥ 155 subjects compared with NGT < 155 patients. On the contrary, s-PAP and PVR were significantly higher. At multiple regression analysis, 1-h glucose was the strongest predictor of TAPSE in NGT ≥ 155, IGT, and T2DM.
Conclusions
The presence of RV impairment in hypertensive NGT ≥ 155 subjects further complicates their CV burden and it may, at least in part, justify the worse clinical outcome in this setting of patients.
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Sciacqua, A., Perticone, M., Miceli, S. et al. Elevated 1-h post-load plasma glucose is associated with right ventricular morphofunctional parameters in hypertensive patients. Endocrine 64, 525–535 (2019). https://doi.org/10.1007/s12020-019-01873-5
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DOI: https://doi.org/10.1007/s12020-019-01873-5