Summary: In this small randomized trial of 80 patients with poorly controlled arterial hypertension and prediabetes, adding sustained-release indapamide or moxonidine to perindopril and metformin produced statistically significant and comparable improvements in left ventricular myocardial structure and function and in intrarenal vascular resistance after 24 weeks. Neither regimen was superior for organ protection; the moxonidine arm showed a more pronounced fall in fasting plasma insulin.
PICO Summary
| Element | Detail |
|---|---|
| Population | 80 patients with poorly controlled arterial hypertension and prediabetes (diagnosed by oral glucose tolerance test); single-centre randomized controlled trial, Russian Federation. |
| Intervention | Perindopril 5 mg/day, sustained-release indapamide 1.5 mg/day, and metformin 1000 mg/day; perindopril titrated to maximum tolerated dose (group 1, n=40). |
| Comparison | Perindopril 5 mg/day, moxonidine 0.2 mg/day, and metformin 1000 mg/day; perindopril and moxonidine titrated to maximum tolerated dose (group 2, n=40). |
| Outcome | At 24 weeks, among patients reaching target blood pressure, both groups had statistically significant and comparable improvements in all measured left ventricular structural and functional indices and in intrarenal vascular resistance, with comparable normalization of LV geometry and diastolic function. The moxonidine combination produced a significantly greater decrease in fasting plasma insulin than the diuretic combination. No effect sizes, 95% confidence intervals, between-group p values, or ARR/NNT were reported in the abstract. |
Expert Commentary
This is a small single-centre randomized trial, and its central message is one of equivalence rather than advantage: an indapamide-based and a moxonidine-based regimen, each built on perindopril and metformin, delivered comparable improvements in left ventricular geometry, diastolic function, and intrarenal vascular resistance over 24 weeks. The headline therefore should not be read as one combination protecting organs better than the other. The only consistent between-arm difference was metabolic, with moxonidine producing a more pronounced reduction in fasting plasma insulin, which is mechanistically plausible for a centrally acting sympatholytic in an insulin-resistant population. The limitations are substantial and should temper any firm conclusion. With only 40 patients per arm, the study is underpowered to exclude clinically meaningful differences, the surrogate imaging endpoints were assessed without reported blinding, and the abstract provides no effect sizes, confidence intervals, or between-group p values to gauge precision. Can I use this with my patients? Not as a basis for choosing one regimen over the other on organ-protection grounds; both remain reasonable add-ons to an ACE inhibitor in hypertension with early dysglycaemia, and the modest insulin signal favouring moxonidine is hypothesis-generating only. Larger, adequately powered and blinded trials with hard cardiovascular and renal endpoints are needed before the metabolic edge translates into a practice recommendation.
References
Skibitsky VV, Gutova SR, Fendrikova AV. Potential of Combination Pharmacotherapy in Patients with Arterial Hypertension and Prediabetes: Focus on Organ Protection. Kardiologiia. 2025;65(3):26-34. doi:10.18087/cardio.2025.3.n2902