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Sitagliptin e scompenso cardiaco

Gli inibitori della DPP-4 stanno avendo un buon successo grazie alla loro efficacia nel controllo metabolico del diabete, alla buona tolleranza ed al fatto che alcuni studi attribuiscono loro un effetto positivo sulla funzione cardio-renale, e su alcuni fattori di rischio per l'aterosclerosi quali LDL, HDL e pressione arteriosa. Dati discordanti però emergono dagli studi che hanno valutato l'incidenza di eventi cardiovascolari. Da alcuni di questi studi emergono effetti positivi, da altri un effetto neutro. In uno studio recente, la terapia con saxagliptin è risultata associata ad un aumento del rischio di insufficienza cardiaca, uno studio con alogliptin non ha invece trovato alcuna relazione tra l'uso del farmaco e lo scompenso cardiaco in diabetici con cardiopatia ischemica. Nello studio della Weir, solo nei pazienti diabetici con già una storia di insufficienza cardiaca, la terapia con sitagliptin è risultata associata ad un rischio aumentato di ricovero per scompenso cardiaco. Lo studio soffre però di alcuni aspetti discutibili, primo dei quali la raccolta dei dati basata su archivi delle assicurazioni.

Sitagliptin Use in Patients With Diabetes and Heart Failure. A Population-Based Retrospective Cohort Study.

Daniala L. Weir, McAlister FA, Senthilselvan A, Minhas-Sandhu JK, Eurich DT

J Am Coll Cardiol HF 2014;2:573-582

Objectives: The study objective was to evaluate the effects of sitagliptin in patients with type 2 diabetes (T2D) and heart failure (HF).
Background: There is uncertainty in the literature about whether dipeptidyl peptidase (DPP)-4 inhibitors cause harm in patients with HF and T2D.
Methods: We analyzed data from a national commercially insured U.S. claims database. Patients with incident HF were identified from individuals with T2D initially treated with metformin or sulfonylurea and followed over time. Subjects subsequently using sitagliptin were compared with those not using sitagliptin in the 90 days before our primary outcome of all-cause hospital admission or death using a nested case-control analysis after adjustment for demographics and clinical and laboratory data. HF-specific hospital admission or death also was assessed.
Results: A total of 7,620 patients with diabetes and incident HF met our inclusion criteria. Mean (SD) age was 54 years (9), and 58% (3,180) were male. Overall, 887 patients (12%) were exposed to sitagliptin therapy (521 patient years of exposure) after incident HF. Our primary composite endpoint occurred in 4,137 patients (54%). After adjustment, sitagliptin users were not at an increased risk for the primary endpoint (7.1% vs. 9.2%, adjusted odds ratio [aOR]: 0.84, 95% confidence interval [CI]: 0.69 to 1.03) or each component (hospital admission 7.5% vs. 9.2%, aOR: 0.93, 95% CI: 0.76 to 1.14; death 6.9% vs. 9.3%, aOR: 1.16, 95% CI: 0.68 to 1.97). However, sitagliptin use was associated with an increased risk of HF hospitalizations (12.5% vs. 9.0%, aOR: 1.84, 95% CI: 1.16 to 2.92).
Conclusions: Sitagliptin use was not associated with an increased risk of all-cause hospitalizations or death, but was associated with an increased risk of HF-related hospitalizations among patients with T2D with pre-existing HF.

J Am Coll Cardiol HF 2014;2:573-582