The development of heart failure (HF) is a common problem in patients with adult congenital heart disease (ACHD) and is one of the leading causes of death in this population. Therefore, timely diagnosis and management to reduce symptoms and improve survival rates is crucial. However, HF management in this heterogenous group of patients is challenging; the drug therapies with proven survival benefits in the general HF population are of limited value in ACHD. Sodium-glucose cotransporter 2 inhibitors (SGLT2I) represent one of the cornerstones of medical-therapy in patients with HF (1,2). Although the morbidity and mortality benefits of SGLT2I have been well demonstrated in general HF patients with reduced and preserved ejection fraction, data supporting the use of these agents in ACHD patients is scarce (3,4).
Kheiwa et al (5) evaluated the safety of SGLT2I in patients with ACHD. In this retrospective, single centre study, 18 patients with ACHD and HF who were started on SGLT2I as part of routine clinical care were included. All patients in this cohort received dapagliflozin 10 mg. 11 (61%) had moderate congenital heart disease (CHD), and 7 (39%) had severe CHD, including 4 with single ventricle physiology (3 post Fontan procedure, 1 with palliated single ventricle and Eisenmenger pathophysiology). Patients were assessed at baseline, prior to initialisation of SGLT2I, and within 6-month follow-up period. The primary safety endpoints included stable systolic blood pressure and renal function (including serum creatinine and sodium). The secondary endpoints included changes in weight, natriuretic peptides (NT-proBNP), and ejection fraction (EF).
No significant reduction in systolic blood pressure was observed (121.8 ± 20.8 mmHg before SGLT2I vs 114.0 ± 14.9 mmHg post SGLT2I initiation, p = 0.06). Renal function also remained stable during follow-up period (average creatinine at baseline 0.85 ± 0.18 mg/dL vs 0.89 ± 0.18 mg/dL on follow up, p = 0.07). Although serial NT-proBNP was available in only 5 of the included patients, the average value of NT-proBNP on follow-up was lower compared to baseline (1358 ± 2735 pg/mL vs 601 ± 786.1 pg/mL, p = 0.36). Similarly to previously published results on the use of SGLT2I in the general HF population, authors observed a significant decline in weight (78.9 ± 22.9 kg vs 76.0 ± 23.0 kg, p = 0.0039), which is attributed to loss of plasma volume with increased diuresis of extracellular volume, reduction in adipose tissue and daily urine negative calorie loss.
In summary, in this study published in the International Journal of Cardiology Congenital Heart Disease (5), the use of SGLT2I was well-tolerated during short term follow up in the heterogenous cohort of ACHD patients, which for the first time also included the most complex CHD, including single ventricle physiology. These promising results add to the scarce data on the use of SGLT2I in ACHD patients with HF. Nevertheless, longer, prospective, multicentric studies are needed to better characterise the safety and potential efficacy of SGLT2I in patients with ACHD.
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