Sodium-glucose cotransporter-2 inhibitors reduce cardiovascular outcomes in patients with congestive heart failure and a biventricular circulation. Congestive heart failure in Fontan univentricular circulation is distinctly different. Experience with sodium-glucose cotransporter-2 inhibitors in this group has not yet been well described.

This work describes safety and tolerability of sodium-glucose cotransporter-2 inhibitors in patients with Fontan circulation.

Single-centre review of patients with Fontan circulation prescribed a sodium-glucose cotransporter-2 inhibitors for congestive heart failure. Primary outcome was tolerability or need for discontinuation. Secondary outcomes were changes in New York Heart Association class, congestive heart failure hospitalisation, ventricular function, exercise performance, and laboratory values.

We identified 25 patients with Fontan circulation prescribed an sodium-glucose cotransporter-2 inhibitors, most with a systemic right ventricle. Over a third of subjects had at least moderately reduced baseline ventricular function. Baseline catheterisation showed a mean Fontan pressure of 17.1 ± 3.7 mmHg and pulmonary capillary wedge pressure 11.7 ± 3.2 mmHg at rest; 59% had occult diastolic dysfunction with abnormal pulmonary capillary wedge pressure elevation following volume expansion. Most were on congestive heart failure medications and/or a pulmonary vasodilator prior to sodium-glucose cotransporter-2 inhibitors addition, and three had a congestive heart failure hospitalisation within the previous year. All reported good medication tolerance except one patient was nonadherent to medications and two discontinued sodium-glucose cotransporter-2 inhibitors for perceived side effects. There were no significant differences in secondary outcomes. There was, however, a downward trend of serum brain natriuretic peptide (n = 13) and improved peak VO2 (n = 6), though neither statistically significant (p > 0.05).

This series, the largest published to date, suggests that sodium-glucose cotransporter-2 inhibitors are safe and tolerable congestive heart failure therapy in Fontan circulation. Further research is warranted to explore therapy in this unique population.

In the National Institutes of Health (NIH) Clinical Center, patients colonized or infected with vancomycin-resistant Enterococcus (VRE) are placed in contact isolation until they are deemed “decolonized,” defined as having 3 consecutive perirectal swabs negative for VRE. Some decolonized patients later develop recurrent growth of VRE from surveillance or clinical cultures (ie, “recolonized”), although that finding may represent recrudescence or new acquisition of VRE. We describe the dynamics of VRE colonization and infection and their relationship to receipt of antibiotics.

In this retrospective cohort study of patients at the National Institutes of Health Clinical Center, baseline characteristics were collected via chart review. Antibiotic exposure and hospital days were calculated as proportions of VRE decolonized days. Using survival analysis, we assessed the relationship between antibiotic exposure and time to VRE recolonization in a subcohort analysis of 72 decolonized patients.

In total, 350 patients were either colonized or infected with VRE. Among polymerase chain reaction (PCR)-positive, culture (Cx)-negative (PCR+/Cx−) patients, PCR had a 39% positive predictive value for colonization. Colonization with VRE was significantly associated with VRE infection. Among 72 patients who met decolonization criteria, 21 (29%) subsequently became recolonized. VRE recolonization was 4.3 (P = .001) and 2.0 (P = .22) times higher in patients with proportions of antibiotic days and antianaerobic antibiotic days above the median, respectively.

Colonization is associated with clinical VRE infection and increased mortality. Despite negative perirectal cultures, re-exposure to antibiotics increases the risk of VRE recolonization.