Renal and cardiac effects of salt loading in ambulatory heart failure patients

Abstract

73 p < 0.01) and, moreover, we also documented a higher sacubitril/valsartan prescription (67% vs 55%; p = 0.06) instead of lower loop diuretics use (47% vs 35%, p = 0.05). Mineralocorticoid receptor antagonist (77% vs 83%; p = 0.19) and beta blockers (94% in both groups) therapy did not change. With a total median follow-up of 19 months (Q1-Q3: 9-36), Kaplan-Meier mortality analysis was represented in Figure 1. Conclusions: In our centers, since SGLT2-i approval for HFrEF, there exists a fast joining of SGLT2-i to HFrEF therapy. It could help us to accomplish lower rates of loop diuretics prescription enabling a better titration of drugs with proven positive impact in remodelling and morbimortality. These results support in real-world the provider role of SGLT2-i, explaining a higher increase of left ventricular ejection fraction in post SGLT2-i group, with a non-statistically significant trend to lower mortality probably due to a small follow-up. Follow-up clinical visit Figure 1. Funding Acknowledgements: Type of funding sources: None. Background: Patients with hypotension have consistently been excluded from heart failure (HF) randomized controlled trials. This group of HF patients is largely unstudied. We aimed to characterize HF patients with hypotension. Methods: We retrospectively studied adult outpatients with systolic dysfunction followed in our HF clinic from January 2012 to December 2020. Patients without blood pressure measurement on the index visit (first medical visit) were excluded. We defined hypotension as systolic blood pressure (SBP) of less than 100 mmHg. The endpoint under analysis was all-cause mortality. Patients were followed until January 2023. Patients with hypotension were compared with the remaining. A Cox-regression analysis was used to assess the prognostic impact of hypotension and to study the prognostic impact of evidence-based therapy separately in HF patients with SPB < 100mmHg and those with SPB ≥ 100mmHg. Adjustments were made considering potential confounders. Results: We studied 1206 chronic ambulatory HF patients, 64.9% male, mean age 71 years, 47.4% with severe systolic dysfunction. Regarding the medication in use, 91.4% were on beta blockers (BB), 82.8% were on renin angiotensin system inhibitors (RASi), including angiotensin converting enzyme inhibitors, angiotensin receptor blockers or angiotensin receptor neprilysin inhibitors; 29.6% were on min-eralocorticoid receptor antagonists (MRA). A total of 157 patients (13.0%) presented SBP < 100mmHg on the index visit. Hypotensive patients more often presented atrial fibrillation and severe systolic dysfunction; they had lower haemoglobin values and higher brain natriuretic peptide (BNP) levels. Patients with hypotension were less medicated with RASi (70.7% vs 84.6%, p < 0.001) but more with MRA (39.6% vs 28.1%, p = 0.004) and diuretics (86.6% vs 78.6%, p = 0.02). There were no differences regarding BB use between both groups. During a median follow-up of 47 (27-85) months 645 (53.5%) patients died, 61.1% in those with hypotension and 52.3% in the remaining, p = 0.04. The use of RASi in hypotensive patients was associated with better survival (HR = 0.42 (0.26-0.69)) as in those with SPB ≥ 100mmHg (HR = 0.64 (0.51-0.80)). Contrarily to patients with SPB ≥ 100mmHg, in those with hypotension, BB use was not associated with survival benefit (HR = 0.61 (0.46-0.81) and 0.98 (0.48-1.97), respectively). MRA use showed no prognostic impact in either group. Conclusions: Hypotension was associated with poor prognosis in HF patients. In HF patients with SBP < 100mmHg, BB and MRA use did not impact prognosis, however, RASi use portended a survival benefit. Despite their exclusion from most HF therapy trials, hypotensive patients might benefit from RASi drugs. Renal and cardiac effects of salt loading in ambulatory heart failure patients Funding Acknowledgements: Type of funding sources: Public grant(s)-National budget only. Main funding source(s): Hartfalenfonds ZOL-UHasselt Limburg Sterk Merk Background: Current guidelines recommend to limit sodium intake in heart failure (HF) patients. However, stringent sodium restriction can increase neurohormonal activation, decrease quality of life and was not advantageous in recent trials. In addition, recent studies suggest that the skin can function as a sodium buffer. Purpose: To study effects and handling of an increased salt load in patients with HF and reduced ejection fraction. Methods: Eighteen patients with HF and left ventricular ejection fraction < 40% and 10 age-and sex-matched healthy volunteers without cardiovascular disease were included. HF patients with severe right ventricular dysfunction, eGFR < 30 mL/min/1.73 m 2 or severe valvular dysfunction were excluded. After 2 weeks of run-in, all study participants received 3 grams of sodium chloride (capsules of 1 g three times daily) on top of their usual diet for 4 weeks. Patients were evaluated at inclusion, at 2 weeks (end of run-in), 4 weeks (2 weeks of sodium chloride intake) and 6 weeks (4 weeks of sodium chloride intake). At each evaluation, clinical parameters, Everest congestion score, lab, echocardiography, 24-hour urine collection and bio-impedance measurements of total body water were performed. Blood volume and plasma volume were assessed using a radio-labeled red blood cells dilution technique before salt loading (at 2 weeks) and and the end of the study (at 6 weeks). At the same time points, a skin biopsy was taken at the lower leg to assess skin sodium content and glycosaminoglycan content. Results: Mean age was 66 ± 8 years, 2 (11.1%) were female, median LVEF was 35 (31-39) %, median eGFR was 68 (51-74) mL/min/1.73 m 2 and median NT-proBNP was 431 (275-961) ng/L at baseline and all patients were optimally treated medically. Salt loading did not influence weight, blood pressure, congestion score or NT-proBNP (Figure 1). There was no significant change in total body water (from 46.87 L to 44.41 L; p = 0.780), plasma volume (2735 mL vs. 2904 mL; p = 0.231) and total blood volume (4748 mL vs. 4885 mL; p = 0.327). Renal sodium excretion increased from 150 ± 55 mmol/24h to 173 ± 58 mmol/24h (p = 0.024), while plasma renin decreased from 286 (25-550) í µí¼ U/L to 88 (19-362) í µí¼ U/L (p = 0.002) (Figure 2). Salt loading did not significantly influence LVEF (from 35% to 35%; p = 0.801), left