AI Article Synopsis

  • Sodium-glucose transport protein 2 inhibitors (SGLT2i) are beneficial for slowing kidney issues and improving outcomes in heart failure patients, but specific effects on amyloidosis are not well-studied.
  • A review of 79 patients with cardiac amyloidosis treated with dapagliflozin or empagliflozin showed minimal side effects, such as a low incidence of urinary tract infections and stable cardiac function over time.
  • The findings support the potential use of SGLT2i for treating amyloidosis-related heart and kidney problems, but more thorough studies are needed to verify safety and effectiveness.

Article Abstract

Sodium-glucose transport protein 2 inhibitors (SGLT2i) slow the progression of renal dysfunction and improve the prognosis of patients with heart failure. Amyloidosis constitutes an important subgroup for which evidence is lacking. Amyloidotic fibrils originating from misfolded transthyretin and light chains are the causal agents in ATTR and AL amyloidosis. In these most frequent subtypes, cardiac involvement is the most common organ manifestation. Because cardiac and renal function frequently deteriorate over time, even under best available treatment, SGLT2i emerge as a promising treatment option due to their reno- and cardioprotective properties. We retrospectively analyzed patients with cardiac amyloidosis, who received either dapagliflozin or empagliflozin. Out of 79 patients, 5.1% had urinary tract infections; 2 stopped SGLT2i therapy; and 2.5% died unrelated to the intake of SGLT2i. No genital mycotic infections were observed. As expected, a slight drop in the glomerular filtration rate was noted, while the NYHA functional status, cardiac and hepatic function, as well as the 6 min walk distance remained stable over time. These data provide a rationale for the use of SGLT2i in patients with amyloidosis and concomitant cardiac or renal dysfunction. Prospective randomized data are desired to confirm safety and to prove efficacy in this increasingly important group of patients.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10780141PMC
http://dx.doi.org/10.3390/jcm13010283DOI Listing

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