In 40 patients undergoing transcatheter aortic valve implantation (TAVI), circulating short-chain fatty acid (SCFA) profiles shifted significantly within three months post-procedure, driven primarily by selective reductions in butyrate and isovalerate — despite minimal restructuring of overall gut microbial community composition. Critically, greater butyrate decline was inversely correlated with IL-18 elevation (rho=0.668, p<0.001), independent of valve calcification burden, hemodynamic improvement, and cardiac medications. Baseline isovalerate showed exploratory predictive value for 30-day adverse events (AUC 0.77).
This preprint — not yet peer-reviewed — opens a compelling mechanistic window into post-procedural cardiovascular inflammation. Butyrate is an established immunomodulator, known to suppress inflammasome activation and regulate intestinal barrier integrity. The butyrate-IL-18 connection is particularly noteworthy: IL-18 is a pro-inflammatory cytokine implicated in atherosclerosis progression and adverse cardiac remodeling, and its elevation post-TAVI may partly reflect gut metabolic disruption rather than purely hemodynamic stress. The finding that metabolite output changes while microbial community structure stays relatively stable suggests functional remodeling precedes compositional shifts — a distinction often missed in microbiome studies.
Limitations are significant: single-center design, small cohort of 40 patients, and observational methodology preclude causal conclusions. Whether butyrate supplementation or dietary fiber interventions could blunt post-TAVI inflammatory responses remains entirely untested. If confirmed in larger trials, however, this gut-metabolite-immune axis could represent a genuinely novel therapeutic target in structural heart disease recovery — an incremental but meaningfully directional finding.
