Thamali Ayagama

Abstract Atrial fibrillation (AF) increases energy demand in atrial myocytes, yet the mitochondrial mechanisms underlying this stress remain poorly defined. Using previously published proteomic data from left atrial tissue of AF and sham-operated goats, we performed organelle-specific bioinformatic analyses of the mitochondrial fraction. Over-representation and consensus pathway analyses consistently highlighted enrichment of oxidative phosphorylation (OXPHOS) subunits.

1 INTRODUCTION Congestive cardiac failure (CHF) is associated with high resting sympathetic drive, leading to increased release of noradrenaline (Cohn et al., 1984) and the cotransmitter neuropeptide Y (NPY) (Ajijola et al., 2020; Hulting et al., 1990; Maisel et al., 1989; McDowell et al., 2024), in addition to vagal withdrawal (La Rovere et al., 1998; Nolan et al., 1998), which are indicators of poor prognosis for morbidity and mortality (Herring, Kalla et al., 2019).

In 1902, Bayliss first described that an isolated blood vessel responds to an increase in intravascular pressure with a paradoxical decrease in diameter, and vice versa (Bayliss, 1902). Thus was borne the concept of autoregulation of blood flow and, indeed, even today, the assessment of myotonic tone through pressure myography remains the gold standard for measuring blood vessel reactivity (Wilson et al., 2022).