Gouty tophi predict cardiovascular remodeling

By Lynda Williams, Senior medwireNews Reporter

Research shows that the severity of gout, rather than uric acid level, is significantly associated with changes in left ventricular (LV) diastolic function and left atrial volume (LAV).

The study, published in Rheumatology, reveals that serum uric acid levels did not significantly differ between 30 patients with asymptomatic hyperuricemia, 58 patients with gouty arthritis but no tophi, and 50 patients with gouty tophi.

LV mass was significantly higher in patients with tophi than patients with less advanced gout and when compared with 35 individuals without elevated uric acid, report Kuo-Li Pan (Chang Gung Memorial Hospital, Taiwan) and co-workers.

There was no significant difference in LV or right ventricular systolic function between the four groups, diastolic peak early or late transmitral flow velocity, or the ratio of early to late velocities.

However, both the ratio of transmitral and myocardial peak early diastolic velocities (E/e') – a marker of LV filling pressure – and the left atrial volume (LAV) significantly progressed with severity of gout.

E/e' was 10.5 for patients with tophi compared with 9.7 for those with gouty arthritis and 8.8 for asymptomatic patients, while individuals with normal uric acid levels had an E/e' of 8.6.

And maximal, minimal, and precontraction LAV index values significantly increased with gout progression, peaking in patients with tophi at 29.6, 9.6, and 19.1 mL/m², respectively.

Indeed, the researchers calculated that for patients with gouty arthritis, each 1 mL/m² increase in maximal LAV index was associated with a 6.8% increase in the likelihood for tophi.

Noting that there was no significant correlation between LAV index and uric acid, the researchers write that “the severity of gout, not serum [uric acid] levels per se, affects LA volume remodelling.”

They therefore conclude: “Thus several factors may play an important role in LA remodelling in gout patients, including oxidative stress mediated by active xanthine oxidase, the duration of inflammation and inflammation mediated by monosodium urate crystals.”

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