BMC Cardiovascular Disorders (Mar 2004)

Reversibility of stress-echo induced ST-segment depression by long-term oral n-3 PUFA supplementation in subjects with chest pain syndrome, normal wall motion at stress-echo and normal coronary angiogram

  • Ziacchi Vigilio,
  • Gaibazzi Nicola

DOI
https://doi.org/10.1186/1471-2261-4-1
Journal volume & issue
Vol. 4, no. 1
p. 1

Abstract

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Abstract Background Normal coronary arteries may coexist with abnormal coronary and systemic endothelial function in patients with chest pain. Recent work by the renowned Pisa echo-group elegantly suggests that isolated ST-segment depression during stress-echo (SE) can be used as a marker of coronary endothelial dysfunction, in the absence of stress-inducible wall motion abnormalities and in the absence of angiographically-significant coronary artery disease (CAD). The long chain n-3 polyunsaturated fatty acids (PUFAs) have been reported to possess several properties that may positively influence vascular function. The present study's hypothesis is that a 4 month-course of oral supplementation with n-3 PUFAs can reverse endothelial dysfunction. Methods Subjects were selected on the basis of the following criteria: 1) reported chest pain syndrome, 2) significant ST-segment depression during an otherwise normal SE, 3) absence of angiographically-significant CAD. Subjects underwent a 4-month course of oral supplementation with commercially available n-3 PUFA, 1 g once a day. Normalization of endothelial dysfunction was defined, at the end of the supplementation period, by the absence of significant ST-segment depression during repeat SE. We tested the aforementioned hypothesis in a very small series of consecutive subjects, with the intent to produce a hypothesis-generating study. Results Seven out of the total nine subjects enrolled (77.8%) had normal ST-segment during repeat SE performed after the 4 month course of therapy. Conclusions A striking rate of reversion of SE-induced ST-segment depression after oral n-3 PUFAs suggests reversion of coronary endothelial dysfunction; nonetheless these data need to be validated in larger, placebo-controlled studies.

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