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# L-carnitine supplements help ventricular fibrosis, heart failure
- URL: https://www.foodconsumer.org/l-carnitine_0718120904/
- Published: 2012-07-17T22:03:00.000Z
- Updated: 2026-09-22T16:09:09.000Z
- Description: In rats with hypertensive heart failure with preserved ejection fraction, L-carnitine restored left-ventricular free carnitine, eased fibrosis and stiffening, prevented pulmonary congestion and improved survival. The authors tie the effect to arachidonic acid and prostacyclin production.
- Author: Food Consumer
- Tags: Supplements, Nutrition, #vivvo-import

By David Liu, PHD

Tuesday July 18, 2012 (foodconsumer.org) -- Prognosis of heart failure with preserved ejection fraction (HPpEF) remains poor, but L-carnitine supplementation may help the patients, according to a anew study published in the July 12, 2012 issue of Journal of Hypertension.

The study led by Y. Omori of Osaka University in Japan and colleagues showed that after receiving L-carnitine supplements, rats with hypertensive HPpEF and decreased free-carnitine levels "restored left-ventricular free-carnitine levels, attenuated left-ventricular fibrosis and stiffening, prevented pulmonary congestion, and improved survival in the HFpEF model independent of the antihypertensive effects, accompanied with increased expression of fatty acid desaturase (FADS) 1/2, rate-limiting enzymes in forming arachidonic acid, and enhanced production of arachidonic acid, a precursor of prostacyclin, and prostacyclin in the LV. (left ventricle )."

The researcher also found that "In cultured cardiac fibroblasts, L-carnitine attenuated the angiotensin II-induced collagen production with increased FADS1/2 expression and enhanced production of arachidonic acid and prostacyclin" and "L-Carnitine-induced increase of arachidonic acid was canceled by knock-down of FADS1 or FADS2 in cultured cardiac fibroblasts."

They concluded "L-carnitine supplementation attenuates cardiac fibrosis by increasing prostacyclin production through arachidonic acid pathway, and may be a promising therapeutic option for HFpEF."