Abstract
Background—During heart failure (HF), cardiac metabolic substrate preference changes from fatty acid (FA) toward glucose oxidation. This change may cause progression toward heart failure. We hypothesize that a diet rich in FAs may prevent this process, and that dietary ¿3-FAs have an added antiarrhythmic effect based on action potential (AP) shortening in animals with HF.
Methods and Results—Rabbits were fed a diet containing 1.25% (w/w) high oleic sunflower oil (HF-¿9, N=11), 1.25% fish oil (HF-¿3, N=11), or no supplement (HF-control, N=8). Subsequently, HF was induced by volume and pressure overload. After 4 months, HF-parameters were assessed, electrocardiograms were recorded, and blood and ventricular tissue were collected. Myocytes were isolated for patch clamp or intracellular Ca2+- recordings to study electrophysiologic remodeling and arrhythmogenesis. Both the HF-¿9 and the HF-¿3 groups had larger myocardial FA oxidation capacity than HF control. The HF-¿3 group had significantly lower mean (± SEM) relative heart and lung weight (3.3±0.13 and 3.2±0.12 g kg-1, respectively) than HF control (4.8±0.30 and 4.5±0.23), and shorter QTc intervals (167±2.6 versus 182±6.4). The HF-¿9 also displayed a significantly reduced relative heart weight (3.6±0.26), but had similar QTc (179±4.3) compared with HF control. AP duration in the HF-¿3 group was ˜20% shorter due to increased Ito1 and IK1 and triggered activity, and Ca2+-aftertransients were less than in the HF-¿9 group.
Conclusions—Dietary unsaturated FAs started prior to induction of HF prevent hypertrophy and HF. In addition, fish oil FAs prevent HF-induced electrophysiologic remodeling and arrhythmias.
Methods and Results—Rabbits were fed a diet containing 1.25% (w/w) high oleic sunflower oil (HF-¿9, N=11), 1.25% fish oil (HF-¿3, N=11), or no supplement (HF-control, N=8). Subsequently, HF was induced by volume and pressure overload. After 4 months, HF-parameters were assessed, electrocardiograms were recorded, and blood and ventricular tissue were collected. Myocytes were isolated for patch clamp or intracellular Ca2+- recordings to study electrophysiologic remodeling and arrhythmogenesis. Both the HF-¿9 and the HF-¿3 groups had larger myocardial FA oxidation capacity than HF control. The HF-¿3 group had significantly lower mean (± SEM) relative heart and lung weight (3.3±0.13 and 3.2±0.12 g kg-1, respectively) than HF control (4.8±0.30 and 4.5±0.23), and shorter QTc intervals (167±2.6 versus 182±6.4). The HF-¿9 also displayed a significantly reduced relative heart weight (3.6±0.26), but had similar QTc (179±4.3) compared with HF control. AP duration in the HF-¿3 group was ˜20% shorter due to increased Ito1 and IK1 and triggered activity, and Ca2+-aftertransients were less than in the HF-¿9 group.
Conclusions—Dietary unsaturated FAs started prior to induction of HF prevent hypertrophy and HF. In addition, fish oil FAs prevent HF-induced electrophysiologic remodeling and arrhythmias.
Original language | English |
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Pages (from-to) | 376-384 |
Number of pages | 9 |
Journal | Circulation. Heart Failure |
Volume | 5 |
Issue number | 3 |
Early online date | 2 Apr 2012 |
DOIs | |
Publication status | Published - 2012 |