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A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload
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| Zeitschriftentitel: | Circulation: Heart Failure |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , |
| In: | Circulation: Heart Failure, 5, 2012, 3, S. 376-384 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Den Ruijter, Hester M. Verkerk, Arie O. Schumacher, Cees A. Houten, Sander M. Belterman, Charly N.W. Baartscheer, Antonius Brouwer, Ingeborg A. van Bilsen, Marc de Roos, Baukje Coronel, Ruben Den Ruijter, Hester M. Verkerk, Arie O. Schumacher, Cees A. Houten, Sander M. Belterman, Charly N.W. Baartscheer, Antonius Brouwer, Ingeborg A. van Bilsen, Marc de Roos, Baukje Coronel, Ruben |
|---|---|
| author |
Den Ruijter, Hester M. Verkerk, Arie O. Schumacher, Cees A. Houten, Sander M. Belterman, Charly N.W. Baartscheer, Antonius Brouwer, Ingeborg A. van Bilsen, Marc de Roos, Baukje Coronel, Ruben |
| spellingShingle |
Den Ruijter, Hester M. Verkerk, Arie O. Schumacher, Cees A. Houten, Sander M. Belterman, Charly N.W. Baartscheer, Antonius Brouwer, Ingeborg A. van Bilsen, Marc de Roos, Baukje Coronel, Ruben Circulation: Heart Failure A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload Cardiology and Cardiovascular Medicine |
| author_sort |
den ruijter, hester m. |
| spelling |
Den Ruijter, Hester M. Verkerk, Arie O. Schumacher, Cees A. Houten, Sander M. Belterman, Charly N.W. Baartscheer, Antonius Brouwer, Ingeborg A. van Bilsen, Marc de Roos, Baukje Coronel, Ruben 1941-3289 1941-3297 Ovid Technologies (Wolters Kluwer Health) Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1161/circheartfailure.111.963116 <jats:sec> <jats:title>Background—</jats:title> <jats:p>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 ω3-FAs have an added antiarrhythmic effect based on action potential (AP) shortening in animals with HF.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods and Results—</jats:title> <jats:p> Rabbits were fed a diet containing 1.25% (w/w) high oleic sunflower oil (HF-ω9, N=11), 1.25% fish oil (HF-ω3, 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 Ca <jats:sup>2+</jats:sup> - recordings to study electrophysiologic remodeling and arrhythmogenesis. Both the HF-ω9 and the HF-ω3 groups had larger myocardial FA oxidation capacity than HF control. The HF-ω3 group had significantly lower mean (± SEM) relative heart and lung weight (3.3±0.13 and 3.2±0.12 g kg <jats:sup>−1</jats:sup> , 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-ω9 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-ω3 group was ≈20% shorter due to increased I <jats:sub>to1</jats:sub> and I <jats:sub>K1</jats:sub> and triggered activity, and Ca <jats:sup>2+</jats:sup> -aftertransients were less than in the HF-ω9 group. </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions—</jats:title> <jats:p>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.</jats:p> </jats:sec> A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload Circulation: Heart Failure |
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10.1161/circheartfailure.111.963116 |
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Ovid Technologies (Wolters Kluwer Health), 2012 |
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Ovid Technologies (Wolters Kluwer Health), 2012 |
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1941-3289 1941-3297 |
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1941-3289 1941-3297 |
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denruijter2012adietrichinunsaturatedfattyacidspreventsprogressiontowardheartfailureinarabbitmodelofpressureandvolumeoverload |
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2012 |
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Ovid Technologies (Wolters Kluwer Health) |
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ai |
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Circulation: Heart Failure |
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49 |
| title |
A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_unstemmed |
A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_full |
A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_fullStr |
A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_full_unstemmed |
A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_short |
A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_sort |
a diet rich in unsaturated fatty acids prevents progression toward heart failure in a rabbit model of pressure and volume overload |
| topic |
Cardiology and Cardiovascular Medicine |
| url |
http://dx.doi.org/10.1161/circheartfailure.111.963116 |
| publishDate |
2012 |
| physical |
376-384 |
| description |
<jats:sec>
<jats:title>Background—</jats:title>
<jats:p>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 ω3-FAs have an added antiarrhythmic effect based on action potential (AP) shortening in animals with HF.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Methods and Results—</jats:title>
<jats:p>
Rabbits were fed a diet containing 1.25% (w/w) high oleic sunflower oil (HF-ω9, N=11), 1.25% fish oil (HF-ω3, 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 Ca
<jats:sup>2+</jats:sup>
- recordings to study electrophysiologic remodeling and arrhythmogenesis. Both the HF-ω9 and the HF-ω3 groups had larger myocardial FA oxidation capacity than HF control. The HF-ω3 group had significantly lower mean (± SEM) relative heart and lung weight (3.3±0.13 and 3.2±0.12 g kg
<jats:sup>−1</jats:sup>
, 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-ω9 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-ω3 group was ≈20% shorter due to increased I
<jats:sub>to1</jats:sub>
and I
<jats:sub>K1</jats:sub>
and triggered activity, and Ca
<jats:sup>2+</jats:sup>
-aftertransients were less than in the HF-ω9 group.
</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Conclusions—</jats:title>
<jats:p>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.</jats:p>
</jats:sec> |
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| author | Den Ruijter, Hester M., Verkerk, Arie O., Schumacher, Cees A., Houten, Sander M., Belterman, Charly N.W., Baartscheer, Antonius, Brouwer, Ingeborg A., van Bilsen, Marc, de Roos, Baukje, Coronel, Ruben |
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| author_sort | den ruijter, hester m. |
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| description | <jats:sec> <jats:title>Background—</jats:title> <jats:p>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 ω3-FAs have an added antiarrhythmic effect based on action potential (AP) shortening in animals with HF.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods and Results—</jats:title> <jats:p> Rabbits were fed a diet containing 1.25% (w/w) high oleic sunflower oil (HF-ω9, N=11), 1.25% fish oil (HF-ω3, 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 Ca <jats:sup>2+</jats:sup> - recordings to study electrophysiologic remodeling and arrhythmogenesis. Both the HF-ω9 and the HF-ω3 groups had larger myocardial FA oxidation capacity than HF control. The HF-ω3 group had significantly lower mean (± SEM) relative heart and lung weight (3.3±0.13 and 3.2±0.12 g kg <jats:sup>−1</jats:sup> , 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-ω9 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-ω3 group was ≈20% shorter due to increased I <jats:sub>to1</jats:sub> and I <jats:sub>K1</jats:sub> and triggered activity, and Ca <jats:sup>2+</jats:sup> -aftertransients were less than in the HF-ω9 group. </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions—</jats:title> <jats:p>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.</jats:p> </jats:sec> |
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| spelling | Den Ruijter, Hester M. Verkerk, Arie O. Schumacher, Cees A. Houten, Sander M. Belterman, Charly N.W. Baartscheer, Antonius Brouwer, Ingeborg A. van Bilsen, Marc de Roos, Baukje Coronel, Ruben 1941-3289 1941-3297 Ovid Technologies (Wolters Kluwer Health) Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1161/circheartfailure.111.963116 <jats:sec> <jats:title>Background—</jats:title> <jats:p>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 ω3-FAs have an added antiarrhythmic effect based on action potential (AP) shortening in animals with HF.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods and Results—</jats:title> <jats:p> Rabbits were fed a diet containing 1.25% (w/w) high oleic sunflower oil (HF-ω9, N=11), 1.25% fish oil (HF-ω3, 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 Ca <jats:sup>2+</jats:sup> - recordings to study electrophysiologic remodeling and arrhythmogenesis. Both the HF-ω9 and the HF-ω3 groups had larger myocardial FA oxidation capacity than HF control. The HF-ω3 group had significantly lower mean (± SEM) relative heart and lung weight (3.3±0.13 and 3.2±0.12 g kg <jats:sup>−1</jats:sup> , 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-ω9 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-ω3 group was ≈20% shorter due to increased I <jats:sub>to1</jats:sub> and I <jats:sub>K1</jats:sub> and triggered activity, and Ca <jats:sup>2+</jats:sup> -aftertransients were less than in the HF-ω9 group. </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions—</jats:title> <jats:p>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.</jats:p> </jats:sec> A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload Circulation: Heart Failure |
| spellingShingle | Den Ruijter, Hester M., Verkerk, Arie O., Schumacher, Cees A., Houten, Sander M., Belterman, Charly N.W., Baartscheer, Antonius, Brouwer, Ingeborg A., van Bilsen, Marc, de Roos, Baukje, Coronel, Ruben, Circulation: Heart Failure, A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload, Cardiology and Cardiovascular Medicine |
| title | A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_full | A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_fullStr | A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_full_unstemmed | A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_short | A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| title_sort | a diet rich in unsaturated fatty acids prevents progression toward heart failure in a rabbit model of pressure and volume overload |
| title_unstemmed | A Diet Rich in Unsaturated Fatty Acids Prevents Progression Toward Heart Failure in a Rabbit Model of Pressure and Volume Overload |
| topic | Cardiology and Cardiovascular Medicine |
| url | http://dx.doi.org/10.1161/circheartfailure.111.963116 |