Obesity modifies the energetic phenotype in dilated cardiomyopathy
<p><strong>Aims:</strong> We sought to determine if myocardial energetics could distinguish obesity cardiomyopathy as a distinct entity from dilated cardiomyopathy.</p> <p><strong>Methods and Results:</strong> 16 normal weight participants with dilated card...
| Main Authors: | , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
Oxford University Press
2021
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| _version_ | 1826300374988881920 |
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| author | Rayner, JJ Peterzan, M Clarke, W Rodgers, C Neubauer, S Rider, O |
| author_facet | Rayner, JJ Peterzan, M Clarke, W Rodgers, C Neubauer, S Rider, O |
| author_sort | Rayner, JJ |
| collection | OXFORD |
| description | <p><strong>Aims:</strong> We sought to determine if myocardial energetics could distinguish obesity cardiomyopathy as a distinct entity from dilated cardiomyopathy.</p>
<p><strong>Methods and Results:</strong> 16 normal weight participants with dilated cardiomyopathy (DCMNW), and 27 with DCM and obesity (DCMOB), were compared to 26 normal weight controls (CTLNW). All underwent cardiac magnetic resonance imaging and 31 P spectroscopy to assess function and energetics. 19 DCMOB underwent repeat assessment after a dietary weight loss intervention. ATP delivery through creatine kinase (CK flux) was 55% lower in DCMNW than in CTLNW (p=0.004), correlating with left ventricular ejection fraction (LVEF, r=0.4, p=0.015). In contrast, despite similar LVEF (DCMOB 41±7%,DCMNW 38±6%, p=0.14), CK flux was two-fold higher in DCMOB (p<0.001), due to higher rate through CK (median kf 0.21(0.14) vs 0.11(0.12)s -1, p=0.002). During increased workload, the CTLNW heart increased CK flux by 97% (p<0.001). In contrast, CK flux was unchanged in DCMNW and fell in DCMOB (by >50%, p<0.001). Intentional weight loss was associated with positive left ventricular remodelling, with reduced left ventricular end-diastolic volume (by 8%, p<0.001) and a change in LVEF (40±9% vs 45±10%, p=0.002). This occurred alongside a fall in ATP delivery rate with weight loss (by 7%, p=0.049).
<p><strong>Conclusions:</strong> In normal weight, DCM is associated with reduced resting ATP delivery. In obese DCM, ATP demand through CK is greater, suggesting reduced efficiency of energy utilisation. Dietary weight loss is associated with significant improvement in myocardial contractility, and a fall in ATP delivery, suggesting improved metabolic efficiency. This highlights distinct energetic pathways in obesity cardiomyopathy which are both different from dilated cardiomyopathy, and may be reversible with weight loss.</p> |
| first_indexed | 2024-03-07T05:16:12Z |
| format | Journal article |
| id | oxford-uuid:dd474e24-dcea-4d1a-9cd7-99570db58be2 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T05:16:12Z |
| publishDate | 2021 |
| publisher | Oxford University Press |
| record_format | dspace |
| spelling | oxford-uuid:dd474e24-dcea-4d1a-9cd7-99570db58be22022-03-27T09:23:59ZObesity modifies the energetic phenotype in dilated cardiomyopathyJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:dd474e24-dcea-4d1a-9cd7-99570db58be2EnglishSymplectic ElementsOxford University Press2021Rayner, JJPeterzan, MClarke, WRodgers, CNeubauer, SRider, O<p><strong>Aims:</strong> We sought to determine if myocardial energetics could distinguish obesity cardiomyopathy as a distinct entity from dilated cardiomyopathy.</p> <p><strong>Methods and Results:</strong> 16 normal weight participants with dilated cardiomyopathy (DCMNW), and 27 with DCM and obesity (DCMOB), were compared to 26 normal weight controls (CTLNW). All underwent cardiac magnetic resonance imaging and 31 P spectroscopy to assess function and energetics. 19 DCMOB underwent repeat assessment after a dietary weight loss intervention. ATP delivery through creatine kinase (CK flux) was 55% lower in DCMNW than in CTLNW (p=0.004), correlating with left ventricular ejection fraction (LVEF, r=0.4, p=0.015). In contrast, despite similar LVEF (DCMOB 41±7%,DCMNW 38±6%, p=0.14), CK flux was two-fold higher in DCMOB (p<0.001), due to higher rate through CK (median kf 0.21(0.14) vs 0.11(0.12)s -1, p=0.002). During increased workload, the CTLNW heart increased CK flux by 97% (p<0.001). In contrast, CK flux was unchanged in DCMNW and fell in DCMOB (by >50%, p<0.001). Intentional weight loss was associated with positive left ventricular remodelling, with reduced left ventricular end-diastolic volume (by 8%, p<0.001) and a change in LVEF (40±9% vs 45±10%, p=0.002). This occurred alongside a fall in ATP delivery rate with weight loss (by 7%, p=0.049). <p><strong>Conclusions:</strong> In normal weight, DCM is associated with reduced resting ATP delivery. In obese DCM, ATP demand through CK is greater, suggesting reduced efficiency of energy utilisation. Dietary weight loss is associated with significant improvement in myocardial contractility, and a fall in ATP delivery, suggesting improved metabolic efficiency. This highlights distinct energetic pathways in obesity cardiomyopathy which are both different from dilated cardiomyopathy, and may be reversible with weight loss.</p> |
| spellingShingle | Rayner, JJ Peterzan, M Clarke, W Rodgers, C Neubauer, S Rider, O Obesity modifies the energetic phenotype in dilated cardiomyopathy |
| title | Obesity modifies the energetic phenotype in dilated cardiomyopathy |
| title_full | Obesity modifies the energetic phenotype in dilated cardiomyopathy |
| title_fullStr | Obesity modifies the energetic phenotype in dilated cardiomyopathy |
| title_full_unstemmed | Obesity modifies the energetic phenotype in dilated cardiomyopathy |
| title_short | Obesity modifies the energetic phenotype in dilated cardiomyopathy |
| title_sort | obesity modifies the energetic phenotype in dilated cardiomyopathy |
| work_keys_str_mv | AT raynerjj obesitymodifiestheenergeticphenotypeindilatedcardiomyopathy AT peterzanm obesitymodifiestheenergeticphenotypeindilatedcardiomyopathy AT clarkew obesitymodifiestheenergeticphenotypeindilatedcardiomyopathy AT rodgersc obesitymodifiestheenergeticphenotypeindilatedcardiomyopathy AT neubauers obesitymodifiestheenergeticphenotypeindilatedcardiomyopathy AT ridero obesitymodifiestheenergeticphenotypeindilatedcardiomyopathy |