Article Text

Mechanisms responsible for cardiac energetic impairment in type 1 diabetes
  1. G Nallur Shivu,
  2. TT Phan,
  3. K Abozguia,
  4. I Ahmed,
  5. R Weaver,
  6. U Naidoo,
  7. A Wagenmakers,
  8. P Narendran,
  9. M Stevens,
  10. MP Frenneaux
  1. University of Birmingham, Birmingham, UK


Background Heart failure occurs frequently in individuals with diabetes and is commonly caused by epicardial coronary artery disease (CAD) and/or hypertension. However, in some patients left ventricular dysfunction occurs in the absence of significant epicardial CAD or hypertension. Asymptomatic individuals with diabetes have impaired cardiac energetic status, as reflected in a reduced phosphocreatine/beta adenosine triphosphate (PCr/βATP) ratio on cardiac magnetic resonance spectroscopy (MRS) that may play a significant role in the development of heart failure in diabetes. In this study we assessed the role of metabolic impairment and microvascular dysfunction in the development of impaired cardiac energetics in patients with type1 diabetes (T1D).

Methods 25 asymptomatic subjects with T1D (mean ± 1 SD, age 32.6 ± 8.2 years) and 26 age-matched healthy controls (HC) (age 32.3 ± 8.0 years) were recruited into the study. We studied two age-matched groups of T1D. The first group was newly diagnosed (10 subjects with an average of 4 years since diagnosis) and the second group was subjects with long-term diabetes (15 subjects with an average of 18 years since diagnosis). All subjects underwent history, echocardiogram and exercise ECG to rule out significant CAD or heart failure. Following this, subjects had MRS to determine the cardiac energetic status and adenosine stress magnetic resonance imaging (MRI) with gadolinium to determine their myocardial perfusion reserve index, which is a measure of coronary flow reserve. Stress MRI was done only in a subgroup of HC (six subjects).

Results Baseline characteristics are summarised in the table. A typical cardiac spectrum in T1D and HC is shown in fig 1. The PCr/βATP ratio was significantly reduced in T1D (1.5 ± 0.3 vs 2.1 ± 0.5 in HC, p<0.001). There was no significant difference between subjects with long-term and newly diagnosed diabetes in the PCr/βATP ratio (1.49 ± 0.44 vs 1.60 ± 0.19, p = 0.44). However, the PCr/βATP ratio was significantly reduced compared with healthy volunteers in both long-term (2.23 ± 0.56 vs 1.49 ± 0.44, p<0.001) and newly diagnosed subjects with diabetes (2.23 ± 0.56 vs 1.60 ± 0.19, p<0.001). The mean myocardial perfusion reserve index (MPRI) in T1D subjects was 1.8 ± 0.5 and 2.3 ± 0.6 in HC. The mean MPRI in subjects with long-term diabetes (1.7 ± 0.6) was significantly reduced compared with both newly diagnosed subjects (2.1 ± 0.2, p<.05) and HC (2.3 ± 0.3, p = 0.05). Pearson correlation showed no significant relationship between MPRI and PCr/βATP in patients with diabetes (r  =  0.24, p = ns). However, there was a significant negative correlation between PCr/βATP and fasting glucose levels (r  =  0.34, p<0.05). There was an insignificant correlation between PCr/βATP and haemoglobin A1C (r  =  0.27, p = ns; fig 2).

Abstract 109 Figure 1.

HC, healthy control; PCr, phosphocreatine; ATP, adenosine triphosphate; T1D, type 1 diabetes.

Abstract 109 Figure 2.

HBA1C, haemoglobin A1C; MPRI, myocardial perfusion reserve index; PCr/βATP, phosphocreatine/beta adenosine triphosphate ratio.

Abstract 109 Table

Conclusions We demonstrate that young patients with uncomplicated T1D have impaired myocardial energetics and that impaired cardiac energetics is independent of coronary microvascular function. We postulate that impairment of cardiac energetics in these subjects primarily results from metabolic dysfunction rather than microvascular impairment.

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