Abstract
Aims Patients with type 2 diabetes mellitus (T2DM) are known to have impaired resting myocardial energetics and impaired myocardial perfusion reserve, even in the absence of obstructive epicardial coronary artery disease (CAD). Whether or not the pre-existing energetic deficit is exacerbated by exercise, and whether the impaired myocardial perfusion causes deoxygenation and further energetic derangement during exercise stress, is uncertain. Methods and results Thirty-one T2DM patients, on oral antidiabetic therapies with a mean HBA1c of 7.4 ± 1.3%, and 17 matched controls underwent adenosine stress cardiovascular magnetic resonance for assessment of perfusion [myocardial perfusion reserve index (MPRI)] and oxygenation [blood-oxygen level-dependent (BOLD) signal intensity change (SIΔ)]. Cardiac phosphorus-MR spectroscopy was performed at rest and during leg exercise. Significant CAD (>50% coronary stenosis) was excluded in all patients by coronary computed tomographic angiography. Resting phosphocreatine to ATP (PCr/ATP) was reduced by 17% in patients (1.74 ± 0.26, P = 0.001), compared with controls (2.07 ± 0.35); during exercise, there was a further 12% reduction in PCr/ATP (P = 0.005) in T2DM patients, but no change in controls. Myocardial perfusion and oxygenation were decreased in T2DM (MPRI 1.61 ± 0.43 vs. 2.11 ± 0.68 in controls, P = 0.002; BOLD SIΔ 7.3 ± 7.8 vs. 17.1 ± 7.2% in controls, P < 0.001). Exercise PCr/ATP correlated with MPRI (r = 0.50, P = 0.001) and BOLD SIΔ (r = 0.32, P = 0.025), but there were no correlations between rest PCr/ATP and MPRI or BOLD SIΔ. Conclusion The pre-existing energetic deficit in diabetic cardiomyopathy is exacerbated by exercise; stress PCr/ATP correlates with impaired perfusion and oxygenation. Our findings suggest that, in diabetes, coronary microvascular dysfunction exacerbates derangement of cardiac energetics under conditions of increased workload.
Highlights
Diabetes mellitus (DM) is associated with increased risk of congestive heart failure[1] and cardiovascular mortality.[2]
There were no significant differences in age, gender, systolic blood pressure (BP), and body mass index (BMI) between diabetic patients and controls
Using Cardiovascular magnetic resonance (CMR) and 31P-MRS to study patients with type 2 diabetes mellitus (T2DM) free of significant obstructive epicardial coronary artery disease (CAD), we assessed the effects of diabetes on cardiac metabolic reserve and how metabolic reserve relates to both myocardial oxygenation and perfusion reserve
Summary
Diabetes mellitus (DM) is associated with increased risk of congestive heart failure[1] and cardiovascular mortality.[2]. Myocardial energy depletion in patients with diabetes is a multifactorial phenomenon, related to limitations in uptake and utilization of substrates,[6] mitochondrial dysfunction,[7] and impaired energy transfer from mitochondria to myofibrils.[8]. These metabolic changes, in combination with impaired myocardial. Phosphorus-magnetic resonance spectroscopy (31P-MRS) allows non-invasive assessment of the myocardial phosphocreatine to ATP concentration ratio (PCr/ATP), which is a sensitive indicator of the myocardial energy status.[11] Using 31P-MRS, we, and others, have shown that the diabetic heart is energetically compromised, with a decreased PCr/ATP, at rest.[3,4] changes in cardiac metabolic reserve and energy metabolism in diabetic patients under conditions of increased workload have not been studied
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