Quick Fire Session
SCMR 22nd Annual Scientific Sessions
Louise Brown, BSc, MB
CMR Research Fellow
University of Leeds
Christopher Saunderson
Clinical Research Fellow
University of Leeds
Pei Chew
CMR Research Fellow/Cardiology SpR
University of Leeds
Arka Das
Clinical Research Fellow
Multidisciplinary Cardiovascular Research Centre & Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom
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Hui Xue, PhD
Staff Scientist
National Heart Lung and Blood Institute (NHLBI), National Institutes of Health
Kristopher Knott, MA
Clinical Fellow
University College London
Erica Dall'Armellina, PhD
BHF Intermediate Clinical Research Fellow
University of Leeds
Eylem Levelt, PhD
Cardiologist
University of Leeds
James Moon, MD
Clinical Director, Imaging
Barts Heart Centre and UCL
Peter Kellman, PhD
Senior Scientist
NHLBI, NIH
.jpg "John Greenwood, PhD photo")
John Greenwood, PhD
Professor of Cardiology
University of Leeds
Sven Plein, MD, PhD
BHF Professor of Cardiovascular Imaging; Consultant Cardiologist
University of Leeds
Peter Swoboda, PhD
NIHR Clinical Lecturer
University of Leeds
Background:
Type 2 diabetes mellitus is an independent risk factor for the development of heart failure. Patients with diabetes and heart failure have worse prognosis and higher mortality than normoglycaemic heart failure patients. We hypothesised that diabetic heart failure patients are more likely to have cardiac microvascular dysfunction.
Methods:
We recruited 146 patients with a new diagnosis of left ventricular systolic dysfunction of unknown aetiology from cardiology outpatient clinics. Patients were excluded if they had known ischaemic heart disease or symptoms suggestive of angina.
142 patients underwent adenosine stress perfusion cardiovascular magnetic resonance (CMR) imaging (Siemens 3T). First pass stress and rest myocardial perfusion CMR data were acquired in three short axis slices with 0.05mmol/kg intravenous Gadovist injection. A free-breathing motion corrected in-line quantification of perfusion maps using the Gadgetron framework was used. To achieve stress, adenosine was administered at 140mcg/kg/min increased up to a maximum of 210mcg/kg/min as required to achieve symptoms or haemodynamic response. Segments showing regional perfusion defects on visual assessment or containing scar on LGE imaging were excluded from further quantitative analysis. Myocardial blood flow (MBF) was averaged globally for the remaining left ventricle at stress and rest, and myocardial perfusion reserve (MPR) was calculated from these results.
HbA1c was measured on the day of the scan, and patients categorised by glycaemic status: normoglycaemic (HbA1c<42mmol/mol), pre-diabetes (HbA1c 42-47 mmol/mol) and diabetes (HbA1c ≥48 mmol/mol or pre-existing diagnosis).
Results:
Baseline characteristics were evenly matched between the three groups with all groups showing a significant increase in heart rate and rate pressure product at stress compared to rest (p<0.01). The prevalence of newly identified ischaemic cardiomyopathy was not significantly different between the groups (Table 1). No significant difference was seen in resting MBF between the groups (0.71±0.29 vs 0.64±0.17 vs 0.74±0.27ml/g/min, p=0.19 for diabetes, prediabetes and normoglycaemic). However, patients with diabetes and prediabetes both had significantly lower stress MBF (1.42±0.52 vs 1.45±0.49 vs 1.84±0.71 ml/g/min, p=0.001) and MPR (2.13±0.85 vs 2.31±0.76 vs 2.61±0.95, p=0.03) than normoglycaemic patients (Figure 1). There was no difference in either stress MBF or MPR between patients with diabetes and prediabetes.
Conclusion:
Patients with heart failure and dysglycaemia (either diabetes of prediabetes) have impaired stress myocardial blood flow but show similar prevalence of occult ischaemic cardiomyopathy as normoglycaemic patients. These findings suggest microvascular dysfunction may have a role in the poor prognosis observed in patients with diabetes and heart failure.