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Original article
Subclinical LV dysfunction and 10-year outcomes in type 2 diabetes mellitus
  1. David J Holland1,2,3,
  2. Thomas H Marwick4,
  3. Brian A Haluska1,
  4. Rodel Leano1,
  5. Matthew D Hordern3,
  6. James L Hare5,6,
  7. Zhi You Fang1,
  8. Johannes B Prins1,7,
  9. Tony Stanton1
  1. 1School of Medicine, The University of Queensland, Brisbane, Queensland, Australia
  2. 2School of Medicine, The University of Notre Dame Australia, Sydney, New South Wales, Australia
  3. 3School of Human Movement Studies, The University of Queensland, Brisbane, Queensland, Australia
  4. 4Menzies Research Institute Tasmania, Hobart, Tasmania, Australia
  5. 5Heart Centre, The Alfred Hospital, Melbourne, Victoria, Australia
  6. 6Baker IDI Heart and Diabetes Research Institute, Melbourne, Victoria, Australia
  7. 7Mater Medical Research Institute Brisbane, Brisbane, Queensland, Australia
  1. Correspondence to Dr Tony Stanton, School of Medicine, The University of Queensland, Level 4, The Princess Alexandra Hospital, Ipswich Road, Woolloongabba, QLD 4102, Australia; t.stanton{at}uq.edu.au

Abstract

Objective New imaging techniques have permitted the detection of subclinical LV dysfunction (LVD) in up to half of patients with type 2 diabetes mellitus (DM) with a normal EF. However, the connection between early LVD and prognosis is unclear. This study aimed to define the long-term outcome of LVD associated with type 2 DM.

Methods In this prospective cohort study, 230 asymptomatic patients with type 2 DM underwent measurement of global longitudinal 2D strain (GLS) for detection of LVD and were followed for up to 10 years. All subjects had normal EF (≥50%) and no evidence of coronary artery disease at recruitment. Outcome data were obtained through centralised state-wide death and hospital admission registries. The primary endpoint was all-cause mortality and hospitalisation.

Results On study entry, almost half (45%) of the cohort had evidence of LVD as detected by GLS. Over a median follow-up of 7.4±2.6 years (range 0.6–9.7 years), 68 patients (30%) met the primary endpoint (LVD: 37%; normal LV function: 24%). GLS was independently associated with the primary endpoint (HR=1.10; p=0.04), as was systolic blood pressure (HR=1.02; p<0.001) and levels of glycosylated haemoglobin (HR=1.28; p=0.011). Patients with LVD had significantly worse outcome than those without (χ2=4.73; p=0.030).

Conclusions Subclinical LVD is common in asymptomatic patients with type 2 DM, is readily detectable by GLS imaging and is independently associated with adverse outcome.

Trial registration number Australian and New Zealand Clinical Trials Registry (ACTRN12612001178831).

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