Prevalence, predictors and evolution of echocardiographically defined cardiac abnormalities in adults with type 1 diabetes: an observational cohort study☆,☆☆,★
Introduction
Cardiovascular (CV) disease is a major cause of death in type 1 diabetes (Laing et al., 2003, Soedamah-Muthu et al., 2006), yet non-invasive identification of subclinical cardiac abnormalities, such as left ventricular hypertrophy (LVH) (Levy, Garrison, Savage, Kannel, & Castelli, 1990), a known and modifiable risk factor, or diastolic dysfunction, a risk factor for the development of heart failure (Redfield et al., 2003), is not part of diabetes complications surveillance programs (American Diabetes Association, 2013). Diastolic dysfunction in the absence of coronary artery disease (CAD) or hypertension is the earliest manifestation of diabetic cardiomyopathy in young type 1 diabetes patients (Schannwell, Schneppenheim, Perings, Plehn, & Strauer, 2002). To date, most echocardiographic studies have been in children and adolescents or in younger adults (age < 40 years) (Adal et al., 2006, Kim and Kim, 2010, Salem et al., 2009, Schannwell et al., 2002, Shivalkar et al., 2006, Vazeou et al., 2008), and many excluded anyone with comorbidities and/or diabetes complications, or those on medications other than insulin (Gul et al., 2009, Karamitsos et al., 2007, Konduracka et al., 2007).
Given the high relative risk of a CV death in type 1 diabetes, identification and treatment of subclinical cardiac abnormalities such as LVH and diastolic dysfunction, may be one approach to improve CV outcomes. Currently, the prevalence and predictors of cardiac structural and functional abnormalities on echocardiography in ‘real-world’, asymptomatic adults with type 1 diabetes seen in the ambulatory care setting are unknown. As previous studies have been cross-sectional in nature, it is also unclear whether changes are progressive. We addressed both these issues in a prospective cohort study of 136 asymptomatic adults with type 1 diabetes attending a specialty Diabetes Outpatient Clinic in Melbourne, Australia. The evolution of echocardiographic changes was assessed in 65 subjects with a second echocardiogram to determine the predictors of progression from a normal to an abnormal echocardiogram.
Section snippets
Methods
Subjects with type 1 diabetes aged ≥ 18 years were prospectively recruited, after referral for a transthoracic echocardiogram as part of a complications surveillance program at Austin Health, Melbourne. Subjects with a clinically indicated study were not recruited. The study was approved by the Human Research Ethics Committee at Austin Health, Melbourne. All participants provided written informed consent.
Results
We recruited 141 subjects with a single echocardiogram, and excluded five due to moderate/severe valvular dysfunction (n = 1) or an indeterminate echocardiogram (n = 4). Of the 136 subjects in Study 1, 65 had been referred for a second echocardiogram (Study 2).
Discussion
Subclinical cardiac abnormalities of structure and function, detectable using myocardial TDI and conventional echocardiographic imaging were common in this prospective study of adults with type 1 diabetes. Nearly 30% of asymptomatic adults had an abnormal study, with diastolic dysfunction in 69%, LVH in 38% and systolic dysfunction in 10%. Whilst systolic dysfunction could be predicted from the past history of CAD, diastolic dysfunction would not have been diagnosed without rigorous
Acknowledgments
We thank the sonographers at Repatriation Campus who performed the echocardiograms.
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2017, EBioMedicineCitation Excerpt :Glycosylated hemoglobin (HbA1c) and kidney function were measured and whole blood was collected in EDTA tubes and stored at − 80 °C for DNA extraction. Transthoracic echocardiography was performed as previously described (Wai et al., 2014) according to the recommendations of the American Society of Echocardiography (ASE) (Lang et al., 2015). LV mass was calculated by LV cavity dimensions and wall thickness at end-diastole with the ASE recommended formula as follows (Lang et al., 2015): LV mass (g) = 0.8 × {1.04[(LVEDD + PWTd + SWTd)3 – (LVEDD)3]} + 0.6 g, where LVEDD is the LV end diastolic dimension, PWTd is the posterior wall thickness diameter and SWT is the septal wall thickness.
Take a deep breath and check your heart
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Funding: This study was supported by research grants from the Heart Foundation of Australia and an Australian Diabetes Society — Servier, National Diabetes Strategy grant in memory of Barry Young. B.W. was supported by an NHMRC/Heart Foundation of Australia PhD Scholarship.
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Duality of interest: The authors have no conflicts of interest.
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Author contributions: B.W. and S.P. collected the data, performed the statistical analyses and wrote and edited the manuscript. M.O. assisted with the questionnaires and reviewed the manuscript. L.B. conceived the study, and contributed to writing and editing the manuscript. P.S., R.M. and G.J. contributed to collecting and interpreting the data, and reviewed and edited the manuscript.
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Contributed equally.