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. 2014 Mar;35(10):657-64.
doi: 10.1093/eurheartj/eht193. Epub 2013 Jun 11.

Myocardial extracellular volume fraction quantified by cardiovascular magnetic resonance is increased in diabetes and associated with mortality and incident heart failure admission

Timothy C Wong  1 , Kayla M Piehler, Ian A Kang, Ajay Kadakkal, Peter Kellman, David S Schwartzman, Suresh R Mulukutla, Marc A Simon, Sanjeev G Shroff, Lewis H Kuller, Erik B Schelbert
Affiliations

Myocardial extracellular volume fraction quantified by cardiovascular magnetic resonance is increased in diabetes and associated with mortality and incident heart failure admission

Timothy C Wong et al. Eur Heart J. 2014 Mar.

Abstract

Aims: Diabetes may promote myocardial extracellular matrix (ECM) expansion that increases vulnerability. We hypothesized that: (i) type 2 diabetes would be associated with quantitative cardiovascular magnetic resonance (CMR) measures of myocardial ECM expansion, i.e. extracellular volume fraction (ECV); (ii) medications blocking the renin-angiotensin-aldosterone system (RAAS) would be associated with lower ECV; and (iii) ECV in diabetic individuals would be associated with mortality and/or incident hospitalization for heart failure.

Methods and results: We enrolled 1176 consecutive patients referred for CMR without amyloidosis and computed ECV from measures of the haematocrit and myocardial and blood T1 pre- and post-contrast. Linear regression modelled ECV; Cox regression modelled mortality and/or hospitalization for heart failure. Diabetic individuals (n = 231) had higher median ECV than those without diabetes (n = 945): 30.2% (IQR: 26.9-32.7) vs. 28.1% (IQR: 25.9-31.0), respectively, P < 0.001). Diabetes remained associated with higher ECV in models adjusting for demographics, comorbidities, and medications (P < 0.001). Renin-angiotensin-aldosterone system blockade was associated with lower ECV (P = 0.028) in multivariable linear models. Over a median of 1.3 years (IQR: 0.8-1.9), 38 diabetic individuals had events (21 incident hospitalizations for heart failure; 24 deaths), and ECV was associated with these events (HR: 1.52, 95% CI: 1.21-1.89 per 3% ECV increase) in multivariable Cox regression models.

Conclusion: Diabetes is associated with increased ECV. Extracellular volume fraction detects amelioration of ECM expansion associated with RAAS blockade, and is associated with mortality and/or incident hospitalization for heart failure in diabetic individuals. Extracellular matrix expansion may be an important intermediate phenotype in diabetic individuals that is detectable and treatable.

Keywords: MRI; collagen; diabetes; extracellular matrix; extracellular volume fraction; fibrosis.

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Figures

Figure 1
Figure 1
Frequency histograms of myocardial extracellular volume fraction indicate higher extracellular volume fraction in those with diabetes. The shapes of the distributions are similar, but the histogram for diabetic individuals is shifted rightward towards higher extracellular volume fraction.
Figure 2
Figure 2
In 231 individuals with diabetes and 945 individuals without diabetes, extracellular matrix expansion in myocardium quantified by extracellular volume fraction is associated with increased risks of: death or heart failure admission (top panel); heart failure admission ignoring or censoring for death (middle panel); or all-cause mortality (lower panel). Event rates were higher for those with diabetes. The numbers of events are shown in Table 3.
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References

    1. Kannel WB, Hjortland M, Castelli WP. Role of diabetes in congestive heart failure: the Framingham study. Am J Cardiol. 1974;34:29–34. doi:10.1016/0002-9149(74)90089-7. - DOI - PubMed
    1. Jouven X, Lemaitre RN, Rea TD, Sotoodehnia N, Empana JP, Siscovick DS. Diabetes, glucose level, and risk of sudden cardiac death. Eur Heart J. 2005;26:2142–2147. doi:10.1093/eurheartj/ehi376. - DOI - PubMed
    1. Schelbert EB, Cao JJ, Sigurdsson S, Aspelund T, Kellman P, Aletras AH, Dyke CK, Thorgeirsson G, Eiriksdottir G, Launer LJ, Gudnason V, Harris TB, Arai AE. Prevalence and prognosis of unrecognized myocardial infarction determined by cardiac magnetic resonance in older adults. JAMA. 2012;308:890–896. doi:10.1001/2012.jama.11089. - DOI - PMC - PubMed
    1. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Fibrosis and renin-angiotensin-aldosterone system. Circulation. 1991;83:1849–1865. doi:10.1161/01.CIR.83.6.1849. - DOI - PubMed
    1. Schwartzkopff B, Brehm M, Mundhenke M, Strauer BE. Repair of coronary arterioles after treatment with perindopril in hypertensive heart disease. Hypertension. 2000;36:220–225. doi:10.1161/01.HYP.36.2.220. - DOI - PubMed

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