The Association between Arterial Stiffness and LV Diastolic Function in T2DM: 8-Year Follow-up to the Hoorn Study

Summary

This article discusses data that addressed the issue of whether arterial stiffness was prospectively associated with a higher left ventricular (LV) mass and worse LV diastolic function (indicated by increasing left atrial volume index) and whether this differed in individuals with or without type 2 diabetes mellitus.

  • Diabetes & Endocrinology Clinical Trials
  • Diabetes Mellitus
  • Heart Failure

Individuals with diabetes are more likely to develop congestive heart failure (HF), particularly left-sided HF, than those without diabetes, but the underlying mechanisms remain controversial [Nichols GA et al. Diabetes Care 2004]. Arterial stiffness, which is more common in type 2 diabetes mellitus (T2DM), has been suggested as a potential cause of HF, while left ventricular (LV) mass has been shown to be a predictor [Stehouwer CD et al. Diabetologia 2008; de Simone G et al. Eur Heart J 2008]. Katja van den Hurk, PhD candidate, EMGO Institute for Health and Care Research, VU University Medical Center, Amsterdam, The Netherlands, presented data that addressed the issue of whether arterial stiffness was prospectively associated with a higher LV mass and worse LV diastolic function (indicated by increasing left atrial volume index [LAVI]) and whether this differed in individuals with or without T2DM.

These results were from an 8-year follow-up to the Hoorn Study, a population-based cohort study of diabetes and diabetes complications that began in 1989 [Henry RM et al. Diabetes Care 2004]. Echocardiography and arterial ultrasonography were performed in 2000 and again in 2008. Linear regression analyses were performed to investigate associations between baseline carotid, brachial, and femoral artery distensibility coefficients (DCs, arterial stiffness) with LV mass index (LVMI, g/m27) and LAVI (mL/m2). The results were adjusted for age, gender, and mean arterial pressure (MAP). Individuals with moderate or severe mitral or aortic valve disease, or tachycardia (heart rate >90 beats per minute) were excluded.

Of the 796 individuals for whom baseline echocardiograms were available, 394 were included in the present analysis. Subjects with T2DM (n=128; 32%) were older, had a higher LAVI and blood pressure, and stiffer arteries (lower arterial DCs) at baseline compared with those without T2DM. After adjusting for age and gender, more arterial stiffness at baseline was significantly (p<0.05) associated with higher LVMI and LAVI. Additional adjustment for baseline MAP showed that blood pressure only partly explained these associations.

Subjects with T2DM have a significantly (p<0.05) higher LVMI and LAVI [van den Hurk et al. Eur J Heart Fail. 2010]. However, associations between arterial stiffness and LVMI or LAVI were not different for individuals with or without T2DM (p for interaction >0.10). Adjustments for HbA1C, heart rate, LVMI, systolic blood pressure, or use of antihypertensive medication did not change the results.

Arterial stiffness was prospectively associated with worse LV diastolic function, regardless of T2DM. However, individuals with T2DM commonly have stiffer arteries compared with those without T2DM, suggesting that arterial stiffening might be one of the causes of worse LV diastolic function in T2DM.

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