INTRODUCCIÓN: REVISIÓN CRITICA DEL PROBLEMA

CAPÍTULO IX
Dear editor,
We read with interest the elegantly written paper by Rubin et al. [1] relating to the
analysis of the association between categories of glycated haemoglobin (HbA1c)
and high-sensitivity cardiac troponin-T (hs-cTnT) in participants without coronary
heart disease in the ARIC (Atherosclerosis Risk in Communities) study. In a
community-based population of almost 10,000 subjects without clinically evident
CHD, chronic hyperglycemia was independently associated with subclinical
myocardial injury, as assessed by elevated levels of hs-cTnT in both persons with
and without diabetes.
We congratulate the authors for this research. However, we have some major
concerns regarding the explanation that the authors find to this relationship. In
particular, although the authors already refer in the discussion that advanced
glycation end-products (AGE) may play an important role in the association
between HbA1c and hs-cTnT, we would like to emphasize this interaction.
Interestingly, within the DCCT study [2], AGE levels were a better predictor of
progression to complications than HbA1C, with over a third of the variance in
complications attributed to differences in AGE indices. The influence of AGE levels
was even more evident in the intensive glycaemic control cohort, suggesting that,
while glycaemic control is important, it is not sufficient to prevent progressive
complications
AGE are molecules that appear in plasma and tissues and are generated non-
enzymatically by glycation and oxidation of proteins as a consequence of the
Maillard reaction, which is driven by oxidative stress in its final step.
Arteriosclerosis and diastolic dysfunction are more prevalent in both diabetic
patients and those with renal impairment; in this context, AGEs may provide the
common pathophysiological link. An increase in AGEs can be determined
fundamentally by two factors: the existence of chronic hyperglycaemia and/or a
high degree of oxidative stress [3]. Although AGEs occur as a result of
hyperglycaemia, their effects can occur independently of glycaemic control. This
finding may explain the paradoxical progression of diabetic complications in some
patients with comparatively good glycaemic control. Results from the DCCT are
consistent with the hypothesis that other factors such as oxidative stress may be
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