Comment on: Koivikko et al. Autonomic Cardiac Regulation During Spontaneous Nocturnal Hypoglycemia in Patients With Type 1 Diabetes. Diabetes Care 2012;35:1585–1590
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Abstract
We read with great interest the article published in Diabetes Care by Koivikko et
al. (1) showing that in patients with type 1 diabetes, spontaneous episodes of hypoglycemia
are associated with reduced values of heart rate variability (HRV) parameters, indicating
sympatho-vagal imbalance toward sympathetic predominance.
The data by Koivikko et al. confirm in type 1 diabetic patients what we already demonstrated—for
the first time—in type 2 diabetic patients (2). In our study we performed simultaneous
48-h electrocardiogram Holter monitoring and continuous interstitial glucose measurements
in 12 type 2 diabetic patients with documented stable coronary artery disease. The
highest and the lowest glucose levels for each 3-h segment of the 2 days were identified,
and HRV parameters were measured on Holter recordings at 5-min intervals centered
on the corresponding times. The results showed that HRV parameters (in particular
low frequency and high frequency power) were significantly lower in correspondence
of the lowest glucose blood levels. Of note, we also showed that the decrease in HRV
parameters in association with the lowest glucose blood levels was abolished or significantly
blunted in those who were taking β-blocking agents, suggesting that these drugs might
contrast the hypoglycemia-induced cardiac sympatho-vagal imbalance with potential
protective effects.
In the last years, several studies have fueled the relationship between hypoglycemia
and cardiovascular death (3). By activating sympathetic activity, hypoglycemia might
trigger life-threatening ventricular arrhythmias and sudden cardiac death, which might
be favored by an increased arrhythmogenic substrate, as in case of severe coronary
artery disease or impaired left ventricular function (4). Acute vascular complications
and thrombosis, however, also might be triggered by the hypoglycemia-mediated activation
of adrenergic activity (5).
Our data (2) and those by Koivikko et al. (1) suggest a potential way to assess the
hypoglycemia-related risk. Only prospective studies, however, may establish whether
the depressed hypoglycemia related HRV is actually associated with an increased risk
of acute cardiovascular events, and whether interventions aimed at avoiding the hypoglycemia-related
sympatho-vagal imbalance, as we showed for β-blockers, may reduce this risk.
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