The aim of the study was to assess the role of altered autonomic regulation on changes in the QT interval. Fifty-three diabetic patients, comprising 32 men and 21 women with a mean age of 49.4 +/- 15.9 years (range 13-73 years), underwent sympathetic and parasympathetic stimulatory tests (changes in heart rate between clino- and orthostatism, lying to standing, while deep breathing, Valsalva's manoeuvre, changes of arterial pressure related to posture) to study cardiovascular reflexes. Patients who were positive for at least two of the tests were considered to be affected by autonomic neuropathy. Ten non-diabetic age-matched subjects (44.8 +/- 14.8 years) with no cardiovascular diseases were included in the study as a control group. The QTc interval was measured in basal conditions and during sympathetic and parasympathetic stimulatory tests, in clino- and orthostatism, during deep breathing and Valsalva's manoeuvre. A significantly greater QTc interval (p less than 0.05) was found in neuropathic patients compared to controls and non-neuropathic patients both in basal conditions and following stimulatory tests at the lowest heart rate (phase IV of Valsalva's manoeuvre and slow exhalation during deep breathing), while at a higher heart rate (orthostatism, L-S, deep inhalation during deep breathing, phase II of Valsalva's manoeuvre) there was no difference in QTc between controls, and neuropathic and non-neuropathic patients due to a lesser extension of the QTc in neuropathic patients. This difference appears to be the expression of autonomic dysregulation in neuropathic patients, given the lack of correlation with diabetes or duration of disease, and is only conditioned by the presence or absence of autonomopathic damage. Among other causes, the observed extension of the QT interval might therefore justify the increased frequency of sudden death in diabetic patients with cardiovascular autonomic neuropathy.

Changes in the QT interval caused by autonomic cardiovascular involvement in diabetes mellitus

SAITTA, Antonino;BONAIUTO, Michele;MILETO, Angelo;CINQUEGRANI, Maurizio;SQUADRITO, Giuseppe
1991-01-01

Abstract

The aim of the study was to assess the role of altered autonomic regulation on changes in the QT interval. Fifty-three diabetic patients, comprising 32 men and 21 women with a mean age of 49.4 +/- 15.9 years (range 13-73 years), underwent sympathetic and parasympathetic stimulatory tests (changes in heart rate between clino- and orthostatism, lying to standing, while deep breathing, Valsalva's manoeuvre, changes of arterial pressure related to posture) to study cardiovascular reflexes. Patients who were positive for at least two of the tests were considered to be affected by autonomic neuropathy. Ten non-diabetic age-matched subjects (44.8 +/- 14.8 years) with no cardiovascular diseases were included in the study as a control group. The QTc interval was measured in basal conditions and during sympathetic and parasympathetic stimulatory tests, in clino- and orthostatism, during deep breathing and Valsalva's manoeuvre. A significantly greater QTc interval (p less than 0.05) was found in neuropathic patients compared to controls and non-neuropathic patients both in basal conditions and following stimulatory tests at the lowest heart rate (phase IV of Valsalva's manoeuvre and slow exhalation during deep breathing), while at a higher heart rate (orthostatism, L-S, deep inhalation during deep breathing, phase II of Valsalva's manoeuvre) there was no difference in QTc between controls, and neuropathic and non-neuropathic patients due to a lesser extension of the QTc in neuropathic patients. This difference appears to be the expression of autonomic dysregulation in neuropathic patients, given the lack of correlation with diabetes or duration of disease, and is only conditioned by the presence or absence of autonomopathic damage. Among other causes, the observed extension of the QT interval might therefore justify the increased frequency of sudden death in diabetic patients with cardiovascular autonomic neuropathy.
1991
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/2189902
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