Increased QTc Dispersion Is Related to Blunted Circadian Blood Pressure Variation in Normoalbuminuric Type 1 Diabetic Patients

Increased QTc Dispersion Is Related to Blunted Circadian Blood Pressure Variation in Normoalbuminuric Type 1 Diabetic Patients Per Løgstrup Poulsen 1 , Eva Ebbehøj 1 , Hanne Arildsen 2 , Søren Tang Knudsen 1 , Klaus Würgler Hansen 1 , Henning Mølgaard 2 and Carl Erik Mogensen 1 1 Medical Department...

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Published inDiabetes (New York, N.Y.) Vol. 50; no. 4; pp. 837 - 842
Main Authors Poulsen, Per Logstrup, Ebbehoj, Eva, Arildsen, Hanne, Knudsen, Soren Tang, Hansen, Klaus Wurgler, Molgaard, Henning, Mogensen, Carl Erik
Format Journal Article
LanguageEnglish
Published Alexandria, VA American Diabetes Association 01.04.2001
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Summary:Increased QTc Dispersion Is Related to Blunted Circadian Blood Pressure Variation in Normoalbuminuric Type 1 Diabetic Patients Per Løgstrup Poulsen 1 , Eva Ebbehøj 1 , Hanne Arildsen 2 , Søren Tang Knudsen 1 , Klaus Würgler Hansen 1 , Henning Mølgaard 2 and Carl Erik Mogensen 1 1 Medical Department M (Diabetes and Endocrinology), Aarhus Kommunehospital, Aarhus 2 Department of Cardiology, Skejby University Hospital, Aarhus, Denmark Abstract A reduced nocturnal fall in blood pressure (BP) and increased QT dispersion both predict an increased risk of cardiovascular events in diabetic as well as nondiabetic subjects. The relationship between these two parameters remains unclear. The role of diabetic autonomic neuropathy in both QT dispersion and circadian BP variation has been proposed, but data have been conflicting. The aim of the present study was to describe associations between QT dispersion and circadian BP variation as well as autonomic function in type 1 diabetic patients. In 106 normoalbuminuric (urinary albumin excretion <20 μg/min) normotensive patients, we performed 24-h ambulatory BP (Spacelabs 90207) and short-term (three times in 5 min) power spectral analysis of RR interval oscillations, as well as cardiovascular reflex tests (deep breathing test, postural heart rate, and BP response). No patient had received (or had earlier received) antihypertensive or other medical treatment apart from insulin. In a resting 12-lead electrocardiogram, the QT interval was measured by the tangent method in all leads with well-defined T-waves. The measurement was made by one observer blinded to other data. The QT interval was corrected for heart rate using Bazett’s formula. The QTc dispersion was defined as the difference between the maximum and the minimum QTc interval in any of the 12 leads. When comparing patients with QTc dispersion below and above the median (43 ms), the latter had significantly higher night BP (114/67 vs. 109/62 mmHg, P < 0.003/ P < 0.001), whereas day BP was comparable (129/81 vs. 127/79 mmHg). Diurnal BP variation was blunted in the group with QTc dispersion >43 ms with significantly higher night/day ratio, both for systolic (88.8 vs. 86.2%, P < 0.01) and diastolic (83.1 vs. 79.5%, P < 0.01) BP. The association between QTc dispersion and diastolic night BP persisted after controlling for potential confounders such as sex, age, duration of diabetes, urinary albumin excretion, and HbA 1c . Power spectral analysis suggested an altered sympathovagal balance in patients with QTc dispersion above the median (ratio of low-frequency/high-frequency power: 1.0 vs. 0.85, P < 0.01). In normoalbuminuric type 1 diabetic patients, increased QTc dispersion is associated with reduced nocturnal fall in BP and an altered sympathovagal balance. This coexistence may be operative in the ability of these parameters to predict cardiovascular events. AMBP, ambulatory blood pressure BP, blood pressure ECG, electrocardiogram HF, high-frequency LF, low-frequency UAE, urinary albumin excretion Footnotes Address correspondence and reprint requests to Per Løgstrup Poulsen, Department of Medicine M (Diabetes and Endocrinology), Aarhus Kommunehospital, DK 8000 Aarhus C, Denmark. E-mail: logstrup{at}dadlnet.dk . Received for publication 23 May 2000 and accepted in revised form 8 December 2000.
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ISSN:0012-1797
1939-327X
DOI:10.2337/diabetes.50.4.837