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Lippincott, Williams & Wilkins, Journal of Hypertension, Supplement 1(33), p. e476, 2015

DOI: 10.1097/01.hjh.0000468885.98906.1f

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Pp.37.25

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Objective: In patients with sleep apnea increased sympathetic activity during waking life is accompanied by sustained reduction in vagal tone which leads to the reduction of total heart rate variability. Heart rate has been designated as independent cardiovascular risk factor. Several studies have shown that reduced HRV can predict increased risk for subsequent cardiac events. Aim was to investigate the level of heart rate and heart rate variability in patients with sleep apnea-hypopnea syndrome and without documented CV events. Design and method: Research included 100 patients who underwent polysomnograpic examination in UCC Kragujevac. According to apnea-hypopnea index (AHI) all patients were divided into 3 equal groups, 25 patients in each group (AHI 5-15; 15-30 and >30). Fourth group was a control with 25 patients without sleep apnea. 24 h ECG Holter monitoring was performed and all patients were divided in 3 groups according to the heart rate (low, normal and high). Additionally, we divided patients in low and high-risk group (HR <80/bpm and >80/bpm). HRV represents a measure of cyclic variations of beat-to-beat (RR) intervals assessed using time domain analysis and SDNN (standard deviation of the normalized N-N interval) as global index for HRV. All data were statistically analyzed in the SPSS for Windows. Results: Mean age of study population was 55.05 +/- 11.16 years. More than a half of patients had normal heart rate (60-80/bpm) - 69% (x2 = 61.58; p = 0.000), 24% of patients were in a high-risk vs 76% in low-risk group (x2 = 27.04; p = 0.000). Average mean heart rate during 24 h monitoring was 74.80 +/- 10.90 (51-123/bpm) with average minimal HR 48.00 +/- 6.59 bpm and average maximal HR 124.63 +/- 23.57 bpm. Mean SDNN was 136.14 +/- 44.87 ms. Majority of patients had normal heart rate variability - 71% (x2 = 69.26; p = 0.000), and only 5% had moderate low HRV, with no patients with low/reduced HRV. Conclusions: Although HRV was normal in majority of patients we cannot exclude it's influence in further development of cardiovascular events. Lack of reduction of HRV could be explained by small study sample, mean age of participants, use of therapy and other cofounding factors. Copyright