Original Articles


An Analysis of Periodic Leg Movements During Sleep, 24-Hour Blood Pressure, and Heart Rate

 

Análisis del movimiento periódico de las piernas durante el sueño, la presión arterial de 24 horas y la frecuencia cardíaca

 

Análise dos movimentos periódicos das pernas durante o sono, pressão arterial de 24 horas e frequência cardíaca

 

Stella Maris Valiensi1, Agustin Folgueira2, Marcela Ponce de León2, José Alfie3

 

1- Neurologist. Sleep Medicine. Hospital Italiano de Buenos Aires. Instituto Universitario del HIBA. ORCID: https://orcid.org/0000-0003-3977-2457. Contact email: svaliensi@gmail.com

2- Neurologists. Sleep Laboratory, Hospital Italiano de Buenos Aires.

3- Hospital Italiano de Buenos Aires. Clinical Medicine Department. Arterial Hypertension Service.

 

 

 

 

 

 

Periodic leg movements during sleep, which are diagnosed by nighttime polysomnography, are associated with increases in arterial blood pressure and heart rate caused by sympathetic nervous system activity. In this work we study a sample of patients with pathological degree periodic leg movements, measuring arterial pressure during a 24-hour period while monitoring associated variables and heart rate.

 

 

 

 

KEY CONCEPTS:

Background

A recent study including hypertensive patients found no difference between daytime and nighttime averages or nighttime dips in arterial pressure between patients with periodic leg movments syndrome and controls.

 

Contributions

We found an inverse relation between arterial pressure and the severity of periodic leg movments in affected patients, contrary to expectations.

 

 

Abstract

Introduction: Periodic leg movements during sleep (PLMS), which are diagnosed by polysomnography, consist of stereotypical leg movements that occur repeatedly during sleep. Every event is accompanied by a micro-awakening and an increase in heart rate, arterial pressure and sympathetic nervous system activity. Objectives: To analyze the association between pathological PLMS indices and 24-hour arterial pressure in normotensive patients and compare it to that of patients with normal PLMS. To assess the association between pathological PLMS indices and changes in pulse wave velocity and heartrate. Methods: Observational study of cases and controls. We studied data from 19 normotensive patients by nighttime polysomnography and outpatient monitoring of arterial pressure who had pathological PLMS indices. The variables we considered were age, sex, weight and body mass index. Daytime, nighttime and 24-hour arterial pressure and heart rates were measured by 24-hour outpatient monitoring. We excluded patients with apnea / hypopnea ≥ 5 e/h. These variables were used to compare patients with and without PLMS, setting p-value tresholds of 0.05 and using correlation analysis to determine statistical significance. Results: We studied 11 patients with pathological PLMS and 7 controls (PLMS index 35.6±15 vs 7.9±5, respectively). Patients with PLMS were younger (57 ± 14 years vs 64±6 years; p=0.284). 24-hour arterial blood pressure was lower in the PLMS group than in controls (systolic 114.2±11 versus 123±11; p=0.095; and dyastolic 65.7±5 versus 74.4±11, p=0.027). Conclusion: We found a statistically significant negative correlation between pathological PLMS, 24-hour systolic blood pressure, daytime and nighttime systolic pressure, and average nighttime arterial pressure, and found a similar negative correlation between 24-hour pulse pressure and daytime pulse pressure in normotensive patients, which was lower in patients in the control group, who had normal PLMS indices. We did not find differences in heart rate. Collecting data from a larger sample is necessary.

Keywords: polysomnography; arterial pressure; heart rate; systolic arterial pressure.

 

 

Resumo

Introdução: Os Movimentos Periódicos das Pernas Durante o Sono (PLMS), diagnosticados por polissonografia, são caracterizados por movimentos estereotipados das pernas que aparecem repetidamente à noite. Cada PLMS está associado a microdespertar e aumentos na frequência cardíaca, pressão arterial e atividade simpática. Objetivos: Analisar a associação entre o índice patológico de MPMS e PA de 24 horas em pacientes normotensos. Avaliar a associação entre índice patológico de MPMS, com alterações na velocidade da onda de pulso. Métodos: Estudo observacional de casos e controles. 19 indivíduos normotensos foram estudados por Polissonografia Noturna e Monitorização Ambulatorial da Pressão Arterial. As variáveis ​​foram determinadas: Idade, sexo, peso, índice de massa corporal. A pressão arterial e a frequência cardíaca de 24 horas, diurnas e noturnas foram avaliadas com monitorização ambulatorial da pressão arterial de 24 horas. Foram excluídos pacientes com índice de apneia/hipopneia ≥ 5 e/h. As variáveis ​​foram descritas e sujeitos com e sem PLMS foram comparados, considerando-se significante um p<0,05, além de análise de correlação. Resultados: Onze pacientes com PLMS patológicos e 7 controles foram estudados. Índice de PLMS 35,6±15 versus 7,9±5, respectivamente. Os pacientes com PLMS eram mais jovens 57±14 versus 64±6; p=0,284. A pressão arterial de 24 horas foi menor no grupo PLMS do que nos controles (sistólica 114,2±11 versus 123±11; p=0,095; e diastólica 65,7±5 versus 74,4±11, p=0,027). Conclusão: Encontramos uma relação inesperada, inversa e estatisticamente significativa ao correlacionar movimentos periódicos das pernas de grau patológico durante o sono com pressão arterial sistólica e média de 24 horas, pressão arterial sistólica diurna e noturna e pressão arterial média. A pressão de pulso de 24 horas e a pressão de pulso diurna e noturna que foram inferiores ao grupo controle. Não encontramos alterações na frequência cardíaca.

Palavras-chave: polissonografia; pressão arterial; frequência cardíaca; pressão arterial sistólica.

 

 

 

 

Introduction

Periodic leg movements during sleep (PLMS) consist of regular, very stereotypical involuntary movements, including repeated extensions of the first toe, generally accompanied by hip, knee and ankle flexions, lasting from 0.5 to 10 seconds, which appear every five to ninety seconds and must be produced in series of at least 4 consecutive rounds. Polysomnography is necessary for diagnosis. PLMS is considered pathological when more than 5 PLMS events per hour occur, in the case of children, and 15 PLMS events per hour, for adult patients. These are the current values, but formerly values were lower (10 or more per hour). (1,2).

In general, patients with PLMS present no symptoms, especially when leg movements do not interrupt sleep. Fluctuations in occurence from one night to another is significant (3,4).

Given patients are rarely aware of suffering the disease, diagnoses are usually made by accident, when polysomnography studies are requested because of other sleep-related pathologies. Sometimes, patients "kick" repeatedly during sleep and find sheets spread on the floor or at their bedside.

The prevalence of PLMS in the general population is estimated to be around 5% or 6% in patients between ages 30 and 40, and 30% in patients older than 50 years, increasing with age. In total, it affects around 5% to 15% of the population, is more frequent in women, and is found in 85% of patients suffering from restless leg syndrome (now termed Willis Ekbom disease(5-7)), which is a syndrome characterized by sensory-motor anomalies (8) occuring while in a state of wakeful rest, improves with exercise, and can be diagnosed by a clinician.

There is a higher prevalence of periodic leg movement during sleep in hypertensive patients, when compared to the general population (9-11).

The impact of nighttime periodic leg movements in arterial pressure over the whole day is not known (12). We conjecture the number of leg movement events could have a sustained impact in sympathetic system activity and increase arterial pressure over the whole day, as well as affect how rigid arterial walls are, as measured by pulse wave velocity.

Thus, we analyzed the association between pathological periodic leg movement syndrome and 24-hour arterial pressure in normotensive patients.

As a secondary objective, we aimed to assess the association between pathological PLMS indices, pulse wave velocity, and heart rate.

 

Methods

Cases and controls study, with informed consent, approved with protocol number 2264 by Comité de Estudios de Protocolos de Investigación of our hospital. Both arterial pressure and polysomnography studies (level 2) were carried out by the outpatient department of Hospital Italiano de Buenos Aires.

Our sample consisted of patients who were referred to the sleep laboratory of the adult neurology service by their general practitioners in order to conduct a polysomnography for diagnosing some sleep disorder.

 

Selection criteria split the sample into:

 

Inclusion criteria

Patients older than 18 years

Pathological degree PLMS as measured by a nighttime polysomnography, with or without oximetry, with PLMS indices ≥ 10 per hour.

 

Exclusion criteria

Patients with a history of:

 

Variable definitions:

We defined periodic leg movements during sleep as the presence of 4 (four) or more consecutive inferior limb movements separated by intervals lasting at least 5 seconds and at most 90 seconds. Patients with ≥ 10 periodic leg movements per hour were considered cases. PLMs were measured by polysomnography, with or without oximetry.

Electromyogram electrodes were placed in both anterior tibial muscles. Patients were monitored following the habitual protocol for conducting polysomnography studies, defined in the AASM (American Academy of Sleep Medicine) standards (1), and PLMS were determined using criteria established by the International Restless Legs Syndrome Study Group (IRLSSG) (2).

Office Arterial Pressure Monitoring (PAC) was carried out by the arterial hypertension service of our hospital, arterial pressure was measured while sitting after 15 minutes of rest in standardized conditions, three times, set apart by two minute intervals, using calibrated and validated automatic equipment (HEM-705 CP OMROM®) using an adequate-size cuff.

For 24-Hour Outpatient Arterial Pressure Monitoring, a calibrated and validated Spacelabs Healthcare® model 90207 was used, with cuffs that were appropriate for the study participants' arm circumference. The device was programmed to collect measures every 15 minutes from 6:00 to 22:00 hours, and every 20 minutes from 22:00 to 6:00 hours, respecting sleep time as much as possible. Studies were carried out during business days, instructing patients to carry out their regular activities while keeping a record in a journal. Once the study finished, measures were considered valid when at least 70% of all samples were satisfactory and there was at least one valid measure per hour. Daytime and nighttime periods were determined based on the sleep times recorded by the patient. Averages and standard deviations were computed for 24-hour arterial pressure, Daytime and nighttime arterial pressure (diastolic and systolic values). Arterial hypertension was defined as 24-hour records with, ³ 130 and / or 80 mmHg; Daytime arterial hypertension³ 135 and / or 85 mmHg and Nighttime arterial hypertension as values of ³ 120 and / or 70 mmHg.  

It is known that arterial pressure decreases during the night (because of cyrcadian rhythms regulating arterial pressure). Normal nighttime decreases are between 10% and 20%. Patients whose blood pressure dips within this range are said to be dipping patients. Patients whose pressure drops are below 10% are considered nondipping, and patients whose drops are above 20% are said to have hyper-dipping.

In order to estimate the impact that medications frequently administered during the outpatient protocol have on sleep quality, patients were asked to fill a self-reported questionnaire aimed at comparing habitual sleep and protocol sleep subjectively. To this end, we instructed the patient to indicate if: their sleep was the same, was altered for less than two hours, for two to four hours, or more than four hours.

To calculate femoral-carotid pulse wave velocity (VOP) carotídeo-femoral, we used specialized equipment (Aortic®) that measured PWV (m/seg) in a single step, since it registered carotid and femoral wave pulse simultaneously. To this end, the equipment uses two tonometric transducers, which are placed simultaneously over the carotid artery on the neck and the femoral artery on the inguinal region. After that, the time between both wave foots is measured using the "foot to foot" method. Wave foots are identified via intersecting tangets. The most frequently applied method for measuring the distance between two pulses requires two measurements, the first from the sternal notch to the place where pulse was detected in the carotid artery (E-C) and the second from the notch to the place where femoral pulse was detected. The final distance measurment used in our computation of pulse wave velocity was (E-F) distance – (E-C) distance, in meters (substractive method).

Changes in arm arterial pressure do not always correspond to changes in aortic arterial blood pressure. Hence, central arterial pressure analysis, is required to obtain infromation about arterial rigidity. Central wave pulse measuring can be used to obtain the augmentation index, which measures increases in central systolic arterial blood pressure, using the effect of wave reflection. Measuring central aortic pressure, or rather analyzing

central wave pulse , makes it possible to infer several other quantities asides from systolic arterial pressure, diastolic arterial pressure, and central pulse pressure. Pressure waves are composed of an incident wave, starting with ventricular ejection, and a reflection wave formed by reflection in sites where arteriae branch. Central aortic blood pressure measures and augmentation indices are obtained non-invasively by peripheral arterial tonometry.

When patients are young, and hence have elastic arteriae, pulses occur during diastole, given which they have no effect on maximum systolic pressure . On the contrary, as patients age and vessels become more rigid, pulses are transmitted to the aorta first (in systole), increasing central systolic arterial pressure; the ratio between that increase and total pulse pressure is known as augmentation index, which is defined as the difference between the second and first systolic peaks, expressed as percentages. There is evidence that increases in augmentation index are associated with greater risk of cardiovascular disease. Wave pulse velocity and age are known to be two other fundamental factors. Increases in systolic pressure and augmentation indices were computed based on radial pulse.

 

Procedures and data collection

 

Case patients were selected by diagnosis of periodic leg movements during sleep based on polysomnography. They were invited to participate and those who accepted were asked to fill in an informed consent form, their questions about the procedure and meaning of informed consent were answered, and their signature was requested. We recorded some of the data gathered during polysomnography. Since normally healthy individuals do not require examination by polysomnography, a small control group was included. Each control patient was matched based on sex and age. Patients were cited for taking office and outpatient protocol measurements of blood pressure within the next 30 days. Costs derived from this study did not involve any sepending on the part of the study subjects or their healtchare service providers, given only commonly used diagnostic tests were required.

 

Statistical analysis

 

Continuous variables were described as averages or medians. Categorical variables were expressed as percentages. For comparing data from case and control patients collected with the outpatient protocol we used the t-test for matched samples. For comparing continous data we used Pearson bivariate correlation adjusted by age. We considered differences with p-values below 0.05 as statistically significant. Statistical analysis was carried out using SPSS version 20.

 

Results

We studied 11 patients with PLMS (PLMS group) and n=7 controls. Most patients in both groups were women.

The general characteristics of each group are summarized in table 1. We show a descriptive analysis of the variables under consideration in the PLMS group, were median age was 59 years and BMI was 26.93. We also show the descriptive analysis of several variables analyzed by the control group, whose average age was 64 years and BMI was 27.13 (considered overweight).

In table 2, we observe the comparative analysis of variables associated with arterial pressure, pulse pressure and heart rate between the PLMS group and the control group. We found significant differences. The control group had higher values in 24-hour dyastolic arterial pressure, 24-hour average arterial pressure, daytime dyastolic arterial pressure and daytime average arterial pressure. We found no significant differences regarding pulse pressure and heart rate. We found patients with PLMS had lower 24-hour arterial pressure than controls, and day-night arterial pressure rhythms were preserved.

Table 3 summarizes the Pearson correlation between general quantitative variables and PLMS indices, and shows no statistically significant associations were found.

Table 4 shows correlations between variables linked to arterial pressure and PLMS indices. We found a statistically significant inverse relation between 24-hour systolic arterial pressure, 24-hour average arterial pressure, daytime dyastolic arterial pressure, nighttime systolic arterial pressure and nighttime average arterial pressure and PLMS indices, and made similar findings when analysing pulse pressure (PP 24, PP D, PP N). Age did not have a significant effect on PLMS index.

 

 

 

 

 

 

Table N° 1: Descriptive analysis of quantiative variables in the abnormal PLMS group (n=11) and the control group (n=7). Comparative analysis (T-test)

 

PLMS Group (n=11)

Control group (n=7)

p

 

 

Min

Max

Average

Number of awakenings

Min

Max

Average

Number of awakenings

 

General Variables

PLMS indices

15

66

34.67

15.7

0

13

7.91

5.3

0.001

 

Number of Awakenings

1

35

17.57

11.2

11

40

24.33

14.6

0.442

 

Age

24

73

58.27

14.6

53

71

63.71

6.5

0.37

 

Weight

54

89

69.32

11.7

63

95

76.37

10.9

0.252

 

Height

151

170

160.3

5.4

161

171

167.83

3.7

0.01

 

Abdominal perimeter

65

102

86.3

12.4

79

110

89.33

11.5

0.634

 

Neck perimeter

32

43

37.5

3.5

33

42

38.4

3.6

0.647

 

BMI

21

35

26.93

4.2

22

34

27.13

4

0.925

 

PLMS Index: Periodic Leg Movement During Sleep Index.

MBI: Body-Mass Index.

 

 

 

 

 

Table N° 2: Comparative Analysis (T-test) of quantitative variables related to arterial pressure in the PLMS group and the control group.

 

PLMS Group (n=11)

Control group (n=7)

p

 

Min

Max

Average

Number of awakenings

Min

Max

Average

Number of awakenings

Variables Linked to Arterial Pressure

24-Hour systolic arterial pressure

101

133

115.27

10.3

108

134

123

10.5

0.143

24-hour diastolic arteriall pressure

55

72

65.82

5.4

57

90

74.43

10.8

0.03

24-hour pulse pressure

73

93

83.64

6.8

82

104

91.86

8.7

0.038

24-hour diastolic arterial pressure

37

63

49.45

8.2

39

54

44.29

5

0.154

24-hour heart rate

57

84

67.55

8

59

84

66.71

8.9

0.839

Daytime SAP

103

137

119.09

10.5

113

138

128

9.9

0.091

Daytime diastolic arterial pressure

57

77

69

5.6

58

96

79

11.9

0.028

Daytime diastolic arterial pressure

78

97

87.45

7.1

85

110

96.57

8.9

0.028

Daytime diastolic blood pressure

37

65

50

8.1

40

74

49.29

12

881

Daytime heart rate

57

88

70.73

9.4

62

88

69.43

9.3

0.778

Nighttime systolic arterial pressure

84

120

104.64

10.2

93

126

109.71

12.5

0.357

Nighttime diastolic arterial pressure

48

63

56.09

5.5

52

76

62.71

9.4

0.076

Nighttime diastolic arterial pressure

61

83

73.91

6.5

69

89

79.71

8.3

0.117

Nighttime diastolic arterial pressure 

35

59

48.36

8.9

39

74

47.14

12.4

0.811

Nighttime heart rate

51

67

58,09

6

52

74

59,86

8.2

0,605

Office systolic arterial pressure

92

116

107,5

8,4

93

122

107,83

11.7

0,948

Office diastolic arterial pressure

58

82

68.7

7.5

68

88

77

7.3

0.048

Office pulse pressure

27

50

38.9

8.7

24

42

31

7.9

0.091

Au mmHg

6

22

12

5.1

6

12

8.67

2.5

0.157

Lau %

18

43

30.7

8.7

22

31

28

3.7

0.487

Systolic blood pressure - Pulse wave velocity

98

142

112.11

14

103

126

114.33

9.6

0.741

Diastolic arterial pressure - Pulse wave velocity (PAD vop)

52

67

60.56

5,2

62

89

71.83

10.4

0.015

Heart rate - Pulse wave velocity (FC vop)

45

68

57.78

6.7

44

72

56.83

11.1

0.84

Radial pulse wave velocity

6

8

6.53

0.8

5

8

6.6

1.1

0.886

Femoral pulse wave velocity

5

10

7.61

1.7

7

11

8.68

1.7

0.248

Daytime average arterial pressure - Nighttime average arterial pressure

9

17

13,55

2,6

6

23

16,86

5,8

0,112

Dipping

11

22

15,49

2,9

7

25

17,37

5,9

0,377

PAS:  Systolic arterial pressure.  PAD:  Diastolic Arterial Pressure. PAM:  Average Arterial Pressure. PP:  Pulse Pressure. Au mmHG: augmentation. I_au%: augmentation indices %. FC: Heart rate. VOP: Pulse wave velocity

 

 

 

Table N° 3. Pearson correlation between quantitative variables and PLMS indices.

General variables of the population under study

Grupo MPP

Grupo Control

PLMS+Control

PLMS (x Edad)

PLMS+Control (x Edad)

 

 

r

p

r

p

r

p

r

p

r

p

 

Number of Awakenings

-0,73

0,06

-0,19

0,88

-0,58

0,08

-0,61

0,39

-0,59

0,22

 

Age

-0,43

0,18

-0,45

0,3

-0,45

0,06

 

 

---

---

 

Weight

0,09

0,81

-0,59

0,22

-0,23

0,39

-0,86

0,14

-0,11

0.84

 

Height

0,58

0,08

-0,48

0,34

-0,22

0,4

0,62

0,38

-0,61

d.d

 

Abdominal perimeter

-0,01

0,97

-0,66

0,15

-0,16

0,54

-0,9

0,1

-0,11

0.84

 

Neck perimeter

0,38

0,28

-0,55

0,34

0,07

0,81

0,7

0,3

0,57

0,23

 

BMI

-0,14

0,7

-0,44

0,38

-0,14

0,62

-0,91

0,09

0,08

0,88

 

 

 

 

Tabla N° 4: Correlación de Pearson de Variables Cuantitativas relacionados con la Presión Arterial contra el Índice de PLMS.

Variables relacionadas con la Presión arterial

Grupo PLMS

Grupo Control 

PLMS+ control 

  Grupo PLMS (x Edad)

PLMS+Control (x Edad)

 

r

p

r

p

r

p

r

p

r

p

PAS 24 hs

-0,7

0,02

0,1

0,83

-0,59

0.01

-0,77

0,23

-0,85

0.03

PAD 24 hs

-0,12

0,73

-0,49

0,27

-0,46

0,05

0,08

0,92

-0,58

0,22

PAM 24 hs

-0,58

0,06

-0,32

0,48

-0,63

0

-0,47

0,53

-0,78

0,07

PP 24 hs

-0,79

0.004

0,24

0,61

-0,17

0,51

-0,84

0,16

-0,25

0,64

FC 24 hs

0,42

0,19

-0,35

0,44

0,21

0,41

-0,23

0,77

0,06

0,91

Daytime SAP

-0,64

0.03

0.03

0,95

-0,61

0.01

-0,54

0,46

-0,79

0,06

Daytime diastolic arterial pressure

-0,06

0,86

-0,5

0,25

-0,46

0,05

0,19

0,81

-0,51

0,3

Daytime diastolic arterial pressure

-0,54

0,09

-0,37

0,41

-0,63

0

-0,31

0,69

-0,71

0,11

Daytime diastolic blood pressure

-0,76

0.01

0,51

0,24

-0,23

0,35

-0,75

0,25

-0,21

0,69

Daytime heart rate

0,49

0,13

-0,33

0,47

0,27

0,27

0.01

0,99

0,28

0,58

Nighttime systolic arterial pressure

-0,81

0

0,26

0,57

-0,52

0.03

-0,91

0,09

-0,85

0.03

Nighttime diastolic arterial pressure

-0,2

0,55

-0,44

0,32

-0,44

0,07

-0,16

0.84

-0,65

0,16

Nighttime diastolic arterial pressure

-0,64

0.03

-0,13

0,77

-0,57

0.01

-0,62

0,38

-0,81

0,05

Nighttime diastolic arterial pressure 

-0,8

0

0,58

0,17

-0,24

0,34

-0,96

0,04

-0,26

0,61

Nighttime heart rate

0

0,991

-0,37

0,41

-0,14

0,58

-0,71

0,29

-0,51

0,3

Office systolic arterial pressure

-0,09

0.8

0,59

0,22

0.01

0,96

0,51

0,49

0,29

0,57

Office diastolic arterial pressure

0,47

0,17

0,21

0,69

-0,14

0,61

0,53

0,47

-0,07

0,9

Office pulse pressure

-0,46

0,18

0,69

0,13

0,16

0,56

-0,53

0,46

0,6

0,21

Au mmHg

-0,072

0,02

0,79

0,06

-0,1

0,72

-0,89

0,11

0.01

0,98

Lau %

-0,78

0.01

0,59

0,22

-0,31

0,24

-0,94

0,05

-0,35

0,49

PAS - VOP

-0,63

0,07

0,4

0,43

-0,4

0,14

-0,41

0,59

-0,4

0,45

PAD - VOP

-0,24

0,54

-0,49

0,32

-0,57

0.03

-0,27

0,73

-0,74

0,09

FC - VOP

0,54

0,17

-0,11

0,83

0,23

0,41

0,71

0,29

0,36

0,48

VOP radial

0,06

0,87

-0,22

0,67

-0,03

0,92

0,13

0,74

0.03

0,92

VOP femoral

-0,57

0,08

0,24

0,64

-0,49

0,05

-0,44

0,23

-0,23

0,42

Daytime average arterial pressure - Nighttime average arterial pressure

0,13

0,7

-0,38

0,4

-0,3

0,23

0,21

0,55

-0,32

0,21

Dipping

0,4

0,23

-0,31

0,49

-0,07

0,79

0,43

0,21

-0,13

0,62

PLMS Index: Periodic Leg Movement During Sleep Index. MBI: Body-Mass Index. PAS:  Systolic arterial pressure.  PAD:  Diastolic Arterial Pressure. PAM:  Presión Arterial Media.  FC: Frecuencia Cardíaca. PP:  Presión de Pulso.  Au mmHG: aumentación

I_au%: índice de aumentación %

VOP: Pulse wave velocity

 

 

 

 

 

Discussion

This work analysed PLMS and sought to determine if it affects blood pressure, heart rate and associated variables during 24 hour periods, in a small population without comorbidities.

The abscence of nighttime arterial pressure dipping is a predictor of cardiovascular mortality(13), coronary disease(14) stroke (15,16), heart failure, Cheyne Stokes(17-33), and heart transplant (18). Fragmented sleep, low sleep efficiency, insomnia, deppression and anxiety, more so when comorbid with metabolic disregulation, like diabetes, obesity and dyslipidemia, have been associated with sympathic hyperactivity, and consequently with increases in blood pressure and SPI (17).

Certain studies have demonstrated a temporal coincidence between PLMS and increases in heart rate and arterial pressure, which are more pronounced when PLMS are accompanied by micro-awakening EEGs, even in the abscence of visible awakenings detectable by EEG (19-21), which are linked to repetitive activation of the autonomic nervous system.

Several efforts have been made to establish a relationship between hypertension and periodic leg movements (22). In a 821 subject sample, the relative risk of hypertension was twice as high for subjects with periodic leg movement indices above 30 per hour (RR 2.26; confidence interval 95%: 1.28-3.99) after controlling for confounding factors such as body-mass index or age. The probability of presenting with arterial hypertension increases in proportion to the severity of periodic leg movements during sleep (23). However, even though an association can be established, many of the studies contributing supporting evidence are transversal, and hence it is hard to establish causal relations. However, speculations can be made about the nature of this relation and possible physiopathologic mechanisms involved.

We found significant differences between PLMS and the control group when comparing variables associated with arterial pressure and heartrate: DAP_24, MAP_24, DAP_D and MAP_D were higher in the the control group, and no significant differences were found for systolic arterial pressure. No significant differences in pulse pressure and heartrate were found either.

It has been suggested that autonomic microawakenings due to sympathetic hyperactivation co-occur with PLMS, confirmed by several authors (24,25), both for NREM and REM sleep(26), being the sympathetic nervous system the main system involved (27-29).

Other studies found changes in heart rate using spectral analyses of EEG (30), even in the abscence of awakenings that were directly visible in EEG. These autonomic changes in sympathetic hyperactivity have been found both during sleep and wakefulness (31) in patients with PLMS. However, in our study we found no changes and/or significant differences in heart rate or wave pulse pressure between both groups. Correlation analysis of all variables showed the PLMS group had lower values of 24-hour systolic arterial pressure, pulse pressure, systolic pressure, average 24-hour arterial pressure and average nighttime arterial pressure.

In the literature, there is evidence that confounding factors associated to both Willis-Ekbom disease, which include the simultaneous prescence of diabetic polyneuropathy, anemia, or kidney failure, which could increase cardiovascular and cerebrovascular morbidity(13). Since our inclusion criteria were strict, it is possible that our patients were in good health during the study, and hence had lower values as compared to the control group.

More recently, another study (starting later than ours) gathered a large sample, included hypertensive patients, and found no correlation between PLMS and 24-hour, nighttime and daytime arterial pressure and heartrate. Decreases in arterial pressure between cases and controls(33).

As regards treatment, Manconi et al speculate that D3 receptors in sympathetic preganglionar neurons in the intermediolateral horn of the spinal chord could be involved in responses to pramipexol, a dopaminergic agonist, and suggested that the risk of cardiovascular disease and autonomic dysfunction affecting patients with restless leg syndrome and periodic leg movement syndrome could be significantly reduced by treatment, given that in their study (which so far has not been reproduced) they observed a decrease in arterial pressure (32), which was something we took into account in our sample, given none of our patients was being treated with dopaminergic agonists.

 

Limitations

The results obtained by the present study must be interpreted in the light of several limitatons, such as: 

First, the number of patients affected by PLMS who were analyzed in this study was small. Although polysomnography studies are requested routinely, patients suffering from it have many comorbid conditions, given which it is hard to find patients who are not affected by disease and agree to undergo all the required examinations, which are cumbersome in terms of schedule, transportation costs, and other practical issues.

Second, it must be considered that PLMS, as a disease, is usually associated to other disorders which could act together to raise arterial pressure and cardiovascular risk. We did, however, make an effort to exclude all other confounding factors. However, since 25% of patients affected by PLMS are casual findings, this work could be used as a small model.

Third, the protocol was started in 2013/2014, when pathological PLMS indices were defined as 10 movements per hour or above, and international standards changed the year we put this protocol into practice.

It could be argued that one of the strong points of this article is that it only included normotensive patients without obstructive sleep apnea. The work that is most similar to ours is (33), which started on a later date and included a larger sample with hypertensive patients, did not find an association between arterial pressure and 24-hour heart rate, during both sleeptime and waketime, and did not observe the arterial pressure dip from day to night between cases and controls.

 

Conclusions

 

The analysis of periodic leg movement during sleep in pathological degree and its association to arterial pressure, pulse pressure and heartrate did not exhibit the expected inverse relationship between arterial pressure and the severity of periodic leg movement syndrome. In our analysis, we did find a significant association between pathological PLMS, reduced 24-hour systolic arterial pressure, systolic pressure, pulse pressure, and average 24 hour arterial pressure and nighttime arterial pressure. We found patients with pathological PLMS did not show the expected arterial pressure dip. We consider it necessary to analyze a larger sample in order to reassess these results.

 

Ethical considerations, data confidentiality and safety

This study was carried out in total agreement with national and international norms currently in force: the Helsinki declaration and the world medical association and the norms for good clinical practice ICH E6.

Participation in this study was in all cases voluntary and certified by the process of informed consent. At all times, the right to nonparticipation was respected, without that implying any form of discrimination, mistreatment or differential treatment, for any patient.

At all times patient identity and data were protected following national law 25.326 on personal data protection (Habeas Data), in accordance with international norms regulating the storage of disease data and personal and private data, following the 18th world medical assembly in Helsinki (1964), where applicable. Data confidentiality was guaranteed, since data that enabled patient identification was separate from clinical data obtained in the study, and an ID number was used in all databases and spreadsheets, instead of the patient's name. All practices were noninvasive and carried out during daily clinical practice, and did not bear any additional risk for patients, given which hiring insurance was not required.

 

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Limitations of liability:

Responsibility for this work lies exclusively with those who collaborated in conducting this study.

 

Conflict of interest:

None.

 

Funding:

The present work did not receive any funding

 

Originality:

This article contains original work exclusively and has not been sent for publication to any other scientific media outlet, nor in partial nor in total form.

 

Grant of rights:

Those who participated in conducting this study grant authorship rights to Universidad Nacional de Córdoba for publication in Revista de la Facultad de Ciencias Médicas and translation into english.

 

Authors' contributions:

All authors participated in the design and conduction of this study, collected data and helped in writing the manuscript, and claim responsibility for its content and the contents and approve its final version.

Derivative work notice:

Obra derivada: Traducción del artículo "Análisis del movimiento periódico de las piernas durante el sueño, la presión arterial de 24 horas y la frecuencia cardíaca", escrito por Valiensi et al, publicada en Rev Fac Cien Med Univ Nac Cordoba. 2023; 80 (3), realizada por la Revista de la Facultad de Ciencias Médicas de Córdoba

This derivative work is a translation of the article "Análisis del movimiento periódico de las piernas durante el sueño, la presión arterial de 24 horas y la frecuencia cardíaca", authored by Valiensi et al, published in Rev Fac Cien Med Univ Nac Cordoba. 2023; 80 (3), produced by Revista de la Facultad de Ciencias Médicas de Córdoba

 

 

 

 

Recibido: 2022-02-19 Accepted: 2022-04-11

 

DOI: http://dx.doi.org/10.31053/1853.0605.v80.n1.36765 

  

https://creativecommons.org/licenses/by-nc/4.0/

 

©Universidad Nacional de Córdoba