Trastornos respiratorios durante el sueño en pacientes con hipertensión arterial de difícil control

doi:10.1157/13083275

Archivos de Bronconeumología

Volume 42, Issue 1, January 2006, Pages 14-20

https://doi.org/10.1157/13083275 Get rights and content

Objetivo

Analizar la relación existente entre los trastornos respiratorios durante el sueño y la hipertensión arterial de difícil control (HTAr).

Pacientes y métodos

Se consideró HTAr cuando las cifras medias de la presión arterial sistólica (PAS) eran mayors o iguales a 125 mmHg y/o la diastólica (PAD) era igual o superior a 80 mmHg según el registro de 2 estudios de monitorización ambulatoria durante 24 h a pesar de la utilización de 3 o más fármacos antihipertensivos. Se realizó posteriormente una poligrafía respiratoria (Autoset) para el estudio de los trastornos respiratorios durante el sueño en todos los pacientes.

Resultados

Se incluyó en el estudio a 49 pacientes con una media (± desviación estándar) de edad de 68,1±9,1 años, PAS/PAD media de 152,5±13/89,2 ±8,5 mmHg y una media de 3,5 fármacos prescritos. El índice de apneas-hipopneas (IAH) fue de 26,2±19,5, de predominio obstructivo. Los pacientes con síndrome de apneas-hipopneas durante el sueño (SAHS) grave (IAH ≥ 30; 40,8%) presentaron mayor descontrol de la PAS tanto diurna (p = 0,017) como nocturna (pp = 0,033) que el resto de pacientes, así como mayor PAD diurna (p = 0,035) y toma de un mayor número de fármacos que quienes no lo presentaban (IAH<10; 28,6%) (p = 0,041). Tomados en su conjunto, los pacientes presentaron una correlación significativa entre las cifras de la presión arterial y la obesidad, además de existir una correlación ajustada significativa con el IAH sólo en los pacientes con SAHS. El IAH se mostró como el predictor independiente que más influyó en las cifras de la presión arterial de estos pacientes.

Conclusiones

En pacientes con HTAr la prevalencia de SAHS fue muy elevada. En los pacientes con SAHS, el IAH se mostró como el factor predictivo independiente más importante de las cifras de presión arterial.

Objective

To analyze the relationship between sleep-disordered breathing and difficult-to-control arterial hypertension.

Patients and methods

Patients were considered to have difficult-to-control hypertension when mean systolic blood pressure was 125 mm Hg or higher and/or mean diastolic blood pressure was more than or equal to 80 mm Hg (as recorded during 2 24-hour ambulatory monitoring studies) despite the use of 3 or more antihypertensive drugs. Respiratory polygraphy using the AutoSet device (ResMed Corp, Sydney, Australia) was then performed to study sleep-disordered breathing in all patients.

Results

Forty-nine patients with a mean (SD) age of 68.1 (9.1) years, mean systolic and diastolic pressures of 152.5 (13)/89.2 (8.5) mm Hg, and an average of 3.5 prescribed drugs were included in the study. The mean apnea-hypopnea index (AHI) was 26.2 (19.5) and events were predominantly obstructive. Patients with severe sleep apnea-hypopnea syndrome (SAHS) (AHI ≥ 30; 40.8%) showed more uncontrolled daytime (P=.017) and nighttime (P=.033) systolic pressure than the rest, as well as higher daytime diastolic pressure (P=.035) and a greater consumption of drugs than those without severe SAHS (AHI < 0; 28.6%) (P=.041). The study population as a whole showed a significant correlation between blood pressure and obesity. There was a significant correlation (adjusted for age and sex) with AHI only in patients with SAHS. AHI was found to be the independent predictor with the greatest effect on blood pressure in these patients.

Conclusions

Prevalence of SAHS was very high in patients with difficult-to-control hypertension. In patients with SAHS, AHI was found to be the independent predictor with the greatest affect on arterial blood pressure.

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Cited by (29)

Can pulse transit time be useful for detecting hypertension in patients in a sleep unit?
2014, Archivos de Bronconeumologia
Citation Excerpt :
This phenomenon is known as resistant HT11 and is associated with a greater incidence of cardiovascular episodes and complications.12 Several studies show a high rate of OSAHS (greater than 70%) in patients with resistant HT.10,13 The aim of early detection of hypertension and appropriate control with medication is to prevent cardiovascular complications and reduce high healthcare costs.14
Pulse transit time (PTT) is the time that a pulse wave takes to travel between two different arterial points, and may be useful in estimating blood pressure. This noninvasive technique, which does not add any cost to the procedure, offers the advantage of avoiding ‘arousals’ during sleep measurement as it occurs with ambulatory blood pressure monitoring (ABPM). We aim to confirm the usefulness of PTT for the detection of hypertension, and to study the correlation between both the measurements.
Prospective observational study in a multidisciplinary sleep unit. We recruited 30 consecutive patients attending a sleep clinic and ran a baseline polysomnography followed by an ABPM the following day. Average systolic and diastolic blood pressure (SBP, DBP) by PTT were calculated and compared with ABMP results. In accordance with international guidelines, patients with mean nocturnal ABMP≥120/70 mmHg were diagnosed as having arterial hypertension.
Mean age was of 60 years; 66% were male, of whom 80% suffered from sleep apnoea (OSAS). Taking the ABPM as the reference technique, we found that the diagnostic sensitivity of PTT is 85% with a specificity of 88% in the case of SBP, with a positive predictive value of 85% and negative predictive value of 88%. By studying the relationship between mean SBP measured by ABPM and PTT, we found a linear correlation coefficient (R) of 0.88, showing a distribution of all subjects with a difference of ±15 mmHg between the tests. There is also a positive correlation between mean DBP measured for the two tests and with a weaker linear correlation.
Pulse transit time shows a strong correlation with blood pressure (measured by ABPM). PTT provides continuous, non-invasive, cuffless blood pressure monitoring free of additional cost and could be an alternative for screening hypertension.
La relación causal entre el síndrome de apneas e hipopneas de sueño (SAHS) y la hipertensión arterial (HTA) es un hecho establecido en la literatura. El tiempo de tránsito de pulso (PTT) representa el tiempo que tarda el pulso en viajar entre 2 puntos arteriales diferentes, y puede ser útil en la estimación de la presión arterial (PA). Con este estudio se pretende valorar la utilidad del PTT en la estimación de la PA, ya que además de ser una técnica no invasiva y exenta de coste adicional, ofrece la ventaja de evitar arousals, como sucede con la monitorización ambulatoria de la PA (MAPA).
Estudio prospectivo y observacional realizado en una unidad multidisciplinar de sueño con la colaboración del servicio de Nefrología. Se reclutaron 30 pacientes consecutivos que acuden a consulta de sueño por sospecha de SAHS a los que se les realiza una polisomnografía (PSG) basal seguida de MAPA al día siguiente. Se calcula la PA sistólica (PAS) y la diastólica (PAD) media por PTT en la PSG y se compara con los resultados de la MAPA. Se diagnosticaron como pacientes con hipertensión arterial aquellos con cifras medias de MAPA durante la noche iguales o superiores a 120/70 mmHg, siguiendo normativas internacionales.
Edad media de 60 años (66% varones). El 80% eran SAHS (36% SAHS grave). La validez diagnóstica de HTA del PTT con respecto a la MAPA considerada como técnica de referencia fue: sensibilidad, 85%; especificidad, 88%; valor predictivo positivo, 85%, y valor predictivo negativo, 88%. El coeficiente de correlación lineal (R) entre la PAS media medida por MAPA durante la noche (desde las 24:00 h del día siguiente hasta las 6:00 h) y por PTT fue de 0,88, con un coeficiente de correlación intraclase de 0,88 (intervalo de confianza: 0,76–0,94), observándose una distribución de todos los sujetos entre ±15 mmHg de diferencia entre las pruebas.
Existe una correlación positiva entre el PTT y la MAPA en la HTA sistólica. El PTT podría ser una alternativa capaz de ofrecer una medición continua y no invasiva de cribado de HTA no conocida o mal controlada.
Hypertension and sleep apnea-hypopnea syndrome: changes in echocardiographic abnormalities depending on the presence of hypertension and treatment with CPAP
2009, Sleep Medicine
Citation Excerpt :
Recent studies have shown that patients with SAHS have a higher prevalence of hypertension than the general population, even after adjusting for different confounding variables, such as BMI, age and gender [6–8]. Furthermore, the apnea–hypopnea index (AHI) has been shown to be an independent predictor of difficult-to-control hypertension in patients with SAHS [9]. Cardiac dysfunction can be detected by echocardiography [10–12].
Sleep apnea–hypopnea syndrome (SAHS) is an emerging disease with high prevalence. There is controversy as to whether cardiac abnormalities are due to the disease itself or to the arterial hypertension frequently associated with this disease.
To analyze echocardiographic abnormalities in a population of SAHS patients depending on the presence or absence of hypertension at the time of diagnosis and after six months of treatment with continuous positive airway pressure (CPAP).
We studied 85 consecutive patients diagnosed with SAHS who required treatment with CPAP (Hypertensive: 43, nonhypertensive: 42). We performed a baseline echocardiogram after six months of treatment. We analyzed morphological (wall thickness, diameters, ejection fraction) and functional (peak E- and A-wave velocities, deceleration time, Tei index) parameters of the left and right ventricles.
Hypertensive patients were older and had higher blood pressure values, but there were no differences between groups in other clinical parameters. The hypertensive group had greater septal thickness (hypertensive: 12.1 ± 2.3; nonhypertensive: 10.8 ± 2.1 mm; p = 0.01). There were also differences in impairment of left (hypertensiveHT: 92.9%, nonhypertensive: 65%, p = 0.002) and right (hypertensive: 74.4%, nonhypertensive: 42.1%, p = 0.006) ventricular filling.
After six months of treatment, an improvement of the myocardial performance index was noted in nonhypertensive patients (baseline Tei: 0.55 ± 0.1 vs. 6-month Tei: 0.49 ± 0.1; p = 0.01), whereas no significant change was observed in hypertensive patients.
Cardiac abnormalities in SAHS patients are increased in the presence of associated hypertension. Treatment with CPAP for six months improves cardiac abnormalities in nonhypertensive patients but not in hypertensive patients.
Analysis of echocardiographic alterations observed in sleep apnea-hypopnea syndrome and how they are influenced by hypertension
2008, Revista Espanola de Cardiologia
El síndrome de apneas e hipopneas del sueño (SAHS) conlleva importantes repercusiones cardiacas que se pueden evaluar mediante métodos no invasivos como la ecocardiografía transtorácica; sin embargo, está por dilucidar si se deben a la propia enfermedad o a la influencia de factores concomitants como la hipertensión arterial (HTA). El objetivo de este estudio es analizar las alteraciones ecocardiográficas en pacientes con SAHS y si se modifican en caso de HTA concomitante.
Estudiamos a 103 pacientes consecutivos diagnosticados de SAHS e indicación de presión positive continua en la vía aérea (HTA, 49 pacientes; sin HTA, 54) frente a 24 controles ajustados por edad e índice de masa corporal. Realizamos ecocardiograma-Doppler por un observador para el que la asignación estaba enmascarada. Analizamos variables morfológicas (grosor de paredes y diámetros) y funcionales (fracción de eyección, velocidad máxima de ondas E y A, tiempo de deceleración mitral e índice Tei). Se compararon los resultados mediante ANOVA y test de Bonferroni.
Los pacientes hipertensos tuvieron más alteraciones morfológicas tipo hipertrofia ventricular izquierda (mayor grosor de septo y pared posterior) que los no hipertensos, y éstos más que los controles. Grosor del septo: SAHS-HTA (1), 12 ± 2; SAHS sin HTA (2), 11 ± 2, y controles (3), 9,5 ± 5 mm (1 frente a 2, p = 0,038; 1 frente a 3, p = 0,0001, y 2 frente a 3, p = 0,034). Pared posterior: SAHS-HTA, 11 ± 2; SAHS sin HTA, 10 ± 1, y controles, 9 ± 1,5 mm (1 frente a 2, p = 0,5; 1 frente a 3, p = 0,0001, y 2 frente a 3, p = 0,001). También hubo más alteraciones en el patrón de llenado ventricular izquierdo (SAHS-HTA, 92%; SAHS sin HTA, 72%, y controles, 29%; p = 0,0001) y derecho (SAHS-HTA, 72%; SAHS sin HTA, 58%, y controles, 25%; p = 0,001). Los valores del índice Tei del VI tuvieron tendencia a incrementarse (SAHS-HTA, 0,56 ± 0,2; SAHS sin HTA, 0,54 ± 0,12, y controles, 0,5 ± 0,1; 1 frente a 2, p = 0,8; 1 frente a 3, p = 0,09; 2 frente a 3, p = 0,7).
El SAHS presenta signos de hipertrofia ventricular izquierda y alteración del llenado biventricular aun en ausencia de HTA concomitante, y desde el momento de su diagnóstico. Las alteraciones detectadas son mayores cuando se asocia HTA.
Sleep apnea-hypopnea syndrome (SAHS) is associated with significant effects on the heart, which can be assessed using noninvasive methods such as transthoracic echocardiography. However, it is not clear whether these effects are due to the condition itself or are influenced by associated factors, such as high blood pressure (HBP). The objective of this study was to investigate the echocardiographic alterations observed in SAHS patients and how they are affected by the presence of concomitant HBP.
The study involved 103 consecutive patients (49 with HBP and 54 without) with SAHS and an indication for continuous positive airways pressure treatment and 24 controls matched for age and body mass index. Doppler echocardiography was performed in a blinded manner. Both morphology (i.e., wall thickness, and diameters) and function (i.e., ejection fraction, peak E and A wave velocities, mitral deceleration time, and Tei index) were assessed. Results were compared using ANOVA and Bonferroni's test.
Hypertensive patients had larger morphological changes characteristic of left ventricular hypertrophy (i.e., increased septal and posterior wall thicknesses) than nonhypertensive patients, who in turn had larger changes than controls (septal thickness: HBP-SAHS, 12 [2] mm; non-HBP SAHS, 11 [2] mm, and controls, 9.5 [5] mm; 1 vs. 2, P=.038; 1 vs. 3, P=.0001, 2 vs. 3, P=.034) (posterior wall thickness: HBP-SAHS, 11 [2] mm; non-HBP SAHS, 10 [1] mm, and controls, 9 [1.5] mm; 1 vs. 2, P=.5; 1 vs. 3,P=.034) (posterior wall thickness: HBP-SAHS, 11 [2] mm; non-HBP SAHS, 10 [1] mm, and controls, 9 [1.5] mm; 1 vs. 2, P=.5; 1 vs. 3, P=.0001; 2 vs. 3, P=.001). In addition, there were also greater changes in ventricular filling patterns on the left (HBP-SAHS, 92%; non-HBP SAHS, 72%, controls, 29%; P=.0001) and on the right (HBP-SAHS, 72%; non-HBP SAHS, 58%; controls, 25%; P=.001). There was a trend towards a larger left ventricular Tei index (HBP-SAHS, 0.56 [0.2]; non-HBP SAHS, 0.54 [0.12]; controls, 0.5 [0.1]; 1 vs. 2, P=.8; 1 vs. 3, P=.09; 2 vs. 3, P=.7).
From the time of diagnosis, SAHS was associated with left ventricular hypertrophy and impaired biventricular filling, even in the absence of concomitant HBP. The abnormalities observed were more severe when HBP was present.
Obstructive sleep apnea and resistant hypertension: A case-control study
2007, Chest
Citation Excerpt :
In a case series,9 OSAS was diagnosed in 83% of patients with resistant hypertension; this study did not have a control group and therefore could not exclude other factors associated with resistant hypertension. In another uncontrolled study,18 the AHI among patients with difficult-to-control hypertension was 26/h. In our study, case patients and control subjects were well matched for other risk factors for resistant hypertension, and the risk was independent of them in a multivariate analysis.
Obstructive sleep apnea syndrome (OSAS) has been linked to resistant hypertension, but the magnitude of this association and its independence of confounding have not been established.
Case patients were 63 patients with resistant hypertension (BP ≥ 140/90 mm Hg using at least three BP-lowering drugs, including a diuretic), and control subjects were 63 patients with controlled BP receiving drug treatment. The primary outcome was the frequency of OSAS (apnea-hypopnea index [AHI] ≥ 10 episodes per hour) determined with a portable home monitor. The comparison of AHI episodes in patients truly normotensive, truly hypertensive, and in patients with white coat or masked hypertension, based on BP determined at office and by ambulatory BP monitoring (ABPM) was a secondary outcome.
Case patients and control subjects were well matched for confounding factors. OSAS was present in 45 case patients (71%) and in 24 control subjects (38%) [p < 0.001]. In a logistic regression model, OSAS was strongly and independently associated with resistant hypertension (odds ratio, 4.8; 95% confidence interval, 2.0 to 11.7). The AHI of case patients with normal BP in ABPM (white coat hypertension) and control subjects with abnormal BP in ABPM (masked hypertension) was intermediate between the AHI of individuals with normal and abnormal BP measures in both settings (p < 0.001).
The magnitude and independence of the risk of OSAS for resistant hypertension strengthen the concept that OSAS is a risk factor for resistant hypertension. Comorbid OSAS should be considered in patients with resistant hypertension.
The ArchivosArchive, 2006: An overview of research published in archivos de bronconeumología
2007, Archivos de Bronconeumologia
Association of modifiable risk factors with obstructive sleep apnea: a Mendelian randomization study
2023, Aging

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OriginalesTrastornos respiratorios durante el sueño en pacientes con hipertensión arterial de difícil controlSleep-Disordered Breathing in Patients With Difficult-to-Control Hypertension

Objetivo

Pacientes y métodos

Resultados

Conclusiones

Objective

Patients and methods

Results

Conclusions

Association of sleep apnea, and hypertension in a large community-based study

JAMA

Population-based study of sleep-disordered breathing as a risk factor for hypertension

Arch Intern Med

Sleep apnea and hypertension. The role of peripheral chemoreceptors and the sympathetic system

Chest

Sympathetic over activity in the etiology of hypertension of obstructive sleep apnea

Sleep

Prospective study of the association between sleep-disordered breathing and hypertension

N Engl J Med

Sleep apnea syndrome: a possible contributing factor to resistant

Sleep

Detection and control of high blood pressure in the community. Do we need a wake-up call?

Hypertension

Inadequate management of blood pressure in a hypertensive population

N Engl J Med

Refractory hypertension

N Engl J Med

Prognosis in therapy-resistant hypertension

J Int Med

2003 European Society of Hypertension-European Society of Cardiology guidelines for the management of arterial hypertension World Health Organization-International Society of Hypertension Guidelines for the Management of Hypertension

J Hypertens

High prevalence of unrecognized sleep apnea in drug resistant hypertension

J Hypertens

Sleep-related breathing disorder is an independent risk factor for uncontrolled hypertension

J Hypertens

Obstructive sleep apnoea/ hypopnoea syndrome and hypertension

Thorax

1999 World Health Organization-International Society of Hypertension guidelines for the management of hypertension

J Hypertens

Validez de 6 métodos indirectos para valorar el cumplimiento del tratamiento farmacológico en la hipertensión arterial

Aten Primaria

Originales
Trastornos respiratorios durante el sueño en pacientes con hipertensión arterial de difícil controlSleep-Disordered Breathing in Patients With Difficult-to-Control Hypertension