RESUMEN
Untreated obstructive sleep apnea (OSA) is common in patients with hypertension and may impair blood pressure (BP) and target-organ damage responses to antihypertensive therapy. In this study, we recruited hypertensive patients who underwent treatment with a 30-day regimen of hydrochlorothiazide 25 mg plus enalapril (20 mg BID) or losartan (50 mg BID) and were assessed with a baseline clinical evaluation, polysomnography, 24-hour ambulatory BP monitoring, and carotid-femoral pulse wave velocity. All the examinations except for polysomnography were repeated at 6 and 18 months of follow-up. We studied 94 hypertensive patients (mean age, 55±9 years). The frequency of OSA was 55%. Compared with baseline, we did not observe significant differences between groups in 24-hour BP, daytime systolic and diastolic BPs, or night-time systolic BP at 6 and 18 months. The BP control rate at 24 hours (<130/80 mm Hg) was similar between the groups (baseline, 42.3% versus 45.2%; 6 months, 46.9% versus 57.5%; 18 months, 66.7% versus 61.5%). However, patients with OSA had higher night-time diastolic BP decrease than did the non-OSA group (6 months, -4.9±11.8 versus -0.3±10.3 mm Hg; 18 months, -6.7±11.1 versus -1.2±10.6 mm Hg; P=0.027). There were no differences in the number and class of antihypertensive medications prescribed during follow-up. In terms of arterial stiffness, patients with OSA had higher pulse wave velocity than did patients without OSA at baseline (10.3±1.9 versus 9.2±1.7 m/s; P=0.024), but both groups had similar decreases in pulse wave velocity during follow-up. In conclusion, with combined antihypertensive treatment aimed at controlling BP, hypertensive patients with OSA had similar 24-hour BP and arterial stiffness to those without OSA.
Asunto(s)
Antihipertensivos/uso terapéutico , Presión Sanguínea/fisiología , Hipertensión/tratamiento farmacológico , Apnea Obstructiva del Sueño/etiología , Rigidez Vascular/fisiología , Presión Sanguínea/efectos de los fármacos , Monitoreo Ambulatorio de la Presión Arterial , Femenino , Estudios de Seguimiento , Humanos , Hipertensión/complicaciones , Hipertensión/fisiopatología , Masculino , Persona de Mediana Edad , Polisomnografía , Pronóstico , Análisis de la Onda del Pulso , Estudios Retrospectivos , Apnea Obstructiva del Sueño/fisiopatología , Factores de Tiempo , Rigidez Vascular/efectos de los fármacosRESUMEN
Whether sex influences the association of obstructive sleep apnea (OSA) with markers of cardiovascular risk in patients with hypertension is unknown. In this study, 95 hypertensive participants underwent carotid-femoral pulse wave velocity, 24-hour ambulatory blood pressure monitoring, echocardiogram, and polysomnography after a 30-day standardized treatment with hydrochlorothiazide plus enalapril or losartan. OSA was present in 52 patients. Compared with non-OSA patients, pulse wave velocity values were higher in the OSA group (men: 11.1±2.2 vs 12.7±2.4 m/s, P=.04; women: 11.8±2.4 vs 13.2±2.2 m/s, P=.03). The proportion of diastolic dysfunction was significant in men and women with OSA. Compared with non-OSA patients, nondipping systolic blood pressure in OSA was higher in men (14.3% vs 46.4%) and in women (41.4% vs 65.2%). OSA was independently associated with pulse wave velocity (ß=1.050; P=.025) and nondipping systolic blood pressure (odds ratio, 3.03; 95% confidence interval, 1.08-8.55; P=.035) in the regression analysis. In conclusion, OSA is independently associated with arterial stiffness and nondipping blood pressure in patients with hypertension regardless of sex.
Asunto(s)
Presión Sanguínea/fisiología , Enfermedades Cardiovasculares/epidemiología , Hipertensión/complicaciones , Apnea Obstructiva del Sueño/complicaciones , Rigidez Vascular/fisiología , Adulto , Anciano , Bloqueadores del Receptor Tipo 1 de Angiotensina II/uso terapéutico , Inhibidores de la Enzima Convertidora de Angiotensina/uso terapéutico , Monitoreo Ambulatorio de la Presión Arterial/métodos , Brasil/epidemiología , Enfermedades Cardiovasculares/fisiopatología , Diuréticos/normas , Diuréticos/uso terapéutico , Ecocardiografía/métodos , Enalapril/administración & dosificación , Enalapril/uso terapéutico , Femenino , Humanos , Hidroclorotiazida/administración & dosificación , Hidroclorotiazida/normas , Hidroclorotiazida/uso terapéutico , Hipertensión/tratamiento farmacológico , Hipertensión/epidemiología , Hipertensión/fisiopatología , Losartán/administración & dosificación , Losartán/uso terapéutico , Masculino , Persona de Mediana Edad , Polisomnografía/métodos , Análisis de la Onda del Pulso/métodos , Factores de Riesgo , Apnea Obstructiva del Sueño/epidemiología , Apnea Obstructiva del Sueño/fisiopatologíaRESUMEN
Obstructive sleep apnea (OSA) is an extremely common comorbid condition in patients with hypertension, with a prevalence of ~50%. There is growing evidence suggesting that OSA is a secondary cause of hypertension, associated with both poor blood pressure (BP) control and target organ damage in patients with hypertension. The application of continuous positive airway pressure (CPAP) during sleep is the gold standard treatment of moderate- to-severe OSA and very effective in abolishing obstructive respiratory events. However, several meta-analyses showed that the overall impact of CPAP on BP is modest (~2 mmHg). There are several potential reasons for this disappointing finding, including the heterogeneity of patients studied (normotensive patients, controlled, and uncontrolled patients with hypertension), non-ideal CPAP compliance, clinical presentation (there is some evidence that the positive impact of CPAP on lowering BP is more evident in sleepy patients), and the multifactorial nature of hypertension. In this review, we performed a critical analysis of the literature evaluating the impact of CPAP on BP in several subgroups of patients. We finally discussed perspectives in this important research area, including the urgent need to identify predictors of BP response to CPAP and the importance of precision medicine in this scenario.
RESUMEN
A apneia obstrutiva do sono (AOS) é uma condição caracterizadapor episódios recorrentes de obstrução das vias aéreas superiores,levando à fragmentação do sono e hipóxia intermitente. Sendo umdistúrbio altamente prevalente (dados epiderniológicos recentesapontam que 1/3 da população adulta de São Paulo apresentaalgum grau de AOS), esta condição clínica está despontandocomo um novo fator de risco cardiovascular. Quando não tratada,AOS é associada de forma independente à hipertensão, isquemiamiocárdica e acidente vascular encefálico. Os mecanismos deassociação entre a AOS e doenças cardiovasculares ainda nãoestão bem elucidados, mas há evidências consistentes de que AOSpromove disfunção endotelial (por meio da alteração do tônusvasomotor e por episódios repetitivos de hipóxia/reoxigenaçãoque causam estresse oxidativo e ativação inflamatória) e alteraçãoda capacidade de reparo das células endoteliais. Estudos nãorandomizados e randomizados mostram que o tratamento daAOS com a pressão positiva contínua de vias aéreas superiores(CPAP) promove reversão da disfunção endotelial, melhoria nosmarcadores de atividade inflamatória e aumento da capacidaderegenerativa do endotélio. Como o subdiagnóstico ainda éfrequente, estas evidências claramente indicam a necessidade deestratégias para o melhor reconhecimento e tratamento da AOS.O entendimento detalhado dos mecanismos envolvidos podefavorecer a criação de potenciais biomarcadores específicos delesão vascular na AOS. Em última análise, estes biomarcadorespodem servir tanto para a identificação da AOS como para predizereventos cardiovasculares em pacientes com AOS...
Obstructive sleep apnea (OSA) is a condition characterized byrecurrent episodes of obstruction of the upper airway, leadingto sleep fragmentation and intermittent hypoxia during sleep.Being a widely prevalent sleep disorder (recent epidemiologicdata suggest that 1/3 of adult population of São Paulo has somedegree of OSA), this clinical condition is an emerging riskfactor for cardiovascular diseases. OSA is independently associatedwith hypertension, myocardial ischemia and stroke. Themechanisms whereby OSA leads to cardiovascular diseasesare not fully elucidated, but there are consistent data that OSApromotes endothelial dysfunction (through dysregulation invasomotor tone, recurrent episodes of hypoxia-reoxygenationsleading to oxidative stress and inflammation) and alters endothelialrepair capacity. Randomized and non-randomizedstudies have shown that OSA treatment with continuouspositive airway pressure (CPAP) promotes improvement inendothelial function, inflammatory markers and enhancesendothelial repair capacity. These evidences support the needfor better recognition and treatment of OSA.Improving ourcurrent knowledge of the potential mechanisms involved inthe cardiovascular risk induced by OSA has the potential tostimulate development of specific biomarkers of vasculardamage in OSA. Lastly, these biomarkers may be useful notonly for identifying OSA as for predicting cardiovasculardiseases in OSA patients...