RESUMEN
OBJECTIVES: Given the neurocognitive hyperarousal observed in patients with insomnia disorder and associations of nocturnal hot flashes with cardiovascular disease risk, we examined whether women with hot flash-associated insomnia disorder demonstrate exaggerated cardiovascular responsivity to acute stressors, and also a profile of psychological hyperarousal. METHODS: Peri and postmenopausal women with and without hot flash-associated insomnia disorder underwent assessments of cardiovascular autonomic responsivity to acute stress paradigms and psychological hyperarousal. Hemodynamic responses (heart rate, blood pressure) to nociceptive, social-evaluative, and cognitive stress paradigms were measured in the morning. Psychological hyperarousal was evaluated using questionnaires assessing daytime and presleep hyperarousal, anxiety, and sleep-related cognitions. RESULTS: Women (25 with and 15 without hot flash-associated insomnia) aged 53.4â±â4.8 years reported a range of insomnia symptoms. Resting-state hemodynamics were similar between groups. Heart rate and blood pressure responses to stress paradigms did not differ by group nor did they correlate with insomnia severity. Women with insomnia disorder had higher generalized anxiety disorder scores (mean 2.7â±â3.0 vs 1.0â±â1.4; Pâ=â0.05) and sleep-related cognitions than those without insomnia (Pâ≤â0.05). Insomnia symptom severity was moderately correlated with presleep and daytime hyperarousal, anxiety, and sleep-related cognition (all râ≥â0.43). CONCLUSIONS: Though hot flash-associated insomnia is characterized by psychological hyperarousal before sleep and during the daytime, it does not relate to cardiovascular responsiveness to acute stressors. Our findings do not support the hypothesis that altered cardiovascular control is a potential mechanism by which hot flash-associated insomnia confers higher cardiovascular disease risk.
Asunto(s)
Nivel de Alerta/fisiología , Sistema Cardiovascular/fisiopatología , Sofocos/complicaciones , Trastornos del Inicio y del Mantenimiento del Sueño/etiología , Trastornos del Inicio y del Mantenimiento del Sueño/fisiopatología , Anciano , Trastornos de Ansiedad/epidemiología , Trastornos de Ansiedad/fisiopatología , Presión Sanguínea , Enfermedades Cardiovasculares , Cognición/fisiología , Femenino , Frecuencia Cardíaca , Humanos , Menopausia/fisiología , Persona de Mediana Edad , Factores de Riesgo , Sueño/fisiología , Trastornos del Despertar del Sueño/fisiopatología , Trastornos del Despertar del Sueño/psicología , Trastornos del Inicio y del Mantenimiento del Sueño/psicología , Encuestas y CuestionariosRESUMEN
STUDY OBJECTIVES: To examine whether patients with restless legs syndrome demonstrate specific alterations in cardiovascular autonomic control. METHODS: Patients with moderate-severe restless legs syndrome (n = 20, 80% female) and controls (n = 20) matched for age, sex, body mass index, and free of hypertension and cardiovascular disease were enrolled. We assessed cardiovagal baroreflex gain via the modified Oxford technique, sympathetically mediated vascular responses to isometric exercise to fatigue, bradycardiac response to Valsalva maneuver, and respiratory sinus arrhythmia during paced breathing. Standard electrocardiography, beat-by-beat arterial pressure, respiration, and popliteal blood flow velocity were recorded continuously. RESULTS: Resting blood pressure and heart rate were similar between groups. However, baroreflex gain averaged 14.3 ± 1.4 msec/mm Hg in restless legs syndrome and was lower than in controls (22.6 ± 3.5 msec/mm Hg, P = 0.04). Hemodynamic responses to isometric exercise were similar between groups, though participants with restless legs syndrome had lower leg blood flow (P < 0.001), with greater leg vascular resistance (P < 0.0001), before and during isometric exercise. Respiratory sinus arrhythmia and Valsalva ratios were similar between groups. Neither baroreflex gain nor vascular resistance was correlated with sleep duration, sleep quality, or symptom duration. CONCLUSION: Patients with restless legs syndrome demonstrate compromised cardiovagal control, specific to the arterial baroreflex, with greater peripheral vascular resistance, potentially due to heightened sympathetic outflow. These autonomic alterations may directly relate to the higher prevalence of cardiovascular disease in restless legs syndrome.