RESUMO
Obstructive sleep apnea (OSA) is characterized by recurrent episodes of partial (hypopnea) or complete interruption (apnea) in breathing during sleep due to airway collapse in the pharyngeal region. OSA and its cardiovascular consequences have been widely explored in observational and prospective studies. Most evidence verifies the positive relationship between OSA and hypertension, coronary artery disease, atrial fibrillation, stroke and heart failure. However, more studies are needed to better assess the impact of OSA, and possible benefit of treatment with continuous positive airway pressure (CPAP) on dyslipidemia, type 2 diabetes, insulin resistance and cardiovascular mortality. The leading pathophysiological mechanisms involved in the changes triggered by OSA, include intermittent hypoxemia and re-oxygenation, arousals and changes in intrathoracic pressure. Hypertension is strongly related with activation of the sympathetic nervous system, stimulation of the renin-angiotensin-aldosterone system and impairment of endothelial function. The high prevalence of OSA in the general population, hypertensive patients and especially obese individuals and patients resistant to antihypertensive therapy, highlights the need for effective screening, diagnosis and treatment of OSA to decrease cardiovascular risk.
Assuntos
Hipertensão/etiologia , Apneia Obstrutiva do Sono/complicações , Humanos , Hipertensão/epidemiologia , Respiração com Pressão Positiva , Apneia Obstrutiva do Sono/epidemiologia , Apneia Obstrutiva do Sono/terapiaRESUMO
Obstructive sleep apnea (OSA) is characterized by recurrent episodes of partial (hypopnea) or complete interruption (apnea) in breathing during sleep due to airway collapse in the pharyngeal region. OSA and its cardiovascular consequences have been widely explored in observational and prospective studies. Most evidence verifies the positive relationship between OSA and hypertension, coronary artery disease, atrial fibrillation, stroke and heart failure. However, more studies are needed to better assess the impact of OSA, and possible benefit of treatment with continuous positive airway pressure (CPAP) on dyslipidemia, type 2 diabetes, insulin resistance and cardiovascular mortality. The leading pathophysiological mechanisms involved in the changes triggered by OSA, include intermittent hypoxemia and re-oxygenation, arousals and changes in intrathoracic pressure. Hypertension is strongly related with activation of the sympathetic nervous system, stimulation of the reninangiotensinaldosterone system and impairment of endothelial function. The high prevalence of OSA in the general population, hypertensive patients and especially obese individuals and patients resistant to antihypertensive therapy, highlights the need for effective screening, diagnosis and treatment of OSA to decrease cardiovascular risk.
Assuntos
Apneia Obstrutiva do Sono , Doença da Artéria Coronariana , Doença das Coronárias , HipertensãoRESUMO
Resistant hypertension (RHTN) includes both patients whose blood pressure (BP) is uncontrolled on three or more medications (uncontrolled RHTN (UCRH)) and patients whose BP is controlled with use of four or more drugs (controlled RHTN (CRH)). It is unknown whether endothelial function and nocturnal drop demonstrate a similar pattern in patients with CRH and UCRH. We examined circadian BP patterns and vascular function in these patients. In all, 40 CRH and 26 UCRH patients, and 25 normotensives underwent biochemical testing, ambulatory BP monitoring, determination of brachial artery responses to endothelial-dependent (flow-mediated; dilation (FMD)) and independent (nitroglycerin mediated) stimuli. The nighttime drop in systolic BP (SBP) and diastolic BP (DBP) was less pronounced in UCRH than in CRH (SBP, 1.9±1.6 versus 4.9±1.7%; DBP, 7.5±1.8 versus 10.9±1.8%, UCRH and CRH, respectively; P<0.05). FMD was greater in control group compared with RHTN patients. Patients with UCRH had significantly impaired FMD compared with CRH (5.9±2.3% versus 7.1±5.1%; P<0.0001). Therefore, UCRH patients have less nocturnal dipping and a more impaired endothelial response compared with CRH patients. These findings suggest that important differences among patients with RHTN may allow identify subgroups with increased cardiovascular risk.
Assuntos
Pressão Sanguínea , Artéria Braquial/fisiopatologia , Ritmo Circadiano , Endotélio Vascular/fisiopatologia , Hipertensão/fisiopatologia , Vasodilatação , Adulto , Análise de Variância , Anti-Hipertensivos/administração & dosagem , Pressão Sanguínea/efeitos dos fármacos , Monitorização Ambulatorial da Pressão Arterial , Artéria Braquial/diagnóstico por imagem , Artéria Braquial/efeitos dos fármacos , Brasil , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/fisiopatologia , Resistência a Medicamentos , Quimioterapia Combinada , Endotélio Vascular/diagnóstico por imagem , Endotélio Vascular/efeitos dos fármacos , Feminino , Humanos , Hipertensão/sangue , Hipertensão/complicações , Hipertensão/diagnóstico , Hipertensão/tratamento farmacológico , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Nitroglicerina/administração & dosagem , Medição de Risco , Fatores de Risco , Falha de Tratamento , Ultrassonografia , Vasodilatação/efeitos dos fármacos , Vasodilatadores/administração & dosagemRESUMO
Resistant hypertension (RHTN) includes patients whose blood pressure (BP) is controlled with the use of four or more antihypertensive medications, and is referred to as 'controlled resistant hypertension' (CRH). While specifically comparing patients with CRH and uncontrolled resistant hypertension (UCRH), we hoped to identify distinguishing characteristics that would provide insight into factors contributing to resistance to antihypertensive therapies. RHTN patients were identified as controlled (CRH, n=43) or uncontrolled (UCRH, n=47). No statistical differences were observed between the CRH and UCRH subgroups with respect to age and gender. The body mass index, aldosterone-renin ratio and pulse wave velocity (PWV) were significantly higher in UCRH patients. Although both subgroups showed increased cardiac mass, left ventricular mass index was significantly higher in UCRH compared with CRH patients. Multivariate linear regression analysis indicated that PWV was significantly dependent on age in both UCRH and CRH patients; however, the influence of ageing was more pronounced in the former subgroup. Older age, greater vascular stiffness, higher aldosterone levels and greater left ventricular hypertrophy were significantly associated with lack of BP control in patients with RHTN. These findings suggest important possibilities in terms of preventing and better treating RHTN.
Assuntos
Envelhecimento/fisiologia , Índice de Massa Corporal , Cardiomegalia/complicações , Hiperaldosteronismo/complicações , Hipertensão/tratamento farmacológico , Hipertensão/etiologia , Rigidez Vascular , Idoso , Resistência a Medicamentos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Obesidade/complicaçõesRESUMO
A meta-analysis was used to determine whether administering recombinant granulocyte colony-stimulating factor (rG-CSF) to neonates with bacterial septicemia reduces mortality. Five studies were identified, involving 73 rG-CSF recipients and 82 control subjects. Mortality was lower among the rG-CSF recipients (odds ratio, 0.17; CI, 0.03-0.70; P <.05). However, when the non-randomized studies were excluded, the P value was.13. For the subgroups "<2000 g" or "neutropenia," the P value was <.02. Thus the routine use of rG-CSF cannot be recommended for all neonates with sepsis.
Assuntos
Fator Estimulador de Colônias de Granulócitos/uso terapêutico , Sepse/terapia , Humanos , Recém-Nascido , Proteínas RecombinantesRESUMO
OBJECTIVE: To prospectively investigate the incidence, significance, and kinetic mechanism responsible for leukemoid reactions in patients in the neonatal intensive care unit (NICU). DESIGN: We prospectively studied all infants admitted to the NICU at the University of Florida who, during a period of 12 consecutive months, had a leukemoid reaction. All those identified had a standardized evaluation consisting of (1) karyotype analysis, (2) bacterial cultures, (3) evaluations for toxoplasmosis, other (congenital syphilis and viruses), rubella, cytomegalovirus, and herpes simplex virus) (TORCH), (4) determination of blood viscosity, (5) use of marrow aspirates for morphology, clonogenic progenitor cell assays, and cell-cycle analysis of progenitors, (6) determination of serum concentrations of granulocyte and granulocyte-macrophage colony-stimulating factors, and (7) serial complete blood cell counts until the leukemoid reaction remitted. RESULTS: During 12 months, 707 patients were admitted to the NICU and 4262 complete blood cell counts were performed on samples from these patients. A leukemoid reaction was identified in nine patients, all of whom were preterm (born at 24 to 38 weeks' gestation). Peak blood leukocyte concentrations were 51.7 +/- 15.6 x 10(3)/microl (mean +/- SD). The leukemoid reactions were detected during the first 4 days of life in seven patients, on day 9 in one, and on day 25 in one. An abnormal karyotype (47, XY, +21) was present in one infant. Mothers of four infants had received betamethasone antenatally. None had elevated whole blood viscosity or positive findings on bacterial or TORCH evaluations. None of the bone marrow findings were consistent with steroid-induced leukocytosis; all studies indicated accelerated neutrophil production. Serum concentrations of granulocyte-macrophage colony-stimulating factor were either negligible or nondetectable. Serum granulocyte colony-stimulating factor was elevated in three patients, low in two, and nondetectable in four. The leukemoid reactions persisted for 5 to 32 days, the longest being in the patient with trisomy 21. CONCLUSIONS: Leukemoid reactions were not particularly rare in our NICU (1.3% of patients). The reactions were not associated with hyperviscosity and, except in one patient with a karyotype abnormality, were transient. The responsible kinetic mechanism was increased neutrophil production, not steroid-induced leukocytosis.