Obstructive sleep apnea and hypertension-mediated organ damage in nonresistant and resistant hypertension.

The potential role of obstructive sleep apnea (OSA) in hypertension-mediated organ damage (HMOD) may be influenced by the presence of resistant hypertension (RH). Herein, we enrolled patients with hypertension from a tertiary center for clinical evaluation and performed a sleep study to identify OSA (apnea-hypopnea index ≥15 events/h) and a blinded analysis of four standard HMOD parameters (left ventricular hypertrophy [LVH], increased arterial stiffness [≥10 m/s], presence of retinopathy, and nephropathy). RH was diagnosed based on uncontrolled blood pressure (BP) (≥140/90 mmHg) despite concurrent use of at least three antihypertensive drug classes or controlled BP with concurrent use of ≥4 antihypertensive drug classes at optimal doses. To avoid the white-coat effect, ambulatory BP monitoring was performed to confirm RH diagnosis. One-hundred patients were included in the analysis (mean age: 54 ± 8 years, 65% females, body mass index: 30.4 ± 4.5 kg/m²). OSA was detected in 52% of patients. Among patients with non-RH (n = 53), the presence of OSA (52.8%) was not associated with an increased frequency of HMOD. Conversely, among patients with RH, OSA (51.1%) was associated with a higher incidence of LVH (RH-OSA,61%; RH + OSA,87%; p = 0.049). Logistic regression analysis using the total sample revealed that RH (OR:7.89; 95% CI:2.18-28.52; p = 0.002), systolic BP (OR:1.04; 95% CI:1.00-1.07; p = 0.042) and OSA (OR:4.31; 95% CI:1.14-16.34; p = 0.032) were independently associated with LVH. No significant association was observed between OSA and arterial stiffness, retinopathy, or nephropathy. In conclusion, OSA is independently associated with LVH in RH, suggesting a potential role of OSA in RH prognosis.

Effects of CPAP on Metabolic Syndrome in Patients With OSA: A Randomized Trial.

BACKGROUND: OSA is associated with metabolic syndrome (MS), but it is unclear whether OSA treatment with CPAP can revert MS. RESEARCH QUESTION: Does OSA treatment with CPAP per se have effects on the MS reversibility and the associated metabolic, adiposity and vascular parameters? STUDY DESIGN AND METHODS: The TREATOSA-MS trial is a randomized placebo-controlled trial that enrolled adult patients with a recent diagnosis of MS and moderate or severe OSA (apnea-hypopnea index [AHI], ≥ 15 events/h) to undergo therapeutic CPAP or nasal dilator strips (placebo group) for 6 months. Before and after each intervention, we measured anthropometric variables, BP, glucose, and lipid profile. To control potential-related mechanisms and consequences, we also measured adiposity biomarkers (leptin and adiponectin), body composition, food intake, physical activity, subcutaneous and abdominal fat (visceral and hepatic fat), and endothelial function. RESULTS: One hundred patients (79% men; mean age, 48 ± 9 years; BMI, 33 ± 4 kg/m2; AHI, 58 ± 29 events/h) completed the study (n = 50 per group). The mean CPAP adherence was 5.5 ± 1.5 h/night. After 6 months, most patients with OSA randomized to CPAP retained the MS diagnosis, but the rate of MS reversibility was higher than observed in the placebo group (18% vs 4%; OR, 5.27; 95% CI, 1.27-35.86; P = .04). In the secondary analysis, CPAP did not promote significant reductions in the individual components of MS, weight, hepatic steatosis, lipid profile, adiponectin, and leptin, but did promote a very modest reduction in visceral fat and improved endothelial function (all analyses were adjusted for baseline values). INTERPRETATION: Despite the higher rate of MS reversibility after CPAP therapy as compared with placebo, most patients retained this diagnosis. The lack of significant or relevant effects on adiposity biomarkers and depots supports the modest role of OSA in modulating MS. TRIAL REGISTRATION: ClinicalTrials.gov; No.: NCT02295202; URL: www. CLINICALTRIALS: gov.

Diastolic and systolic left ventricular dysfunction and mortality in chronic kidney disease patients on haemodialysis.

AIMS: Left ventricular diastolic dysfunction (LVDD) and LV systolic dysfunction (LVSD) are prevalent in CKD, but their prognostic relevance is debatable. We intent to verify whether LVDD and LVSD are independently predictive of all-cause mortality and if they have comparable or different effects on outcomes. METHODS: A retrospective analysis was conducted of the echocardiographic data of 1285 haemodialysis patients followed up until death or transplantation. LVDD was classified into 4 grades of severity. Endpoint was all-cause mortality. RESULTS: During a follow-up of 30 months, 419/1285 (33%) patients died, 224 (53%) due to CV events. LVDD occurred in 75% of patients, grade 1 DD was the prevalent diastolic abnormality, and pseudonormal pattern was the predominant form of moderate-severe DD. Moderate-severe LVDD (HR 1.379, CI% 1.074-1.770) and LVSD (HR 1.814, CI% 1.265-2.576) independently predicted death; a graded, progressive association was found between LVDD categories and the risk of death; and the impact of isolated severe-moderate LVDD on the risk of death was comparable to that exercised by isolated compromised LV systolic function. CONCLUSION: Moderate-severe LVDD and LVSD were independently associated with a higher probability of death and had a similar impact on survival. A progressive association was observed between LVDD grades and mortality.

Clinical-care protocol for preventing mediastinitis after coronary artery bypass graft surgery: A quality improvement initiative from a private hospital.

BACKGROUND: Surgical site infections after cardiac surgery are associated with severe outcomes, including reoperation and death. We aimed to describe the effect of a standardized clinical-care protocol for preventing mediastinitis in patients who underwent coronary artery bypass graft surgery (CABG). METHODS: In a hospital certified by Joint Commission International, all patients who underwent CABG from January 2011 to December 2016 were compared in two periods according to the moment of implementation of a standardized clinical-care protocol for prevention of mediastinitis (CCPPM): pre-protocol (January 2011-December 2012) and post-protocol (January 2013-December 2016). The CCPPM consisted of the patient using a kit containing chlorhexidine 2% for bathing, mupirocin 20 mg/g for nasal topical use and chlorhexidine 0.12% for oral hygiene for 5 days before surgery, in addition to prophylaxis with a glycopeptide antimicrobial and strict glucose control (110-140 mg/dL) during surgery and immediate postoperative. RESULTS: We evaluated 1760 patients who underwent CABG in both periods. The occurrence of mediastinitis before protocol implementation was 1.44% (10 of 692 CABG). After the implementation of the protocol, there was an important reduction in the incidence of mediastinitis to 0.09% (1 of 1068 CABG) (P = 0.002). Although we did not observe a significant difference in mortality between the groups (2.3% vs 1%, P = 0.77), there was fewer in-hospital mortality due to mediastinitis after the CCPPM (0.2% vs 0%, P < 0.001). CONCLUSION: Implementation of a standardized CCPPM was associated with a significant reduction in the incidence of mediastinitis after CABG and reduction of mortality in the group of patients with mediastinitis.

Higher arterial stiffness is associated with lower cognitive performance in patients with hypertension.

Cognitive impairment and elevated arterial stiffness have been described in patients with arterial hypertension, but their association has not been well studied. We evaluated the correlation of arterial stiffness and different cognitive domains in patients with hypertension compared with those with normotension. We evaluated 211 patients (69 with normotension and 142 with hypertension). Patients were age matched and distributed according to their blood pressure: normotension, hypertension stage 1, and hypertension stage 2. Cognitive function was assessed using the Mini-Mental State Examination, Montreal Cognitive Assessment, and a battery of neuropsychological evaluations that assessed six main cognitive domains. Pulse wave velocity was measured using a Complior device, and carotid properties were assessed by radiofrequency ultrasound. Central arterial pressure and augmentation index were obtained using applanation tonometry. The hypertension stage 2 group had higher arterial stiffness and worse performance either by Mini-Mental State Examination (26.8±2.1 vs 27.3±2.1 vs 28.0±2.0, P=.003) or the Montreal Cognitive Assessment test (23.4±3.5 vs 24.9±2.9 vs 25.6±3.0, P<.001). On multivariable regression analysis, augmentation index, intima-media thickness, and pulse wave velocity were the variables mainly associated with lower cognitive performance at different cognitive domains. Cognitive impairment in different domains was associated with higher arterial stiffness.

Impact of hypertension severity on arterial stiffness, cerebral vasoreactivity, and cognitive performance / Impacto da gravidade da hipertensão na rigidez arterial, vasorreatividade cerebral e desempenho cognitivo

ABSTRACT. Aging, hypertension (HTN), and other cardiovascular risk factors contribute to structural and functional changes of the arterial wall. Objective: To evaluate whether arterial stiffness (AS) is related to cerebral blood flow changes and its association with cognitive function in patients with hypertension. Methods: 211 patients (69 normotensive and 142 hypertensive) were included. Patients with hypertension were divided into 2 stages: HTN stage-1 and HTN stage-2. The mini-mental state examination (MMSE), Montreal Cognitive Assessment (MoCA) and a battery of neuropsychological (NPE) tests were used to determine cognitive function. Pulse wave velocity was measured using the Complior®. Carotid properties were assessed by radiofrequency ultrasound. Central arterial pressure and augmentation index were obtained using applanation tonometry. Middle cerebral artery flow velocity was measured by transcranial Doppler ultrasonography. Results: Both arterial stiffness parameters and cerebral vasoreactivity worsened in line with HTN severity. There was a negative correlation between breath holding index (BHI) and arterial stiffness parameters. Cognitive performance worsened in line with HTN severity, with statistical difference occurring mainly between the HTN-2 and normotension groups on both the MMSE and MoCA. The same tendency was observed on the NPE tests. Conclusion: Hypertension severity was associated with higher AS, worse BHI, and lower cognitive performance.

RESUMO. A idade, hipertensão arterial (HA), e outros fatores de risco cardiovascular contribuem para as alterações estruturais e funcionais da parede arterial. Objetivo: Avaliar o quanto a rigidez arterial está relacionada com as alterações do fluxo sanguíneo cerebral e sua associação com a função cognitiva em pacientes com hipertensão. Métodos: Foram incluídos 211 pacientes (69 normotensos e 142 hipertensos). Os pacientes com hipertensão foram divididos em dois estágios: HA-1 e HA-2. O mini exame do estado mental (MEEM), Montreal Cognitive Assessment (MoCA) e uma bateria de testes neuropsicológicos foram usados para avaliar a função cognitiva. A velocidade da onda de pulso foi medida usando o Complior®. As propriedades da artéria carótida foram avaliadas usando o ultrassom de radiofrequência. A pressão arterial central e o índice de incremento foram obtidos usando a tonometria de aplanação. A velocidade de fluxo sanguíneo da arterial cerebral média foi medida pelo ultrassom com Doppler Transcraniano. Resultados: Tanto os parâmetros da rigidez arterial quanto a vasorreatividade cerebral foram piores com a gravidade da hipertensão. Houve uma correlação negativa entre o índice de apnéia e os parâmetros da rigidez arterial. O desempenho cognitivo foi pior com a gravidade de hipertensão arterial com diferença estatística ocorrendo principalmente entre os grupos HA-2 e normotensão tanto no MEEM quanto no MoCA. A mesma tendência foi observada em relação aos testes neuropsicológicos. Conclusão: A gravidade de hipertensão arterial foi associada com maior rigidez arterial, pior índice de apneia, e menor desempenho cognitivo.

OSA and Prognosis After Acute Cardiogenic Pulmonary Edema: The OSA-CARE Study.

BACKGROUND: Acute cardiogenic pulmonary edema (ACPE) is a life-threatening condition. OSA may be a modifiable risk factor for ACPE recurrence. This study was designed to evaluate the impact of OSA on the incidence of cardiovascular events following ACPE recovery. METHODS: Consecutive patients with confirmed ACPE from 3 centers underwent a sleep study following clinical stabilization. OSA was defined as an apnea-hypopnea index (AHI) ≥ 15 events/h. The mean follow-up was 1 year, and the primary outcome was ACPE recurrence. RESULTS: A total of 104 patients were included in the final analysis; 61% of the patients had OSA. A higher rate of ACPE recurrence (25 vs 6 episodes; P = .01) and a higher incidence of myocardial infarction (15 vs 0 episodes; P = .0004) were observed in patients with OSA than in those without OSA. All 17 deaths occurred in the OSA group (P = .0001). In a Cox proportional hazards regression analysis, OSA was independently associated with ACPE recurrence (hazard ratio [HR], 3.3 [95% CI, 1.2-8.8]; P = .01), incidence of myocardial infarction (HR, 2.3 [95% CI, 1.1-9.5]; P = .02), cardiovascular death (HR, 5.4 [95% CI, 1.4-48.4]; P = .004), and total death (HR, 6.5 [95% CI, 1.2-64.0]; P = .005). When the analysis was limited only to patients with OSA, levels of AHI and hypoxemic burden and rates of sleep-onset ACPE were significantly higher in those who presented with ACPE recurrence or who died than in those who did not experience these events. CONCLUSIONS: OSA is independently associated with higher rates of ACPE recurrence and both fatal and nonfatal cardiovascular events.

Hypertension Severity Is Associated With Impaired Cognitive Performance.

BACKGROUND: Most evidence of target-organ damage in hypertension (HTN) is related to the kidneys and heart. Cerebrovascular and cognitive impairment are less well studied. Therefore, this study analyzed changes in cognitive function in patients with different stages of hypertension compared to nonhypertensive controls. METHODS AND RESULTS: In a cross-sectional study, 221 (71 normotensive and 150 hypertensive) patients were compared. Patients with hypertension were divided into 2 stages according to blood pressure (BP) levels or medication use (HTN-1: BP, 140-159/90-99 or use of 1 or 2 antihypertensive drugs; HTN-2: BP, ≥160/100 or use of ≥3 drugs). Three groups were comparatively analyzed: normotension, HTN stage 1, and HTN stage 2. The Mini-Mental State Examination, Montreal Cognitive Assessment, and a validated comprehensive battery of neuropsychological tests that assessed 6 main cognitive domains were used to determine cognitive function. Compared to the normotension and HTN stage-1, the severe HTN group had worse cognitive performance based on Mini-Mental State Examination (26.8±2.1 vs 27.4±2.1 vs 28.0±2.0; P=0.004) or Montreal Cognitive Assessment (23.4±3.7 vs 24.9±2.8 vs 25.5±3.2; P<0.001). On the neuropsychological tests, patients with hypertension had worse performance in language, processing speed, visuospatial abilities, and memory. Age, hypertension stage, and educational level were the best predictors of cognitive impairment in patients with hypertension in different cognitive domains. CONCLUSIONS: Cognitive impairment was more frequent in patients with hypertension, and this was related to hypertension severity.

Impact of hypertension severity on arterial stiffness, cerebral vasoreactivity, and cognitive performance.

Aging, hypertension (HTN), and other cardiovascular risk factors contribute to structural and functional changes of the arterial wall. OBJECTIVE: To evaluate whether arterial stiffness (AS) is related to cerebral blood flow changes and its association with cognitive function in patients with hypertension. METHODS: 211 patients (69 normotensive and 142 hypertensive) were included. Patients with hypertension were divided into 2 stages: HTN stage-1 and HTN stage-2. The mini-mental state examination (MMSE), Montreal Cognitive Assessment (MoCA) and a battery of neuropsychological (NPE) tests were used to determine cognitive function. Pulse wave velocity was measured using the Complior®. Carotid properties were assessed by radiofrequency ultrasound. Central arterial pressure and augmentation index were obtained using applanation tonometry. Middle cerebral artery flow velocity was measured by transcranial Doppler ultrasonography. RESULTS: Both arterial stiffness parameters and cerebral vasoreactivity worsened in line with HTN severity. There was a negative correlation between breath holding index (BHI) and arterial stiffness parameters. Cognitive performance worsened in line with HTN severity, with statistical difference occurring mainly between the HTN-2 and normotension groups on both the MMSE and MoCA. The same tendency was observed on the NPE tests. CONCLUSION: Hypertension severity was associated with higher AS, worse BHI, and lower cognitive performance.

A idade, hipertensão arterial (HA), e outros fatores de risco cardiovascular contribuem para as alterações estruturais e funcionais da parede arterial. OBJETIVO: Avaliar o quanto a rigidez arterial está relacionada com as alterações do fluxo sanguíneo cerebral e sua associação com a função cognitiva em pacientes com hipertensão. MÉTODOS: Foram incluídos 211 pacientes (69 normotensos e 142 hipertensos). Os pacientes com hipertensão foram divididos em dois estágios: HA-1 e HA-2. O mini exame do estado mental (MEEM), Montreal Cognitive Assessment (MoCA) e uma bateria de testes neuropsicológicos foram usados para avaliar a função cognitiva. A velocidade da onda de pulso foi medida usando o Complior®. As propriedades da artéria carótida foram avaliadas usando o ultrassom de radiofrequência. A pressão arterial central e o índice de incremento foram obtidos usando a tonometria de aplanação. A velocidade de fluxo sanguíneo da arterial cerebral média foi medida pelo ultrassom com Doppler Transcraniano. RESULTADOS: Tanto os parâmetros da rigidez arterial quanto a vasorreatividade cerebral foram piores com a gravidade da hipertensão. Houve uma correlação negativa entre o índice de apnéia e os parâmetros da rigidez arterial. O desempenho cognitivo foi pior com a gravidade de hipertensão arterial com diferença estatística ocorrendo principalmente entre os grupos HA-2 e normotensão tanto no MEEM quanto no MoCA. A mesma tendência foi observada em relação aos testes neuropsicológicos. CONCLUSÃO: A gravidade de hipertensão arterial foi associada com maior rigidez arterial, pior índice de apneia, e menor desempenho cognitivo.

OSA and prognosis after acute cardiogenic pulmonary edema: the OSA-care study

BACKGROUND: Acute cardiogenic pulmonary edema (ACPE) is a life-threatening condition. OSA may be a modifiable risk factor for ACPE recurrence. This study was designed to evaluate the impact of OSA on the incidence of cardiovascular events following ACPE recovery. METHODS: Consecutive patients with confirmed ACPE from 3 centers underwent a sleep study following clinical stabilization. OSA was defined as an apnea-hypopnea index (AHI) ≥ 15 events/h. The mean follow-up was 1 year, and the primary outcome was ACPE recurrence. RESULTS: A total of 104 patients were included in the final analysis; 61% of the patients had OSA. A higher rate of ACPE recurrence (25 vs 6 episodes; P = .01) and a higher incidence of myocardial infarction (15 vs 0 episodes; P = .0004) were observed in patients with OSA than in those without OSA. All 17 deaths occurred in the OSA group (P = .0001). In a Cox proportional hazards regression analysis, OSA was independently associated with ACPE recurrence (hazard ratio [HR], 3.3 [95% CI, 1.2-8.8]; P = .01), incidence of myocardial infarction (HR, 2.3 [95% CI, 1.1-9.5]; P = .02), cardiovascular death (HR, 5.4 [95% CI, 1.4-48.4]; P = .004), and total death (HR, 6.5 [95% CI, 1.2-64.0]; P = .005). When the analysis was limited only to patients with OSA, levels of AHI and hypoxemic burden and rates of sleep-onset ACPE were significantly higher in those who presented with ACPE recurrence or who died than in those who did not experience these events...

Renal artery stenosis predicts coronary artery disease in patients with hypertension.

In hypertensive patients with indication of renal arteriography to investigate renal artery stenosis (RAS) there are no recommendations regarding when to investigate coronary artery disease (CAD). Moreover, the predictors of CAD in patients with RAS are not clear. We aimed to evaluate the frequency and the determinants of CAD in hypertensive patients referred to renal angiography. Eighty-two consecutive patients with high clinical risk suggesting the presence of RAS systematically underwent renal angiography and coronary angiography during the same procedure. Significant arterial stenosis was defined by an obstruction ≥ 70% to both renal and coronary territories. Significant CAD was present in 32/82 (39%) and significant RAS in 32/82 (39%) patients. Both CAD and RAS were present in 25.6% from the 82 patients. Patients with severe CAD were older (63 ± 12 vs. 56 ± 13 years; p = 0.03) and had more angina (41 vs. 16%; p = 0.013) compared to patients without severe CAD. Significant RAS was associated with an increased frequency of severe CAD compared to patients without significant RAS (66% vs. 22%, respectively; p<0.001). Myocardial scintigraphy showed ischemia in 21.8% of the patients with CAD. Binary logistic regression analysis showed that RAS ≥ 70% was independently associated with CAD ≥ 70% (OR: 11.48; 95% CI 3.2-40.2; p<0.001), even in patients without angina (OR: 13.48; 95%CI 2.6-12.1; p<0.001). Even considering a small number of patients with significant RAS, we conclude that in hypertensive patients referred to renal angiography, RAS ≥ 70% may be a strong predictor of severe CAD, independently of angina, and dual investigation should be considered.