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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with a blunted fall in nocturnal BP (known as non-dippers) have a high risk of micro- and macrovascular complications, particularly if they have hypertension, but also in normotensive patients with diabetes. A blunted fall in nocturnal BP reflects the high level of CV risk in these patients. ABPM data indicating an altered circadian BP rhythm reverse circadian BP profile should alert the physician to the potential risk of complications and should lead to efforts to treat hypertension effectively, especially at night, and to check for sleep apnoea syndrome, particularly in cases of resistant hypertension, or autonomic neuropathy (postural hypotension), a well known risk factor for cardiovascular (CV) events. Patients should be carefully screened for nephropathy. However, the definitions of "non-dipper" vary widely. Suitable treatments are poorly defined, but angiotensin-converting enzyme inhibitors (ACEi), diuretics, salt restriction and the maintenance of continuous positive airway pressure (CPAP) can be used as non-specific treatments. The efficacy of taking blood pressure-lowering drugs at bedtime rather than in the morning is still debated but deserves attention. In the diabetic population, brachial pulse pressure (PP) is an independent predictor of cardiovascular mortality, but not of all-cause mortality. It is also associated with complications of both type 2 and type 1 diabetes, this effect being stronger for nocturnal than for diurnal PP, and is strongly predictive of coronary heart disease in patients with type 2 diabetes. The stronger association between PP and age in diabetic than in non-diabetic populations suggests that diabetes accelerates vascular ageing. In patients with incipient nephropathy or overt renal failure, PP increases CV risk. However, misinterpretation could be related to confusion between brachial PP and central PP. The therapeutic implications of PP measurement remain poorly documented in diabetes.
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PMID:Should pulse pressure and day/night variations in blood pressure be seen as independent risk factors requiring correction or simply as markers to be taken into account when evaluating overall vascular risk? 1793 63

The purpose of this study was to examine the possible difference in the 24-hr BP profile--including short-term BP variability, assessed as the standard deviation--between diabetic and non-diabetic hypertensives. We measured 24-hr ambulatory BP in 11 diabetic hypertensives (diabetic HT) and 10 non-diabetic hypertensives (non-diabetic HT) who were hospitalized for the educational program in our hospital and were under stable salt intake. Renal function and sleep apnea were also estimated. There were no significant differences in 24-hr systolic BP (141 mmHg vs. 135 mmHg, ns), daytime systolic BP (143 mmHg vs. 138 mmHg, ns), and nighttime systolic BP (135 mmHg vs. 130 mmHg, ns) between diabetic HT and non-diabetic HT. The values of 24-hr HR (69.7 beats/min vs. 65.2 beats/min, ns) and 24-hr HR variability (9.9 beats/min vs. 10.1 beats/min, ns) were also similar between the groups. Interestingly, diabetic HT had a significantly greater 24-hr systolic and diastolic BP variability than non-diabetic HT (18.2 mmHg vs. 14.5 mmHg, p < 0.05; 11.5 mmHg vs. 9.6 mmHg, p < 0.05, respectively). The values for creatinine clearance, urinary protein excretion, and apnea-hypopnea index were similar between the groups. Bivariate linear regression analysis demonstrated that fasting blood glucose was the primary determinant of 24-hr diastolic BP variability (r = 0.661, p < 0.01). Multiple stepwise regression analysis revealed that fasting blood glucose was a significant and independent contributor to 24-hr systolic BP variability (r = 0.501, p < 0.05). Taken together, these results demonstrate that BP variability is increased in diabetic hypertensives. Furthermore, it is possible that an elevation of fasting blood glucose may contribute to the enhanced BP variability in hypertensives.
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PMID:Ambulatory blood pressure variability is increased in diabetic hypertensives. 1842 1

Masked hypertension has been drawing attention recently because this condition is often seen in untreated and treated individuals and is associated with target organ damage and a poor cardiovascular prognosis. Although masked hypertension is defined as normal office blood pressure with elevated ambulatory or home blood pressure, there are several subtypes. Morning hypertension is the most common form of masked hypertension, and is caused by natural circadian variation, evening alcohol consumption, and the use of short-acting antihypertensive drugs. Daytime hypertension may be caused by lifestyle factors such as habitual smoking and mental or physical stress. Nighttime hypertension is seen in various conditions that produce non-dipping status, including a high salt intake, renal dysfunction, obesity, sleep apnea, and autonomic failure. Advanced target organ damage such as increases in the left ventricular mass, carotid artery intima-media thickness, and urinary albumin excretion, is often present both in untreated and treated subjects with masked hypertension. In our study, the presence of the reverse white-coat effect is independently associated with those indices of organ damage among treated hypertensive patients. It is important to identify individuals with masked hypertension, to evaluate them with including the search for the subtype, and to treat each patient appropriately according to the cause of this condition.
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PMID:Masked hypertension: subtypes and target organ damage. 1842 8

Resistant hypertension is defined as uncontrolled blood pressure despite the use of three antihypertensive drugs, including a diuretic, in optimal doses. Treatment resistance can be attributed to poor adherence to antihypertensive drugs, excessive salt intake, physician inertia, inappropriate or inadequate medication, and secondary hypertension. Drug-induced hypertension, obstructive sleep apnoea, primary aldosteronism, and chronic kidney disease represent the most common secondary causes of resistant hypertension. Several drugs can induce or exacerbate pre-existing hypertension, with non-steroidal anti-inflammatory drugs being the most common due to their wide use. Obstructive sleep apnoea and primary aldosteronism are frequently encountered in patients with resistant hypertension and require expert management. Hypertension is commonly found in patients with chronic kidney disease and is frequently resistant to treatment, while the management of renovascular hypertension remains controversial. A step-by-step approach of patients with resistant hypertension is proposed at the end of this review paper.
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PMID:Common secondary causes of resistant hypertension and rational for treatment. 2142 78

Importance of strict blood pressure control in hypertension is stressed in guidelines. But rates of achieving target blood pressure in several surveillance studies are less than 50%. Poor compliance to medication, life style related problems such as obesity, excess salt and alcohol intake, sleep apnea and coadministered drugs such as NSAIDs or licorice, and physicians attitude to blood pressure control can be reasons for resistant hypertension. First step to improve the blood pressure control status is identifying reasons. To solve the identified problems, comprehensive approaches by health professionals are necessary.
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PMID:[Current status of blood pressure control in Japan and strategies for the better control]. 2211 16

Heart failure is increasing in prevalence around the world, with hospitalization and re-hospitalization as a result of acute decompensated heart failure (ADHF) presenting a huge social and economic burden. The mechanism for this decompensation is not clear. Whilst in some cases it is due to volume expansion, over half of patients with an acute admission for ADHF did not experience an increase in total body weight. This calls into question the current treatment strategy of targeting salt and water retention in ADHF. An alternative hypothesis proposed by Fallick et al. is that an endogenous fluid shift from the splanchnic bed is implicated in ADHF, rather than an exogenous fluid gain. The hypothesis states further that this shift is triggered by an increase in sympathetic tone causing vasoconstriction in the splanchnic bed, a mechanism that can translocate blood rapidly into the effective circulating volume, generating the raised venous pressure and congestion seen in ADHF. This hypothesis encourages a new clinical paradigm which focuses on the underlying mechanisms of congestion, and highlights the importance of fluid redistribution and neurohormonal activation in its pathophysiology. In this article, we consider the concept that ADHF is attributable to episodic sympathetic hyperactivity, resulting in fluid shifts from the splanchnic bed. Chemosensitivity is a pathologic autonomic mechanism associated with mortality in patients with systolic heart failure. Tonic and episodic activity of the peripheral chemoreceptors may underlie the syndrome of acute decompensation without total body salt and water expansion. We suggest in this manuscript that chemosensitivity in response to intermittent hypoxia, such as experienced in sleep disordered breathing, may explain the intermittent sympathetic hyperactivity underlying renal sodium retention and acute volume redistribution from venous storage sites. This hypothesis provides an alternative structure to guide novel diagnostic and treatment strategies for ADHF.
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PMID:Chemohypersensitivity and autonomic modulation of venous capacitance in the pathophysiology of acute decompensated heart failure. 2350 1

In Asian populations, a high prevalence of stroke, high salt intake and high salt sensitivity, the effects of which are partly augmented by epidemic obesity, are associated with hypertension. These factors are closely associated with resistant hypertension, especially with the disrupted circadian rhythm of blood pressure (BP), that is, non-dipper and riser patterns. An ambulatory BP profile-based strategy combined with medication and devices (renal denervation and baroreceptor activation therapy) would help to achieve 'perfect 24-h BP control', consisting of strict reduction of the 24-h BP level, restoring disrupted circadian BP rhythms and reducing excess BP variability. Such BP control would protect high-risk patients with resistant hypertension against systemic hemodynamic atherothrombotic syndrome (which involves systemic atherothrombotic vascular diseases and target-organ damage, advanced by the composite risks of pulsatile hemodynamic stress from central pressure and blood flow and by thrombometabolic risk factors). Information technology-based home sleep BP pressure monitoring may be useful for assessing the risk during sleep in high-risk patients with resistant hypertension and sleep apnea syndrome.
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PMID:Proposal of a new strategy for ambulatory blood pressure profile-based management of resistant hypertension in the era of renal denervation. 2351 17

Blood pressure exhibits a robust circadian rhythm in health. In hypertension, sleep apnea, and even shift work, this balanced rhythm is perturbed via elevations in night-time blood pressure, inflicting silent damage to the vasculature and body organs. Herein, we examined the influence of circadian dysfunction during experimental hypertension in mice. Using radiotelemetry to measure ambulatory blood pressure and activity, the effects of angiotensin II administration were studied in wild-type (WT) and period isoform knockout (KO) mice (Per2-KO, Per2, 3-KO, and Per1, 2, 3-KO/Per triple KO [TKO] mice). On a normal diet, administration of angiotensin II caused nondipping blood pressure and exacerbated vascular hypertrophy in the Period isoform KO mice relative to WT mice. To study the endogenous effects of angiotensin II stimulation, we then administered a low-salt diet to the mice, which does stimulate endogenous angiotensin II in addition to lowering blood pressure. A low-salt diet decreased blood pressure in wild-type mice. In contrast, Period isoform KO mice lost their circadian rhythm in blood pressure on a low-salt diet, because of an increase in resting blood pressure, which was restorable to rhythmicity by the angiotensin receptor blocker losartan. Chronic administration of low salt caused vascular hypertrophy in Period isoform KO mice, which also exhibited increased renin levels and altered angiotensin 1 receptor expression. These data suggest that circadian clock genes may act to inhibit or control renin/angiotensin signaling. Moreover, circadian disorders such as sleep apnea and shift work may alter the homeostatic responses to sodium restriction to potentially influence nocturnal hypertension.
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PMID:Low-Salt Diet and Circadian Dysfunction Synergize to Induce Angiotensin II-Dependent Hypertension in Mice. 2678 Dec 74

An understanding of the potential mechanisms underlying recurrent upper airway collapse may help anesthesiologists better manage patients in the postoperative period. There is convincing evidence in the sleep medicine literature to suggest that a positive fluid and salt balance can worsen upper airway collapse in patients with obstructive sleep apnea through the redistribution of fluid from the legs into the neck and upper airway while supine, in a process known as "rostral fluid shift." According to this theory, during the day the volume from a fluid bolus or from fluid overload states (i.e., heart failure and chronic kidney disease) accumulates in the legs due to gravity, and when a person lies supine at night, the fluid shifts rostrally to the neck, also owing to gravity. The fluid in the neck can increase the extraluminal pressure around the upper airways, causing the upper airways to narrow and predisposing to upper airway collapse. Similarly, surgical patients also incur large fluid and salt balance shifts, and when recovered supine, this may promote fluid redistribution to the neck and upper airways. In this commentary, we summarize the sleep medicine literature on the impact of fluid and salt balance on obstructive sleep apnea severity and discuss the potential anesthetic implications of excessive fluid and salt volume on worsening sleep apnea.
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PMID:Is Perioperative Fluid and Salt Balance a Contributing Factor in Postoperative Worsening of Obstructive Sleep Apnea? 2776 17

Sleep apnea is a common condition associated with increased morbidity and mortality. Continuous positive airway pressure and oral appliances are efficient for treating sleep apnea; however, they are often poorly tolerated. Therefore, alternative therapies are needed. Overnight rostral fluid shift has been implicated in the pathogenesis of sleep apnea, particularly in conditions associated with fluid overload. Fluid shift predisposes to both obstructive and central sleep apnea, with the type of sleep apnea being related to whether the fluid shifts from the legs into the neck or chest, respectively. The amount of fluid that shifts from the legs to the upper part of the body at night is correlated with the severity of sleep apnea. As a result of this observation, it has been suggested that the prevention of overnight fluid shift may reduce sleep apnea severity. It has recently been shown that interventions targeting fluid overload and daytime fluid accumulation in the legs consistently attenuate nocturnal fluid shift and sleep apnea, as greater reductions in fluid shift are correlated with greater reductions in sleep apnea severity. This review will focus on interventions that counteract fluid shift, such as diuretics, ultrafiltration/dialysis, physical activity, compression stockings and salt/fluid restriction, which have been shown to have efficacy in reducing sleep apnea severity.
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PMID:Targeting volume overload and overnight rostral fluid shift: A new perspective to treat sleep apnea. 3017 46


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