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Query: UMLS:C0037315 (sleep apnea)
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Resistant hypertension is an increasingly common problem faced by primary care physicians and specialists and will undoubtedly become even more common as the adult population ages and gains weight. In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), at least 8% of subjects were resistant to treatment based on the need for three or more antihypertensive agents. Characteristics of patients with resistant hypertension include being older, black, obese, and diabetic, and having chronic kidney disease as well as untreated sleep apnea. Hyperaldosteronism is common in patients with resistant hypertension, with a prevalence of approximately 20%. This, however, is likely an underestimation of the role aldosterone excess plays in causing drug resistance. In subjects with resistant hypertension, suppressed renin levels are common, exceeding 75% in our studies, suggesting aldosterone excess effects beyond cases of true primary hyperaldosteronism. Recent studies indicate that aldosterone antagonists provide significant blood pressure reduction when added to antihypertensive regimens of patients with resistant hypertension. Interestingly, the blood pressure reduction with use of spironolactone is not limited to patients with hyperaldosteronism, consistent with the concept of aldosterone excess as a continuum from low-renin hypertension with normal aldosterone levels to true primary hyperaldosteronism.
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PMID:The role of aldosterone antagonists in the management of resistant hypertension. 1615 75

The treatment of patients with congestive heart failure has markedly improved over the past 25 years. The most successful therapy has been attenuation of neurohumoral overactivation with antagonists of the renin-angiotensin-aldosterone system, as well as beta-adrenergic blockade. Cardiac surgical interventions, which include not only aortocoronary artery bypass surgery but also interventions that remodel the heart and repair the mitral valve, have also been advocated. However, randomized clinical trials to prove their benefit and to identify which patients could derive the most benefit from these interventions are lacking. Cardiac devices, such as biventricular pacemakers (for cardiac resynchronization) and implantable cardiac defibrillators, have proved useful in improving survival and quality of life. The treatment of sleep apnea with continuous positive airway pressure has shown some promise, as has immune modulation therapy, but more research to conclusively prove their efficacy is necessary. Cell therapy with skeletal myoblasts or pluripotential stem cells is an interesting and emerging area of research that shows enormous promise. However, fundamental questions regarding the optimal use of this therapy remain unanswered. Finally, although exciting, these developments, along with the changing demographics of the Canadian population, will require a change in the way we provide care for patients with congestive heart failure. These changes will require greater involvement of health care professionals other than physicians, and greater emphasis on outpatient care, early detection and prevention, and evidence-based practice.
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PMID:Treatment of congestive heart failure: present and future. 1623 94

The association between hypertension and chronic renal disease is well known. The pathogenesis of hypertension in patients with chronic kidney disease (CKD) is complex and multifactorial, which may explain why it is resistant to treatment. The traditional paradigm is that hypertension in CKD is due either to an excess of intravascular volume (volume dependent) or to excessive activation of the renin-angiotensin system in relation to the state of sodium/volume balance (renin-dependent hypertension). This review focuses on the importance of less established mechanisms, such as increased activity of the sympathetic nervous system, increased endothelin production, decreased availability of endothelium-derived vasodilators and structural changes of the arteries, renal ischemia, and sleep apnea.
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PMID:Hypertension in renal parenchymal disease: why is it so resistant to treatment? 1652 45

Cardiovascular risk in a patient with obesity hypertension increases with the extent of risk factor clustering. It is therefore important to determine the global risk of a patient with hypertension rather than to focus solely on blood pressure. Every hypertensive should be screened for other than blood pressure risk factors, target organ damage and concomitant diseases or accompanying clinical conditions. Assessment of blood pressure and target organ damage might be more difficult in obese hypertensives than in normal-weight patients. Intensive lifestyle interventions can reduce weight, and decrease blood pressure and cardiovascular risk in obese hypertensive patients. Current guidelines do not provide specific recommendation for pharmacological management of the hypertensive patients with obesity. Recent trials have consistently shown that therapy involving beta-blockers and diuretics may induce more new-onset diabetes compared with other combination therapies. Several lines of evidence suggest that anti-hypertensive agents that block the renin-angiotensin system may be especially beneficial in treating obese hypertensive patients. Hypertension management in obese individuals is complicated by poorer response to treatment, and the increased need for multiple medications. It is important to consider obstructive sleep apnoea in the differential diagnosis of hypertensive patients who respond poorly to combination therapy with anti-hypertensive medications.
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PMID:Diagnosis and management of hypertension in obesity. 1662 72

Resistant hypertension affects approximately 10% of the hypertensive patient population. It should be differentiated from white-coat hypertension and pseudo-resistant hypertension. Non-compliance to anti-hypertensive therapy remains the most common cause of resistant hypertension. Primary hyperaldosteronism is not as uncommon as previously thought, but its prevalence depends on the selected population. Low-renin resistant hypertension responds to aldosterone blockade when other drugs are apparently inadequately effective. Sleep apnea syndrome can also contribute to the development of resistant hypertension by stimulating aldosterone secretion, which leads to vascular damage and may promote scarring through more direct actions. Normal blood levels of potassium in resistant hypertension do not exclude the possible presence of hyperaldosteronism.
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PMID:Resistant hypertension: a methodological approach to diagnosis and treatment. 1767 42

Resistance to antihypertensive drugs is common in hypertensive patients with type 2 diabetes. This is unfortunate because hypertension is one of the most important risk factors for development of cardiovascular events, and the goal blood pressure level is set lower in diabetic subjects than in nondiabetic subjects. Previous outcome trials in diabetic subjects have mainly focused on end points such as microalbuminuria or the incidence of cardiovascular events rather than on reduction of blood pressure; some reports, however, have suggested mechanisms for the drug resistance. These include several clinical conditions known to be associated with difficulty in reducing blood pressure specifically in diabetes mellitus: change in the renin-angiotensin system and chymase, volume overload, central sympathetic hyperactivity, sleep apnea, secondary hypertension, pseudoresistance (white coat hypertension), and poor compliance related to subclinical depression. In this review, the authors focus on the mechanisms of resistance to antihypertensive therapy (particularly for monotherapy with either angiotensin-converting enzyme inhibitors or angiotensin II antagonists) in the treatment of diabetic hypertension.
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PMID:Why is blood pressure so hard to control in patients with type 2 diabetes? 1768 64

Management of resistant hypertension (RH), defined as uncontrolled blood pressure on three or more antihypertensive medications including a diuretic, begins initially with identifying and addressing contributors such as medication adherence, lifestyle factors and the use of interfering substances. Evaluation for the "white-coat" phenomenon, or associated conditions and secondary causes such as sleep apnea, primary aldosteronism, chronic kidney disease or renovascular disease may be indicated. Inadequate dosing, lack of using long-acting diuretics, and suboptimal combinations are observed as causes in nearly half of patients with RH. Appropriate pharmacotherapy of RH begins first with insuring the patient is receiving appropriate therapy for compelling indications, as outlined by the JNC-7 guidelines. Specific regimen enhancements to achieve blood pressure control include the addition of aldosterone antagonists, dual renin-angiotensin system blockade, and dual calcium channel blockade. Addition of centrally acting agents, alpha blockers, or vasodilators may also be necessary.
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PMID:Resistant hypertension: identifying causes and optimizing treatment regimens. 1870 62

Obesity is known to be a major aetiological factor in the development of hypertension. It also leads to dyslipidaemia and raised blood glucose. All of these are components of the metabolic syndrome. Thus, hypertension, as part of the syndrome, is often found together with these other abnormalities. Obesity raises blood pressure by a number of mechanisms, including activation of the sympathetic nervous system and the renin- angiotensin system. Apart from cardiovascular disease and diabetes, the metabolic syndrome is also associated with fatty liver disease, sleep apnoea and some malignancies. Measures to reduce obesity through lifestyle changes are therefore highly desirable, not because of reductions in blood pressure alone.
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PMID:Hypertension as part of the metabolic syndrome. 1854 89

Obesity is related to multiple comorbidities, including hypertension, diabetes, hypercholesterolemia, and sleep apnea. Comorbidities burden the health care system, such that in the United States, 6% to 8% of health care costs are related to obesity. Obesity-induced hypertension has multiple potential etiologic pathways, the most well established being increased renal sodium reabsorption with impaired pressure natriuresis via (1) activation of the renin-angiotensin system, (2) stimulation of the sympathetic nervous system, and (3) altered intrarenal physical forces. Weight loss is the best means to reduce obesity-related hypertension. For every 3 patients who lose 10 pounds of weight and maintain the weight loss for 4 years, 1 of them will eliminate the use of antihypertensive medication. Whereas nonsurgical therapy ineffectually treats extreme obesity, bariatric surgery yields durable weight loss, as well as resolution of some of the comorbidities associated with obesity, including hypertension. Increase in anti-inflammatory factors secreted by adipocytes may explain some of the improvement in blood pressure in the first 3 years post-procedure. Bariatric surgery safely and effectively improves and may improve or eliminate obesity-related hypertension. More data need to be collected to substantiate the same results over periods of time longer than 3 years.
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PMID:Is surgery the next answer to treat obesity-related hypertension? 1949 Feb 86

Nasal continuous positive airway pressure (CPAP) is generally recommended for the treatment of obstructive sleep apnoea. CPAP lowers the cardiovascular morbidity and mortality associated with severe obstructive sleep apnoea. At least 50% of patients presenting with chronic heart failure (HF) have sleep apnoea; a subset of these patients may have obstructive sleep apnoea and may derive a survival benefit from CPAP. However, this population is also prone to developing central sleep apnoea, Cheyne-Stokes respiration or both (CSA/CSR), for which CPAP lowers the apnoea-hypopnoea index only partially and for which the overall effect of CPAP on survival remains to be determined, particularly as it has been observed to increase the mortality rate in subsets of patients. Other treatments may prove effective in patients with chronic HF and CSA/CSR, although none, thus far, has been found to confer a survival benefit. New ventilatory modes include bi-level positive airway pressure and automated adaptive servoventilation, the latter being most effective against CSA/CSR. Measures that can alleviate CSA/CSR indirectly include beta-adrenergic blockers and renin-angiotensin-aldosterone system inhibitors, nocturnal supplemental oxygen and cardiac resynchronization therapy (CRT). The effects of theophylline, acetazolamide and nocturnal CO(2) have also been studied. The second part of this review describes the applications and effects of therapies that are available for sleep apnoea in patients with chronic HF.
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PMID:Sleep apnoea in patients with heart failure: part II: therapy. 1991 72


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