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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EThis article discusses the diagnosis of treatment-resistant hypertension, secondary causes of resistant hypertension, the pharmacologic treatment of resistant hypertension, as well as provides an overview of renal denervation.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ECardiology\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EInterventional Techniques \u0026amp; Devices\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EHypertensive Disease\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ECardiology\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EInterventional Techniques \u0026amp; Devices\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EHypertensive Disease\u003C\/li\u003E\u003C\/ul\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EDIAGNOSIS OF RESISTANT HYPERTENSION\u003C\/h2\u003E\n         \u003Cp id=\u0022p-2\u0022\u003ERoland E. Schmieder, MD, University Hospital of the Friedrich Alexander University, Erlangen\/N\u00fcrnberg, Germany, discussed the diagnosis of treatment-resistant hypertension. While the terminology may differ, a common definition is the failure of treatment that includes antihypertensive drugs and lifestyle modification to lower blood pressure (BP) to appropriate levels [Calhoun DA et al. \u003Cem\u003ECirculation.\u003C\/em\u003E 2008; Mancia G et al. \u003Cem\u003EEur Heart J.\u003C\/em\u003E 2007].\u003C\/p\u003E\n         \u003Cp id=\u0022p-3\u0022\u003EA working definition of resistant hypertension is an office systolic\/diastolic BP \u2265 140\/90 mm Hg despite adequate medical therapy (defined as adequate doses of at least 3 classes of drugs, 1 of which is a diuretic). True treatment-resistant hypertension becomes evident when BP measurements are done at different times of the day, usually involving self-measurements at home or 24-hour ambulatory BP monitoring. In the United States, data from the National Health and Nutrition Examination Survey indicated a rate of resistant hypertension of 8.9% among all hypertensive adults and 12.8% among drug-treated hypertensive adults [Persell SD. \u003Cem\u003EHypertension.\u003C\/em\u003E 2011]. Clinical determinants of resistant hypertension included albuminuria; reduced renal function; and self-reported chronic kidney disease, chronic heart failure, stroke, and diabetes mellitus.\u003C\/p\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EThe estimated rate of apparent resistant hypertension has increased over the past 20 years in the United States [Egan BM et al. \u003Cem\u003ECirculation.\u003C\/em\u003E 2011]. It is clear that treatment-resistant hypertension is associated with a worse long-term cardiovascular prognosis [Kumbhani DJ et al. \u003Cem\u003EEur Heart J.\u003C\/em\u003E 2013].\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EResistant hypertension is treated by identifying and reducing the influence of contributing lifestyle factors, minimizing or discontinuing compounds that exacerbate the hypertension, and screening for secondary causes.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ESECONDARY CAUSES OF RESISTANT HYPERTENSION\u003C\/h2\u003E\n         \u003Cp id=\u0022p-6\u0022\u003EXavier Jeunemaitre, MD, PhD, European Hospital Georges Pompidou, Paris, France, discussed secondary causes of resistant hypertension, which reflect the complexity of BP regulation, with inputs from the structure and function of blood vessels, heart, and kidney and with neuroendocrine influences. The workup of secondary causes of resistant hypertension includes ruling out pseudo treatment-resistant hypertension and nonadherence to prescribed treatments. Evaluation should focus on drug-related causes, lifestyle factors, and volume overload. Other modifiable causes of treatment-resistant hypertension include obstructive sleep apnea, primary aldosteronism, renal artery stenosis, renal parenchymal disease, drug or alcohol abuse, and thyroid disorders (\u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E) [Vongpatanasin W. \u003Cem\u003EJAMA.\u003C\/em\u003E 2014].\u003C\/p\u003E\n         \u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/14997\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/14997\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/14997\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-7\u0022 class=\u0022first-child\u0022\u003ESecondary Causes of Resistant Hypertension\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EPredictors of sleep apnea include age \u0026gt; 50 years, neck circumference (\u2265 41 cm for women, \u2265 43 cm for men), and snoring [Pedrosa RP et al. \u003Cem\u003EHypertension.\u003C\/em\u003E 2011]. Continuous positive airway pressure, which provides small but significant reductions in BP in patients with obstructive sleep apnea, should be considered for appropriate patients [Schein AS et al. \u003Cem\u003EJ Hypertens.\u003C\/em\u003E 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EPrimary aldosteronism, which is the most frequent cause of secondary hypertension, is caused by excess secretion of aldosterone [Fernandes-Rosa FL et al. \u003Cem\u003EHypertension.\u003C\/em\u003E 2014; Choi M et al. \u003Cem\u003EScience.\u003C\/em\u003E 2011]. Primary aldosteronism has been associated with increasing age, duration of hypertension, systolic and diastolic BP, potassium concentration, plasma aldosterone concentration, and adenoma size [Fernandes-Rosa FL. \u003Cem\u003EHypertension.\u003C\/em\u003E 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EIn summary, secondary forms of hypertension\u2014most frequently, primary aldosteronism\u2014are common in resistant hypertension. Screening for these secondary forms can aid in medication choice and is useful in assessing the feasibility of renal denervation.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EPHARMACOLOGIC TREATMENT\u003C\/h2\u003E\n         \u003Cp id=\u0022p-12\u0022\u003EPharmacologic treatment of resistant hypertension was discussed by Bryan Williams, MD, University College London, London, United Kingdom. At least one-quarter of patients are noncompliant with BP-lowering medications. Noncompliance has been associated with the number of drugs prescribed [Tomaszewski M et al. \u003Cem\u003EHeart.\u003C\/em\u003E 2014; Strauch B et al. \u003Cem\u003EJ Hypertens.\u003C\/em\u003E 2013]. While some of these patients will respond to therapy, others (\u0026lt; 10%) are truly resistant. One potentially efficient way to identify those who have treatment-resistant hypertension may be to screen for renin, given that about two-thirds of patients with proven resistant hypertension have low plasma renin (\u0026lt; 0.5 nmol\/L\/h) despite diuretic therapy [Eide IK et al. \u003Cem\u003EJ Hypertens.\u003C\/em\u003E 2004].\u003C\/p\u003E\n         \u003Cp id=\u0022p-13\u0022\u003EOf the various drug options, the effect of low-dose spironolactone (25 or 50 mg, twice daily) has been shown in multiple studies [Chapman NC et al. \u003Cem\u003EHypertension.\u003C\/em\u003E 2007; Sharabi Y et al. \u003Cem\u003EAm J Hypertens.\u003C\/em\u003E 2006]. Current European Society of Cardiology\u2014European Society of Hypertension guidelines (2013) for the management of arterial hypertension support the use of spironolactone, eplerenone, or the alpha-1 blocker doxazosin [Mancia G et al. \u003Cem\u003EEur Heart J.\u003C\/em\u003E 2013] in patients with resistant hypertension. Amiloride can also be used but is not recommended in patients with markedly reduced estimated glomerular filtration rate (eGFR).\u003C\/p\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EWhether the effect of spironolactone on resistant hypertension reflects specific blockade of the aldosterone receptor or augmentation of ongoing diuretic therapy is unclear. If spironolactone is not effective, options include boosting the dose of thiazide-like diuretic, use of amiloride, use of frusemide in patients with low eGFR, use of eplerenone despite its comparatively lower efficacy [Parthasarathy HK. \u003Cem\u003EJ Hypertens.\u003C\/em\u003E 2011], or combinations of these agents. Optimal pharmacologic treatment may involve treatment stratification, with spironolactone used in cases of low plasma renin, alpha-blockade medications used for intermediate-level renin, and beta-blockade drugs used in cases of high plasma renin. More evidence is needed to inform this strategy.\u003C\/p\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EIn summary, the pharmacologic treatment of resistant hypertension needs more study, but poor compliance to therapy and undetected secondary causes are both important and underappreciated. Low plasma renin is likely important, and it is possible that sodium overload may contribute to resistant hypertension. Careful screening for secondary causes is essential, especially for adrenal adenoma in those with low plasma renin activity. Spironolactone is the first-choice therapy, with other diuretic therapy as warranted.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-4\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ERENAL DENERVATION 4 YEARS ON: FOCUS ON LONG-TERM RESULTS\u003C\/h2\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EMurray Esler, PhD, Baker IDI Heart and Diabetes Institute, Melbourne, Australia, provided an overview of renal denervation, a 7-year-old technique in which a catheter is used to deliver radiofrequency ablation to renal arteries. Neurogenic hypertension is claimed to be the basis of half the cases of high BP [Easler M. \u003Cem\u003EJ Appl Physiol.\u003C\/em\u003E 2010]. Some studies suggest that renal denervation can lower BP and reduce renal sympathetic afferent and efferent activity.\u003C\/p\u003E\n         \u003Cp id=\u0022p-17\u0022\u003ERegistry data from a number of globally conducted trials of renal denervation have revealed the 1- and 6-month safety of the approach. Yet, the SYMPLICITY HTN-3 study\u2014which was the first placebo-controlled cardiovascular outcomes trial of renal denervation\u2014indicated no reduction in BP with renal denervation [Bhatt DL et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2014]. The trial included 535 patients allocated 2:1 in a blinded fashion to active and sham treatment. The trial\u0027s primary end point was the mean change in office systolic BP at 6 months, and treatment with renal denervation had no effect on this end point. At 6 months, the change in 24-hour ambulatory systolic BP was not significantly different between the groups.\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EProf Esler noted that SYMPLICITY HTN-3 exemplifies the weak spot in renal denervation research. Animal studies have provided evidence of the effectiveness of the approach, but similar outcomes have not been shown in clinical trials performed in well-treated humans. The catheter-based process is not easy and is usually incomplete, and success relies on the experience and talent of the operator. In the trial, the interventionalists performing the procedure had little experience in renal denervation, and there was no way to determine if renal denervation actually occurred. Thus, the trial may have failed because of the execution of the procedure, not necessarily because renal denervation does not work for resistant hypertension [Henegar JR et al. \u003Cem\u003EAm J Hypertens.\u003C\/em\u003E 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-19\u0022\u003EThe development of a more reliable molecular test of renal denervation is needed. One target being explored is fragments of tyrosine hydroxylase excreted in urine.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2014 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/14\/27\/38.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzoule\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzoule\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}