Treatment Of Drug-resistant Hypertension Research Articles

Role of eplerenone in the threatment of cardiovascular diseases.

Eplerenone is a selective mineralocorticoid receptor antagonist. Its approved for the therapy of patients with chronic heart failure with left ventricular systolic dysfunction and for the patients after myocardial infarction complicated by heart failure and left ventricular dysfunction. It´s also recommended for the therapy of primary hyperaldosteronism and the treatment of drug resistant hypertension.

Technical advance in silico and in vitro development of a new bipolar radiofrequency ablation device for renal denervation

BackgroundRenal denervation with radiofrequency ablation has become an accepted treatment for drug-resistant hypertension. However, there is a continuing need to develop new catheters for high-accuracy, targeted ablation. We therefore developed a radiofrequency bipolar electrode for controlled, targeted ablation through Joule heating induction between 60 and 100 °C. The bipolar design can easily be assembled into a basket catheter for deployment inside the renal artery.MethodsFinite element modeling was used to determine the optimum catheter design to deliver a minimum ablation zone of 4 mm (W) × 10 mm (L) × 4 mm (H) within 60 s with a 500 kHz, 60 Vp-p signal, and 3 W maximum. The in silico model was validated with in vitro experiments using a thermochromic phantom tissue prepared with polyacrylamide gel and a thermochromic ink additive that permanently changes from pink to magenta when heated over 60 °C.ResultsThe in vitro ablation zone closely matched the size and shape of the simulated area. The new electrode design directs the current density towards the artery walls and tissue, reducing unwanted blood temperature increases by focusing energy on the ablation zone. In contrast, the basket catheter design does not block renal flow during renal denervation.ConclusionsThis computational model of radiofrequency ablation can be used to estimate renal artery ablation zones for highly targeted renal denervation in patients with resistant hypertension. Furthermore, this innovative catheter has short ablation times and is one of the lowest power requirements of existing designs to perform the ablation.

Abstract MP23: Arterial Depressor Responses Induced By Neuromodulation Of Deep Peroneal Nerve In Spontaneously Hypertensive Rats

Hypertension affects nearly half of the US population but only 43% achieved blood pressure control with medication alone. Medical devices for hypertension include implantable lead electrodes that stimulate the carotid baroreceptors with promising results, albeit with significant adverse complications. To address these limitations, we have proposed the use of deep peroneal nerve stimulation (DPNS), which elicited a depressor response in anesthetized, breathing supported, spontaneously hypertensive rats (SHR). In this study, we further define the electrical stimulation parameters that optimize the DPNS depressor response, and demonstrated that increasing the pulse duration from 0.15 ms to 1ms, of 1.0 mA pulses at 2 Hz for 10 sec, significantly reduced the mean arterial pressure (MAP) by 8±4 mmHg (p<0.005; n=4) in this animal model. DPNS also caused an immediate increase in renal nerve activity (RNA; p< 0.004, n=5), which may represent afferent sensory axons from the kidney, although this possibility needs to be further investigated. In a separate cohort of anesthetized SHR animals, breathing spontaneously, we demonstrated that optimal DPNS stimulation reduced the MAP from 121±3 to 108±4; p=0.02; n=10). To confirm if DPNS is able to evoke a depressor response in fully awake SHR animals, we developed a novel miniaturized wireless microchannel electrode (w-μCE) with a L-shaped microchannel, through which the DPN slides and locks into a recording/stimulation chamber, causing no discomfort to the animal during locomotion. Two weeks after implantation of the w-μCE neural stimulation device, animals were movement-retrained to received wireless DPNS for 10 min daily for 2 weeks. Blood pressure was measured by tail-cuff at baseline, 10 days after device implantation, and 1 and 2-hr 15 days after DPNS. After two weeks of DPNS, the acute neuromodulation treatment reduced the initial systolic BP of 154±20 mmHg to 127±7 and 119±2 mmHg at 1 and 2 hr; respectively (p< 0.001, n=15-19 measurements; n=2 animals). These results provide evidence of the effectiveness and reliability of DPN neuromodulation as a possible treatment for drug-resistant hypertension.

Stretching the carotid sinus to treat resistant hypertension

Around a quarter of adults have hypertension, and by 2025, the number affected might be more than 1·5 billion people worldwide. 1 Olsen MH Angell SY Asma S et al. A call to action and a lifecourse strategy to address the global burden of raised blood pressure on current and future generation: the Lancet Commission on hypertension. Lancet. 2016; 388: 2665-2712 Summary Full Text Full Text PDF PubMed Scopus (484) Google Scholar Despite important advances in pharmacotherapy in the past 40 years, resistant hypertension—that is, persistently raised ambulatory blood pressure despite treatment with at least three antihypertensive drugs, including a diuretic—occurs in about 13% of treated adults. 2 Calhoun DA Jones D Textor S et al. Resistant hypertension: diagnosis, evaluation, and treatment. A scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Hypertension. 2008; 51: 1403-1419 Crossref PubMed Scopus (1230) Google Scholar Optimisation of treatment is crucial in people with resistant hypertension because of the increased risk of cardiovascular disease. Two main pathophysiological mechanisms can be targeted: volume excess related to dietary sodium, reduced renal function, or aldosterone excess; and vascular resistance increased by overactivity of the renin–angiotensin–aldosterone system (RAAS) or sympathetic nervous system. Excess volume may be counterbalanced by use of high-dose diuretics or by adding a mineralocorticoid-receptor antagonist. 3 Williams B MacDonald TM Morant S et al. Spironolactone versus placebo, bisoprolol, and doxazosin to determine the optimal treatment for drug resistant hypertension (PATHWAY-2): a randomised, double-blind, crossover trial. Lancet. 2015; 386: 2059-2068 Summary Full Text Full Text PDF PubMed Scopus (676) Google Scholar Vascular resistance may be reduced with RAAS blockers, β blockers, or interventional strategies. The baroreflex, which is controlled by the sympathetic nervous system, is mainly directed at short-term control of blood pressure. Several concepts have emerged suggesting that strong interactions between the sympathetic nervous system, the kidneys, and the RAAS contribute to long-term regulation of blood pressure. 4 Lohmeier TE Iliescu R The baroreflex as a long-term controller of arterial pressure. Physiology. 2015; 30: 148-158 Crossref PubMed Scopus (78) Google Scholar Device therapies have been developed to target the sympathetic nervous system by baroreceptor stimulation or renal denervation. 5 Courand PY Feugier P Workineh S et al. Baroreceptor stimulation for resistant hypertension: first implantation in France and literature review. Arch Cardiovasc Dis. 2014; 107: 690-696 Crossref PubMed Scopus (10) Google Scholar Endovascular baroreflex amplification for resistant hypertension: a safety and proof-of-principle clinical studyIn patients with resistant hypertension, endovascular baroreceptor amplification with the MobiusHD device substantially lowered blood pressure with an acceptable safety profile. Randomised, double-blind, sham-controlled trials are warranted to investigate the use of this treatment further. Full-Text PDF

Evaluation of Adherence Should Become an Integral Part of Assessment of Patients With Apparently Treatment-Resistant Hypertension.

Since the publication of the first Symplicity studies in 2009 to 2010, renal sympathetic denervation gained acceptance as a novel treatment of drug-resistant hypertension. The latter has been defined as a blood pressure (BP) >140/90 mm Hg, despite appropriate lifestyle measures plus a diuretic and 2 other antihypertensive drugs belonging to different classes at adequate doses.1 According to the US definition, patients with controlled BP on ≥4 antihypertensive drugs are also considered as resistant hypertensives.2 However, a substantial proportion of patients with apparently resistant hypertension are in fact poorly adherents to drug treatment. The highly variable BP response to renal denervation (RDN)3–5 prompted to a more rigorous evaluation of eligible patients, with the goal to exclude false resistant hypertension, because of poor adherence to drug treatment.6–8 In particular, several publications documented a high proportion of low drug adherence in patients with apparently resistant hypertension (23%–66%), using witnessed drug intake9 or plasma/urine drug determinations10–18 (Figure 1). Figure 1. Proportion of poor or nonadherence according to drug monitoring in different cohorts of patients with apparently resistant hypertension. Black indicates total nonadherence, whereas gray indicates partial adherence. Partial adherence was defined as the presence of at least one undetectable drug10–12,14,16–18 or as the presence of fewer medications than prescribed.13,15 Furthermore, RDN studies shed the light on the dynamic character of drug adherence. Inclusion in RDN trials may influence drug adherence in various, unpredictable directions.6 In some patients, close follow-up and massive attention devoted to them may lead to improved adherence to lifestyle measures and drug treatment, particularly in the RDN arm (Hawthorne effect). Other patients may stop their medications after RDN according to their perception that the intervention cured their …

Renal Denervation for Treatment of Hypertension: a Second Start and New Challenges.

Following the publication of the randomized controlled but open-label trial Symplicity HTN-2, catheter-based renal sympathetic denervation was proposed as a novel treatment for drug-resistant hypertension. Thousands of procedures were routinely performed in Europe, Australia and Asia, and many observational studies were published. A sudden shift from overoptimistic views to radical scepticism occurred later, when the large US randomized sham-controlled trial Symplicity HTN-3 failed to meet its primary blood pressure lowering efficacy endpoint. Experts are divided on the reasons accounting for the large discrepancy between the results of initial studies and those of Symplicity HTN-3. Indeed, the blood pressure lowering effect associated with renal denervation was overestimated in initial trials due to various patient and physician-related biases, whereas it could have been underestimated in Symplicity HTN-3, which was well designed but not rigorously executed. Still, there is a large consensus on the need to further study catheter-based renal denervation in more controlled conditions, with particular emphasis on identification of predictors of blood pressure response. US and European experts have recently issued very similar recommendations on design of upcoming trials, procedural aspects, drug treatment, patient population and inclusion-exclusion criteria. Application of these new standards may represent a second chance for renal denervation to demonstrate--or not--its efficacy and safety in various patient populations. With its highly standardized treatment regimen, the French trial DENERHTN paved the way for this new approach and may inspire upcoming studies testing novel renal denervation systems in different populations.

Inferences Beyond a Study Design's Grasp: A Cautionary Case Study From the Recent Renal Sympathetic Denervation Literature.

During the past 6 years, the technique of renal sympathetic denervation has been proposed as a treatment for drug-resistant hypertension, and several studies have been published that claimed to provide supportive evidence of its efficacy. There is no question that resistant hypertension is a major medical concern: hypertension has been authoritatively designated as the greatest threat to the global burden of disease, and approximately 8% of hypertensive individuals have resistant hypertension. However, the first studies reporting the efficacy of renal sympathetic denervation were not methodologically capable of supporting such claims. Subsequently, in March 2014, the most appropriately designed clinical trial failed to provide supportive evidence of the intervention's efficacy. This Commentary presents a cautionary case study to exemplify the need for optimal methodologic rigor in all experimental clinical research and highlights the pitfalls should claims from less than optimally rigorous studies be afforded more weight than is scientifically appropriate.

Abstract 526: Blood Pressure in the SHR Following Renal Denervation or Etamicastat, a Novel Dopamine-β-Hydroxylase Inhibitor

Overactivity of the sympathetic nervous system plays an important role in the development and progression of hypertension. Catheter-based renal nerve ablation for treatment of drug-resistant hypertension has been recently developed. An alternative strategy for modulation of sympathetic nerve function is to reduce the biosynthesis of norepinephrine (NE) via inhibition of dopamine β-hydroxylase (DβH), the enzyme that catalysis the conversion of dopamine to NE in sympathetic nerves. Renal denervation (RDN) was performed in spontaneously hypertensive rats (SHR) to evaluate the effect of RDN on NE levels and blood pressure throughout a 28-day period. Chronic oral treatment with the peripheral selective DβH inhibitor etamicastat (30 mg/kg/day) was performed in another cohort of SHR. RDN and chronic oral treatment with etamicastat did not affect renal function, as assessed by urinary protein, creatinine and urea levels. RDN significantly decreased mean arterial blood pressure (MAP, in mm Hg) 7 days post-surgery (139±6, P<0.01) versus baseline values (158±6). A gradual MAP return to high baseline levels was observed overtime; 139±7 at day 14, 151±12, at day 21 and 155±12 at day 28 after RDN. Treatment with etamicastat decreased baseline MAP (150±5) in a sustained and significant (P<0.01) manner at all-time points: 141±5 at day 7, 139±5 at day 14, 138±5 at day 21 and 143±5 at day 28. At day 28, NE levels (in pmol/mg tissue) in renal tissue were significantly decreased in both RDN (0.12±0.08, P=0.001) and etamicastat-treated group (0.48±0.04, P=0.01) as compared to vehicle group (0.88±0.13). On the other hand, left ventricle NE levels were decreased only after treatment with etamicastat (1.24±0.12, P=0.04) but not in the RDN group (2.53±0.24, P=0.9) when compared to controls (2.59±0.58). It is concluded that RDN produces transitory decreases in MAP, whereas prolonged down regulation of sympathetic drive with the DβH inhibitor etamicastat results in sustained decreases in MAP.

Recurrent pulmonary oedema after percutaneous radiofrequency renal denervation

Renal denervation is an emerging treatment of drug resistant hypertension. However there are theoretical concerns that renal artery stenosis may develop following this procedure. We report the first known case of bilateral renal artery stenosis occurring post renal denervation.

Sympathetic Nervous System Moves Toward Center Stage in Cardiovascular Medicine

In 1664, the first anatomically correct depiction of the sympathetic nervous system came from Thomas Willis and his circle of London anatomists,1 included in The Anatomy of the Brain and Nerves , 1664 (Figure 1). This, the first work dedicated completely to the nervous system, also described the arterial loops at the base of the brain, which we now know as the Circle of Willis.1 Christopher Wren, an anatomist member of the group, was the principal illustrator1 before being asked by the City Fathers to turn his talents to town planning, architecture, and cathedral building after the 1666 Great Fire of London. Figure 1. An illustration of the human sympathetic nerves of the neck and thorax, from The Anatomy of the Brain and Sympathetic Nerves , published in 1664 by Thomas Willis and reproduced in Soul Made Flesh .1 Almost 2 centuries later, subsequent microscopic examination demonstrated that blood vessel walls were densely innervated, leading Stelling in 18402 to correctly conclude that these vasomotor fibers were in fact sympathetic nerves that were carried from the central nervous system to the blood vessels. In the mid-19th century, celebrated European physiologists, including Brown-Sequard, Waller, and Bernard,2 built on these observations, demonstrating vasoconstriction with electrical stimulation of the cut nerves and vasodilatation on nerve section, which indicated that the sympathetic fibers exerted a tonic, vasoconstrictor influence. The pressor nerves had gained recognition. Identification of the sympathetic neurotransmitter proved to be difficult. Claims for epinephrine3,4 and the hypothetical sympathins I and E confused the picture. Ulf von Euler compared bioassay responses of epinephrine, norepinephrine, and dihydroxy norephedrine with those of cattle splenic nerve extract, by testing blood pressure (BP) responses in the anesthetized cat and contractile responses in the isolated pregnant rabbit uterus, to definitively demonstrate the …

Abstract 454: Hypertension Control by Decrease of Sympathetic Hyperactivity in SHR Rats: Comparison Between Renal Denervation and Dopamine ß-hydroxylase Inhibition

Activation of the sympathetic nervous system has been described in the development and progression of systemic hypertension. Recently, catheter-based renal nerve ablation for treatment of drug-resistant hypertension has been developed. An alternative strategy for modulation of sympathetic nerve function is to reduce the biosynthesis of norepinephrine (NE) via inhibition of dopamine β-hydroxylase (DβH), the enzyme that catalysis the conversion of dopamine (DA) to NE in sympathetic nerves. Renal denervation was assessed in the rat by transient (90 sec) ischemia of renal tissues. Bilateral renal artery occlusion (RAO) was assessed in spontaneously hypertensive rats (SHR) to evaluate the effect of renal denervation on NE levels and blood pressure throughout a 28-day period. Oral treatment with the selective peripheral DβH inhibitor etamicastat (30 mg/Kg body weight) was performed in a second cohort of SHR and NE levels and blood pressure was assessed. Renal denervation resulted in marked depletion of NE levels, selective for the renal sympathetic innervations, 5 days after RAO in renal cortex (16.5±7.7% of control values, P<0.0001). Decreased NE levels persisted up to 28 days after RAO (40.8±19.4% of control values, P<0.0001). No differences in left ventricle NE levels were observed. Renal denervation significantly decreased systolic blood pressure (SBP) 5 days (165±6 vs. 187±2 mmHg, P<0.05) and 14 days post-surgery (194±3 vs. 204±2 mmHg, P<0.05), but had no effect on heart rate. Systolic blood pressure recovered to basal values 28 days post-surgery. Likewise, etamicastat treatment resulted in a depletion of NE levels in both renal cortex (70.9±9.1% of control values, P<0.05) and left ventricle (55.8±3.9% of control values, P<0.01). Etamicastat treatment decreased SBP (228±7 vs. 174±9 mmHg, P<0.001) without effects on heart rate. In conclusion, these results suggest that renal denervation and DβH inhibition similarly decreases sympathetic hyperactivity and high blood pressure in the SHR. Downregulation of sympathetic drive with DβH inhibitors may be useful in the treatment of hypertension.

Novel Approaches for the Treatment of the Patient with Resistant Hypertension: Renal Nerve Ablation.

Sympathetic innervation of the kidneys plays a major role in the pathogenesis of hypertension through modulation of renin secretion, glomerular filtration rate and renal absorption of sodium. Targeted interventions for renal nerve ablation are being developed for treatment of drug resistant hypertension in the USA and rest of the world. Early studies with the use of radiofrequency based renal denervation systems have shown encouraging results with significant reduction of blood pressure in patients inadequately controlled despite nearly maximal drug therapy regimens. Thus far, the renal denervation procedure has been associated with minimal side effects. Long term efficacy and safety beyond 3 years needs to be determined for renal nerve ablation. This review focuses on the physiology of the renal sympathetic system, the rationale for renal nerve ablation and current evidence in support of the available therapeutic renal denervation systems.

Renal denervation in the treatment of drug-resistant hypertension: current knowledge and future perspectives

Resistant hypertension remains a challenging issue even for modern medicine. Therefore, research is focusing on the development of new technologies to optimize the treatment of this condition. It has been demonstrated that the dysfunction of the sympathetic nervous system is crucial in the development and maintenance of advanced stages of hypertension. Based on these findings, clinical trials have recently shown that catheter-based percutaneous renal denervation therapy is safe and effective in the treatment of resistant hypertension. This review discusses the current scientific knowledge of renal denervation therapy in resistant hypertension, including the different methods that have been described in the literature so far, as well as limitations of the available data. Furthermore, new potential targets for this fascinating therapy will be addressed.

Renal Sympathetic Denervation for the Treatment of Systemic Hypertension

Systemic hypertension is a common cardiovascular problem that often cannot be fully treated with existing nonpharmacologic and pharmacologic measures. A catheter-based strategy which denervates the renal afferent and efferent autonomic nervous system has been developed for the treatment of drug-resistant hypertension. In early clinical trials, this procedure was shown to be both feasible and safe in reducing blood pressure in patients with uncontrolled hypertension receiving treatment with a minimum of 3 antihypertensive drugs. In addition, this procedure has been associated with decreased renin secretion, preservation of renal function, improved glucose tolerance, and a reduction in left ventricular hypertrophy. The long-term effects of this procedure (beyond 3 years) still need to be determined. A large 530-patient sham-controlled trial is now in progress.

Timing and Efficacy of Alternative Methods of Sympathetic Blockade

Despite the presence of seven different antihypertensive drug classes and over 120 different antihypertensive medications, about 48% of the 75 million people with hypertension are not reaching their target blood pressure goals. One of the reasons for this lack of control is the failure to adequately inhibit the sympathetic nervous system. Consequently, alternative therapies have been attracting interest. Recent technical advances targeting the sympathetic over-activity of the carotid sinuses (baroreflex activation therapy, BAT) and the renal sympathetic nerves (renal denervation therapy, RDT) have renewed interest in invasive therapies for the treatment of drug-resistant hypertension. Encouraging results from the recent Rheos Pivotal and Symplicity HTN-2 trials on the safety and efficacy of BAT and RDT, respectively, indicate that invasive approaches can safely reduce blood pressure in patients with resistant/refractory hypertension. These approaches, while still experimental in the US, are appropriate for those on more than three fully tolerated doses of antihypertensive medications whose blood pressure is not at goal, i.e. <140/90 mmHg. The present review is focused on the clinical implications of these two technics and when they are appropriate.

Drug-resistant Hypertension: Is Renal Sympathetic Denervation the Answer?

Trial: Symplicity HTN-2 Investigators, Esler MD, Krum H, et al.: Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomized controlled trial. Lancet 2010, 376:1903–1909. Rating: ••Of major importance. Introduction: Sympathetic overactivity is thought to be a major contributor to the pathogenesis and progression of human hypertension [1, 2]. In particular, renal sympathetic activation results in renal vasoconstriction, increased renin secretion, and enhanced sodium and water reabsorption, all of which contribute to the development of hypertension [3]. Despite this mechanistic understanding, attempts at modulating sympathetic tone with antiadrenergic drug therapy have been limited by their poor clinical performance and undesirable side-effect profile [1, 4]. Additionally, historic surgical approaches for the treatment of hypertension with renal sympathectomy have long been abandoned due to a high perioperative morbidity and mortality [5, 6]. In recent years, the advent of a catheter-based technique using radiofrequency to destroy the renal nerves has revitalized these long abandoned thoughts of treating hypertension with renal denervation. Following encouraging results of an uncontrolled feasibility trial and a case report [7, 8], a recent randomized controlled trial (Symplicity HTN-2 [Renal Denervation in Patients With Uncontrolled Hypertension]) has further demonstrated the potential for catheter-based renal denervation in the treatment of drug-resistant hypertension. Aims: The Symplicity HTN-2 trial was designed to determine the safety and effectiveness of catheter-based renal artery denervation with the Symplicity Catheter System (Ardian, Palo Alto, CA) in reducing blood pressure in patients with drug-resistant hypertension. Methods: In this multicenter trial (involving 24 centers in Europe, Australia, and New Zealand), 106 patients ages 18 to 85 years with a systolic blood pressure of 160 mm Hg or more (≥150 mm Hg in patients with type 2 diabetes), despite treatment with three or more antihypertensive medications were randomized to undergo renal denervation while continuing prior drug therapy or to continue prior drug therapy alone. Patients who met initial screening criteria were subsequently excluded from the trial if their blood pressure fell below eligibility criteria at a second clinic visit after a 2-week screening phase. During this phase, patients were required to document medication compliance and twice-daily home blood pressure monitoring. Patients were also excluded if they were found to have unfavorable renal artery anatomy on imaging; other exclusion criteria included an estimated glomerular filtration rate of less than 45 mL/min/1.73 m2 and type 1 diabetes. The trial’s primary end point was the change from baseline in seated office-based measurement of systolic blood pressure at 6 months. During the intervention, the catheter was advanced into the renal arteries and four to six discrete low-power radiofrequency treatments were applied along the length of both renal arteries. Background use of antihypertensive drugs was held constant for the duration of the trial in both groups. Results: At baseline, the groups were well matched on most characteristics: office blood pressure was 178/96 mm Hg in the intervention group (n = 52) and 178/97 mm Hg in the control group (n = 54). Office-based blood pressure fell by 32/12 mm Hg (SD 23/11; P < 0.001) in the patients who underwent renal denervation versus no change in the control group (1/0 mm Hg, SD 21/10; P = NS). Home blood pressure fell by 20/12 mm Hg (SD 17/11) in the renal denervation group (n = 32) versus no change in the control group (n = 40). Twenty-four-hour ambulatory blood pressure fell by 11/7 mm Hg (SD 15/11; P < 0.006) in the renal denervation group (n = 20) versus no change in the control group (n = 25). There were no serious procedural complications in the denervation group and no between-group differences in renal function or in the incidence of adverse events. Discussion: The authors concluded that renal artery denervation is safe and effective in reducing office blood pressure, home blood pressure, and 24-h blood pressure at 6 months in patients with drug-resistant hypertension.

Interventionelle renale Sympathikusdenervation

The pathophysiology of resistant hypertension is complex. Activation of the sympathetic nervous system has been suggested to be one of the main contributors for maintenance of blood pressure elevation and the development of comorbidities. Catheter-based renal denervation - by ablation of the efferent and afferent renal sympathetic nerves - is a new approach to selectively denervate the kidneys from their sympathetic control. Renal denervation is associated with substantial and sustained blood pressure reduction (24 months), lowers central sympathetic outflow, and reduces whole-body norepinephrine spillover. The procedure is feasible and safe. The randomised controlled Symplicity-HTN-2 trial (results reported at AHA 2010, Nov 13-17) provides important information to determine the role of this new method for the treatment of drug resistant hypertension.

Vascular compliance and arterial calcification: impact on blood pressure reduction

The aim of this article is to review the relationship between vascular calcification and difficult to control hypertension. This does not address antihypertensive treatment of drug resistant hypertension per se. Vascular calcification occurs in a variety of common hypertension scenarios. Basic mechanisms of how and why vessels calcify are reviewed including new genetic insights. The potential for contributing to or improving calcification through drug therapies for nonhypertensive disorders is reviewed. Vascular calcification is common and easily recognized. Studies that target its clinical consequences (arterial stiffness) as primary treatment goals are needed.

CONTROL OF HYPERTENSION AFTER RENAL TRANSPLANTATION BY EMBOLISATION OF HOST KIDNEYS

A percutaneous embolisation technique was used for host kidney ablation in 13 patients with renal allografts and hypertension. Markedly improved blood pressure control was achieved in 9 of them, and morbidity was minimal. All patients have been followed from 12 to 25 months. Embolisation of the host kidneys appears to be a simple, effective, and less hazardous alternative to surgery in the treatment of drug-resistant hypertension after renal transplantation in some patients.