Refractory Hypertension Patients Research Articles

Prevalence and Clinical Characteristics of Refractory Hypertension.

BackgroundWe aimed to estimate the prevalence of refractory hypertension (RfH) and to determine the clinical differences between these patients and resistant hypertensives (RH). Secondly, we assessed the prevalence of white‐coat RfH and clinical differences between true‐ and white‐coat RfH patients.Methods and ResultsThe present analysis was conducted on the Spanish Ambulatory Blood Pressure Monitoring Registry database containing 70 997 treated hypertensive patients. RH and RfH were defined by the presence of elevated office blood pressure (≥140 and/or 90 mm Hg) in patients treated with at least 3 (RH) and 5 (RfH) antihypertensive drugs. White‐coat RfH was defined by RfH with normal (<130/80 mm Hg) 24‐hour blood pressure. A total of 11.972 (16.9%) patients fulfilled the standard criteria of RH, and 955 (1.4%) were considered as having RfH. Compared with RH patients, those with RfH were younger, more frequently male, and after adjusting for age and sex, had increased prevalence of target organ damage, and previous cardiovascular disease. The prevalence of white coat RfH was lower than white‐coat RH (26.7% versus 37.1%, P<0.001). White‐coat RfH, in comparison with those with true RfH, showed a lower prevalence of both left ventricular hypertrophy (22% versus 29.7%; P=0.018) and microalbuminuria (28.3% versus 42.9%; P=0.047).ConclusionsThe prevalence of RfH was low and these patients had a greater cardiovascular risk profile compared with RH. One out of 4 patients with RfH have normal 24‐hour blood pressure and less target organ damage, thus indicating the important role of ambulatory blood pressure monitoring in guiding antihypertensive therapy in difficult‐to‐treat patients.

Comparison of ambulatory blood pressure-lowering effects of higher doses of different calcium antagonists in uncontrolled hypertension: the Calcium Antagonist Controlled-Release High-Dose Therapy in Uncontrolled Refractory Hypertensive Patients (CARILLON) Study

Background: Data are sparse regarding ambulatory blood pressure (BP) reduction of up-titration from a standard dose to a high dose in both nifedipine controlled-release (CR) and amlodipine. This was a prospective, randomized, multicenter, open-label trial.Patients and methods: Fifty-one uncontrolled hypertensives medicated by two or more antihypertensive drugs including a renin-angiotensin system inhibitor and a calcium antagonist were randomly assigned to either the nifedipine CR (80 mg)/candesartan (8 mg) group or the amlodipine (10 mg)/candesartan (8 mg) group.Results: The changes in 24-hr BP were comparable between the groups. The nifedipine group demonstrated a significant decrease in their urinary albumin creatinine ratio, whereas the amlodipine group demonstrated a significant decrease in their NTproBNP level. However, there was no significant difference in any biomarkers between the two groups.Conclusion: Nifedipine showed an almost equal effect on ambulatory blood pressure as amlodipine. Their potentially differential effects on renal protection and NTproBNP should be tested in larger samples.

PP.09.02] ACCESSORY RENAL ARTERIES IN RESISTANT HYPERTENSION

Objective: Refractory hypertension (RHT) is a major health care concern affecting 20 to 30% of hypertensive patients and increasing cardiovascular risk. Recent renal denervation trials suggest a high prevalence of accessory renal arteries (ARA) in RHT. Previous publications report a putative role of ARA in triggering hypertension through renin secretion in underperfused renal segments. Our objective was to compare the prevalence of ARA in RHT vs non-refractory hypertension (NRHT). Design and method: 86 essential hypertensive patients who benefited from an abdominal CT-scan or MRI during their initial work-up were retrospectively recruited in 6 french hypertension centers. At the end of a minimal 6 months of follow up, patients were classified between RHT or NRHT. RHT was defined as blood pressure that remains above goal in spite of 3 antihypertensive agents at optimal dose including a diuretic, or controlled by more than 3 medications (Calhoun, 2008). Other patients were classified as NRHT. Blinded independant central review of all radiologic renal artery charts was performed. Results: Baseline characteristics were: age 50 ± 15 years, 62% males, BP 145 ± 23 / 87 ± 13 mmHg. 53 (62%) patients had RHT and 25 (29%) had at least one ARA. Prevalence of ARA was comparable between RHT (25%) and NRHT patients (33%, p = 0,62), but there were significantly more ARA per patient in NRHT (2 ± 0,9) vs RHT (1,3 ± 0,5, p = 0,03). ARA were similar in diameter or length between the 2 groups. Patients with ARA had a significative increase in renin plasma levels at baseline (51,6 ± 49,3 mUI/l) versus patients without ARA (20,3 ± 25,1 mUI/l, p = 9x10-3), but this did not translate into a worse blood pressure control or a raise in medication number, especially in renin angiotensin system inhibitors at the end of follow up. Conclusions: In this retrospective series of 86 essential hypertensive patients, we found no difference in the prevalence of ARA in RHT and NRHT, but NRHT patients had significantly more ARA per patients than RHT patients. This study confirms elevated renin plasma levels at baseline in hypertensive patients with ARA, but limits its clinical relevance in terms of blood pressure control.

Effects of Renal Sympathetic Denervation in Diastolic Heart Function in CKD Refractory Hypertensive Patients

&lt;p&gt;Diastolic heart failure (HF) is an important factor that increases mortality related to the cardiovascular system in patients with chronic kidney disease (CKD) whose extent of kidney function deterioration differs. As a non-invasive method to allow early assessment, the E/e’ ratio estimated by tissue Doppler imaging can predict mortality and cardiovascular events in CKD patients with diastolic dysfunction. The current study evaluated 15 patients with CKD and left ventricular hypertrophy (LVH), who were selected according to a previously published protocol. In the present study, we reported for the first time the improvement in diastolic parameters measured by echocardiography in CKD patients with resistant hypertension and left ventricular hypertrophy 6 months after renal sympathetic denervation (RSD). Our results suggest that RSD in this kind of patients seems to avoid the progression to diastolic HF.&lt;/p&gt;

Proof of concept study: Improvement of echocardiographic parameters after renal sympathetic denervation in CKD refractory hypertensive patients

AimEvaluation of the effectiveness of the renal sympathetic denervation (RSD) in reducing lesions of target organs such as the heart and kidneys, in resistant hypertensive CKD patients. Methods and resultsForty-five patients were included and treated with an ablation catheter with open irrigated tip. RSD was performed by a single operator following the standard technique. Patients included with CKD were on stages 2 (n=22), 3 (n=16), and 4 (n=7). Data were obtained at baseline and monthly until the 6th month of follow-up. Twenty-six out of the 45 patients had LVH and nineteen did not present LVH. The LV mass index decreased from 123.70±38.44g/m2 at baseline to 106.50±31.88g/m2 at the 6th month after RSD, P<0.0001. The end-diastolic left ventricular internal dimension (LVIDd) reduced from 53.02±6.59mm at baseline to 51.11±5.85mm 6months post procedure, P<0.0001. The left ventricular end-diastolic posterior wall thickness (PWTd) showed a reduction from 10.58±1.39mm at baseline to 9.82±1.15mm at the 6th month of follow-up, P<0.0001. The end-diastolic interventricular septum thickness (IVSTd) also decreased from 10.58±1.39mm at baseline to 9.82±1.15mm 6months post procedure, P<0.0001. The left ventricular ejection fraction (LVEF) improved from 58.90±10.48% at baseline to 62.24±10.50% at the 6th month of follow-up, P<0.0001. When the ∆ between baseline and the 6th month post RSD in LVH patients and non LVH patients were compared to the same parameters no significant difference was found. ConclusionsThe RSD seemed to be feasible, effective, and safe resulting in an improvement of echocardiographic parameters in LVH and non LVH CKD refractory hypertensive patients.

Effects of renal sympathetic denervation in left ventricular hypertrophy in CKD refractory hypertensive patients

Effects of renal sympathetic denervation in left ventricular hypertrophy in CKD refractory hypertensive patients

Improvement of the renal function after renal sympathetic denervation in refractory hypertensive patients with chronic kidney disease: Possible predictors

Improvement of the renal function after renal sympathetic denervation in refractory hypertensive patients with chronic kidney disease: Possible predictors

Refractory Hypertension: Evidence of Heightened Sympathetic Activity as a Cause of Antihypertensive Treatment Failure.

Refractory hypertension is an extreme phenotype of treatment failure defined as uncontrolled blood pressure in spite of ≥5 classes of antihypertensive agents, including chlorthalidone and a mineralocorticoid receptor antagonist. A prospective evaluation of possible mechanisms of refractory hypertension has not been done. The goal of this study was to test for evidence of heightened sympathetic tone as indicated by 24-hour urinary normetanephrine levels, clinic and ambulatory heart rate (HR), HR variability, arterial stiffness as indexed by pulse wave velocity, and systemic vascular resistance compared with patients with controlled resistant hypertension. Forty-four consecutive patients, 15 with refractory and 29 with controlled resistant hypertension, were evaluated prospectively. Refractory hypertensive patients were younger (48±13.3 versus 56.5±14.1 years; P=0.038) and more likely women (80.0 versus 51.9%; P=0.047) compared with patients with controlled resistant hypertension. They also had higher urinary normetanephrine levels (464.4±250.2 versus 309.8±147.6 µg per 24 hours; P=0.03), higher clinic HR (77.8±7.7 versus 68.8±7.6 bpm; P=0.001) and 24-hour ambulatory HR (77.8±7.7 versus 68.8±7.6; P=0.0018), higher pulse wave velocity (11.8±2.2 versus 9.4±1.5 m/s; P=0.009), reduced HR variability (4.48 versus 6.11; P=0.03), and higher systemic vascular resistance (3795±1753 versus 2382±349 dyne·s·cm(5)·m(2); P=0.008). These findings are consistent with heightened sympathetic tone being a major contributor to antihypertensive treatment failure and highlight the need for effective sympatholytic therapies in patients with refractory hypertension.

Acute effect of renal sympathetic denervation on blood pressure in refractory hypertensive patients with chronic kidney disease

a Renal Division, Department of Medicine, Universidade Federal Fluminense, Niteroi, RJ, Brazil b Hospital Regional Darcy Vargas, Rio Bonito, RJ, Brazil c Department of Cardiology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China d Fellowship of European Heart Rhythm Association/European Society of Cardiology, Department of Cardiology, Elisabethinen University Teaching Hospital Linz, Linz, Austria e Abteilung Elektrophysiologie, Herzzentrum, Universitat Leipzig, Leipzig, Sachsen, Germany

Henry Krum: resisting the pressure

Henry Krum: resisting the pressure

High-Risk Clinical Presentations in Atherosclerotic Renovascular Disease: Prognosis and Response to Renal Artery Revascularization

Current trial data may not be directly applicable to patients with the highest risk presentations of atherosclerotic renovascular disease, including flash pulmonary edema, rapidly declining kidney function, and refractory hypertension. We consider the prognostic implications of these presentations and response to percutaneous revascularization. Single-center prospective cohort study; retrospectively analyzed. 467 patients with renal artery stenosis ≥50%, managed according to clinical presentation and physician/patient preference. Presentation with flash pulmonary edema (n = 37 [7.8%]), refractory hypertension (n = 116 [24.3%]), or rapidly declining kidney function (n = 46 [9.7%]) compared to low-risk presentation with none of these phenotypes (n = 230 [49%]). Percutaneous revascularization (performed in 32% of flash pulmonary edema, 28% of rapidly declining kidney function, and 28% of refractory hypertension patients) compared to medical management. Death, cardiovascular (CV) event, end-stage kidney disease. During a median follow-up of 3.8 (IQR, 1.8-5.8) years, 55% died, 33% had a CV event, and 18% reached end-stage kidney disease. In medically treated patients, flash pulmonary edema was associated with increased risk of death (HR, 2.2; 95% CI, 1.4-3.5; P < 0.001) and CV event (HR, 3.1; 95% CI, 1.7-5.5; P < 0.001), but not end-stage kidney disease, compared to the low-risk phenotype. No increased risk for any end point was observed in patients presenting with rapidly declining kidney function or refractory hypertension. Compared to medical treatment, revascularization was associated with reduced risk for death (HR, 0.4; 95% CI, 0.2-0.9; P = 0.01), but not CV event or end-stage kidney disease, in patients presenting with flash pulmonary edema. Revascularization was not associated significantly with reduced risk for any end point in rapidly declining kidney function or refractory hypertension. When these presentations were present in combination (n = 31), revascularization was associated with reduced risk for death (HR, 0.15; 95% CI, 0.02-0.9; P = 0.04) and CV event (HR, 0.23; 95% CI, 0.1-0.6; P = 0.02). Observational study; retrospective analysis; potential treatment bias. This analysis supports guidelines citing flash pulmonary edema as an indication for renal artery revascularization in atherosclerotic renovascular disease. Patients presenting with a combination of rapidly declining kidney function and refractory hypertension also may benefit from revascularization and may represent a subgroup worthy of further investigation in more robust trials.

Non‐surgical periodontal treatment reduces cardiovascular risk in refractory hypertensive patients: a pilot study

To evaluate the effects of non-surgical periodontal treatment on left ventricular mass (LVM), arterial stiffness, systolic and diastolic blood pressure and plasma levels of inflammatory markers (C-reactive protein (CRP), fibrinogen and interleukin-6) in refractory hypertension patients. This interventional prospective cohort pilot study included 26 patients (53.6±8.0years old) diagnosed with refractory hypertension and generalized chronic periodontitis. Subjects received non-surgical periodontal treatment according to their needs. Plasma levels of systemic inflammation (CRP; fibrinogen and interleukin-6) and established cardiovascular risk factors [systolic and diastolic blood pressure (SBP and DBP), left ventricular mass (LVM) and arterial stiffness] were assessed at three time points (baseline, 3months after baseline and 6months after periodontal therapy). Periodontal therapy significantly reduced all cardiovascular risk markers evaluated. Median values of SBP and DBP were reduced by 12.5mmHg and 10.0mmHg, respectively, whereas left ventricular mass (LVM) reduced by 12.9g and pulse wave velocity reduced by 0.9m/s (p<0.01). Levels of CRP, IL-6 and fibrinogen lowered by 0.5mg/dl, 1.4pg/dl and 37.5mg/dl (p<0.01), respectively, 6months after periodontal therapy. Periodontal therapy significantly reduced levels of CRP, IL-6, fibrinogen, blood pressure, LVM and arterial stiffness, lowering cardiovascular risk in refractory hypertensive patients.

Abstract 19101: Increased Sympathetic Nervous System Activity in Refractory Hypertensive Patients in Contrast to Controlled and True Resistant Hypertensive Patients

Within the population of patients with resistant hypertension (RHTN), a unique phenotype with unexplained mechanisms of treatment failure has been identified. This phenotype remains uncontrolled despite optimal medical therapy who we refer to as having refractory hypertension (RefHTN) in contrast to true or controlled RHTN. The current study prospectively compared biochemical parameters, indices of arterial compliance, endothelial function and cardiohemodynamics in patients with RefHTN and a matched cohort of controlled and true resistant hypertensive patients. From 2009 to 2012, refractory patients were identified in a referral hypertension clinic using the following criteria: uncontrolled blood pressure (BP) on 5 or more antihypertensive medications (including chlorthalidone and spironolactone) after ≥ 3 visits within a minimum 6-month follow-up period. All 40 patients underwent measurement of 24-hr BP, heart rate (HR); pulse wave analysis (PWA); augmentation index (AIx75); aortic pulse pressure (APP); pulse wave velocity (PWV); arterial flow-mediated dilation (FMD), electrocardiogram, and impedance cardiogram. Baseline characteristics were similar; although, refractory patients were younger and were treated with an average of 7 different antihypertensive classes. ABPM confirmed a difference in systolic (177±29 vs 133±6 mm Hg, p&lt;0.001) and diastolic BP (101±17 vs 79±10 mm Hg, p&lt; 0.001) in the true or controlled vs refractory groups. Average 24-hr HR was higher in patients with RefHTN (78±8 vs 69±7 bpm, p=0.039) despite being on more β-blockers. PWV was greater(12±3 vs 10±3 m/s, p=0.044), as was AIx75 (31±7 vs 17±12 %). Brachial artery FMD was more reduced in patients with RefHTN (6.6 vs 9.4%). Impedance electrocardiogram showed significantly increased systemic vascular resistance(supine 3876.4 vs 1372.9 , p&lt;0.001 and standing 1980.1 vs 1197.7 dyne sec cm-5,p=0.037). Patients with RefHTN have increased arterial stiffness, central blood pressure,systemic vascular resistance, and endothelial dysfunction compared to patients with controlled and true RHTN, consistent with higher sympathetic activity in his group suggesting that increased adrenergic output contributes importantly to antihypertensive treatment failure.

Role of renal sympathetic denervation in a refractory arterial hypertension patient.

Despite advances in the pharmacological treatment of arterial hypertension (AHT) and the use of multiple antihypertensive drugs, a small but significant percentage of true severe refractory arterial hypertension patients are still not reaching their target blood pressure. In these cases, renal sympathetic denervation (RSD) seems to be a safe and effective method for severe hypertensive patients who are resistant to multiple drug treatment. We present the case of a 52-year-old patient diagnosed with essential hypertension, resistant to treatment with seven antihypertensive drugs. After 10 hospitalisations without achieving adequate blood pressure control, we decided to propose renal sympathetic denervation as an addition to medical treatment. The procedure was performed without complications in the short to medium-long term, achieving a significant improvement in blood pressure with the intention of reducing overall vascular risk.

Treatment of carvedilol for refractory hypertension in patients with renal diseases: A multicentre, prospective clinical trial

Hypertension is one of the main risk factors for cardiovascular diseases. In this study we aimed to evaluate efficiency and safety of carvedilol treatment in refractory hypertensive patients with renal diseases, including chronic kidney disease (CKD), polycystic kidney disease (PKD), dialysis and post-transplantation population. A multicentre, prospective, open label, self-compared trial was conducted in the east area of China in 2005. Two hundred and seventeen patients were enrolled in this study. Mean arterial blood pressure (systolic/diastolic) at 4 weeks significantly reduced in comparison with that before the use of carvedilol (142.6 ± 14.4/84.2 ± 10.1 mmHg vs 166.2 ± 18.1/90.4 ± 11.0 mmHg, P < 0.05), and then it continued to drop to 136.9 ± 12.4 mmHg/80.1 ± 10.6 mmHg at the completion of trial (week 8). Total efficiency (subjects with a BP less or equal to 130/80 mmHg or having a fall of greater or equal to 10 mmHg in DBP or greater or equal to 30 mmHg in systolic blood pressure) was 57.1% at 4 weeks and 79.7% at 8 weeks, and dominant efficiency (subjects with a BP of less or equal to 130/80 mmHg and those showing a fall of greater or equal to 10 mmHg in diastolic blood pressure) was 11.5% and 26.7%, respectively. Mean heart rate declined from 79.3 ± 10.2/min to 75.9 ± 7.6/min at 4 weeks and 75.0 ± 8.5/min at 8 weeks ( P < 0.05). Plasma norepinephrine level decreased from 38.7 pg/mL before this trial to 17.6 pg/mL ( P < 0.05). The total number of patients experiencing at least one adverse event was 13. None resulted in withdrawal of the patient from study. This study suggests that carvedilol is an efficient and safe drug in treatment of refractory hypertensive patients with renal diseases.

ENDOTHELIAL DYSFUNCTION IN REFRACTORY HYPERTENSION: CORRELATION BETWEEN BLOOD PRESSURE LEVELS AND NOCTURNAL DIPPING BP IMPAIRMENT: PP.6.261

Introduction: There is marked association between hypertensive disease and the absence of the nocturnal blood pressure (BP) fall. There is also evidence of correlation between endothelial dysfunction and the non-dipping pattern which is associated with increased cardiovascular mortality. In this study we aimed to evaluate the influence of BP levels on endothelium dependent (Flow Mediated Dilation – FMD) and non-dependent (Nitroglycerin – NTG) vasodilation and on the presence of dipping profile (evaluated by ABPM) in resistant hypertensive patients controlled (CRH) or uncontrolled (UCRH). Methods: Refractory hypertensive (RH) patients (n = 76) were divided in 2 groups: CRH (n = 40; M14/ F26; 50,3 + 6,4 yrs) and UCRH (n = 36; M9/F27; 48 + 5,1 yrs). Normotensive individuals (NT, n = 29; M11/F17; 46,1 ± 10,2 yrs) constituted the third group. BP was measured by using ABPM in two occasions. FMD was performed and evaluated by non participating viewers. Statistics: Variables were compared by ANOVA test and Dunn's test was used for multiple comparisons. Pearson's coefficient was used to correlate variable. Results: The UCRH group presented the highest BP levels of the three groups. The FMD tests unveiled that the UCRH patients had a greater impairment of the endothelial function (6,9 + 0,5%) in comparison to the CRH patients (7,5 + 0,5%) (p < 0,05) and that also occurred when comparing the latter group to control subjects (12,0 + 1,4%) (p < 0.001). A positive correlation (Pearson) between 24 hour BP and endothelial dysfunction in the UCRH (p < 0,001; R = 63%) and CRH (p < 0,0001; r = 71%) groups was also noted. In addition, the data revealed nocturnal BP decline in UCRH subjects was less evident than in CRH (10,8 + 4,9 vs. 22,4 + 7,2 mmHg). Conclusions: We concluded that there is a direct correlation between BP levels and endothelial dysfunction both greater in UCRH patients than in CRH patients. The vascular function impairment probably determines the attenuated dipping blood pressure pattern in the hypertensive groups, especially the former.

HYPOTENSIVE DRUGS EFFECT AND LIVER MONOOXIGENASE FUNCTION IN ARTERIAL HYPERTENSION PATIENTS AFTER ADRENAL HYPERFUNCTION CORRECTION

Hypotensive drug tolerance and liver monooxygenase activity were investigated in 24 refractory arterial hypertension patients before and after surgical suppression of adrenal hyperfunction. Liver monooxygenase activity was studied using antipyrine test. It was found that hypotensive drug tolerance was decreased after one and two side operations on adrenal glands. In parallels halftime of antipyrine elimination was shown to be prolonged by 88.5% in 3 months - 3 years after suppression of adrenal hyperfunction. Our findings suggest that the hypotensive drug tolerance diminution may be the consequence of liver monooxygenase activity reduction. This assumption is in accordance with well known the hypotensive drug metabolism by microsomal liver monooxygenases

Cyclic guanosine monophosphate phosphodiesterase-5 inhibitor promotes an endothelium NO-dependent-like vasodilation in patients with refractory hypertension

The nitric oxide/cyclic-guanosine 3′,5′-monophosphate signaling cascade plays an essential role in cardiovascular homeostasis but its involvement in the pathophysiology of refractory hypertension is unclear. The acute vasodilatory effect of a single oral dose of a phosphodiesterase-5 inhibitor (sildenafil citrate) on the brachial artery dilatation was evaluated in 25 normal healthy volunteers (NL) and in 25 refractory hypertensive patients (RH). Endothelial and vascular smooth muscle functions were assessed two times. First, the brachial artery response to endothelium-dependent (flow-mediated dilatation [FMD]) and independent (glyceryl trinitrate [GTN]) stimuli was examined. The FMD in NL was 14.2 ± 3.2% compared to 10.3 ± 3.5% in RH ( P < 0.001) and the GTN-induced responses were 23.5 ± 6.3 in NL compared to 18.4 ± 5.7% in RH ( P < 0.001). Two weeks later, the brachial artery responses to FMD were determined before and after the administration of sildenafil citrate. Sildenafil caused a significant, slow and progressive dilatation of the brachial artery until 45 min after administration (4.7 ± 3.0%, 6.7 ± 3.0% and 9.4 ± 3.9% after 15′, 30′ and 45′, respectively, in RH and 3.7 ± 1.9%, 7.4 ± 2.7% and 10.1 ± 3.0%, respectively, in NL). A second FMD stimulus, applied 45 min after ingesting 50 mg of sildenafil resulted in an additional significant increase in the vasodilatory response (from 9.4 ± 3.9% to 13.0 ± 4.0% in RH; P < 0.001 and from 10.1 ± 3.0 to 14.6 ± 4.1 in NL; P < 0.001), but this was still significantly less than the response to GTN. Sildenafil citrate caused brachial artery vasodilatation similar to that caused by NO released during FMD in patients with refractory hypertension.

Noninvasive Hemodynamic Measurements

It has been well established that effective blood pressure (BP) lowering, using various antihypertensive agents with different mechanisms of action, lowers the risk for cardiovascular morbidity and mortality.1–4 However, when hypertensive populations are partitioned into subgroups by race, sex, geography, and age, differences in BP responses to single antihypertensive drugs emerge, albeit at the group level, that have been used to guide therapy for individuals within these contrasted groups.1,5,6 With respect to race, perhaps the most widely used group characteristic used to guide individual therapy, we5 and Sehgal6 have argued that the observed racial differences in BP response overlap to such a large degree that, by far, the greatest source of variation in BP response is within rather than between groups. This observation renders the use of group characteristics as grossly suboptimal criterion on which to base therapy for all individuals of a group. The inaccuracy of blanket extrapolation of group characteristics to predict BP responses for individuals is also likely to be true for traits such as geographic residence, age, and sex. Thus, the findings reported by Smith et al7 in this issue of Hypertension were very encouraging. These investigators showed that consideration of hemodynamic parameters, as determined noninvasively by impedance cardiography (IC) (BioZ, Cardiodynamics), in the selection of antihypertensive therapy in primary care practice settings improved rates of BP control and normalization of selected hemodynamic parameters in drug-treated hypertensives with BP >140/90 mm Hg. They …

Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex.

This study was undertaken to determine whether abolition of obstructive sleep apnoea (OSA) by continuous positive airway pressure (CPAP) could reduce blood pressure (BP) in patients with refractory hypertension. In 11 refractory hypertensive patients with OSA, the acute effects of CPAP on nocturnal BP were studied during sleep and its longer term effects on 24-h ambulatory BP after 2 months. During a single night's application, CPAP abolished OSA and reduced systolic BP in stage 2 sleep from 138.3 +/- 6.8 to 126.0 +/- 6.3 mmHg. There was also a trend towards a reduction in average diastolic BP (from 77.7 +/- 4.5 to 72.9 +/- 4.5). CPAP usage for 2 months was accompanied by an 11.0 +/- 4.4 mmHg reduction in 24-h systolic BP. In addition, both the nocturnal and daytime components of systolic BP fell significantly by 14.4 +/- 4.4 and 9.3 +/- 3.9 mmHg, respectively. Diastolic BP was reduced significantly at night by 7.8 +/- 3.0 mmHg. In patients with refractory hypertension, acute abolition of obstructive sleep apnoea by continuous positive airway pressure reduces nocturnal blood pressure. These data also suggest that continuous positive airway pressure may reduce nocturnal and daytime systolic blood pressure chronically. Randomised trials are needed to confirm the latter results.