Masked arterial hypertension in a 64-year-old man with primary aldosteronism.

PURPOSE: Primary aldosteronism is one of the most frequent causes of secondary arterial hypertension, and whether primary aldosteronism is associated with masked hypertension is unknown. MATERIALS AND METHODS: We describe a 64-year-old man with a history of hypothyroidism, recurring hypokalaemia, and normal home and office blood pressure values. Ambulatory blood pressure monitoring revealed masked hypertension with strikingly high systolic blood pressure variability and typical hypertension-mediated organ damage. RESULTS: The patient required gradual escalation of antihypertensive medication to four drugs. During the diagnostic process we identified primary aldosteronism, cobalamin deficiency, severe obstructive sleep apnoea, and low baroreflex sensitivity (1.63 ms/mmHg). Following unilateral adrenalectomy, cobalamin supplementation and continuous positive airway pressure, we observed a spectacular improvement in the patient's blood pressure control, baroreflex sensitivity (4.82 ms/mmHg) and quality of life. CONCLUSIONS: We report an unusual case of both masked arterial hypertension and primary aldosteronism. Elevated blood pressure values were masked in home and office measurements by coexisting hypotension which resulted most probably from deteriorated baroreflex sensitivity. Baroreflex sensitivity increased following treatment, including unilateral adrenalectomy. Hypertension can be masked by coexisting baroreceptor dysfunction which may derive from structural but also functional reversible changes.

Long-term effects of device-guided slow breathing in stable heart failure patients with reduced ejection fraction.

BACKGROUND: Slow breathing (SLOWB) alleviates symptoms of chronic heart failure (HF) but its long-term effects are unknown. We examined the acute and long-term impact of device-guided breathing on hemodynamics and prognostic parameters in HF patients with reduced ejection fraction (HFrEF). METHODS AND RESULTS: Twenty-one patients with HFrEF (23.9 ± 5.8%, SD ± mean) on optimal medical therapy underwent blood pressure (BP), heart rate (HR), HR variability, 6-min walk test (6MWT), cardiopulmonary exercise testing (CPET), and echocardiography measurements before and 3 months after SLOWB home training (30 min daily). After 3 months, all patients were assigned to continue SLOWB (Group 1) or no-SLOWB (Group 2). All tests were repeated after 6 months. Acute SLOWB (18 ± 5 vs 8 ± 2 breaths/min, P < 0.001) had no influence on BP and HR but improved saturation (97 ± 2 vs 98 ± 2%, P = 0.01). Long-term SLOWB reduced office systolic BP (P < 0.001) but not central or ambulatory systolic BP. SLOWB reduced SDNN/RMSSD ratio (P < 0.05) after 3 months. One-way repeated measures of ANOVA revealed a significant increase in 6MWT and peak RER (respiratory exchange ratio) from baseline to 6-month follow-up in group 1 (P < 0.05) but not group 2 (P = 0.85 for 6MWT, P = 0.69 for RER). No significant changes in echocardiography were noted at follow-up. No HF worsening, rehospitalisation or death occurred in group 1 out to 6-month follow-up. Two hospitalizations for HF decompensation and two deaths ensued in group 2 between 3- and 6-month follow-up. CONCLUSIONS: SLOWB training improves cardiorespiratory capacity and appears to slow the progression of HFrEF. Further long-term outcome studies are required to confirm the benefits of paced breathing in HFrEF.

Insufficiency of the zona glomerulosa of the adrenal cortex and progressive kidney insufficiency following unilateral adrenalectomy - case report and discussion.

BACKGROUND: Primary aldosteronism (PA) is the most common cause of secondary hypertension and bilateral adrenal hyperplasia (BAH) and aldosterone-producing adenoma (APA) seem to be the most common causes of PA. Unilateral adrenalectomy (UA) is the preferred treatment for APA, although the benefits are still difficult to assess. CASE REPORT: We present a case report of a 69-year old man with a 30 year history of hypertension and probably long-standing PA due to APA, with typical organ complications. Since repeated abdominal CT scans were equivocal, not showing radiological changes characteristic for PA, the diagnosis of APA was delayed and was only finally confirmed by adrenal venous sampling which demonstrated unilateral aldosteronism. The patient underwent UA, complicated by mineralocorticoid deficiency syndrome and increased creatinine and potassium levels. At 12 months follow-up the patient still had hyperkalemia and was fludrocortisone dependent. CONCLUSIONS: Older patients and patients with long-lasting PA who are treated with UA may demonstrate deterioration of renal function and develop transient or persistent insufficiency of the zona glomerulosa of the remaining adrenal gland necessitating fludrocortisone supplementation. Transient hyperkalemia may be observed following UA as a result of the prolonged effects of aldosterone antagonists and/or transient mineralocorticoid/glucocorticoid insufficiency. Additionally, the level of progression of chronic kidney disease after UA is difficult to predict. There likely exists a group of patients who might paradoxically have higher cardiovascular risk due to significant deterioration in kidney function not only resulting from the removal of the aldosterone induced glomerular hyperfiltration phenomenon. Identification of such a group requires further detailed investigation.

Recent advances in the pathophysiology of arterial hypertension: potential implications for clinical practice.

Hypertension remains a major and growing public health problem associated with the greatest global rate of cardiovascular morbidity and mortality. Although numerous factors contribute to poor control of blood pressure (BP) and to pseudoresistance (eg, unawareness, lifestyle habits, nonadherence to medication, insufficient treatment, drug­induced hypertension, undiagnosed secondary causes), true resistant hypertension (RH) is reported in 10.1% of patients treated for elevated BP. While the mechanisms underlying RH remain complex and not entirely understood, sympathetic activation involved in the pathophysiology of hypertension, disease progression, and adverse complications is further augmented in patients with drug­resistant hypertension. The well­established contribution of neurogenic component of hypertension has led to the introduction of new alternative therapies aimed specifically at modulating central and neural reflexes mechanisms involved in BP control. Although clinical benefits of lowering BP with renal denervation, baroreflex activation therapy, carotid body denervation, central arteriovenous anastomosis, and deep brain stimulation have advanced our knowledge on uncontrolled hypertension, the variable BP response has prompted extensive ongoing research to define predictors of treatment effectiveness and further investigation of pathophysiology of RH. Very recently, research on the role of vasopressinergic neurons, masked tachycardia, and impaired brain neural activity has provided novel insights into hypertension. This review briefly summarizes the role of the centrally mediated sympathetic nervous system in hypertension, the therapeutic strategies that distinctively target impaired neural reflex mechanisms, and potential implications for future clinical research and therapies.

Optimizing the Management of Uncontrolled/Resistant Hypertension. The Importance of Sleep Apnoea Syndrome.

INTRODUCTION: Obstructive Sleep Apnoea (OSA) constitutes the most prevalent form of abnormal respiratory control during sleep in adults. Evidence linked OSA to cardiovascular disease, and the role of OSA in abnormal Blood Pressure (BP) control has been extensively studied. Although longitudinal trials suggest a causative role of OSA in the development of hypertension, the evidence is not fully consistent. Nasal continuous positive airway pressure (nCPAP) applied during sleep is well documented and a highly efficient therapeutic aid to eliminate OSA. It has been repeatedly shown that nCPAP-therapy is also associated with modest BP lowering effect in hypertensive OSA-patients, and the magnitude of the observed effect correlates with the severity of OSA. However, it is unlikely that nCPAP would normalize BP. CONCLUSION: There are few studies which tested the interplay between OSA, nCPAP and certain BPlowering drug classes. Angiotensin receptor blockers may show synergistic hypotensive effect with nCPAP, whereas mineralocorticoid receptor blocker has been shown to modestly attenuate the severity of OSA. Additionally, the application of chronotherapy may be of special use in such patients. The current evidence is sufficient to promote persistent and effective nCPAP-therapy as a standard in all eligible OSA-patients with difficult-to-control hypertension.

Effects of acute and long-term slow breathing exercise on muscle sympathetic nerve activity in untreated male patients with hypertension.

OBJECTIVE: Acute slow breathing (SLOWB) affects sympathetic cardiovascular regulation, but its long-term effects are unknown. Using device-guided breathing we explored short-term and long-term SLOWB effects on blood pressure (BP), heart rate (HR) and muscle sympathetic nerve activity (MSNA) in essential hypertension. METHODS: We measured BP, HR and MSNA in 10 hypertensive individuals at rest, during laboratory stressors, before and after acute SLOWB, and 8 weeks after SLOWB exercise. Twelve matched hypertensive controls underwent a similar protocol excluding SLOWB intervention. Office and 24-h BP were obtained at baseline and at follow-up. RESULTS: Acute SLOWB had no influence on BP, HR, but decreased MSNA (P < 0.01). BP, HR, MSNA responses to handgrip were comparable before and after acute SLOWB. Acute SLOWB tended to reduce SBP (P = 0.09), HR (P = 0.08), but not MSNA (P = 0.20) responses to mental stress. Long-term SLOWB decreased office SBP (P < 0.001), DBP (P < 0.01), HR (P = 0.004), but not 24-h BP. Resting MSNA was unchanged after long-term SLOWB (P = 0.68). Long-term SLOWB did not influence BP, HR or MSNA responses to handgrip and cold pressor, but reduced SBP (P = 0.03), HR (P = 0.03) responses to mental stress without MSNA changes. In controls BP, HR, MSNA responses to laboratory stressors remained unchanged at baseline and at follow-up. CONCLUSION: In essential hypertension, MSNA is reduced during acute SLOWB, but remains unaltered following long-term SLOWB. Long-term SLOWB reduces office, but not ambulatory BP and HR. SLOWB attenuates cardiovascular response to mental stress, but not physical stressors. These findings may be indicative of beneficial SLOWB effects on stress reduction in essential hypertension.

Novel baroreflex activation therapy in resistant hypertension: results of a European multi-center feasibility study.

OBJECTIVES: This study assessed the safety and efficacy of a novel implantable device therapy in resistant hypertension patients. BACKGROUND: Despite the availability of potent antihypertensive drugs, a substantial proportion of patients remain hypertensive. A new implantable device (Rheos system, CVRx, Inc., Minneapolis, Minnesota) that activates the carotid baroreflex may help these patients. METHODS: Forty-five subjects with systolic blood pressure ≥160 mm Hg or diastolic ≥90 mm Hg despite at least 3 antihypertensive drugs were enrolled in a prospective, nonrandomized feasibility study to assess whether Rheos therapy could safely lower blood pressure. Subjects were followed up for as long as 2 years. An external programmer was used to optimize and individualize efficacy. RESULTS: Baseline mean blood pressure was 179/105 mm Hg and heart rate was 80 beats/min, with a median of 5 antihypertensive drugs. After 3 months of device therapy, mean blood pressure was reduced by 21/12 mm Hg. This result was sustained in 17 subjects who completed 2 years of follow-up, with a mean reduction of 33/22 mm Hg. The device exhibited a favorable safety profile. CONCLUSIONS: The Rheos device sustainably reduces blood pressure in resistant hypertensive subjects with multiple comorbidities receiving numerous medications. This unique therapy offers a safe individualized treatment option for these high-risk subjects. This novel approach holds promise for patients with resistant hypertension and is currently under evaluation in a prospective, placebo-controlled clinical trial.