Renal denervation in patients who do not respond to cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) reduces the morbidity and mortality in advanced heart failure (HF) in about two-thirds of the patients. Approximately one-third of the patients do not respond to CRT. The overactivity of sympathetic nervous system is associated with advanced HF and deteriorates the hemodynamic state. We tested the hypothesis that controlling sympathetic overactivity by renal denervation (RDN) could be beneficial in nonresponders for CRT. In our HeartF-RDN study (ClinalTrials.gov. NCT02638324), RDN could not reverse the progression of HF in subjects with New York Heart Association Classification (NYHA) III-IV stage symptoms.

Intravascular Renal Denervation in Renal Dialysis Patients with Uncontrolled Hypertension: A Case Series of Four Patients.

BACKGROUND Hypertension is a common complication of renal dialysis and is inadequately controlled in approximately one-third of patients. Intravascular renal denervation is an option to control sympathetic overdrive and decrease blood pressure. Four renal dialysis patients are presented with uncontrolled hypertension who were treated with intravascular renal denervation. CASE REPORT In a renal dialysis unit, patients were screened for therapy-resistant hypertension, which was defined as an outpatient blood pressure >160/100 mmHg and a blood pressure by interdialytic ambulatory blood pressure monitoring (ABPM) >130/80 mmHg. Four patients were identified with a mean ABPM of 175/95 mmHg. The four patients included a 24-year-old man with neurogenic bladder undergoing hemodialysis; a 55-year-old woman with a history of type 1 diabetes mellitus undergoing peritoneal dialysis; a 56-year-old woman with a history of autosomal dominant polycystic kidney disease (ADPKD) undergoing peritoneal dialysis; and a 72-year-old man with a history of ADPKD undergoing hemodialysis Following intravascular renal denervation, one patient had antihypertensive medicines withdrawn at 12 months, and he remained normotensive up to renal transplantation at 24 months. In two patients, ABPM did not decrease until renal transplantation was performed. The fourth patient was not a candidate for renal transplantation, and he was also a non-responder for intravascular renal denervation. None of the patients experienced hypotension or other adverse events following intravascular renal denervation. CONCLUSIONS A case series of four patients showed that, for some patients who have unresponsive hypertension while on renal dialysis, intravascular renal denervation is a safe procedure.

Renal sympathetic denervation in treating drug-resistant hypertension in a patient on hemodialysis.

A 26-year-old man had an end-stage renal disease because of a neurogenic urinary bladder with a vesicourinary reflux. The first kidney transplant was lost in consequence of chronic allograft nephropathy. Immunosuppressive medication was withdrawn and transplantectomy was performed in November 2010. After transplantectomy, his blood pressure (BP) slowly increased up to 200/100 mmHg. Antihypertensive medication was intensified and a fluid overload was excluded with body composition bioimpedance measurements. Forty-eight-hour ambulatory BP was 180/109 mmHg in the daytime and 178/108 mmHg in the night-time. Bilateral renal denervation (RDN) was performed with a single electrode Symplicity catheter on May 2013. The effect of RDN became evident at the 6 months visit, and all the antihypertensive medicines were withdrawn at 12 months. Fifteen months after RDN, 48-h ambulatory BP was 120/63 mmHg in the daytime and 108/60 mmHg in the night-time. The patient was without antihypertensive medication until retransplantation in May 2015.

Impaired negative chronotropic response to adenosine in patients with inappropriate sinus tachycardia.

INTRODUCTION: Adenosine is an endogenous nucleoside that has an important role in the diagnosis and treatment of several cardiac arrhythmias. However, its effects on inappropriate sinus tachycardia (IST) are not well established. METHODS AND RESULTS: In this study, the response to intravenous adenosine (0.1 to 0.15 mg/kg) was studied in 18 patients (age 46+/-15 years) with IST. In a subset of patients (n = 5), the direct effects of adenosine were assessed during pharmacologic beta-adrenergic and cholinergic blockade. Atrial cycle length (ACL) was measured before adenosine injection, at the time of the greatest cycle length prolongation, and during the maximum rebound acceleration of heart rate. Eighteen subjects (age 46+/-11 years) with normal sinus rhythm undergoing clinically indicated electrophysiologic study served as controls. Adenosine did not terminate IST in any patient. The maximum dose of adenosine prolonged the sinus interval significantly, from 780+/-128 msec to 985+/-225 msec (P < 0.001) in the control subjects. In contrast, adenosine caused no significant lengthening of atrial cycle length (527+/-69 msec vs 590+/-148 msec; P = NS) in the patients with IST. Similar difference in the response to adenosine was seen during the pharmacologic autonomic blockade. The reflex increase of the sinus rate (rebound effect) was greater in the control subjects than in the patients with IST (21.2%+/-9.7% vs 8.5%+/-8.8%; P < 0.001). CONCLUSION: The usual negative chronotropic effect of adenosine was impaired in the patients with IST. This may have important diagnostic implications and provide new insight into the mechanism(s) of IST.