Abstract

Resistant hypertension is a growing problem in the United States and around the world. Although its pathophysiology is multifactorial and poorly understood, it is invariably associated with increased renal sympathetic activation and central sympathoexcitation. 1–3 Sympathetic nervous system (SNS) regulation is complex and several mechanisms modulate its activity, 4–6 with accumulating evidence pointing to the kidney as a key contributor. The kidney, through efferent and afferent sympathetic fibers, acts as both a generator and a recipient of sympathetic signals. 7 A great deal of basic research 8–11 has pointed out for decades that efferent fibers can modulate sodium and fluid retention by the kidney, control renin release and plasma renin activity, and regulate renal blood flow. On the other hand, afferent fibers can transfer signals generated by mechanoreceptors and chemoreceptors in the kidney to the brain and sequentially modulate heart rate (HR), heart function, and peripheral resistance. 9,10 Recent advances in technology made it possible to percutaneously approach and interrupt transvascularly the sympathetic fibers coursing in the adventitia of the renal artery. A first-in-man study, 12 using a single tip radiofrequency ablation catheter, suggested impressive reductions in office blood pressure (OBP), sustained and improved over time. Other follow-up studies demonstrated similar results, with durable long-term blood pressure (BP) reduction, 13–15 although all published data consistently indicate that response varies among patients. Some patients demonstrate adequate response, some partial response, and some no response at all. 16 It is therefore important to focus our research on response indicators in order to better tailor our therapies. In this brief article we describe a case with impressive BP response early on after sympathetic renal denervation using a multi-electrode ablation catheter. The patient had clinical evidence of sympathetic activation, ie, persistently high BP and HR despite the use of multiple drugs including sympatholytics. CASE The patient was a 52-year-old morbidly obese (body mass index = 43.4 kg/m 2 ) woman with a history of smoking of more than 30 years and uncontrolled severe drug-resistant hypertension diagnosed more than 5 years prior to presentation. She also had a history of hypothyroidism and received levothyroxin replacement therapy, being eythyroid at last follow-up. Extensive workup for secondary causes of hypertension had been negative. On presentation, the patient was treated with 6 antihypertensive medications as follows: olmesartan 40 mg, chlorthalidone 25 mg, nifedipine 60 mg, bisoprolol 15 mg, and eplerenone 50 mg once a day and clonidine 0.15 mg 3 times a day. Systolic OBP was consistently >160 mm Hg despite use of a multidrug regimen and she was referred for renal denervation. During baseline evaluation, office systolic and diastolic OBP were 223 mm Hg and 131 mm Hg, respectively. HR was 97 beats per minute and 24-hour ambulatory BP monitoring (ABPM) averaged 178/102 mm Hg. Laboratory results showed normal complete blood cell count and chemistry, and glomerular filtration rate was estimated at 93 mL/min/1.73 m 2 . Target organ damage was indicated by an albumin to creatinine ratio of 101 mg/g, while findings from transthoracic echocardiography revealed concentric left ventricular hypertrophy (left ventricular mass indexed for body surface area equal to 148.6 g/m 2 ).

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