the cumulative sodium retention. Furthermore, this renal denervation was shown to prevent, markedly attenuate or delay the development of hypertension in a diverse number of models of elevated blood pressure. 4 These promising experimental results of renal sympathetic nerve denervation for the treatment of hypertension prompted the establishment of the first clinical trial of this approach as a proof-of-principle study. 3 In brief, in 45 patients with resistant hypertension a catheter connected to a radiofrequency generator was introduced into renal arteries via femoral access and up to six discrete radiofrequency ablations were delivered within each renal artery. The major aims of this study were to assess firstly the efficacy of blood pressure lowering and s econdly the safety of this procedure. The initial blood pressure in these patients who had been treated with four to seven anti-hypertensive medications was 177/101 mmHg. The highly significant average reduction in office measured systolic/diastolic blood pressure at 1 month after the renal sympathetic denervation procedure was 14/10 mmHg. Blood pressure was further reduced at 3 months by 22/10 mmHg, with this effect persisting on s ubsequent assessments with the reduction 12 months after the procedure being 27/17 mmHg. Only six out of 45 patients did not benefit from this treatment, defined as a s ystolic blood pressure reduction of less than 10 mmHg. In 12 patients, 24 hour ambulatory blood pressure monitoring was performed before and after the denervation procedure. The change in office systolic blood pressure correlated closely with the change in mean ambulatory blood pressure (r 2 50.62, p50.002). Furthermore, renal sympathetic denervation was associated with an increase in the number of n octurnal dippers in the group of patients that had responded to this treatment. The effectiveness of the radiofrequency method in achieving efferent renal denervation was assessed in a subgroup of patients (n 51 0) by measuring renal Arterial hypertension is a major risk factor for an array of cardiovascular diseases, particularly in the context of concomitant diabetes. Furthermore, elevated blood pressure is at least twice as prevalent in type 2 diabetes as in the g eneral population. Clinical data suggest that lower blood pressure may induce even greater cardiovascular benefits in diabetic subjects than in individuals without diabetes. With respect to renal disease, recent data from the Action in Diabetes and Vascular Disease (ADVANCE) study indicate that there is no lower threshold for blood pressure reduction when one is aiming to reduce the burden of renal disease. 1 So far, the major therapeutic strategy for arterial hypertension has focused on pharmacological treatments. Despite the abundance of available antihypertensive drugs, arterial hypertension remains undertreated, in particular in diabetes and specifically in the setting of associated chronic kidney disease. Clinical trials involving patients with diabetes or renal impairment have demonstrated that achieving lower blood pressure goals requires treatment with on average at least three different antihypertensive agents. 2 Moreover, it has been shown that with current standard antihypertensive therapies only one of out seven patients with type 2 diabetes can achieve a target blood pressure of less than 130/80 mmHg. Recently, a multi-centre prospective cohort study has demonstrated the efficacy of a non-pharmacological, minimally invasive percutaneous radiofrequency catheter-based treatment to disrupt renal sympathetic nerves in the management of patients with resistant hypertension, which included a significant subgroup with type 2 diabetes. 3 The rationale for renal sympathetic nerves denervation as a treatment strategy for systemic hypertension lies in the hypothesis that abnormal excretory function is crucial for the initiation, p rogression and maintenance of primary hypertension with sodium and water balance considered to be of central importance in the long-term control of systemic blood pressure. In addition, in animal models it has been confirmed that renal sympathetic nerve stimulation results in a substantial increase in the renin secretion rate and promotes antinatriuresis without affecting glomerular filtration rate and renal plasma flow. Moreover, in animal models renal sympathetic denervation has been used to demonstrate that renal sympathetic nerve activity is responsible for approximately 40% of
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Apr 12, 2011
M El-Mas + 2
Open Access