Percutaneous coronary intervention (PCI) with stent implantation has become the standard of care for myocardial revascularization, especially in the setting of unstable coronary artery disease.¹ Despite the use of dual antiplatelet therapy (DAPT; ie, aspirin and clopidogrel), which reduces cardiovascular events after PCI by more than 80%, definite stent thrombosis remains a concern. Although it is a rare complication, occurring in 0.5% to 4% of patients within the first year of PCI,² the majority of stent thromboses occur in the first month and are defined as early stent thrombosis. It is a devastating complication, with a mortality rate up to 40% and large myocardial infarction in roughly 80% of survivors who remain exposed to frequent recurrence.^2,3 Clinical and angiographic correlates of stent thrombosis have been well described, of which premature interruption of DAPT is the most important risk factor for early stent thrombosis.^2,4 In addition, comorbidities, the initial clinical presentation, diabetes, stent undersizing or underexpansion, complex and/or bifurcation lesions, and coronary dissection have been associated with stent thrombosis.²

Approximately 8–18% of all patients with high blood pressure (BP) are apparently resistant to drug treatment.^1,2 In this situation, new strategies to help reduce BP are urgently needed but the complex pathophysiology of resistant hypertension makes this search difficult. Not surprisingly in this context, the latest non-drug treatment which triggered controversy is catheter-based renal denervation (RDN).^3,4 The method uses radiofrequency energy, or alternatively ultrasound or chemical denervation, to disrupt renal nerves within the renal artery wall, thereby reducing sympathetic efferent and sensory afferent signalling to and from the kidneys.^5,6 Various experimental models of hypertension strongly support this concept^7,8 and available evidence also suggests that sympathetic nervous system activation contributes to the development and progression of hypertension and subsequently to target organ damage.^7–11 Historical observations have shown that surgical sympathectomy can reduce BP as well as morbidity and mortality in patients with uncontrolled hypertension.^12,13 However, the clinical evidence in support of RDN as an effective interventional technique in patients with resistant hypertension is conflicting. A number of observational studies and three randomized, controlled trials (Symplicity HTN-2, Prague-15, and DENERHTN) support both safety and efficacy of this new therapy^14–22 but some smaller studies and the large, single-blind, randomized, sham-controlled symplicity HTN-3 trial failed to show superiority of RDN when compared with medical therapy alone.^23–25