Background: Previous studies in patients with resistant hypertension have reported improvements in left ventricular mass (LVM) and fibrosis following renal denervation (RDN)1-5. Potential mechanistic explanations are responses to changes in afterload, sympathetic activity or neuro-hormonal balance. Methods: We investigated the relationships between left ventricular hypertrophy (LVH) and myocardial strain, office blood pressure (BP) and muscle sympathetic nerve activity (MSNA; recorded from the peroneal nerve), before and after renal denervation in 19 patients. Cardiac magnetic resonance assessed left ventricular mass (LVM) and strain parameters (indexed to body surface area). In four patients, extracellular volume fraction (ECV), myocardial cell volume (MCV) and interstitial volume (IV) were also quantified using T1 mapping. Measurements were performed pre- and 6-12 months post-RDN. Data analysed using Student’s t-test and Pearson’s correlation coefficient, and reported as mean ± SEM. Results: At baseline; age 55 ± 3 years, 53% male, 5.0 ± 0.4 antihypertensive drugs, office BP 193 ± 4/107 ± 5 mmHg. 12/19 patients (63%) responded to RDN (≥10 mmHg drop in office systolic BP; SBP); change in BP -18.3 ± 8.8/-2.2 ± 5.1 mmHg. 12/19 patients had MSNA of sufficient quality to analyse. Following RDN, there was a reduction in LVM (96 ± 6 vs 88 ± 7 g/m2, p<0.05) and improvements in peak myocardial strain (radial strain 29.8 ± 1.9 vs 35.3 ± 2.1 %, p<0.01; longitudinal strain -17.4 ± 0.8 vs -19.3 ± 0.8 %, p<0.05; circumferential strain -16.6 ± 0.7 vs -18.6 ± 0.8 %, p<0.01). However MSNA was unchanged (58.4 ± 6.4 vs 61.6 ± 6.4 bursts/100heartbeats, p=0.67). Whilst there was no correlation between SBP and LVM at baseline (R=-0.36, p=0.12), the change in LVM correlated with the reduction in SBP (R=0.56, p<0.01). There was no correlation between the change in MSNA and changes in SBP or LVM. In the four patients assessed with T1 mapping, there were reductions in LVM (-10.6 ± 3.3 g/m2, p<0.05), and specifically IV and ECV (4.1 ± 1.0 ml/m2, -0.011 ± 0.002 %, both p<0.05), with a borderline fall in MCV (-6.5 ± 2.2 ml/m2, p=0.06). Conclusions: Similar to previous studies, we have shown improvements in LV mass and myocardial strain following RDN. The novel finding is that these were independent of MSNA. In contrast to previous studies2,3, LV mass reduction correlates with SBP reduction in this cohort, and may therefore be dependent on afterload. Preliminary T1 mapping data also demonstrates a reduction in myocardial interstitial fibrosis post-RDN, giving additional insights into the potential mechanisms that contribute to hypertensive heart disease.