Renal Sympathetic Denervation and LV Hypertrophy
Objectives This study investigated the effect of catheter-based renal sympathetic denervation (RD) on left ventricular hypertrophy (LVH) and systolic and diastolic function in patients with resistant hypertension.
Background LVH and diastolic dysfunction are associated with elevated sympathetic activity and increased morbidity and mortality. The effect of RD on LVH and LV function is unclear.
Methods Forty-six patients underwent bilateral RD, and 18 patients served as controls. Transthoracic echocardiography was performed at baseline, and after 1 month and 6 months.
Results Besides reduction of systolic and diastolic blood pressure (–22.5/–7.2 mm Hg at 1 month and –27.8/–8.8 mm Hg at 6 months, p < 0.001 at each time point), RD significantly reduced mean interventricular septum thickness from 14.1 ± 1.9 mm to 13.4 ± 2.1 mm and 12.5 ± 1.4 mm (p = 0.007), and LV mass index from 53.9 ± 15.6 g/m (112.4 ± 33.9 g/m) to 47.0 ± 14.2 g/m (103.6 ± 30.5 g/m) and 44.7 ± 14.9 g/m (94.9 ± 29.8 g/m) (p < 0.001) at 1 month and 6 months, respectively. The mitral valve lateral E/E' decreased after RD from 9.9 ± 4.0 to 7.9 ± 2.2 at 1 month and 7.4 ± 2.7 at 6 months (p < 0.001), indicating reduction of LV filling pressures. Isovolumic relaxation time shortened (baseline 109.1 ± 21.7 ms vs. 85.6 ± 24.4 ms at 6 months, p = 0.006), whereas ejection fraction significantly increased after RD (baseline: 63.1 ± 8.1% vs. 70.1 ± 11.5% at 6 months, p < 0.001). No significant changes were obtained in control patients.
Conclusions Besides the known effect on blood pressure, our study showed for the first time that RD significantly reduces LV mass and improves diastolic function, which might have important prognostic implications in patients with resistant hypertension at high cardiovascular risk.
Hypertension is a risk factor for coronary artery disease, myocardial infarction, and stroke. Patients with therapy-refractory hypertension are at particular risk for cardiovascular events. Even before clinical events occur, hypertension induces changes of the heart, including left ventricular hypertrophy (LVH) and cardiac fibrosis. These structural alterations are associated with functional impairment of the left ventricle (LV), i.e., abnormal diastolic relaxation and increased diastolic filling pressures. Notably, diastolic dysfunction may already be present in hypertensive patients with normal LV mass.
LVH and diastolic dysfunction have been linked to cardiovascular morbidity and mortality. Regression of LVH was shown to improve cardiovascular outcome independently of other risk factors, and thus has been suggested as an intermediate endpoint. However, despite a similar reduction of blood pressure (BP), efficacy on LVH regression varies among different antihypertensive drugs.
The cause of resistant arterial hypertension is multifactorial. Chronic activation of the sympathetic nervous system plays a central role in the pathophysiology of both BP elevation and development of LVH. Reduction of renal sympathetic afferent and efferent activity by percutaneous, catheter-based endovascular radiofrequency ablation of the renal sympathetic nerves effectively decreased systolic blood pressure (SBP) and diastolic blood pressure (DBP) in patients with resistant hypertension. However, the impact of renal sympathetic denervation (RD) on LVH is unclear. Therefore, we evaluated whether this new therapeutic approach has a positive effect on LVH as measured by hypertensive end-organ damage and on diastolic dysfunction.
Abstract and Introduction
Abstract
Objectives This study investigated the effect of catheter-based renal sympathetic denervation (RD) on left ventricular hypertrophy (LVH) and systolic and diastolic function in patients with resistant hypertension.
Background LVH and diastolic dysfunction are associated with elevated sympathetic activity and increased morbidity and mortality. The effect of RD on LVH and LV function is unclear.
Methods Forty-six patients underwent bilateral RD, and 18 patients served as controls. Transthoracic echocardiography was performed at baseline, and after 1 month and 6 months.
Results Besides reduction of systolic and diastolic blood pressure (–22.5/–7.2 mm Hg at 1 month and –27.8/–8.8 mm Hg at 6 months, p < 0.001 at each time point), RD significantly reduced mean interventricular septum thickness from 14.1 ± 1.9 mm to 13.4 ± 2.1 mm and 12.5 ± 1.4 mm (p = 0.007), and LV mass index from 53.9 ± 15.6 g/m (112.4 ± 33.9 g/m) to 47.0 ± 14.2 g/m (103.6 ± 30.5 g/m) and 44.7 ± 14.9 g/m (94.9 ± 29.8 g/m) (p < 0.001) at 1 month and 6 months, respectively. The mitral valve lateral E/E' decreased after RD from 9.9 ± 4.0 to 7.9 ± 2.2 at 1 month and 7.4 ± 2.7 at 6 months (p < 0.001), indicating reduction of LV filling pressures. Isovolumic relaxation time shortened (baseline 109.1 ± 21.7 ms vs. 85.6 ± 24.4 ms at 6 months, p = 0.006), whereas ejection fraction significantly increased after RD (baseline: 63.1 ± 8.1% vs. 70.1 ± 11.5% at 6 months, p < 0.001). No significant changes were obtained in control patients.
Conclusions Besides the known effect on blood pressure, our study showed for the first time that RD significantly reduces LV mass and improves diastolic function, which might have important prognostic implications in patients with resistant hypertension at high cardiovascular risk.
Introduction
Hypertension is a risk factor for coronary artery disease, myocardial infarction, and stroke. Patients with therapy-refractory hypertension are at particular risk for cardiovascular events. Even before clinical events occur, hypertension induces changes of the heart, including left ventricular hypertrophy (LVH) and cardiac fibrosis. These structural alterations are associated with functional impairment of the left ventricle (LV), i.e., abnormal diastolic relaxation and increased diastolic filling pressures. Notably, diastolic dysfunction may already be present in hypertensive patients with normal LV mass.
LVH and diastolic dysfunction have been linked to cardiovascular morbidity and mortality. Regression of LVH was shown to improve cardiovascular outcome independently of other risk factors, and thus has been suggested as an intermediate endpoint. However, despite a similar reduction of blood pressure (BP), efficacy on LVH regression varies among different antihypertensive drugs.
The cause of resistant arterial hypertension is multifactorial. Chronic activation of the sympathetic nervous system plays a central role in the pathophysiology of both BP elevation and development of LVH. Reduction of renal sympathetic afferent and efferent activity by percutaneous, catheter-based endovascular radiofrequency ablation of the renal sympathetic nerves effectively decreased systolic blood pressure (SBP) and diastolic blood pressure (DBP) in patients with resistant hypertension. However, the impact of renal sympathetic denervation (RD) on LVH is unclear. Therefore, we evaluated whether this new therapeutic approach has a positive effect on LVH as measured by hypertensive end-organ damage and on diastolic dysfunction.
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