Márcio Galindo Kiuchi1,2, Gustavo Ramalho E Silva3, Luis Marcelo Rodrigues Paz4, Shaojie Chen5,6, Gladyston Luiz Lima Souto3. 1. Department of Cardiac Surgery and Artificial Cardiac Stimulation, Department of Medicine, Hospital e Clínica São Gonçalo, São Gonçalo, RJ, Brazil. marciokiuchi@gmail.com. 2. Electrophysiology Division, Department of Cardiology, Hospital e Clínica São Gonçalo, São Gonçalo, RJ, Brazil. marciokiuchi@gmail.com. 3. Department of Cardiac Surgery and Artificial Cardiac Stimulation, Department of Medicine, Hospital e Clínica São Gonçalo, São Gonçalo, RJ, Brazil. 4. Interventional Cardiology Section, Department of Cardiology, Hospital e Clínica São Gonçalo, São Gonçalo, RJ, Brazil. 5. Department of Cardiology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 6. Fellowship of European Heart Rhythm Association / European Society of Cardiology, Department of Cardiology, Elisabethinen University Teaching Hospital Linz, Linz, Austria.
Abstract
BACKGROUND OR PURPOSE: Polymorphic premature ventricular complexes (PVCs) are very common, appearing most frequently in patients with hypertension, obesity, sleep apnea, and structural heart disease. Sympathetic hyperactivity plays a critical role in the development, maintenance, and aggravation of ventricular arrhythmias. Recently, the relevance of sympathetic activation in patients with ventricular arrhythmias was reported, and this finding suggested a potential role for catheter-based renal sympathetic denervation in reducing the arrhythmic burden. METHODS: We evaluated the effectiveness of the renal sympathetic denervation (RSD) in comparison to antiarrhythmic pharmacologic therapy in reducing polymorphic PVCs refractory to medication therapy and cardiac parameters assessed by 24-h Holter monitoring and cardiac magnetic resonance (CRM), respectively, in patients with structurally normal heart. RESULTS: Thirty-four patients were included in this study, 14 served as control, and 20 were treated with an ablation cardiac catheter with open irrigated tip. RSD was performed by a single operator following the standard technique. All the patients included had polymorphic PVCs and structurally normal heart. Data were obtained at baseline at the 12th month of follow-up (sixth month after RSD or adjustment of antiarrhythmic dosage). In RSD group, we observed a significant decrease in the number of polymorphic PVCs from baseline 36,091 ± 3327 to 3, 6, 7 (first month after RSD, without drugs), and 12 months (sixth month after RSD, without drugs) of follow-up, 31,009 ± 3251, 20,411 ± 3820, 7701 ± 1549, and 1274 ± 749, respectively, in all patients, P < 0.0001 to all the comparisons between the mean of each time point with the mean of every other time point. No changes in mean 24-h ABPM and renal function in both groups were observed at 12th month of follow-up. However, 24-h Holter mean heart rate decreased in control group at 12th month of follow-up, which did not happen with the RSD group. At the sixth month post-RSD in comparison to baseline, a significant reduction in the number of polymorphic PVCs (∆ = -34,817 ± 3590, P < 0.0001) was observed, as well as, in CRM parameters such as left ventricular mass/body surface area (∆ = -5.4 ± 2.1 g/m2, P < 0.0001) and left ventricular ejection fraction (∆ = +3.0 ± 1.8 %, P < 0.0001). In comparison to control group at the same time point, these findings were statistically superior in RSD group (P > 0.05). A significant correlation was found between the Δ number of polymorphic PVCs at the sixth month (r = -0.6723, P = 0.0012) after the RSD and the total number of RSD ablated spots. CONCLUSIONS: Polymorphic PVCs refractory to medication therapy may be modifiable by RSD in patients without structural heart disease. Although encouraging, our data are preliminary and need to be validated in a large population and in long term.
BACKGROUND OR PURPOSE: Polymorphic premature ventricular complexes (PVCs) are very common, appearing most frequently in patients with hypertension, obesity, sleep apnea, and structural heart disease. Sympathetic hyperactivity plays a critical role in the development, maintenance, and aggravation of ventricular arrhythmias. Recently, the relevance of sympathetic activation in patients with ventricular arrhythmias was reported, and this finding suggested a potential role for catheter-based renal sympathetic denervation in reducing the arrhythmic burden. METHODS: We evaluated the effectiveness of the renal sympathetic denervation (RSD) in comparison to antiarrhythmic pharmacologic therapy in reducing polymorphic PVCs refractory to medication therapy and cardiac parameters assessed by 24-h Holter monitoring and cardiac magnetic resonance (CRM), respectively, in patients with structurally normal heart. RESULTS: Thirty-four patients were included in this study, 14 served as control, and 20 were treated with an ablation cardiac catheter with open irrigated tip. RSD was performed by a single operator following the standard technique. All the patients included had polymorphic PVCs and structurally normal heart. Data were obtained at baseline at the 12th month of follow-up (sixth month after RSD or adjustment of antiarrhythmic dosage). In RSD group, we observed a significant decrease in the number of polymorphic PVCs from baseline 36,091 ± 3327 to 3, 6, 7 (first month after RSD, without drugs), and 12 months (sixth month after RSD, without drugs) of follow-up, 31,009 ± 3251, 20,411 ± 3820, 7701 ± 1549, and 1274 ± 749, respectively, in all patients, P < 0.0001 to all the comparisons between the mean of each time point with the mean of every other time point. No changes in mean 24-h ABPM and renal function in both groups were observed at 12th month of follow-up. However, 24-h Holter mean heart rate decreased in control group at 12th month of follow-up, which did not happen with the RSD group. At the sixth month post-RSD in comparison to baseline, a significant reduction in the number of polymorphic PVCs (∆ = -34,817 ± 3590, P < 0.0001) was observed, as well as, in CRM parameters such as left ventricular mass/body surface area (∆ = -5.4 ± 2.1 g/m2, P < 0.0001) and left ventricular ejection fraction (∆ = +3.0 ± 1.8 %, P < 0.0001). In comparison to control group at the same time point, these findings were statistically superior in RSD group (P > 0.05). A significant correlation was found between the Δ number of polymorphic PVCs at the sixth month (r = -0.6723, P = 0.0012) after the RSD and the total number of RSD ablated spots. CONCLUSIONS: Polymorphic PVCs refractory to medication therapy may be modifiable by RSD in patients without structural heart disease. Although encouraging, our data are preliminary and need to be validated in a large population and in long term.
Entities:
Keywords:
Cardiac magnetic resonance; Polymorphic premature ventricular complexes; Renal sympathetic denervation; Structurally normal heart; Sympathetic hyperactivity; Ventricular arrhythmias
Authors: Manuel D Cerqueira; Neil J Weissman; Vasken Dilsizian; Alice K Jacobs; Sanjiv Kaul; Warren K Laskey; Dudley J Pennell; John A Rumberger; Thomas Ryan; Mario S Verani Journal: Circulation Date: 2002-01-29 Impact factor: 29.690
Authors: Benjamin F Remo; Mark Preminger; Jason Bradfield; Suneet Mittal; Noel Boyle; Anuj Gupta; Kalyanam Shivkumar; Jonathan S Steinberg; Timm Dickfeld Journal: Heart Rhythm Date: 2013-12-31 Impact factor: 6.343
Authors: Luciana V Armaganijan; Rodolfo Staico; Dalmo A R Moreira; Renato D Lopes; Paulo T J Medeiros; Ricardo Habib; Jônatas Melo Neto; Marcelo Katz; Dikran Armaganijan; Amanda G M R Sousa; Felix Mahfoud; Alexandre Abizaid Journal: JACC Cardiovasc Interv Date: 2015-06 Impact factor: 11.195
Authors: Theano Papavassiliu; Harald P Kühl; Willem van Dockum; Mark B M Hofman; Olga Bondarenko; I Aernout M Beek; Albert C van Rossum Journal: J Cardiovasc Magn Reson Date: 2004 Impact factor: 5.364
Authors: Andrew S Levey; Lesley A Stevens; Christopher H Schmid; Yaping Lucy Zhang; Alejandro F Castro; Harold I Feldman; John W Kusek; Paul Eggers; Frederick Van Lente; Tom Greene; Josef Coresh Journal: Ann Intern Med Date: 2009-05-05 Impact factor: 25.391
Authors: Jeanette Schulz-Menger; David A Bluemke; Jens Bremerich; Scott D Flamm; Mark A Fogel; Matthias G Friedrich; Raymond J Kim; Florian von Knobelsdorff-Brenkenhoff; Christopher M Kramer; Dudley J Pennell; Sven Plein; Eike Nagel Journal: J Cardiovasc Magn Reson Date: 2013-05-01 Impact factor: 5.364
Authors: Lukas Stoiber; Felix Mahfoud; Seyedeh Mahsa Zamani; Tomas Lapinskas; Michael Böhm; Sebastian Ewen; Saarraaken Kulenthiran; Markus P Schlaich; Murray D Esler; Tommy Hammer; Knut Haakon Stensæth; Burkert Pieske; Stephan Dreysse; Eckart Fleck; Titus Kühne; Marcus Kelm; Philipp Stawowy; Sebastian Kelle Journal: Clin Res Cardiol Date: 2018-03-08 Impact factor: 5.460