TY - JOUR
T1 - Cardiac resynchronization therapy and cardiac sympathetic function
AU - Martignani, Cristian
AU - Diemberger, Igor
AU - Nanni, Cristina
AU - Biffi, Mauro
AU - Ziacchi, Matteo
AU - Boschi, Stefano
AU - Corzani, Alessandro
AU - Fanti, Stefano
AU - Sambuceti, Gianmario
AU - Boriani, Giuseppe
PY - 2015/8/1
Y1 - 2015/8/1
N2 - Background: Cardiac resynchronization therapy (CRT) is an established therapy for advanced congestive heart failure, improving both survival and hospitalization. The mechanism beneath these improvements still needs to be defined as about one-third of the patients do not benefit from resynchronization. Restoration of sympatho-vagal function can play a significant role in the process, but available data are limited. In this scenario, positron emission tomography scans with 11C-hydroxyephedrine, a noradrenaline analogous, has the potential to characterize the modifications of the sympathetic nervous system induced by CRT in decompensated patients. Materials and methods: Ten patients (six males, age 68 ± 10 years) with primary dilated cardiomyopathy were studied before and after resynchronization (acutely and after 3 months), from a clinical and echocardiographic point of view. Their cardiac sympathetic nerve activity was evaluated by 11C-hydroxyephedrine positron emission tomography before resynchronization, at short and medium term after resynchronization. Results: Responders to CRT (patients showing ≥ 15% decrease in left ventricular end-systolic volume) showed a higher level of left ventricular radiotracer uptake both at baseline and after resynchronization with respect to nonresponders. This was coupled with a progressive improvement in homogeneity in left ventricular tracer uptake mainly in responders. Conclusions: Cardiac resynchronization therapy improves cardiac sympathetic nerve activity in responders since its activation, while nonresponders do not show any significant change at any time of evaluation. CRT seems to be more effective in those patients with a still structurally preserved, yet functionally impaired, neuroautonomic system.
AB - Background: Cardiac resynchronization therapy (CRT) is an established therapy for advanced congestive heart failure, improving both survival and hospitalization. The mechanism beneath these improvements still needs to be defined as about one-third of the patients do not benefit from resynchronization. Restoration of sympatho-vagal function can play a significant role in the process, but available data are limited. In this scenario, positron emission tomography scans with 11C-hydroxyephedrine, a noradrenaline analogous, has the potential to characterize the modifications of the sympathetic nervous system induced by CRT in decompensated patients. Materials and methods: Ten patients (six males, age 68 ± 10 years) with primary dilated cardiomyopathy were studied before and after resynchronization (acutely and after 3 months), from a clinical and echocardiographic point of view. Their cardiac sympathetic nerve activity was evaluated by 11C-hydroxyephedrine positron emission tomography before resynchronization, at short and medium term after resynchronization. Results: Responders to CRT (patients showing ≥ 15% decrease in left ventricular end-systolic volume) showed a higher level of left ventricular radiotracer uptake both at baseline and after resynchronization with respect to nonresponders. This was coupled with a progressive improvement in homogeneity in left ventricular tracer uptake mainly in responders. Conclusions: Cardiac resynchronization therapy improves cardiac sympathetic nerve activity in responders since its activation, while nonresponders do not show any significant change at any time of evaluation. CRT seems to be more effective in those patients with a still structurally preserved, yet functionally impaired, neuroautonomic system.
KW - <sup>11</sup>C-hydroxyephedrine
KW - Cardiac resynchronization therapy
KW - Heart failure
KW - Neuroautonomic system
KW - Positron emission tomography
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U2 - 10.1111/eci.12471
DO - 10.1111/eci.12471
M3 - Article
C2 - 26036750
AN - SCOPUS:84937521653
VL - 45
SP - 792
EP - 799
JO - European Journal of Clinical Investigation
JF - European Journal of Clinical Investigation
SN - 0014-2972
IS - 8
ER -