Abstract
We evaluated whether myocardial β-adrenergic receptor (β-AR) density, as determined by 11C-CGP12177 PET, could predict improvement of cardiac function by β-blocker carvedilol treatment in patients with idiopathic dilated cardiomyopathy (IDC). Methods: Ten patients with IDC (left ventricular ejection fraction [LVEF] < 45%) were studied. Myocardial β-AR density was estimated using 11C-CGP12177 PET before treatment with carvedilol. Changes of LVEF in response to dobutamine infusion (ΔLVEF-dobutamine) were also measured by echocardiography. Changes of LVEF (ΔLVEF-carvedilol) were evaluated after 20 mo of carvedilol treatment. Results: Baseline myocardial β-AR density significantly correlated with ΔLVEF-carvedilol (r = -0.88, P < 0.001). In contrast, ΔLVEF-dobutamine did not correlate with ΔLVEF-carvedilol (P = 0.65). Myocardial β-AR density was the significant multivariate independent predictor of ΔLVEF-carvedilol (β = -0.88, P < 0.001) among univariate predictors, including functional class (r = 0.76, P < 0.05), plasma norepinephrine (r = 0.85, P < 0.01), LVEF (r = -0.64, P < 0.05), and age as confounding factors. Furthermore, myocardial β-AR density was significantly correlated with plasma norepinephrine (r = -0.79, P < 0.01) and LVEF (r = 0.70, P < 0.05). Conclusion: Myocardial β-AR density is more tightly related to improvement of LVEF-carvedilol than is cardiac contractile reserve in patients with IDC. Patients with decreased myocardial β-AR have higher resting adrenergic drive, as reflected by plasma norepinephrine, and may receive greater benefit from being treated by antiadrenergic drugs. COPYRIGHT
| Original language | English |
|---|---|
| Pages (from-to) | 220-225 |
| Number of pages | 6 |
| Journal | Journal of Nuclear Medicine |
| Volume | 50 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 1 2009 |
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All Science Journal Classification (ASJC) codes
- Radiology Nuclear Medicine and imaging
Cite this
Myocardial β-adrenergic receptor density assessed by 11C-CGP12177 PET predicts improvement of cardiac function after carvedilol treatment in patients with idiopathic dilated cardiomyopathy. / Naya, Masanao; Tsukamoto, Takahiro; Morita, Koichi; Katoh, Chietsugu; Nishijima, Kenichi; Komatsu, Hiroshi; Yamada, Satoshi; Kuge, Yuji; Tamaki, Nagara; Tsutsui, Hiroyuki.
In: Journal of Nuclear Medicine, Vol. 50, No. 2, 01.02.2009, p. 220-225.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Myocardial β-adrenergic receptor density assessed by 11C-CGP12177 PET predicts improvement of cardiac function after carvedilol treatment in patients with idiopathic dilated cardiomyopathy
AU - Naya, Masanao
AU - Tsukamoto, Takahiro
AU - Morita, Koichi
AU - Katoh, Chietsugu
AU - Nishijima, Kenichi
AU - Komatsu, Hiroshi
AU - Yamada, Satoshi
AU - Kuge, Yuji
AU - Tamaki, Nagara
AU - Tsutsui, Hiroyuki
PY - 2009/2/1
Y1 - 2009/2/1
N2 - We evaluated whether myocardial β-adrenergic receptor (β-AR) density, as determined by 11C-CGP12177 PET, could predict improvement of cardiac function by β-blocker carvedilol treatment in patients with idiopathic dilated cardiomyopathy (IDC). Methods: Ten patients with IDC (left ventricular ejection fraction [LVEF] < 45%) were studied. Myocardial β-AR density was estimated using 11C-CGP12177 PET before treatment with carvedilol. Changes of LVEF in response to dobutamine infusion (ΔLVEF-dobutamine) were also measured by echocardiography. Changes of LVEF (ΔLVEF-carvedilol) were evaluated after 20 mo of carvedilol treatment. Results: Baseline myocardial β-AR density significantly correlated with ΔLVEF-carvedilol (r = -0.88, P < 0.001). In contrast, ΔLVEF-dobutamine did not correlate with ΔLVEF-carvedilol (P = 0.65). Myocardial β-AR density was the significant multivariate independent predictor of ΔLVEF-carvedilol (β = -0.88, P < 0.001) among univariate predictors, including functional class (r = 0.76, P < 0.05), plasma norepinephrine (r = 0.85, P < 0.01), LVEF (r = -0.64, P < 0.05), and age as confounding factors. Furthermore, myocardial β-AR density was significantly correlated with plasma norepinephrine (r = -0.79, P < 0.01) and LVEF (r = 0.70, P < 0.05). Conclusion: Myocardial β-AR density is more tightly related to improvement of LVEF-carvedilol than is cardiac contractile reserve in patients with IDC. Patients with decreased myocardial β-AR have higher resting adrenergic drive, as reflected by plasma norepinephrine, and may receive greater benefit from being treated by antiadrenergic drugs. COPYRIGHT
AB - We evaluated whether myocardial β-adrenergic receptor (β-AR) density, as determined by 11C-CGP12177 PET, could predict improvement of cardiac function by β-blocker carvedilol treatment in patients with idiopathic dilated cardiomyopathy (IDC). Methods: Ten patients with IDC (left ventricular ejection fraction [LVEF] < 45%) were studied. Myocardial β-AR density was estimated using 11C-CGP12177 PET before treatment with carvedilol. Changes of LVEF in response to dobutamine infusion (ΔLVEF-dobutamine) were also measured by echocardiography. Changes of LVEF (ΔLVEF-carvedilol) were evaluated after 20 mo of carvedilol treatment. Results: Baseline myocardial β-AR density significantly correlated with ΔLVEF-carvedilol (r = -0.88, P < 0.001). In contrast, ΔLVEF-dobutamine did not correlate with ΔLVEF-carvedilol (P = 0.65). Myocardial β-AR density was the significant multivariate independent predictor of ΔLVEF-carvedilol (β = -0.88, P < 0.001) among univariate predictors, including functional class (r = 0.76, P < 0.05), plasma norepinephrine (r = 0.85, P < 0.01), LVEF (r = -0.64, P < 0.05), and age as confounding factors. Furthermore, myocardial β-AR density was significantly correlated with plasma norepinephrine (r = -0.79, P < 0.01) and LVEF (r = 0.70, P < 0.05). Conclusion: Myocardial β-AR density is more tightly related to improvement of LVEF-carvedilol than is cardiac contractile reserve in patients with IDC. Patients with decreased myocardial β-AR have higher resting adrenergic drive, as reflected by plasma norepinephrine, and may receive greater benefit from being treated by antiadrenergic drugs. COPYRIGHT
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U2 - 10.2967/jnumed.108.056341
DO - 10.2967/jnumed.108.056341
M3 - Article
C2 - 19164238
AN - SCOPUS:59249087440
VL - 50
SP - 220
EP - 225
JO - Journal of Nuclear Medicine
JF - Journal of Nuclear Medicine
SN - 0161-5505
IS - 2
ER -