Key result
Antitachycardia therapy improved myocardial glucose metabolism and LVEF in tachycardia-induced cardiomyopathy.
Why the study?
Does antitachycardia therapy improve myocardial glucose metabolism and LV function in patients with tachycardia-induced cardiomyopathy?
Observational (n=47)
Does antitachycardia therapy improve myocardial glucose metabolism and LV function in patients with tachycardia-induced cardiomyopathy?
Antitachycardia therapy improves both left ventricular ejection fraction and myocardial glucose metabolism in patients with tachycardia-induced cardiomyopathy.
Answers are grounded in this paper and cite their sources.
May support antitachycardia therapy in tachycardia-induced cardiomyopathy; hypothesis-generating and requires randomized confirmation.
BACKGROUND: We assessed left ventricular (LV) function and myocardial glucose metabolism by fluoro-18-deoxyglucose (18F-FDG) positron emission tomography (PET) in patients with tachycardia-induced cardiomyopathy (TC). METHODS: The subjects were 42 patients with heart disease, consisting of 7 patients with TC (61.4 +/- 19.0 years, LVEF 34.1%+/- 10.6%) and 35 with ischemic heart disease (IHD) (63.1 +/- 10.8 years, LVEF 49.9%+/- 13.5%). Five volunteers with normal ECG were the control group. All of the patients underwent 18F-FDG PET and echocardiography, and all of the patients with TC underwent 18F-FDG PET and echocardiography before and 6 months after antitachycardia therapy. Six patients underwent radiofrequency catheter ablation (RFCA) and 1 patient was medically treated with antitachycardia therapy. Myocardial glucose metabolism was assessed semiquantitatively by using the % dose uptake of 60 kg of BW (% dose uptake). RESULTS: Mean % dose uptake of the control group was 5.52 +/- 0.54%. After antitachycardia therapy, LVEF significantly improved (34.1 +/- 10.6% vs 54.3 +/- 13.6%, P < 0.01), and % dose uptake also significantly improved (1.26 +/- 0.55% vs 1.49 +/- 0.62%, P < 0.05). Patients with IHD showed higher % dose uptake than those with TC before antitachycardia therapy (3.18 +/- 1.36 vs 1.26 +/- 0.55%, P < 0.01), controls showed higher value of % dose uptake than TC before antitachycardia therapy (5.52 +/- 0.54% vs 1.26 +/- 0.55%, P < 0.01). CONCLUSION: Semiquantitative analysis of 18F-FDG PET showed that antitachycardia therapy improved myocardial glucose metabolism in patients with TC.
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Matsumoto et al. (2006) conducted an observational in Tachycardia-induced cardiomyopathy (n=47). Antitachycardia therapy (radiofrequency catheter ablation or medical therapy) vs. Baseline (before therapy) was evaluated on Myocardial glucose metabolism (% dose uptake) (p=<0.05). Antitachycardia therapy improved myocardial glucose metabolism and LVEF in tachycardia-induced cardiomyopathy.
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