title: Anti-tachycardia therapy can improve altered cardiac adrenergic function in tachycardia-induced cardiomyopathy.
abstract: We investigated whether anti-tachycardia therapy might improve the altered cardiac adrenergic and systolic function in tachycardia-induced cardiomyopathy (TC) in contrast to dilated cardiomyopathy (DCM). The subjects were 23 patients with heart failure, consisting of 8 patients with TC (43.6 +/- 10.0 yrs) and 15 with DCM (45.3 +/- 8.2 yrs). TC was determined as impairment of left ventricular function secondary to chronic or very frequent arrhythmia during more than 10% of the day. All patients were receiving anti-tachycardia treatment. Cardiac 123I-MIBG uptake was assessed as the heart/mediastinum activity ratio (H/M) before and after treatment. LVEF was also assessed. In the baseline study, H/M and LVEF showed no difference between TC and DCM (2.21 +/- 0.44 vs. 2.10 +/- 0.42, 35.3 +/- 13.1 vs. 36.0 +/- 10.9%, respectively). After treatment, the degree of change in H/M and LVEF differed significantly (0.41 +/- 0.34 vs. 0.08 +/- 0.20, 20.5 +/- 14.4 vs. -2.1 +/- 9.6%, p < 0.01). In TC, heart failure improved after a shorter duration of treatment (p < 0.05). In conclusion, anti-tachycardia therapy can improve altered cardiac adrenergic function and systolic function in patients with TC over a shorter period than in those with DCM.
authors.affiliation: Second Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama, Japan. y_ohkusu@yahoo.co.jp
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Ohkusu
authors.forename: Nobukazu
authors.initials: N
authors.lastname: Takahashi
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Ishikawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Oka
authors.forename: Shinichi
authors.initials: S
authors.lastname: Sumita
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Kohei
authors.initials: K
authors.lastname: Matsushita
authors.forename: Youhei
authors.initials: Y
authors.lastname: Yamakawa
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Uchino
authors.forename: Kazuo
authors.initials: K
authors.lastname: Kimura
authors.forename: Tomio
authors.initials: T
authors.lastname: Inoue
authors.forename: Satoshi
authors.initials: S
authors.lastname: Umemura
mesh_terms: D019797:3-Iodobenzylguanidine; D000320:Adrenergic Fibers / Q000000981:diagnostic imaging; D000328:Adult; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D009202:Cardiomyopathies / Q000145:classification / Q000000981:diagnostic imaging / Q000503:physiopathology; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*; D003937:Diagnosis, Differential; D004452:Echocardiography; D005260:Female; D006801:Humans; D008297:Male; D008482:Mediastinum / Q000000981:diagnostic imaging; D008875:Middle Aged; D011877:Radionuclide Imaging; D019275:Radiopharmaceuticals; D015203:Reproducibility of Results; D012189:Retrospective Studies; D012680:Sensitivity and Specificity; D013318:Stroke Volume; D013599:Systole / Q000187:drug effects; D013610:Tachycardia / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy*; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology / Q000628:therapy
chemical_list: D000889:Anti-Arrhythmia Agents; D019275:Radiopharmaceuticals; D019797:3-Iodobenzylguanidine