triiodothyronine--reverse has been researched along with Tachycardia* in 4 studies
4 other study(ies) available for triiodothyronine--reverse and Tachycardia
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Serum reverse T3 and amiodarone efficacy.
The use of serum reverse T3 (rT3) levels in the assessment of amiodarone efficacy is controversial. We prospectively studied 10 patients with frequent ventricular ectopy and symptomatic ventricular tachycardia (VT) treated with amiodarone. Serial 24-h Holter monitor, thyroid function studies including serum rT3, and 12-lead electrocardiogram were performed on each patient at baseline, and at 1, 4, 12, and 24 weeks of oral amiodarone therapy. Serial Holter monitors on therapy were analyzed for 100% suppression of VT, 90% suppression of couplets, and 85% suppression of ventricular ectopic beats (VEBs) compared with baseline Holter, defining patient groups VT-, Co-, and VEB-, respectively. Lack of arrhythmia suppression to this degree defined groups as VT+, Co+, and VEB+. There were no statistically significant differences in rT3 levels between VT+ and VT- groups, Co+ and Co- groups, or the VEB+ and VEB- groups. VT suppression could not be predicted at any rT3 level. We conclude that serum rT3 is an insensitive means of assessing amiodarone efficacy. Topics: Adult; Aged; Aged, 80 and over; Amiodarone; Cardiac Complexes, Premature; Electrocardiography; Female; Humans; Male; Middle Aged; Monitoring, Physiologic; Prospective Studies; Tachycardia; Thyroid Function Tests; Triiodothyronine, Reverse | 1989 |
Thyrotropin hyperresponsiveness to TRH despite hyperthyroxinemia in amiodarone-treated subjects.
Pituitary responsiveness to TRH was assessed prospectively over 24 weeks, in 15 patients receiving 300 mg amiodarone a day. All developed significant hyperthyroxinemia (both total and free), and marked elevations in reverse T3 compared to pretreatment levels. Although basal TSH levels were unchanged in all of them, TSH increased by greater than 50% when compared to pretreatment responses, in eight patients, while they remained unchanged (+/- 15%) in the remaining seven. All eight with exaggerated responses also showed significant reductions (P less than .001) in plasma levels of total and free T3, whereas in the seven who did not show any increase in TSH responses, T3 levels were unchanged. The increase in TSH response to TRH was strongly correlated (r = -.82, P less than .001) with T3 levels. Total and free T4 levels were equally elevated in both groups. These observations indicate that amiodarone effectively blocks the suppressive effect of hyperthyroxinemia on TSH secretion, and that T3 is the mediator of thyroid feedback control in amiodarone treated patients. Topics: Amiodarone; Female; Humans; Male; Tachycardia; Thyrotropin; Thyrotropin-Releasing Hormone; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse | 1987 |
Pharmacokinetic significance of serum reverse T3 levels during amiodarone treatment: a potential method for monitoring chronic drug therapy.
We studied the antiarrhythmic effects of amiodarone, 600-1400 mg/day, in 18 patients with refractory arrhythmias, and related to drug efficacy and side effects to serum levels of T4, reverse T3 (rT3) and the QTc interval. In the 11 patients with ventricular arrhythmias, premature complexes were reduced by 90-98%, and complex ectopy and runs of ventricular tachycardia were abolished; in the seven patients with paroxysmal atrial flutter, there were no recurrences on stable drug therapy. The QTc lengthened by 11.6% (p less than 0.01), T4 increased by 31.6-63.3% (p less than 0.001) and rT3 increased by 82.9-176.8% (p less than 0.001) as a function of dose and duration of amiodarone therapy. A close correlation was found between rT3 (normal up to 50 ng/dl) and drug efficacy and some of the drug side effects; arrhythmia suppression occurred at levels of 55-100 ng/dl, and some of the known side effects at levels of 100-110 ng/dl. When amiodarone was stopped in nine patients, the changes in QTc, T4 and rT3 regressed toward normal and arrhythmia recurred in eight 2-20 weeks (mean 7.4 weeks) and when rT3 levels fell below 55 ng/dl; arrhythmia resuppression was achieved 3-28 days (mean 11 days) after resumption of amiodarone therapy. The indirect therapeutic half-life of amiodarone in seven patients, computed from the semilogarithmic plots of plasma rT3 after cessation of amiodarone therapy, ranged from 25 to 55 days (mean 35 days). The data suggest that rT3 levels may be useful in monitoring the efficacy and certain side effects of amiodarone. Topics: Adult; Aged; Amiodarone; Atrial Flutter; Benzofurans; Electrocardiography; Heart Ventricles; Humans; Male; Middle Aged; Recurrence; Tachycardia; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse | 1982 |
Fetal tachycardia associated with intrauterine fetal thyrotoxicosis.
Tachycardia in both fetuses of a twin gestation was documented in a mother who had undergone subtotal thyroidectomy 8 years prior to her present pregnancy. Maternal and fetal plasma concentrations of long-acting thyroid stimulator (LATS) and amniotic fluid 3,3',5'-triiodothyronine (reverse T3) were determined. All values were consistent with the diagnosis of fetal thyrotoxicosis, as were cord blood studies performed on the fetuses post partum. Significant concentrations of LATS were present in fetal cord blood. The first fetus survived but suffered hyperthyroidism during the first 3 neonatal weeks. The second twin died, possibly of fetal thyrotoxicosis. These studies suggest that in women with a history of thyrotoxicosis, high levels of maternal LATS may in some instances provoke fetal thyrotoxicosis, which can be diagnosed by the measurement of amniotic fluid reverse T3. Topics: Adult; Amniotic Fluid; Female; Fetal Diseases; Fetal Heart; Humans; Hyperthyroidism; Infant, Newborn; Long-Acting Thyroid Stimulator; Male; Pregnancy; Pregnancy Complications; Pregnancy, Multiple; Tachycardia; Triiodothyronine, Reverse; Twins | 1980 |