Cardiac Complications of Ritodrine in Mother and Baby

Brosset, P; Ronayette, D; Pierre, M.; Lorier, Bertrand Le; Bouquier, Julie

doi:10.1016/s0140-6736(82)92476-x

Cited by 19 publications

(7 citation statements)

References 9 publications

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“…Although some studies neither described changes in ECG and laboratory chemical parameters such as CK-MB and serum myoglobin [24] nor long-term effects upon live-born infants who have been exposed to ß-sympatomimetic drugs in utero [25], several reports have documented serious fetal cardiac complications after this tocolytic therapy [4,5]. Briefly, sympathomimetic agents have been associated with heart rate and rhythm disturbances, including paroxysmal superventricular tachycardia and atrial flutter [26][27][28]. Electrocardiographic abnormalities include transient nonspecific T wave changes and ischemic T wave changes [5,[26][27][28].…”

Section: Discussionmentioning

confidence: 99%

“…Briefly, sympathomimetic agents have been associated with heart rate and rhythm disturbances, including paroxysmal superventricular tachycardia and atrial flutter [26][27][28]. Electrocardiographic abnormalities include transient nonspecific T wave changes and ischemic T wave changes [5,[26][27][28]. Prospective studies using M-mode echocardiography have documented interventricular septal thickening [6,7].…”

Section: Discussionmentioning

confidence: 99%

“…More serious fetal complications, e.g. hydrops fetalis, pulmonary edema and neonatal cardiac failure, have also been described and can even cause neonatal death [26,28,29]. Pathologic changes of autopsy specimens were classified as focal necrosis, fatty degeneration, and myocardial cell nuclear enlargement, primarily of the right ventricle [30].…”

Section: Discussionmentioning

confidence: 99%

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Cardiac Troponin T in Neonates after Acute and Long-Term Tocolysis

Adamcová¹,

Kokśtein

Palička³

et al. 2000

Neonatology

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The present study was designed to determine the levels of cardiac troponin T (cTnT) in cord blood of neonates exposed in utero to tocolytic therapy by β-sympathomimetics. cTnT in 40 neonates after acute tocolysis (0.24 ± 0.05 μg/l) was significantly higher (p < 0.05) in comparison with the control group (0.05 ± 0.01 μg/l). The maximal values were reached in about the 3rd day of therapy (0.39 ± 0.11 μg/l). cTnT in 30 neonates after long-term tocolysis was 0.12 ± 0.03 μg/l. No correlation was found between cTnT and CK and its isoenzyme CK-MB or ECG. CK, unlike cTnT, significantly correlated with gestational age (r = 0.57, p < 0.05) and birth weight (r = 0.55, p < 0.05). It is possible to conclude that acute tocolytic therapy by β-sympathomimetics increases the cTnT levels in cord blood and cardiac troponin T is more useful for the laboratory diagnosis of neonatal myocardial injury than CK-MB.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Cardiac Troponin T in Neonates after Acute and Long-Term Tocolysis

Adamcová¹,

Kokśtein

Palička³

et al. 2000

Neonatology

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“…Fetal tachycardia (rates greater than 160 beats/min) has been re ported in 35% of patients treated with isoxsuprine [5] and in 6% treated with the beta-2 selective agent ritodrine [6], Although re lated perinatal morbidity is uncommon, fe tal distress, stillbirths and congestive heart failure have been reported [6][7][8],…”

Section: Introductionmentioning

confidence: 99%

Effects of Isoproterenol-Induced Tachycardia on Myocardial Blood Flow and Glycogen in the Fetal Lamb

Tweed

Davies²,

Alexander³

et al. 1987

Neonatology

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In utero tachycardia is a cause of fetal congestive heart failure and fetal hydrops. We investigated the effects of isoproterenol-induced tachycardia (IIT) on cardiac output and its distribution, on myocardial blood flow and intramyocardial blood flow distribution as well as on regional myocardial glycogen in 8 chronically prepared, near-term fetal lambs and 3 control twins (for myocardial glycogen only). Blood flows were measured by the radioactive microsphere method, myocardial glycogen by an enzymatic method. In animals with IIT (heart rate 200–280), cardiac output (excluding lung flow) increased from 0.399 to 0.544 ml/g/tissue/min (+36%), blood flow to the carcass increased from 0.19 to 0.32 ml/g/tissue/min (+68%) and myocardium increased from 2.31 to 7.72 ml/g/tissue/min (+234%), while kidney blood flow decreased from 1.34 to 0.72 ml/g/tissue/min (––46%). The normal intramyocardial blood flow distribution and predominance of flow to the endocardium of both ventricles was preserved during IIT. In the three sets of twins, glycogen was lower in the right (RV) and left (LV) ventricular walls of each animal stressed by IIT (mean RV = 0.19, mean LV = 0.44) than of its unstressed twin (mean RV = 0.75, mean LV = 0.70). Furthermore, a metabolic acidemia (mean pH 7.21, mean BE -8.4) developed in the stressed animals. Although we were unable to demonstrate regional myocardial ischemia at the maximal fetal heart rates achieved by isoproterenol infusion, our data suggest that metabolic acidemia and myocardial glycogen depletion are consequences of severe inotropic and chronotropic stress in the fetal lamb.

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“…A total of 12.5% of patients who received a 30 mg/day oral ritodrine daily maintenance dose, however, experienced transient tachycardia, palpitation and tremor. 4 Considering the spontaneous termination of transient VT in the present infant with no structural heart disease or primary electrical heart disease, the maximum dose of oral ritodrine could affect fetal and neonatal organs; therefore, ritodrine may produce significant, similar electrophysiological effects on the ventricle, 5 and these alternations may predispose to ventricular arrhythmia. Pediatric providers should be aware that ritodrine use in the pregnant mother can cause significant electrophysiological effects in neonates.…”

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confidence: 99%