28 research outputs found
In utero indomethacin alters O₂ [oxygen] delivery to the fetal ductus arteriosus : implications for persistent postnatal patency
No full textExposure of the fetus to indomethacin produces constriction of the fetal ductus arteriosus (DA) and hypoxia in the avascular muscle media of the vessel wall. Hypoxia induces cell death, which increases the incidence of patent DA in the newborn period. We used a fetal sheep model to determine the factors that were responsible for indomethacin-induced hypoxia at various degrees of DA constriction. Indomethacin produced DA constriction in all fetuses studied in vivo. Cell death in the DA wall was directly related to the degree of indomethacin-induced DA constriction and was present at both moderate (pressure gradient across DA \u3c16 \u3emmHg) and marked (≥16 mmHg) degrees of constriction. Indomethacin did not alter oxygen consumption in DA rings studied in vitro, indicating that oxygen demand in the constricting tissue is not significantly increased by indomethacin. Both moderate and marked degrees of DA constriction reduced vasa vasorum flow to the ductus (moderate = 69±25%; marked = 30±16% of pre-indomethacin exposure values) and increased the thickness of the ductus wall. In contrast, DA luminal blood flow was not affected by moderate degrees of constriction and was reduced only after marked constriction. Our findings suggest that changes in vasa vasorum blood flow and muscle media thickness are the primary contributors to hypoxia-induced cell death at moderate degrees of indomethacin-induced constriction. Diminished luminal blood flow only appears to contribute to the induction of cell death following the development of marked degrees of constriction. These findings help to explain why in utero exposure to indomethacin in late gestation fetuses, which depend on vasa vasorum to supply O2 to the DA muscle media, leads to hypoxia-induced remodeling and and increased incidence of postnatal patent DA. Note: Figures and Diagrams created with Cricket Graph for Macintosh may not open or be legible without the possession of that application
Dofetilide induced torsade de pointes: Mechanism, risk factors and management strategies
No full textAbstractDofetilide is an effective antiarrhythmic agent for conversion of atrial fibrillation and atrial flutter as well as maintenance of sinus rhythm in appropriately selected patients. However, as with other antiarrhythmic agents, proarrhythmia is a known adverse effect. The risk of dofetilide induced torsade de pointes (Tdp) is low when used with strict dosing criteria guided by renal function, QT interval and concomitant drug therapy. Benefit from dofetilide use must be individualized and weighed against the side effects and the role of other available treatment options. In this review, we discuss the underlying mechanism, risk factors and precautionary measures to avoid dofetilide induced QT prolongation and ventricular tachycardia/Tdp. We suggest a scheme for the management of QT prolongation, ventricular arrhythmia and Tdp as well
Left ventricle penetration—A rare complication of transseptal puncture and catheter ablation for supraventricular tachycardia
No full textInappropriate mode switching clarified by using a chest radiograph
No full textAbstractAn 80-year-old woman with a history of paroxysmal atrial fibrillation and atrioventricular node disease status post-dual chamber pacemaker placement was noted to have abnormal pacing episodes during a percutaneous coronary intervention. Pacemaker interrogation revealed a high number of short duration mode switching episodes. Representative electrograms demonstrated high frequency nonphysiologic recordings predominantly in the atrial lead. Intrinsic pacemaker malfunction was excluded. A chest radiograph showed excess atrial and ventricular lead slack in the right ventricular inflow. It was suspected that lead–lead interaction resulted in artifacts and oversensing, causing frequent short episodes of inappropriate mode switching
Coexistent Brugada Syndrome and Wolff-Parkinson-White Syndrome: What is the Optimal Management?
No full textAbstractCoexistent Brugada syndrome and Wolff-Parkinson-White (WPW) syndrome is rare, and as such poses management challenges. The overlap of symptoms attributable to each condition, the timing of ventricular stimulation after accessory pathway ablation and the predictive value of programmed stimulation in Brugada syndrome are controversial. We describe a case of coexistent Brugada syndrome and WPW syndrome in a symptomatic young adult. We discuss our treatment approach and the existing literature along with the challenges in management of such cases
Left ventricle penetration—A rare complication of transseptal puncture and catheter ablation for supraventricular tachycardia
No full textYIELD OF A STANDARD MULTIMODALS IMAGING WORK-UP FOR ACUTE ISCHEMIC STROKE IN A MULTI-ETHNIC PATIENT COHORT
No full textVasa vasorum hypoperfusion is responsible for medial hypoxia and anatomic remodeling in the newborn lamb ductus arteriosus
No full textThis is a non-final version of an article published in final form in KAJINO, HIROKI ; GOLDBARG, SETH ; ROMAN, CHRISTINE ; LIU, BAO MEI ; MAURAY, FRANÇOISE ; CHEN, YAO QI ; TAKAHASHI, YASUSHI ; KOCH, CAMERON J. ; CLYMAN, RONALD I., Vasa vasorum hypoperfusion is responsible for medial hypoxia and anatomic remodeling in the newborn lamb ductus arteriosus, Pediatric research 51(2), 2002 FEB, pp. 228-235.
AuthorPostnatal constriction of the full-term ductus arteriosus produces hypoxia of the muscle media. This is associated with anatomic remodeling (including smooth muscle death) that prevents subsequent reopening. We used late-gestation fetal and neonatal lambs to determine which factors are responsible for the postnatal hypoxia. Hypoxia [measured by 2-(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl) acetamide technique] and cell death (measured by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling technique) were observed in regions of the constricted ductus wall within 4 h after delivery. Although there was a decrease in ductus luminal flow during the first 6 h after delivery (measured by Doppler transducer), the amount of oxygen delivered to the ductus lumen (3070 ± 1880 μmol O_2 · min^ · g^) far exceeded the amount of oxygen consumed by the constricted ductus (0.052 ± 0.021 μmol O2 · min^ · g^, measured in vitro). Postnatal constriction increased the effective oxygen diffusion distance across the ductus wall to >3× the limit that can be tolerated for normal tissue homeostasis. This was owing to both an increase in the thickness of the ductus (fetus, 1.12 ± 0.20 mm; newborn, 1.60 ± 0.17 mm;p · g^; newborn, 0.21 ± 0.08 mL · min^ · g^;p < 0.01). These findings suggest that hypoxic cell death in the full-term ductus is caused primarily by changes in vasa vasorum flow and muscle media thickness and can occur before luminal flow has been eliminated. We speculate that in contrast with the full-term ductus, the preterm ductus is much less likely to develop the degree of hypoxia needed for vessel remodeling inasmuch as it only is capable of increasing its oxygen diffusion distance to 1.3× the maximally tolerated limit
Inappropriate mode switching clarified by using a chest radiograph
No full textAn 80-year-old woman with a history of paroxysmal atrial fibrillation and atrioventricular node disease status post-dual chamber pacemaker placement was noted to have abnormal pacing episodes during a percutaneous coronary intervention. Pacemaker interrogation revealed a high number of short duration mode switching episodes. Representative electrograms demonstrated high frequency nonphysiologic recordings predominantly in the atrial lead. Intrinsic pacemaker malfunction was excluded. A chest radiograph showed excess atrial and ventricular lead slack in the right ventricular inflow. It was suspected that lead–lead interaction resulted in artifacts and oversensing, causing frequent short episodes of inappropriate mode switching
