Transumbilical balloon angioplasty of subclavian artery thrombosis in a neonate.

We present a case of arterial thrombosis of the upper extremity in a 1-day-old neonate. The initial response to thrombolytic and anticoagulant therapy alone was unsuccessful. Distal flow to the extremity was reestablished by combined percutaneous transluminal angioplasty of the subclavian artery using transumbilical access followed by resumption of the thrombolytic and anticoagulant regimen. Cathet. Cardiovasc. Intervent. 49:56-60, 2000.

Transcatheter closure of a patent foramen ovale following mitral valve replacement.

We report the successful closure of a postoperative patent foramen ovale in a patient who underwent coronary artery bypass grafting and mitral valve replacement for severe mitral insufficiency. The postoperative course was complicated by severe hypoxemia due to a large patent foramen ovale. The patient underwent transcatheter closure with the Das Angel Wings transcatheter occluder (Microvena Corporation, White Bear Lake, MN) with immediate improvement.

Pericardial effusion and tamponade as a result of percutaneous silastic catheter use.

Percutaneous Silastic catheters (PSCs) are used in premature infants to deliver total parenteral nutrition. We report two cases in which migration of the catheter into the right atrium resulted in rapid onset of shocklike symptoms. Pericardial effusion and tamponade were diagnosed by echocardiography. Subxiphoid pericardiocenteses were performed, with immediate clinical improvement. In both cases, fluid withdrawn from the pericardial space was analyzed to be hyperalimentation and intravenous fat emulsion. Pericardial effusion and tamponade should be suspected in any infant with a PSC line in place who develops sudden onset of shocklike symptoms.

Right atrial thrombi in children with cancer and indwelling catheters.

OBJECTIVE: To determine the prevalence of right atrial thrombi in children with cancer and indwelling catheters. STUDY DESIGN: We systematically examined 156 children with cancer and indwelling catheters for the presence of a right atrial thrombus when they underwent routine screening of cardiac function by two-dimensional echocardiography. RESULTS: Thirteen children (8.8%) had right atrial thrombi. Of the 13 children, 6 had thrombi adherent to the right atrial wall, and in 5 of these 6 children the clots were considered large enough to require intervention: 2 children with obstruction of venous or tricuspid valve inflow underwent right atriotomy and thrombus removal; they recovered and remained well. The other 3 children had moderate-sized thrombi and were treated with oral anticoagulants; their clots stabilized (2 children) or regressed (1 child). The remaining 7 children had thrombus on the tip of the catheter: 5 of these children were observed; the thrombi spontaneously resolved in 2 of them and did not change in size in the other 3. In the sixth child, the catheter malfunctioned 2 weeks after discovery of the clot and the catheter was removed. The seventh child was treated with warfarin and the clot decreased in size. Thrombi were detected in a greater proportion of children with catheter tips in the right atrium versus the superior vena cava, and in a greater proportion of children with acute lymphoblastic leukemia versus other diagnoses. There was no association between the presence of a clot and duration of time the catheter was in place, the number of catheters placed, treatment with asparaginase, or treatment with total parenteral nutrition. CONCLUSION: The incidence of right atrial thrombi in children with indwelling catheters may be higher than was previously appreciated.

Decrease in vascular TxA2 receptors in a subgroup of rabbits unresponsive to a TxA2 mimetic.

In rabbit pulmonary artery, endothelium-dependent contractions to arachidonic acid and methacholine are mediated by thromboxane (Tx) A2. The TxA2 mimetics U-46619 and (1S-[1 alpha,2 beta(5Z),3 alpha(1E,3R*),4 alpha])-7-[3- [3-hydroxy-4-(4'-iodophenoxy)-1-butenyl]-7-oxabicyclo(2.2.1)hep tan-2-yl]- 5-heptenoic acid (I-BOP), norepinephrine, and endothelin produced endothelium-independent contractions. Arachidonic acid, methacholine, U-46619, and I-BOP failed to produce contractions in a subgroup of rabbits (25%). Nonresponder arteries contracted similarly to norepinephrine and endothelin as responder arteries. The affinity (Kd) and density (Bmax) of TxA2 receptors in crude pulmonary artery membranes were assessed via equilibrium binding studies using 125I-BOP. There was no difference in Kd between the two groups (0.49 +/- 0.17 vs. 0.32 +/- 0.14 nM, responder vs. nonresponder). There was a significant decrease in Bmax (123 +/- 21 vs. 28 +/- 11 fmol/mg protein, responder vs. nonresponder; P < 0.01) of receptors in the nonresponders. Nonresponder aortas also did not contract to U-46619 and exhibited a decrease in TxA2 receptors, indicating that the difference is not specific for the pulmonary artery. Nonresponder platelets aggregated to U-46619, suggesting that the platelet receptor is not altered. TxA2-receptor expression may be regulated in vivo. Nonresponder rabbits may provide a useful model for studying these receptors in vascular disease.

Endothelium-dependent contractions in rabbit pulmonary artery are mediated by thromboxane A2.

This study was designed to characterize the endothelium-dependent contracting factor (EDCF) released by arachidonic acid (AA) and methacholine (MeCH) in the rabbit pulmonary artery. AA and MeCH contract the rabbit pulmonary artery; however, the effects of both are blocked by denuding the vessels and by administration of indomethacin (a cyclooxygenase inhibitor), dazoxiben (a thromboxane [TX] synthase inhibitor), and SQ29548 (a TXA2/prostaglandin [PG] H2 receptor antagonist). When segments of rabbit pulmonary artery were incubated with [14C]AA and the [14C] metabolites were resolved by reverse-phase high-performance liquid chromatography (HPLC), radioactive products were observed that comigrated with 6-keto-PGF1 alpha and TXB2, the stable metabolites of prostacyclin and TXA2. The TXB2 radioactive peak was rechromatographed on normal-phase HPLC and again migrated with TXB2. Finally, the structures of derivatized [14C]6-keto-PGF1 alpha and [14C]TXB2 peaks were confirmed by gas chromatography/mass spectrometry. The synthesis of [14C]6-keto-PGF1 alpha and [14C]TXB2 was inhibited by removal of the endothelium and by indomethacin. Dazoxiben inhibited the synthesis of [14C]TXB2 but not [14C]6-keto-PGF1 alpha. Using specific radioimmunoassays, AA and MeCH stimulated 6-keto-PGF1 alpha and TXB2 release. Indomethacin blocked the production of both 6-keto-PGF1 alpha and TXB2, whereas dazoxiben only blocked TXB2. In a superfusion/bioassay system, AA stimulated an endothelium-intact donor vessel to release a labile substance that contracted an indomethacin-treated endothelium-denuded recipient vessel. The EDCF released by AA had an approximate half-life of 30 seconds. Cultured rabbit pulmonary arterial endothelial cells synthesized 6-keto-PGF1 alpha but not TXB2. Immunohistochemical studies indicated the presence of cyclooxygenase, but not TX synthase, in pulmonary artery endothelial cells. TXA2 appears to be the EDCF released by AA and MeCH in rabbit pulmonary artery; however, TXA2 is not produced by endothelial cells but may arise from cells that adhere to the luminal surfaces, such as platelets or macrophages.