Low weight is not a risk factor for recurrent obstruction after repair of coarctation of the aorta in infants less than 3 months of age. Rather, risk of recoarctation is more a function of the anatomy of the arch. Thus, it is not indicated to delay repair in low weight infants with the goal of achieving growth.

LANIYBNU, A.A., SAIFEDDINE, M., YAIVG, S.-G., and WBLLENBBRG, M.D. 1994. Tyrosine kinase inhibitors and the contractile action of G-protein-linked vascular agonists. Can. J. Physiol. Pharrnacol. 72: 1075-1885. In a porcine coronary artery helical strip preparation, the tyrosine kinase inhibitors genistein and tyrphostin (AG82) attenuated the contractile actions of angiotensin 11, arginine vasopressin, epidermal growth factor -urogastrone, noradrenaline, and prostaglandin F,,, under conditions where contractions due to acetylcholine and KC1 were not affected. Both genistein and typhostin also caused a selective inhibition of angiotensin 11 action in rat aorta helical strips, without affecting KCI-mediated contractions. The HC, , values for the inhibition of contraction in the porcine coronary artery were in the range of 2-5 pM for genistein and 8 -15 pM for tyrphostin. Comparable IC, values were observed for the inhibitory effects of genistein on angiotensin 11 and prostaglandin FZu action in the rat aorta, whereas much higher tyrphostin concentrations (BCSo r 40 pM) were required to block angiotensin III action in this preparation. Angiotensin 11 caused an elevation of phosphotyrosyl protein (antiphosphotyrosine Western blot) in the porcine coronary artery, which was reversed by genistein. In addition, porcine coronary artery derived membrane and cytosolic fractions exhibited sarcoma vims related tyrosine kinase activity, which was inhibited by both genistein and tyrphostin. Our data (i) document the selective inhibition by genistein and tyrphostin of the contractile action of some, but by no means all, G-protein-linked vascular agonists in porcine and rat arterial preparations, (ii) establish the presence of sarcoma vims related tyrosine kinase activity in the porcine coronary artery, and (iii) demonstrate angiotensin II mediated increases in phosphstyrosyl protein content in porcine coronary artery tissue. These data support the hypothesis that selected G-protein-linked contractile vascular agonists may act in part via the stimulation of nonreceptor tyrosine kinases. The data also indicate the complex actions of the tyrosine kinase inhibitors, even for the same agonist acting in vascular preparations obtained from different species.

Intraoperative transesophageal echocardiography (IOTEE) is commonly used to assess for residual defect and the need to return to bypass after repair of ventricular septal defect (VSD). The frequency and significance of residual septal defects as noted on IOTEE has not been well defined. We evaluated the frequency of residual VSD via IOTEE and the relationship between size of a residual VSD and rate of reoperation. In addition, we looked at the relationship between the presence of a residual VSD via IOTEE and the presence of residual VSD at follow-up transthoracic echocardiography (TTE). Residual VSD was measured via the largest width of the Doppler color jet diameter originating at the left ventricular septal surface. Of the 294 patients evaluated with IOTEE after VSD repair, one-third had a residual defect by IOTEE Doppler color flow mapping. Two-thirds of these defects closed spontaneously on TTE by the time of hospital discharge. There was no difference in frequency of residual VSD between simple (VSD closure alone, n = 90) and complex (VSD with associated lesions, n = 204) repair. Return to bypass with immediate reoperation was undertaken in nine patients, all of whom had significant shunt via oximetry (Qp/Qs > 1.5:1.0). All had residual VSD color jet diameters > 3 mm. Seven patients had residual color jet equal to 3 mm; however, hemodynamic studies did not reveal a significant shunt and none of these had reoperation. Seven patients with no VSD or < 3 mm residual VSD via had late reoperation to close residual VSD at 4 days to 5 months after initial operation. These were due to patch dehiscence or development of an "intramural" VSD in patients with conotruncal anomaly. A residual defect on IOTEE color Doppler measuring > or = 4 mm predicts the need for immediate reoperation, while a 3 mm defect may be significant and requires additional intraoperative hemodynamic evaluation. The majority of small defects noted on IOTEE are not present at discharge TTE. Patients with conotruncal defect repair should be followed closely for development of late significant "intramural" defects.