Neonatal aortic arch reconstruction avoiding circulatory arrest and direct arch vessel cannulation.

BACKGROUND: Aortic arch reconstruction in neonates routinely requires deep hypothermic circulatory arrest. We reviewed our experience with techniques of continuous low-flow cerebral perfusion (LFCP) avoiding direct arch vessel cannulation. METHODS: Eighteen patients, with a median age of 11 days (range 1 to 85 days) and a mean weight of 3.2 +/- 0.8 kg, underwent aortic arch reconstruction with LFCP. Seven had biventricular repairs with arch reconstruction, 9 underwent the Norwood operation and 2 had isolated arch repairs. In 1 Norwood and 7 biventricular repair patients, LFCP was maintained by advancing the cannula from the distal ascending aorta into the innominate artery. In 8 of 9 Norwood patients, LFCP was maintained by directing the arterial cannula into the pulmonary artery confluence and perfusing the innominate artery through the right modified Blalock-Taussig shunt fully constructed before cannulation for cardiopulmonary bypass. In 2 patients requiring isolated arch reconstruction, the ascending aorta was cannulated and the cross-clamp was applied just distal to the innominate artery. RESULTS: LFCP was maintained at 0.6 +/- 0.2 L x min(-1) x m(-2) for 41.0 +/- 13.9 minutes at 18.5 degrees C +/- 1.1 degrees C. In 10 of the 18 patients, blood pressure during LFCP was 15 +/- 8 mm Hg remote from the innominate artery (left radial, umbilical or femoral arteries). In 8 of the 18 patients, right radial pressure during LFCP was 24 +/- 10 mm Hg. The mean mixed-venous saturation was 79.8% +/- 10% during LFCP. Two patients had preoperative seizures, whereas none had seizures postoperatively. One patient died. CONCLUSIONS: Neonatal aortic arch reconstruction is possible without circulatory arrest or direct arch vessel cannulation. These techniques maintained adequate mixed-venous oxygen saturations with no associated adverse neurologic outcomes.

Transposition complexes with systemic obstruction.

The arterial switch operation is currently the procedure of choice for transposition of the great arteries and double-outlet right ventricle with subpulmonary ventricular septal defect. While the results of surgical repair have improved tremendously in recent years, the presence of associated lesions continues to make this a surgically challenging malformation. The association of these so-called transposition complexes with systemic obstruction has recently received increased attention. Systemic obstruction may occur at the subaortic level, in the aortic arch, or at both levels. Valvar aortic stenosis or atresia is extremely rare. Resection of hypertrophied muscle bundles with or without pericardial patch augmentation is frequently enough to deal with obstruction at the subaortic level, which becomes the subpulmonary area following arterial switch operation. Aortic arch obstruction associated with intracardiac defects has traditionally been addressed with a staged approach, dealing first with the arch obstruction followed later by intracardiac repair. The results with this approach have been disappointing. At the Montréal Children's Hospital, we have obtained superior results using a single-stage approach. Therefore, we have advocated the use of pulmonary homograft patch aortoplasty for aortic arch reconstruction at the time of intracardiac repair to completely remove any anatomic afterload. Since 1989, in 22 consecutive patients undergoing single-stage anatomic repair of transposition complexes associated with aortic arch obstruction, we have had no early deaths, one late death of a noncardiac cause, and one recoarctation requiring balloon dilatation. In the last 2 years, we have been able to perform all our aortic arch reconstructions avoiding the use of circulatory arrest.

Surgical technique to avoid circulatory arrest and direct arch vessel cannulation during neonatal aortic arch reconstruction.

Deep hypothermic circulatory arrest (DHCA) has been used routinely for surgery involving the aortic arch. Recently, techniques have been developed that avoid circulatory arrest and maintain low-flow cerebral perfusion (LFCP) in an attempt to avoid the potential neurological sequelae associated with DHCA. We describe a technique of LFCP that avoids circulatory arrest and direct cannulation of the arch vessels. Five patients underwent reconstruction of the aortic arch with concomitant biventricular intracardiac repair. The distal ascending aorta was cannulated and patients were systemically cooled. The cannula was advanced into the innominate artery and snared in place prior to opening and reconstructing the aorta with continuous LFCP. In all five patients, we completely avoided circulatory arrest and direct cannulation of the arch vessels. All patients survived and there were no adverse neurological outcomes.

An automated interrupted suturing device for coronary artery bypass grafting: automated coronary anastomosis.

BACKGROUND: The purpose of this study was to have a preliminary assessment of the safety and efficacy of an automated vascular suturing device. METHODS: The device (Heartflo, Perclose/Abbott Labs, Redwood City, CA), which delivers 10 interrupted 7-0 polypropylene sutures between side-to-side arteriotomies, was evaluated in animals (8 Yorkshire pigs). RESULTS: Tissue edge capture and quality of anastomosis were highly rated. Time of anastomoses averaged 22 minutes. This time was prolonged primarily due to suture management, tying of interrupted sutures, and learning curve effects. Six of the anastomoses were hemostatic and two required an additional stitch each. Angiography and histology of the anastomosis confirmed patency and quality of the anastomosis. CONCLUSIONS: Our preliminary results indicate that the Heartflo automated anastomotic device is safe and effective. Preclinical and clinical studies to validate its acute and long-term effectiveness will commence shortly.

Angiogenic response induced by mechanical transmyocardial revascularization.

BACKGROUND: Angiogenesis is the proposed mechanism of transmyocardial revascularization. We evaluated mechanical transmyocardial revascularization in a chronically ischemic porcine model by measuring myocardial angiogenic response. METHODS: Ameroid constrictors were implanted 6 weeks before mechanical transmyocardial revascularization. Group I (n = 5) and group II (n = 3) animals received 30 punctures with an 18-gauge needle and samples were harvested at 1 and 4 weeks, respectively, after the operation. Group III (n = 5) had sternotomy only and served as the control group. Myocardial samples were immunohistochemically stained for vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor beta (TGF-beta) using specific antibodies. Growth factor expression was quantified by means of computer-assisted morphometry. Vascular density was assessed by immunohistochemical stain for VEGF and factor VIII. RESULTS: Compared with group III, increased angiogenic factor levels were found in group I (VEGF 0.47 +/- 0.03 mm(2) vs 0.05 +/- 0.05 mm(2), P =.000; bFGF 0.67 +/- 0.14 mm(2) vs 0.03 +/- 0.03 mm(2), P =. 000; TGF-beta 1.40 +/- 0.18 mm(2) vs 0.09 +/- 0.06 mm(2), P = 0.000), and in group II (VEGF 0.34 +/- 0.06 mm(2) vs 0.05 +/- 0.05 mm(2), P =.003; bFGF 0.06 +/- 0.02 mm(2) vs 0.03 +/- 0.03 mm(2), P =.135; TGF-beta 0.28 +/- 0.09 mm(2) vs 0.09 +/- 0.06 mm(2), P =.042). Vascular densities after mechanical transmyocardial revascularization were also increased (group I, VEGF stain 8.1 +/- 0. 6 vs 1.1 +/- 0.5, P =.000; factor VIII stain 5.1 +/- 2.7 vs 0.4 +/- 0.3, P =.018; group II, VEGF stain 1.9 +/- 0.5 vs 1.1 +/- 0.5, P = 0. 107; factor VIII stain 2.3 +/- 0.4 vs 0.4 +/- 0.3, P =.004). CONCLUSIONS: Mechanical transmyocardial revascularization is associated with increased angiogenic factor expression and concomitant neovascularization at up to 4 weeks. These changes are indistinguishable from those of laser transmyocardial revascularization. Myocardial perfusion studies are needed to establish the functional significance of these angiogenic changes.

Exploring the scientific basis of surgery: transmyocardial revascularization.

Transmyocardial revascularization (TMR) is a new surgical procedure aimed at increasing blood flow to the ischemic myocardium. It has been used for treatment of patients with end-stage coronary artery disease who are not candidates for conventional measures such as medication, percutaneous transluminal coronary angioplasty, and coronary artery bypass grafting. TMR involves creating transmural channels in the myocardium using lasers, in areas shown to be ischemic during preoperative testing. This procedure has shown promising results in clinical trials, but the mechanism of its efficacy remains largely unknown. TMR was originally developed as a means of supplying blood to the ventricular myocardium, directly through channels made in the wall of the ventricle. This was in an attempt to recreate the situation that exists in the reptilian heart, in which the myocardium is perfused directly from the ventricular chamber through a rich network of sinusoids that bathe the myocardial cells. However, the existence of a significant sinusoidal network in the human heart is doubtful. Whether the myocardium can be perfused directly via the TMR channels is controversial; it is becoming clear that other mechanisms such as angiogenesis are also at work. This review will use TMR as an example to illustrate how surgical practice and thinking can be based on theories that have little or no sound experimental evidence to support them. The importance of elucidating the valid scientific basis of surgical procedures in this modern era of evidence-based medicine will be emphasized.

Regional blood flow and the endocrine response to sustained hypoxemia in the preterm ovine fetus.

To determine the circulatory response of the preterm fetus to a sustained hypoxic insult, regional blood flow was measured (microsphere technique) in 12 unanesthetized fetal sheep (0.75 gestation) during a normoxic control period, after 1 h and 8 h of sustained hypoxemia, and after a 1-h recovery period. Associated endocrine changes which might relate to organ-specific changes in blood flow were also assessed. Myocardial and cerebral blood flow were increased by 240 and 90%, respectively, such that oxygen delivery to the heart was well maintained throughout the study, whereas that to the brain was significantly decreased by 8 h of hypoxic study. Regional blood flows for all structures within the brain showed similar percent increases, except that for the pituitary gland, where the increase was much smaller, and that for the choroid plexus, where blood flow actually fell. Whereas blood flow to upper body muscle showed no significant change throughout the study, that to the thyroid was increased by 70% by 1 h of hypoxic study but fell thereafter. Adrenal cortical blood flow relative to that of the medulla was increased 3-fold by 8 h of hypoxic study, indicating a differential effect of sustained hypoxia on these vascular beds. Although pituitary and thyroid blood flows showed no relationship to respective trophic and/or secretory hormones measured, values for adrenal cortical flow relative to medullary flow were well correlated with plasma concentrations of ACTH. It is concluded that the "centralization" of blood flow to vital organs in response to a sustained hypoxic insult is qualitatively similar for both the preterm and near term ovine fetus and that hypoxic regulatory mechanisms may be better protective of the heart. Additionally, a role for the functional activation of the adrenal gland in its blood flow response to sustained hypoxemia is suggested.

Cerebral metabolism during sustained hypoxemia in preterm fetal sheep.

OBJECTIVE: The purpose of this study was to determine the effect of sustained hypoxia with resulting metabolic acidosis on cerebral metabolism in the preterm ovine fetus. STUDY DESIGN: Twelve fetal sheep were studied at 0.75 of gestation during a normoxic control period, after 1 and 8 hours of sustained hypoxemia, and again after a 1-hour recovery period. Cerebral arteriovenous differences were analyzed for oxygen content, blood gases and pH, glucose, and lactate. Cerebral blood flow was measured with the microsphere technique. RESULTS: Induced hypoxemia resulted in a variable degree of fetal acidemia that was entirely metabolic. Although cerebral oxidative metabolism was well maintained throughout the study, cerebral glucose consumption was variably increased when measured after 1 hour of sustained hypoxemia, with a subsequent decrease after 1 hour of recovery. Although lactate was neither consumed nor produced during the control period, by 8 hours of hypoxic study a significant efflux of lactate from the brain was evident, which continued into the recovery period. CONCLUSION: Sustained hypoxemia results in an increase in the anaerobic metabolism of glucose by the preterm fetal brain independent of any change in cerebral oxidative metabolism, which may give rise to an accumulation of lactic acid and contribute to neurologic impairment.