Pediatric near-drowning events: do they warrant trauma team activation?

BACKGROUND: The purpose of this study was to determine the incidence of traumatic injuries, factors associated with mortality, and need for pediatric trauma surgery involvement for drowning and near-drowning events in children. MATERIALS AND METHODS: An institutional review board-approved, retrospective chart review was performed at three American College of Surgeons-verified Pediatric Trauma Centers (2011-2014). Patients with International Classification of Diseases, Ninth Revision, codes or E-codes for fatal-nonfatal drowning, fall into water, accidental drowning, or submersion were included. Bivariate analysis using chi-square or Fisher exact test for nominal variables and Mann-Whitney U test for continuous variables was performed. RESULTS: A total of 363 patients (median 3.17 y [18 d-17 y]) met the inclusion criteria. Drowning sites included pool (81.5%), bathtub (12.9%), and natural water (5.2%). A witnessed fall or dive was reported in 34.9%, 57.9% did not fall or dive, and 7% had an unwitnessed event. Most patients did not undergo cervical spine (83%) or brain imaging (75.5%). Seven patients (1.92%) had associated soft tissue injuries. Two patients (0.006%) received surgical intervention (bronchoscopy and extracorporeal membrane oxygenation) within 24 h of presentation. Only 2.2% were admitted to the pediatric trauma service. The percentage of patients discharged home from the emergency department was 10.2%. Overall mortality was 12.4%. Factors associated with mortality included transfer from outside hospital (P = 0.016), presence of hypothermia on arrival (P < 0.0001), Glasgow Coma Scale of 3 on arrival (P < 0.0001), drowning in a pool (P = 0.013), or undergoing brain cooling at admission (P = 0.011). CONCLUSIONS: This is the largest reported series of pediatric near-drowning events. Only rarely did patients require immediate surgical attention and the majority were admitted to nonsurgical services. These data suggest that routine pediatric trauma surgery service involvement in patients with near-drowning events may be unnecessary.

Surgical management for complications of pediatric lung injury.

The etiologies of pediatric lung injury requiring surgical intervention can be infectious, traumatic, congenital, or iatrogenic. Childhood pneumonia is a significant global health problem affecting 150 million children worldwide. Sequelae of pulmonary infections potentially requiring surgery include bronchiectasis, lung abscess, pneumatocele, and empyema. Trauma, congenital conditions such as cystic fibrosis and iatrogenic injuries can result in pneumothoraces, chylothoraces, or bronchopleural fistulae. Recurrence rates for spontaneous pneumothorax treated non-operatively in pediatric patients approach 50-60%. Chylothoraces in newborns may occur spontaneously or due to birth trauma, whereas in older children the etiology is almost always iatrogenic. This article examines the surgical management for the complications of lung injury in pediatric patients. In addition, we review the available pediatric evidence for early tracheostomy as well as treatment strategies for the negative ramifications of tracheostomy.

Blunt intraabdominal arterial injury in pediatric trauma patients: injury distribution and markers of outcome.

BACKGROUND: The epidemiology of pediatric blunt intraabdominal arterial injury is ill defined. We analyzed a multiinstitutional trauma database to better define injury patterns and predictors of outcome. METHODS: The American College of Surgeons National Trauma Database was evaluated for all patients younger than 16 years with blunt intraabdominal arterial injury from 2000 to 2004. Injury distribution, operative treatment, and variables associated with mortality were considered. RESULTS: One hundred twelve intraabdominal arterial injuries were identified in 103 pediatric blunt trauma patients. Single arterial injury (92.2%) occurred most frequently: renal (36.9%), mesenteric (24.3%), and iliac (23.3%). Associated injuries were present in 96.1% of patients (abdominal visceral, 75.7%; major extraabdominal skeletal/visceral, 77.7%). Arterial control was obtained operatively (n = 46, 44.7%) or by endovascular means (n = 6, 5.8%) in 52 patients. Overall mortality was 15.5%. Increased mortality was associated with multiple arterial injuries (P = .049), intraabdominal venous injury (P = .011), head injury (P = .05), Glasgow Coma Score less than 8 (P < .001), cardiac arrest (P < .001), profound base deficit (P = .007), and poor performance on multiple injured outcomes scoring systems (Revised Trauma Score [P < .001], Injury Severity Score [P = .001], and TRISS [P = .002]). CONCLUSION: Blunt intraabdominal arterial injury in children usually affects a single vessel. Associated injuries appear to be nearly universal. The high mortality rate is influenced by serious associated injuries and is reflected by overall injury severity scores.

Melagatran for thromboprophylaxis after mechanical valve implantation: results in a heterotopic porcine model.

OBJECTIVE: Melagatran, the active form of ximelagatran, is a novel, direct thrombin inhibitor that does not have a narrow therapeutic window regarding hemorrhagic and thromboembolic events. We aimed to determine whether melagatran would be effective in preventing thrombus formation on heterotopically placed mechanical heart valves. METHODS: A graft containing a bileaflet mechanical heart valve was implanted in the descending thoracic aorta of domestic swine. Two groups of 6 animals received daily subcutaneous injections of either melagatran (2.4 mg/kg, 3 times per day) or dalteparin (175 U/kg, 2 times per day) for 30 days. Four control animals received no anticoagulation therapy. Fecal HemoQuant and serum hemoglobin levels were recorded. Thirty days after the procedure, platelets were labeled with indium 111, the abdominal organs were inspected, and thrombi and platelets deposited on the valve were measured. RESULTS: Median thrombus burden on the valves was 0.4 mg (interquartile range, 0.15-5.45 mg) with melagatran, 0.5 mg (interquartile range, 0-14.5 mg) with dalteparin, and 168 mg (interquartile range, 32.5-665.75 mg) for controls (melagatran vs dalteparin and control; P = .04). Median platelet deposition on the valves was 0 (interquartile range, 0-8.9 x 10(4)) with melagatran, 49.9 x 10(4) (interquartile range, 27.9 x 104-191.8 x 10(4)) with dalteparin, and 115.2 x 10(4) (interquartile range, 9.6 x 10(4)-243 x 10(4)) for controls (melagatran vs dalteparin and control; P = .02). Melagatran did not increase the risk of thromboembolism or bleeding. CONCLUSIONS: Thrombus and platelet accumulation on the prosthetic valves was decreased by melagatran and dalteparin. The use of melagatran or other related direct thrombin inhibitors warrants further study in prophylaxis of thromboembolism in patients with mechanical heart valves.

Cardiotropin-1 and myocardial strain change heterogeneously in cardiomyopathy.

BACKGROUND: The pacing model of heart failure produces heterogeneous changes in wall stress and myocyte diameter. The purpose of this study was to measure regional changes in cardiotrophin-1 (CT-1), a cytokine thought to play a role in LV remodeling, and regional changes in LV strain as measured with magnetic resonance imaging. MATERIALS AND METHODS: Dilated cardiomyopathy was induced in nine mongrel dogs over 4 wk by rapid pacing using a right ventricular epicardial lead. Baseline CT-1 was measured from an apical myocardial biopsy, and regional CT-1 was measured from anterior, lateral, inferior, and septal walls after the induction of heart failure and in six control dogs. Tissue tagged images were divided into similar regions and minimal principal strain (MPS), ejection fraction, and ventricular volumes were compared after induction of heart failure. RESULTS: After induction of heart failure, LV ejection fraction and end-diastolic volume differed significantly from baseline (P < 0.01 and P = 0.02, respectively). Additionally, regional CT-1 and MPS were significantly different (P < 0.01 for both). Cardiotrophin-1 increased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Minimum principal strain decreased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). CONCLUSION: The pacing model of heart failure produces heterogeneous changes in regional CT-1 and wall motion as measured by MPS. The greatest regional changes are closest to the pacemaker site: the inferior and septal walls. These differences in regional CT-1 may account for previously noted myocyte hypertrophy and preserved ventricular function in these regions.

Pheochromocytoma and paraganglioma in children: a review of medical and surgical management at a tertiary care center.

OBJECTIVE: The aim of this study was to review our institutional experience managing pheochromocytomas and paragangliomas in children. METHODS: A retrospective chart review of the Mayo Clinic database from 1975 to 2005 identified 30 patients < 18 years of age with histologically confirmed pheochromocytoma or paraganglioma. RESULTS: There were 12 patients with pheochromocytomas and 18 with paragangliomas. The most common presenting symptoms were hypertension (64%), palpitation (53%), headache (47%), and mass-related effects (30%). Nine patients (30%) had a genetic mutation or documented family history of pheochromocytoma or paraganglioma. Fourteen patients (47%) had malignant disease, whereas 16 (53%) had benign disease. Logistic analysis showed that statistically significant risk factors for malignancy were (1) paraganglioma, (2) apparently sporadic, as opposed to familial, pheochromocytoma or paraganglioma, and (3) tumor size of > 6 cm. Surgical resection was performed for 28 patients (93%), with perioperative mortality and major morbidity rates of 0% and 10%, respectively. Resection achieved symptomatic relief for 25 patients (83%). All patients with benign disease appeared cured after resection. For patients with malignant disease, the 5- and 10-year disease-specific survival rates were 78% and 31%, respectively, and the mean survival time was 157 +/- 32 months. CONCLUSIONS: The incidence of malignant pheochromocytoma/paraganglioma was high in children (47%), particularly those with apparently sporadic disease, paraganglioma, and tumor diameters of > 6 cm. Patients with a known genetic mutation or familial pheochromocytoma/paraganglioma were more likely to achieve resection with negative microscopic margins and had improved disease-specific mortality rates. Surgical resection remains the treatment of choice for pheochromocytoma and paraganglioma.

Bilateral staged versus bilateral simultaneous thoracotomy in the pediatric population.

AIM: The aim of the study was to evaluate the safety and outcomes of simultaneous bilateral thoracotomy in pediatric patients compared with traditional bilateral staged thoracotomy. METHODS: This is a retrospective review of 30 consecutive patients 18 years or younger undergoing either bilateral staged or bilateral simultaneous thoracotomy between March 1994 and July 2004. Follow-up (mean, 47 months) was available for all patients. RESULTS: Thirty patients (17 boys, 13 girls; average age, 12 years) underwent bilateral staged or bilateral simultaneous thoracotomy. Eighteen patients underwent staged thoracotomy, 9 patients underwent simultaneous thoracotomy, and 3 patients underwent both procedures. Diagnosis included sarcoma (n = 21), Wilms tumor (n = 4), indeterminate pulmonary nodules (n = 3), and germ cell tumor (n = 2). When we compared outcomes for patients undergoing simultaneous versus staged bilateral thoracotomy, mean hospital stay (5.2 vs 10.6 days; P < .002), intensive care unit stay (1 vs 2 nights; P < .0001), days with tube thoracostomy (4 vs 8 days; P < .0005), and time to initiation of adjuvant chemotherapy (13 vs 30 days; P < .05) were all significantly less for patients undergoing bilateral simultaneous thoracotomy. In addition, postoperative complications were less frequent in patients undergoing simultaneous versus staged thoracotomy (0 vs 3 events; P = .25). CONCLUSIONS: In selected patients, bilateral simultaneous thoracotomy is safe and may lessen morbidity and hospital stay while avoiding delay in initiation of adjuvant chemotherapy.

Irrigated radiofrequency ablation with transmurality feedback reliably produces Cox maze lesions in vivo.

BACKGROUND: Irrigated bipolar radiofrequency ablation has been used to replicate Cox maze surgical scars in pig hearts ex vivo. Impedance monitoring accurately predicted complete transmurality for all lesions. This study aimed to assess the feasibility and reliability of irrigated radiofrequency ablation and impedance monitoring to produce electrically isolating Cox maze lesions in vivo. METHODS: A modified Cox maze procedure was performed in 8 adult sheep during cardiopulmonary bypass using irrigated bipolar and unipolar radiofrequency ablation. For bipolar radiofrequency ablation, atrial tissues were clamped between opposing electrodes; ablation was terminated at the plateau in impedance decline. Unipolar radiofrequency ablation lesions were painted on the endocardium, and transmurality was assessed visually. Animals survived 30 days. RESULTS: Bipolar lesions (n = 48) were thinner (7.4 +/- 2.4 mm versus 12.7 +/- 3.2 mm) and required less time (14.1 +/- 3.4 seconds versus 41.4 +/- 21.8 seconds) and energy (377.5 +/- 99.2 W.s versus 995.1 +/- 547.1 W.s) to create despite being longer (31.7 +/- 8.6 mm versus 19.2 +/- 5.6 mm) than unipolar lesions (n = 26). The left atrial pacing threshold across selected bipolar lesions increased at least fivefold above baseline (1.6 +/- 0.2 mA) at 1 hour (18.4 +/- 4.6 mA; n = 8; p < 0.001) and 30 days (17.2 +/- 5.2 mA; n = 6; p < 0.001), indicating functional conduction block. Bipolar lesions had no adherent thrombus or endocardial defects. Cross-section examination confirmed transmurality in 100% of bipolar lesions and 98.7% of unipolar lesions. CONCLUSIONS: Irrigated bipolar radiofrequency ablation with impedance monitoring safely and reliably produces electrically isolating, transmural Cox maze lesions in vivo.

Prolonged exposure of canine coronary arteries to a nitric oxide donor desensitizes soluble guanylate cyclase.

BACKGROUND: This study investigated the role of soluble guanylate cyclase desensitization in the development of tolerance to organic nitrates. MATERIALS AND METHODS: In organ baths, canine coronary arteries were exposed to either sodium nitroprusside (SNP) (experimental group) or papaverine (control group) at various concentrations (10(-9), 10(-7), or 10(-5) M) for 3 h. Arteries were then compared for response to vascular agonists and for inducible cyclic guanine monophosphate (cGMP) formation. RESULTS: KCl (5 to 50 mM) and prostaglandin F(2alpha) (10(-9) to 10(-5) M) induced similar vascular contractions (n = 7, P > 0.05). Vascular relaxation in response to calcium ionophore A23187 (10(-9) to 10(-6) M) and to authentic nitric oxide (NO) (3 x 10(-9) to 10(-5) M) was attenuated in arteries exposed to SNP at 10(-7) and 10(-5) M concentrations but not at a 10(-9) M concentration (n = 7 each, P < 0.05 versus the respective papaverine group). Pretreatment of arteries with methylene blue (10(-5) M) abolished the responses to authentic NO (n = 4). In cGMP determinations, control arteries demonstrated an increase in cGMP from 364 +/- 89 to 778 +/- 175 pg/mg of protein with A23187 (3 x 10(-5) M) stimulation (n = 5). Conversely, arteries exposed to SNP (10(-5) M) demonstrated similar levels of cGMP before (562 +/- 126 pg/mg of protein) and after (641 +/- 98 pg/mg of protein) A23187 stimulation. CONCLUSIONS: Prolonged exposure of coronary arteries to SNP did not alter vascular smooth muscle function, but it markedly attenuated the relaxation in response to both A23187 and authentic NO at concentrations above 10(-9) M in a concentration-dependent fashion. The constant levels of cGMP in response to an NO donor suggest that the attenuation of relaxation is due to desensitization of soluble guanylate cyclase. Thus, this study supports the role of soluble guanylate cyclase desensitization in the development of tolerance to organic nitrates.

Safety and biocompatibility of the Myosplint system--a passive implantable device that alters ventricular geometry for the treatment of heart failure.

A passive implantable device developed for the treatment of heart failure, the Myosplint System, has demonstrated therapeutic efficacy in a canine model of pacing induced heart failure. The current study sought to demonstrate chronic device safety and biocompatibility, in vivo, in a normal porcine model. Two devices were implanted into each normal, beating heart of 6 juvenile and 15 adult pigs without cardiopulmonary bypass. Animals survived 90 (juvenile and adult) or 180 days (adult only). Serial hematologic and biochemical profiles were evaluated in each pig during the study period. A comprehensive necropsy study was performed in each pig to evaluate device stability, healing response, thromboembolism, hemorrhage, and intravascular hemolysis related to the Myosplint system. Six adult animals died from infectious disease (four) or perioperative (two) complications unrelated to device design or function and were excluded from the final analysis. No clinical, biochemical or pathologic evidence of significant, device related adverse events was observed in surviving animals. The chronic myocardial healing response appeared normal at term, and all devices maintained their structural integrity throughout the study. The Myosplint system was easily implanted in beating hearts and was rapidly incorporated into host tissues without clinically significant morbidity in this porcine model.

Hirudin (desulfated, 54-65) contracts canine coronary arteries: extracellular calcium influx mediates hirudin-induced contractions.

OBJECTIVE: Although the anticoagulatory properties of hirudin are well known, its direct vasoactive effects have not been investigated extensively. Hirudin stimulates nitric oxide and prostacyclin production in noncoronary vascular beds, but its actions on coronary arteries are unknown. MATERIALS AND METHODS: Five-millimeter segments of canine left circumflex coronary arteries were obtained for organ chamber experiments. Some segments were denuded of endothelium before study. Segments were exposed to hirudin (10(-10)-10(-6) mol/L) following precontraction with prostaglandin F(2alpha) with or without pretreatment with indomethacin or calcium channel blockers (verapamil and nifedipine). RESULTS: Hirudin stimulated endothelium-independent contraction in coronary arterial segments. Maximum tension (hirudin 10(-6) mol/L) above precontraction baseline was 33.6 +/- 9.0% (n = 10, P < 0.05) for endothelium-intact and 31.8 +/- 11.5% (n = 8, P < 0.05) for endothelium-denuded arterial segments. Differences between endothelium-intact and endothelium-denuded segments were not significant. Contractile responses to hirudin were unaffected by the presence of indomethacin. Pretreatment with either verapamil or nifedipine (10(-4) mol/L) for 1 h attenuated these contractions. The maximal increase in tension above baseline (hirudin 10(-6) mol/L) for verapamil and nifedipine was only 6.2 +/- 12.4 and 3.8 +/- 7.0% (n = 6, P < 0.05 versus endothelium-intact control), respectively. CONCLUSIONS: Hirudin stimulates endothelium-independent contractions of canine coronary arteries in vitro. Pretreatment with calcium channel blockers attenuates this response, suggesting that extracellular influx of calcium has an important mechanistic role in hirudin-mediated coronary artery constriction.

Endothelium-dependent vasodilation during acute rejection in dogs.

BACKGROUND: Acute rejection, which is a major cause of death after cardiac transplantation, is associated with increased coronary artery resistance and decreased coronary blood flow, leading to congestive heart failure. MATERIALS AND METHODS: To examine the contribution of endothelium-derived vasoactive factors on coronary artery tone during acute rejection, dogs underwent orthotopic heart transplantation without immunosuppression. Plasma levels of endothelin, a potent endogenous vasoconstrictor peptide, and atrial natriuretic peptide, an endogenous coronary vasodilator of cardiac origin, were measured daily by radioimmunoassay until sacrifice. RESULTS: Over 7 days, all animals developed acute rejection accompanied by progressive increases in plasma endothelin (10 +/- 3 to 25 +/- 4 pg/ml, n = 6, P < 0.05) and atrial natriuretic peptide (57 +/- 10 to 188 +/- 42 pg/ml, n = 6, P < 0.05). However, in organ chamber experiments, coronary artery segments from rejecting hearts exhibited normal endothelium-dependent vasodilation to acetylcholine, adenosine diphosphate, and the calcium ionophore A23187. In addition, coronary arteries exhibited normal relaxation to sodium nitroprusside (cyclic guanosine monophosphate-dependent) and isoproterenol (cyclic adenosine monophosphate-dependent). CONCLUSIONS: In early, untreated acute rejection after orthotopic heart transplantation, graft dysfunction is not associated with impaired endothelium-dependent coronary artery vasodilation but may result from enhanced production of endothelin, a potent vasoconstrictor.

Nitric oxide and prostacyclin in ultrasonic vasodilatation of the canine internal mammary artery.

BACKGROUND: Investigators recently demonstrated increased free blood flow from radial artery free grafts harvested using ultrasonic technology. We investigated the mechanism underlying this phenomenon. METHODS: Canine internal mammary artery segments (with and without intact endothelium) were precontracted with norepinephrine and sonicated 3 seconds in organ chambers with ultrasonic coagulating shears (Harmonic Scalpel; Ethicon Endo-Surgery, Cincinnati, OH) functioning at level 2. Vessel tension was continuously measured to examine vasoactivity in response to sonication alone (control) or with N(ù)-Nitro-l-arginine (l-NNA) and indomethacin added to the chamber medium individually or in combination. Tissue heating, acoustic pressure, and endothelial damage as detected by scanning electron micrography were also assessed. RESULTS: In vitro sonication with the Harmonic Scalpel induced predominately endothelium-dependent internal mammary artery vasorelaxation but a small endothelium-independent contribution was also observed. Early vasorelaxation (1 minute after stimulus) was maximally inhibited by l-NNA alone and in combination with indomethacin. Relaxation during this period was insignificantly affected by indomethacin alone. Only the combination of l-NNA and indomethacin maximally inhibited late vasorelaxation (5 minutes after stimulus), whereas inhibitory effects of l-NNA diminished during this time period. Indomethacin inhibited relaxation substantially during this phase, although significantly less than did l-NNA alone. The Harmonic Scalpel minimally heated the tissue surface (0.3 +/- 0.03 degrees C) and did not disrupt endothelial cell integrity while operating at 50 mW/cm(2) intensity (acoustic pressure 40 kPa). CONCLUSIONS: Sonication induces vasorelaxation almost completely by time-dependent endothelial nitric oxide and prostacyclin release, which appears unrelated to tissue heating or endothelial architectural disruption.

A novel antioxidant, EPC-K1, stimulates endothelial nitric oxide production and scavenges hydroxyl radicals.

EPC-K1, a hydroxyl radical scavenger synthesized by phosphate linkage of vitamin E and vitamin C, prevents myocardial reperfusion injury in vivo; however, the direct effects of EPC-K1 on coronary arteries are unknown. These experiments were undertaken to define possible mechanisms through which EPC-K1 imparts its protective action on the coronary vasculature. EPC-K1 (10(-5) to 10(-1) mg/ml) induced concentration-dependent relaxation in contracted canine coronary artery segments with endothelium, but no change in tension of arterial segments without endothelium (p<0.05, ANOVA). Endothelium-dependent relaxation to EPC-K1 was inhibited by N(G)-monomethyl-(L)-arginine ((L)-NMMA) (10(-5) mol/L). Inhibition of relaxation by (L)-NMMA was reversed by the addition of (L)-arginine (10(-4) mol/L), but not by (D)-arginine (10 (-4) mol/L). Subsequent exposure of canine coronary artery segments with intact endothelium to hydroxyl radicals for 30 min (generated by FeSO(4) [0.56 mmol/L] + H(2)O(2) [0.56 mmol/L]) impaired endothelium-dependent relaxation. However, pretreating the vascular segments with EPC-K1 (10(-4) mg/ml) prevented hydroxyl radical-mediated endothelial cell injury and maintained endothelium-dependent relaxation. These experiments indicate that EPC-K1 stimulates the release of endothelium-derived nitric oxide, an endogenous vasodilator and inhibitor of platelet and leukocyte activation and adhesion, from the coronary artery endothelium. Additionally, EPC-K1 scavenges hydroxyl radicals that mediate endothelial cell injury. These 2 independent and important actions are possible mechanisms by which EPC-K1 prevents reperfusion injury in the ischemic heart.

Evaluation of a novel 2 mm internal diameter stainless steel saphenous vein to coronary artery connector: laboratory studies of on-pump and off-pump revascularization.

OBJECTIVE: A second generation, 'easy-load', 2 mm internal diameter (ID), stainless steel, distal anastomotic device has been developed, and design improvements facilitate rapid connector loading with minimal magnification. The reduced size should allow application to most distal coronary vessels currently grafted. This technology may be useful in off-pump and minimally invasive surgical approaches to coronary revascularization. METHODS: Two distinct models were used to evaluate the distal connector. In the first model, a single saphenous vein graft (SVG)-to-LAD procedure (n=18) was used to evaluate long-term patency of the 2 mm ID, stainless steel, distal connector in a chronic canine model. Cardiopulmonary bypass was initiated through an anterolateral thoracotomy. Aortosaphenous vein anastomoses were created using suture. In the second model, an acute off-pump feasibility study of SVG-to-LAD bypass fashioned with both proximal and distal connectors (n=15) was conducted. Aortosaphenous vein anastomoses were performed using a FDA approved vascular connector. Device loading and deployment times, graft blood flow following native LAD ligation, and device-related complications were compared. In the chronic model, the grafts were examined by angiography and gross and microscopic examination at animal sacrifice. RESULTS: All 33 animals survived the procedures. All grafts were widely patent after a minimum 30 (n=8), 90 (n=5), and 180 days (n=5) in the chronic model. Distal graft loading and deployment times, graft blood flow rates, and device-related complications were similar in both procedures. In the off-pump feasibility study, total grafting time including loading and deployment was 10:54+/-2:54 min. CONCLUSIONS: Sutureless SVG-to-coronary artery bypass is feasible, rapid, and reproducible with on- and off-pump surgical techniques using a 2 mm ID, stainless steel, distal connector. In this model, early graft patency was 100% with either procedure, and grafts performed on-pump were widely patent at 30, 90, and 180 days. Few device-related complications occurred, each easily managed without compromising graft integrity, and the incidence of events was similar whether on- or off-pump techniques were employed. This or similar technologies may become an important addition to the management of coronary artery disease, particularly in off-pump or minimally invasive approaches.

Trends in the surgical management of ischemic mitral regurgitation.

The surgical approach to ischemic mitral regurgitation (IMR) remains a topic of considerable controversy. Will coronary artery bypass alone suffice, or should the valve be intervened upon? The poor late survival of patients with IMR is well recognized, but it remains unknown if this can be altered by addressing the valve directly. And if surgery is undertaken, should the valve be repaired or replaced? The underlying mechanisms of IMR remain incompletely understood, and although current theory focuses on the role of alterations in ventricular geometry in its pathogenesis, IMR is most often addressed by annuloplasty alone. Is this sufficient, or does the ventricle itself require "remodeling?" The debate is confounded by imprecise terminology that fails to distinguish between acute and chronic disease, and active ischemia from completed infarction. Available clinical information is from retrospective studies with all of their inherent limitations and potential for bias. Still, progress is being made as increasing attention is focused on this clinically important entity.

Irrigated bipolar radiofrequency ablation with transmurality feedback for the surgical Cox-Maze procedure.

BACKGROUND: Nonirrigated radiofrequency ablation (RFA) has been used to replicate the surgical scars of the Cox-Maze procedure. This study aimed to demonstrate that an irrigated, bipolar RFA energy source could also effectively replicate Cox-Maze lesions with impedance monitoring to predict the transmurality of ablated tissue. METHODS: A complete Cox-Maze lesion pattern was created ex vivo on fresh porcine atria using an irrigated, bipolar RFA system. Tissues were clamped between opposing electrodes with steady pressure to ensure an intimate tissue-electrode interface during ablation. A proprietary feedback and control algorithm monitored tissue impedance and terminated ablation when lesions were deemed transmural by a plateau in impedance decline. Ablation time and power, lesion width and length, and tissue thickness were recorded. Lesions were stained with 1% triphenyltetrazolium chloride and sectioned for gross assessment of transmurality. RESULTS: One hundred thirty-seven lesions were created on 11 porcine hearts. The total ablation time per lesion was 14.8 +/- 1.2 seconds (range, 10.0-19.0 seconds). Lesions averaged 4.2 +/- 1.3 mm (range, 1.3-10.2 mm) in width. Average tissue thickness was 3.0 +/- 1.7 mm (range, 0.5-9.9 mm). Crosssectional examination revealed that 100% of lesions were transmural (n = 718), and no tissue defects were observed. CONCLUSIONS: These results indicate that irrigated bipolar RFA energy can produce transmural Cox-Maze lesions ex vivo on intact porcine atria and that impedance monitoring is a reliable predictor of lesion transmurality. Additional in vivo studies are under way to further demonstrate the efficacy and safety of irrigated, bipolar RFA technology.

Gene transfer to coronary artery bypass conduits.

BACKGROUND: Gene therapy is a rational approach to prevention of stenosis in saphenous vein grafts used as conduits for coronary artery bypass grafting. To explore this possibility we developed methods for adenoviral-mediated gene transfer to canine saphenous veins. METHODS: During a single procedure, autogenous canine saphenous vein segments were transduced ex vivo and used as coronary artery bypass grafts. The proximal end of each vein was ligated, adenovirus containing the Escherichia coli beta-galactosidase gene (Ad.CMVLacZ) was delivered at titers of 2.5 x 10(9) or 5 x 10(9) plaque-forming units (pfu)/mL to the lumen through a distal heparin lock, and the segment was immersed in the viral solution for 1 hour at 37 degrees C. Control segments were exposed to diluent alone in an identical manner. Aortocoronary anastomoses were made using cardiopulmonary bypass. Transgene expression was assessed qualitatively and quantitatively after 3 days. RESULTS: Beta-galactosidase levels showed a dose-dependent increase: 0.00 +/- 0.00 ng/mg total protein for controls; 5.60 +/- 2.27 ng/mg total protein for a viral titer of 2.5 x 10(9) pfu/mL and 11.97 +/- 6.14 ng/mg for 5 x 10(9) pfu/mL. The two dosage groups differed significantly from each other (p = 0.035) and from controls (p = 0.003). X-gal staining demonstrated mostly endothelial and scattered adventitial transgene expression. CONCLUSIONS: Transgene expression after ex vivo gene transfer into saphenous vein grafts in a canine coronary artery bypass model indicates that this method may be useful for delivery of therapeutic genes to prevent or retard vein graft arteriosclerosis.