Monica Robotin
University of Sydney
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The Journal of Thoracic and Cardiovascular Surgery | 1996
A. Serraf; François Lacour-Gayet; Monica Robotin; Jacqueline Bruniaux; Miguel Sousa-Uva; R. Roussin; Claude Planché
Eighty-two consecutive patients with interrupted aortic arch were referred to our institution between 1985 and 1995. Three died before any attempt at operation and 79 underwent surgical repair. Median age at operation was 9 days (range 1 day to 6 years) and median weight was 3.0 kg (range 1.8 to 20 kg). All but one were in severe congestive heart failure and 31.5% had oliguria or anuria. Preoperative pH varied between 6.8 and 7.4 (median 7.3). Sixty-nine received prostaglandin E1 infusion and 54 received mechanical ventilation. Aggressive preoperative ressucitation was necessary in 43 cases. Preoperative transfontanellar echography (performed routinely) since 1987 revealed intracerebral bleeding in six patients. Type A interrupted aortic arch was present in 37 cases, 41 patients had type B, and one had type C. Interrupted aortic arch was associated with single ventricular septal defect in 35 cases, 24 patients had associated complex heart defects, and 30 had significant subaortic stenosis (six had both subaortic stenosis and complex association). Aortopulmonary window was found in four patients, truncus arteriosus was found in eight, and transposition of the great arteries was found in five, double-outlet right ventricle was found in one, single ventricle was found in three, multiple ventricular septal defects were found in two and superior-inferior ventricles were found in one. Sixty-four patients underwent single-stage repair and 15 underwent multistage repair. Aortic arch repair consisted of direct anastomosis in 59 cases, patch augmentation in eight, and conduit interposition in 12. Ten patients underwent associated pulmonary artery banding and 19 underwent concomitant repair of complex associated lesions. The subaortic stenosis was addressed by four surgical techniques: myotomy or myectomy in five patients; creation of a double-outlet left ventricle, aortopulmonary anastomosis, and conduit insertion between the right ventricle and pulmonary artery bifurcation in four; no direct attempt to relieve the subaortic stenosis in six; and left-sided ventricular septal defect patch in 15. Mean duration of deep hypothermic circulatory arrest, crossclamp time, and cardiopulmonary bypass time were 38.8 +/- 15.6 min, 60.5 +/- 24.7 min, and 143 +/- 40.1 min, respectively. Postoperative mortality rate was 18.9% (70% confidence limits 14% to 24.6%), and overall mortality rate was 31% (70% confidence limits 20.9% to 42.2%). The results have improved with time, with an overall operative mortality rate of 12% since 1990. Univariate statistical analysis revealed that early survival was influenced by preoperative renal function, detection of cerebral bleeding by transfontanellar echography, the number of cardioplegic injections, and the date of operation. Multivariate analysis revealed that preoperative renal function and the number of cardioplegic injections were independent risk factors for early mortality. Echocardiographic measurements of the left heart-aorta complex with preoperative Z values as low as-4 demonstrated rapid growth after repair. In the presence of subaortic stenosis, better survival was obtained with a left-sided patch for ventricular septal defect closure (p < 0.05). Twenty-three patients underwent 26 reoperations for recoarctations (seven), left bronchial compression (two), second-stage repair (eight), right ventricle-pulmonary artery conduit replacement (three), and miscellaneous (four). One of the survivors was reoperated on for subaortic membrane. Survival at 5 years for the entire series was 70%. For isolated forms, it was 73.5% (90% for 1990 to 1995), for complex forms it was 70%, and in the presence of subaortic stenosis it was 60%. In conclusion, interrupted aortic arch remains a surgical challenge with continually improving results. Early diagnosis with preoperative resuscitation and adequate myocardial protection seem extremely important for further improvements. Associated subaortic stenosis or complex lesions
The Journal of Thoracic and Cardiovascular Surgery | 1996
Monica Robotin; Jacqueline Bruniaux; A. Serraf; M.Sousa Uva; R. Roussin; François Lacour-Gayet; Claude Planché
Three groups of unusual forms of tracheobronchial compression caused by vascular anomalies are presented. Three patients had an encircling right aortic arch with a left-sided descending aorta and ligamentum arteriosum (group 1), two patients had airway compression caused by a pincer effect between a malposed and enlarged ascending aorta and the descending aorta (group 2), and three patients had airway compression after an arterial switch operation for transposition of the great arteries (group 3). Symptoms developed in all patients before the age of 4 months, and six of them had multiple failed attempts at extubation before the surgical intervention directed at relieving the airway compression. Fiberoptic endoscopy was used in all patients as a first-line diagnostic tool and was 100% accurate in establishing the diagnosis. The operations performed were aortic uncrossing in group 1, dissection and aortopexy of the right or left main bronchus in group 2, and dissection of the left main bronchus and lysis of adhesions in group 3. In group 1 there was one early death, resulting from aspiration, and one late death 4 years later, resulting from an unrelated cause. In this group, bronchomalacia was noted after the operation and resolved gradually in the year after the intervention. In group 2, one patient died of an aortobronchial fistula after placement of a bronchial stent. Group 3 patients had good postoperative results. Two of them are completely symptom-free and one has residual bronchomalacia and may need placement of a bronchial stent.
The Journal of Thoracic and Cardiovascular Surgery | 1997
A. Serraf; Monica Robotin; Nicolas Bonnet; Hélène Détruit; Bruno Baudet; Michel Mazmanian; Philippe Hervé; Claude Planché
OBJECTIVES The purpose of this study was to analyze the mechanisms associated with lung injury after cardiopulmonary bypass and to propose strategies of prevention. METHODS Thirty-two neonatal piglets underwent 90 minutes of hypothermic cardiopulmonary bypass without aortic cross-clamping. Five experimental groups were defined: group I had standard cardiopulmonary bypass (control), group II received continuous low-flow lung perfusion during cardiopulmonary bypass, group III treatment was similar to that of group I with maintenance of ventilation, group IV received pneumoplegia, and group V received nitric oxide ventilation (30 ppm) after cardiopulmonary bypass. Data drawn from hemodynamic and gas exchange values and muscular and pulmonary tissular levels of adenosine triphosphate (in micromoles per gram) and myeloperoxidase (in international units per 100 mg) were used for comparisons before and 30 and 60 minutes after cardiopulmonary bypass. Pulmonary and systemic vascular endothelial functions were assessed in vitro after cardiopulmonary bypass on isolated rings of pulmonary and iliac arteries. RESULTS Pulmonary vascular resistance index, cardiac index, and oxygen tension were better preserved in groups II, IV, and V. All groups disclosed a significant decrease in lung adenosine triphosphate levels and an increase in myeloperoxidase activity whereas these levels stayed within pre-cardiopulmonary bypass ranges in muscular beds. Endothelium-dependent relaxation was preserved in systemic arteries but was strongly affected in pulmonary arteries after cardiopulmonary bypass. None of the methods that aimed to protect the pulmonary vascular bed demonstrated any preservation of pulmonary endothelial function. CONCLUSION Cardiopulmonary bypass results in ischemia-reperfusion injury of the pulmonary vascular bed. Lung protection by continuous perfusion, pneumoplegia, or nitric oxide ventilation can prevent hemodynamic alterations after cardiopulmonary bypass but failed to prevent any of the biochemical disturbances.
Journal of Gastroenterology and Hepatology | 2004
Monica Robotin; Joy Copland; Graham Tallis; David Coleman; Carolien Giele; Louise Carter; Jenean Spencer; John M. Kaldor; Gregory J. Dore
Background: The purpose of the present paper was to determine recent patterns of hepatitis C virus (HCV) transmission in Australia through a national system of enhanced surveillance of newly acquired hepatitis C.
American Journal of Cardiology | 1992
Mark A. McGuire; David C. Johnson; Monica Robotin; David Richards; John B. Uther; David L. Ross
Abstract The atrioventricular (AV) node is situated in the lower atrial septum at the apex of a triangle described by Koch.1 The sides of Kochs triangle are formed by the tendon of Todaro and the tricuspid annulus. The base is marked by the coronary sinus orifice (Figure 1). At the apex of the triangle the AV node penetrates the central fibrous body to become the His bundle. Increasing interest is now focused on this region because several techniques have been developed for the cure of supraventricular arrhythmias arising near the AV node.2–4 Both surgical and catheter ablation techniques make use of the anatomic landmarks of Kochs triangle.2–4 The aim of the current study was to define the size and variability of Kochs triangle in the human.
Journal of the American College of Cardiology | 1994
Mark A. McGuire; Monica Robotin; Alex S.B. Yip; John P. Bourke; David C. Johnson; Barbara Dewsnap; Peter Grant; John B. Uther; David L. Ross
OBJECTIVES This study was designed to examine the effects of destroying the posterior approaches to the atrioventricular (AV) node. BACKGROUND Surgical and catheter ablation procedures have been developed for the cure of AV junctional reentrant tachycardia. Some of these destroy the posterior approaches to the AV node. METHODS Atrioventricular node function and electrical excitation of Kochs triangle and the proximal coronary sinus were examined in 18 dogs. Dissection of the posterior atrionodal connections was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, repeat electrophysiologic and mapping studies were performed to assess changes in AV node function and the routes of AV and ventriculoatrial (VA) conduction. The AV junction was then examined with light microscopy. RESULTS The compact AV node was undamaged in eight cases (80%). In two cases minor fibrosis occurred at the posterior limit of the compact node. The right-sided posterior atrionodal connections lying between the coronary sinus orifice and the tricuspid annulus were replaced by scar tissue in all cases, but the left-sided posterior connections and the anterior connections remained intact. Atrioventricular and VA conduction intervals and refractory periods were not altered. Atrioventricular junctional echoes were present in 10 dogs before and in 7 dogs after dissection (p = 0.06). Posterior (slow pathway) retrograde exists from the AV node were present in seven dogs before and in seven dogs after dissection. However, retrograde atrial excitation was altered in four of these seven dogs, so that the site of exit from the AV node was more leftward than it had been preoperatively. The node remained responsive to autonomic blocking drugs postoperatively. Double atrial electrograms similar to slow pathway potentials were found in all dogs. CONCLUSIONS This procedure ablates the posterior atrionodal connections but rarely damages the compact AV node. Atrioventricular node function is not impaired and the node is not denervated. The mechanism of cure of AV junctional reentrant tachycardia is probably damage to the perinodal atrium. This suggests that part of the slow AV node pathway may lie outside the compact AV node. Dual AV node exits and double atrial electrograms are present in the normal canine heart.
Hiv Medicine | 2004
Monica Robotin; Matthew Law; Sam Milliken; David Goldstein; Roger Garsia; G. Dolan; John M. Kaldor; Andrew E. Grulich
To analyse clinical features and predictors of survival for AIDS‐related non‐Hodgkins lymphoma (NHL) in the era of highly active antiretroviral therapy (HAART), compared to earlier in the HIV epidemic.
Journal of Hepatology | 2009
Monica Robotin; Melanie Q Kansil; Kirsten Howard; Jacob George; Steven Tipper; Gregory J. Dore; Miriam T. Levy; Andrew Penman
BACKGROUND/AIMS In Australia, Asian-born populations are 6-12 times more likely to develop hepatocellular cancer (HCC) than Australian-born individuals. We therefore, modelled the consequences of different management strategies for chronic hepatitis B (CHB) in Asian-born adults aged > or = 35 years. METHODS A Markov model compared (1) enhanced surveillance for HCC alone (HCC surveillance), or (2) enhanced HCC surveillance coupled with CHB treatment (HCC prevention) to the current practice, of low CHB treatment uptake. Patients were stratified and managed according to risk categories, based upon hepatitis B virus (HBV) viral load and alanine aminotransferase (ALT) levels. We measured costs, health outcomes [cases of HCC and deaths averted, quality-adjusted life-years (QALYs) gained] and incremental cost-effectiveness ratios (ICERs). RESULTS HCC surveillance would cost on average AU
Cancer Causes & Control | 2010
Monica Robotin; Sandra C. Jones; Andrew V. Biankin; Louise Waters; Donald C Iverson; Helen Gooden; Bruce Barraclough; Andrew Penman
8479 per person, compared to AU
World Journal of Hepatology | 2011
Monica Robotin
2632 with current clinical practice and result in a gain of 0.014 QALYs (AU