Developing academic cardiothoracic surgeons.
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Publications and source records attributed to E Verrier.
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The hemodynamic performance of stentless aortic bioprostheses has been well described during the first few months after surgery. The purpose of the present study was to describe the hemodynamic performance of the Toronto SPV valve (St. Jude Medical, Inc, St. Paul, MN) in a multicenter trial through 8 years. The long-term study of the Toronto SPV valve includes 447 consecutive patients from 6 investigative centers. Echocardiographic follow-up was performed at specified intervals, with quantitative analysis performed at a centralized core laboratory. Mean transvalvular gradient decreased significantly between discharge and 6 months, between 6 months and 1 year, and between 1 year and 2 years after surgery, without further significant change. The effective orifice area increased significantly early after surgery and continued to increase through 6-year follow-up. The left ventricular (LV) stroke volume increased progressively from discharge through 6-year follow-up. The LV mass index decreased significantly from discharge through 3 years after surgery and stabilized through 5 years. There was a gradual increase in LV outflow tract diameter between 1 year and 6 years after surgery. The prevalence of any aortic regurgitation (AR) (including trivial) and > or = mild AR increased significantly between discharge and 6-year to 8-year follow-up. However, the prevalence of > or = moderate AR remained very low at 6 years (2.6%) and 8 years (4.5%) after surgery. In conclusion, the Toronto SPV stentless tissue aortic valve is associated with excellent hemodynamics early after surgery and through 8 years after surgery. LV mass decreases early, and returns to within the range of normal by 1 year after surgery. There is evidence of continued LV mass regression involving the LV outflow tract, potentially contributing to a small but significant late improvement in hemodynamics. The prevalence of significant AR remains low through 8 years.
The early hemodynamic benefits of stentless aortic valves have been well documented. The issue of long-term functional integrity remains unanswered. We report the clinical results of a multicenter registry with prospective data on 621 patients monitored for 7.1 years. Patient data were collected and analyzed at St Jude Medical Inc, St Paul, Minnesota. In all, 66% of patients were male; the average age was 65.9 years +/-11.0 years, with 39% older than 70 years. Native aortic valves were bicuspid in 40.6%, 91.5% were calcified and 65.7% stenotic. Most valves implanted (83.1%) were sizes 25, 27, or 29 mm. Concomitant coronary bypass was performed in 42% of patients. Total follow-up time for the 621 patients was 1,944.5 valve years (mean 3.1 years per patient). At 5 years, 86.1% (n = 137) and at 6 years 80.4% (n = 51) were in New York Heart Association class I, and 78% had no or trivial atrial insufficiency. The average mean systolic gradient for all valves at 6 years was 4.0 mm Hg, and the peak gradient was 8.6 mm Hg. The effective orifice area varied from 1.4 cm2 (23-mm valve) to 2.7 cm2 (29-mm valve). The decrease in left ventricular mass index was significant and sustained. Actuarial survival at 6 years was 84.2%, and freedom from cardiac-related deaths was 90.1%. Freedom from valve-related deaths was 95.7%, and freedom from prosthetic endocarditis was 98.6%. There were no instances of primary tissue valve failure during follow-up, with 97.2% freedom from reoperation. The early hemodynamic benefits of the TSPV are well maintained during more than 6 years of follow-up, without evident valvular dysfunction. Longer follow-up time is required to validate durability, but there is increasing evidence for well-maintained structural and functional integrity.
Stentless tissue valves may provide more favorable hemodynamics than conventional stented valves. Hemodynamic findings from a large multicenter trial have not been previously reported. The present report describes the hemodynamic findings from a multinational, multicenter study after implantation of the Toronto SPV valve. A total of 577 patients underwent aortic valve replacement with the Toronto SPV valve at 12 sites in 3 countries. Echocardiograms were recorded in the early postoperative period, 3 to 6 months after surgery, 1 year after surgery, and yearly thereafter, with follow-up to 3 years. Gradients decreased and effective orifice area increased in the months after surgery. One year after surgery, mean gradient for valve sizes 20 to 22, 23, 25, 27, and 29 mm was 7.3 +/- 4.4, 7.4 +/- 4.5, 6.1 +/- 3.3, 4.9 +/- 2.4, and 4.0 +/- 2.1 mm Hg, respectively; effective orifice area was 1.3 +/- 0.7, 1.5 +/- 0.5, 1.7 +/- 0.4, 2.0 +/- 0.4, and 2.4 +/- 0.6 cm2, respectively. There was a very low prevalence of significant aortic regurgitation at all time periods. There was significant left ventricular (LV) mass regression between the early and 3- to 6-month periods and between the 3- to 6-month and 1-year postoperative periods. The Toronto SPV valve has an excellent hemodynamic profile supported by significant regression of LV hypertrophy in the year after implantation. Data through 3 years demonstrates maintenance of low gradients and freedom from significant aortic regurgitation.
Two models of heparin coated, hollow fiber membrane oxygenators were tested in vitro to compare gas transfer and transoxygenator pressure drop using an established protocol. Oxygen and carbon dioxide transfer rates were measured at blood flows of 2.5 and 5.0 liters per minute with gas flow: blood flow ratios of 1:1 and 2:1 at both blood flows. All testing was performed under normothermic conditions. The data shows that oxygen transfer increases as blood flow is increased in both oxygenators. Similarly, carbon dioxide transfer is increased by both increased blood and gas flows. Finally, the pressure drop was dependent on blood flow rate alone. This study demonstrated these two oxygenators to be comparable in both oxygen and carbon dioxide transfer and also in transoxygenator pressure drop.
OBJECTIVES: To study the reproducibility of and agreement between perioperative transesophageal echocardiographic (TEE) and radionuclide (RN) assessment of ventricular volumes and ejection fraction (EF). DESIGN: A prospective, blinded comparison of two methods of measurement. SETTING: A surgical intensive care unit in a university hospital. PARTICIPANTS: Patients after coronary artery bypass surgery. INTERVENTIONS: Left ventricular volumes and ejection fraction were simultaneously measured by radionuclide ventriculography and transesophageal echocardiography. Two sets of measurements were made in rapid succession with a third set after an interval. RESULTS: Reproducibilities of EF and ventricular volumes by TEE and RN were similar. At each set of measurements, the bias for radionuclide EF and TEE Simpson's rule EF, 0.03 +/- 0.05, 0 +/- 0.06, -0.01 +/- 0.07, respectively, for radionuclide EF and TEE area length EF 0.01 +/- 0.05, -0.01 +/- 0.05, -0.03 +/- 0.08, respectively, were significantly less than for radionuclide EF and TEE FAC 0.07 +/- 0.05, 0.05 +/- 0.05, 0.03 +/- 0.09. Poor agreement was observed between RNTD-EDV, and both of the TEE EDV measurements. CONCLUSION: EF measured by TEE area length and Simpson's rule method are as reproducible as TEE FAC and are more accurate estimates of RN EF. Poor agreement between methods of measuring end-diastolic volume was observed.
Although previous studies have documented a wide variety of derangements in laboratory measurements of blood coagulation and platelets during cardiopulmonary bypass, limited data are available concerning the magnitude of these changes and any association with excessive bleeding. To determine whether abnormalities in commonly available laboratory tests for the evaluation of coagulation, fibrinolysis and hemostasis correlate with postoperative blood loss and transfusion requirements as measures of clinical outcome, 47 consecutive patients undergoing coronary artery bypass grafting with hypothermic cardiopulmonary bypass (CPB) were studied prospectively at 12 time points before, during, and following CPB. Routine blood coagulation tests, coagulation factor levels (fibrinogen, V, VII, VIII, and IX) and fibrinolysis (FDP) became abnormal within 15 minutes after patients were placed on CPB, remained abnormal for the duration of CPB, and recovered at varying rates after discontinuation of CPB. Mean factor V levels declined by the greatest percentage, to 15% of normal, followed by factor VIII which decreased to 30%. Platelet counts declined to below 100 x 10(9)/L after the initiation of CPB and remained low in the postoperative period. Twenty-eight percent of patients had mediastinal output > or = 100 mL per hour during the immediate postoperative period, and were considered to be "bleeders." There were no clinically relevant differences in any of the laboratory measurements between patients with normal postoperative blood loss and those defined as bleeders. Thus, the absence of significant correlations between various laboratory measurements of hemostasis and actual postoperative bleeding indicates that these laboratory derangements are transient, are not predictive of clinically important hemostatic abnormalities, and should not be used in isolation to guide the use of blood components in these patients. Furthermore, although bleeders received more blood components, there was surprisingly little effect on the coagulation factor levels measured.
The vascular endothelium has a number of functions that may mediate many of the ischemia-reperfusion (IR) phenomena. The gatekeeper function is disturbed and increased capillary permeability results in edema and organ dysfunction. Vasomotor function is altered, with impairment of relaxation and augmentation of constrictor responses. Coagulation becomes imbalanced, favoring the procoagulant pathways that lead to thrombosis. Vascular adhesion molecules (integrins, selectins) are upregulated or expressed to mediate the adherence and subsequent destructive effects of neutrophils as they interact with the endothelium and the underlying organs. Finally, the more chronic vascular endothelial response may be proliferation of all cellular components of the vessel wall, leading, e.g., to intimal hyperplasia or restenosis. Ultimately, the endothelium plays a significant role either in the reparative processes that lead to recovery of the organ (myocardial stunning) or in the destructive processes that lead to cell or organ death (myocardial infarction). Our research group has been interested in the selectins, particularly E-selectin (endothelial) and P-selectin (platelet). E-selectin is not constitutively present on endothelial cells but can be upregulated by inflammatory mediators such as the cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and endotoxin. We have investigated the upregulation of E-selectin with cytokines in both hypoxia and hypothermia. Hypoxia appears to enhance E-selectin upregulation on stimulation with IL-1 or TNF-alpha, although hypothermia (to 25 degrees C) blunts this response. With rewarming to 37 degrees C, the transduction and surface expression return.
A retrospective study was performed to determine the impact of a coagulation and transfusion management program on blood utilization in 1,079 sequential patients for myocardial revascularization and open ventricle or combined procedures. Four hundred and eighty-eight patients (group 1) before, and 591 patients (group 2) after institution of thromboelastography (TEG)-guided coagulation were studied and compared for transfusion requirements, donor exposure, and the incidence of reoperation for hemorrhage. Group 2 patients had a significantly lower incidence of overall transfusion (78.5% v 86.3%) during hospitalization and in total transfusion in the operating room (57.9% v 66.4%). The incidence of each transfusion subtype was also significantly lower in group 2 patients. Actual total median donor exposure was 8 in group 1 patients and 6 exposures in group 2 patients. Mediastinal reexploration for hemorrhage was 5.7% before institution of TEG-based coagulation monitoring and 1.5% in TEG-monitored patients. Use of TEG monitoring before reexploration has decreased the cost and potential risk for patients undergoing CABG surgery.
Depression in electroencephalogram (EEG) has been documented clinically and is reproducible in swine at the initiation of cardiopulmonary bypass (CPB) utilizing a crystalloid prime. The physiological cause of this transient alteration in electrical brain activity appears to be associated with the transient drop in arterial pressure. The etiology is unknown but may be attributable to the bolus of the crystalloid prime or micro emboli, either air or fibrin-platelet. Thirteen swine (17-26 kg) were anesthetized and received 4 mg/kg dexamethasone, and following a tracheotomy were ventilated with halothane in 100% O2. Surgical preparation included: sternotomy and preparation for right atrial-aortic CPB. The CPB circuit consisted of a hollow fiber membrane oxygenator, a hard-shell venous reservoir, a roller pump, and PVC tubing. The circuit was randomly primed with either 1200 ml Plasmalyte-A or 10 ml/kg perfluorocarbon emulsion (PFE) and Plasmalyte-A to total 1200 ml. The animals were monitored continuously for systemic hemodynamics and electrocardiogram, and cerebral monitoring included blood flow and bitemporal EEG. Arterial blood gases were measured and PaCO2 was kept between 30-45 mmHg both before and during CPB. Cerebral blood flow (CBF) was measured pre-CPB and at 10 minutes after initiation of CPB. Bitemporal computerized EEG was analyzed every 60 seconds. Total power of each hemisphere, power in frequency bands, and spectral edge were recorded. All animals demonstrated a relative decrease in EEG total power at the onset of CPB. Animals that received PFE demonstrated a more stable arterial blood pressure, an increased CBF, and a lesser decrease and an earlier recovery of the EEG power.(ABSTRACT TRUNCATED AT 250 WORDS)
Recent data suggest that postbypass and postoperative myocardial ischemia are related to adverse cardiac outcome following myocardial revascularization. Therapeutic trials to suppress postoperative ischemia are warranted. Because anesthetics can suppress a variety of physiologic responses to stress as well as myocardial ischemia intraoperatively, we examined whether use of intensive analgesia in the stressful postoperative period could decrease postoperative ischemia. In 106 patients undergoing elective myocardial revascularization, we standardized the anesthetic prior to bypass (sufentanil 5-10 micrograms/kg [induction] and 4.2-6.0 micrograms.kg-1.h-1 [infusion] supplemented with up to 0.5 mg/kg of diazepam). During bypass, patients were randomly assigned to receive either morphine sulfate (group M, n = 54, up to 2 mg/kg) or sufentanil (group S, n = 52, 1 microgram/kg and 1 microgram.kg-1.h-1). In the intensive care unit (ICU), group M received low-dose analgesia (morphine sulfate 1-10 mg intravenously every 30 min, average dose = 2.2 +/- 2.1 mg/h), while group S continued to receive intensive analgesia (infusion of sufentanil at 1 microgram.kg-1.h-1). Both groups received supplemental midazolam in the ICU (group M = 1.1 +/- 1.1 mg/h; group S = 0.6 +/- 0.6 mg/h; P = 0.01). All analgesic and sedative-hypnotic medications were discontinued at 18 hours following myocardial revascularization. Using continuous two-channel electrocardiographic (ECG) monitoring (CC5 and CM5), we documented and characterized ECG changes consistent with ischemia during the preoperative, intraoperative (pre- and postbypass), and postoperative (on- and off-treatment) periods. The total ECG monitoring time was 8,486 h, averaging 81 h per patient. During the prebypass (anesthetic control) period, groups M and S had a similar incidence, but group S episodes were more severe: maximum ST-segment change (median), S versus M: -1.8 mm versus -1.4 mm (P = 0.04). During the postbypass period, both groups had a similar incidence of ischemia, but episodes in group S were less severe: maximum ST-segment change, S versus M: -1.8 mm versus -2.7 mm (P = 0.0005). During the ICU-on-therapy period, the incidence of ischemic episodes was less in group S patients, and the severity was less: area-under-the-ST-time curve, S versus M: -21 mm.min versus -161 mm.min (P = 0.05). After discontinuation of the drug regimen in the ICU, the incidence and severity of ischemic episodes was similar. The incidence of hypotension, hypertension, and tachycardia was similar in both groups in both the intraoperative and ICU periods.(ABSTRACT TRUNCATED AT 400 WORDS)
Previous studies investigating the incidence of myocardial ischemia in patients undergoing coronary-artery bypass grafting (CABG) surgery have not considered the potential significance of the preoperative ischemic pattern in the development of intra- and postoperative myocardial ischemia and infarction. Accordingly, the authors compared the frequency and severity of pre-, intra-, and postoperative ischemic episodes (ST-segment depression greater than or equal to 0.1 mV or elevation greater than or equal to 0.2 mV) in 50 men with severe coronary artery disease scheduled for elective CABG. All subjects were monitored by continuous electrocardiography (ECG) (Holter monitor) for 2 preoperative days, intraoperatively, and 2 postoperative days (total monitoring time = 4,363 h). Routine anti-anginal medications were continued until the morning of surgery, and the anesthetic management of the patient was not controlled. During the preoperative period, 42% of the patients had ECG ischemic episodes, 87% of which were clinically silent. Only 18% developed intraoperative ischemia. Postoperatively, the incidence increased to 40%. The number of ischemic episodes/hour (epis/h) of monitoring among the three monitoring periods was similar (0.09 +/- 0.12 epis/h preoperatively, 0.11 +/- 0.20 epis/h intraoperatively, and 0.05 +/- 0.08 epis/h postoperatively; P = NS). The median duration of ischemic episodes was similar pre- and intraoperatively (16 vs. 18.5 min, P = NS), but greater postoperatively (41 min, P less than 0.05). Seventy-six per cent of the perioperative ECG ischemia occurred without acute change (+/- 20% of control) in blood pressure or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Hepatic and renal failure developed in association with severe enteritis and hemorrhagic proctocolitis in a patient who had had a jejunoileal bypass 8 yr previously for morbid obesity. Parenteral antibiotic treatment abolished the systemic manifestations of the enteritis, but did not change the course of the hepatic and renal failure, and prolonged hemodialysis was necessary. Liver function improved in response to hyperalimentation. Take-down of the jejunoileal bypass resulted in immediate improvement of renal function, and hemodialysis could be discontinued. Although there is no direct evidence supporting this theory, the course of this patient suggested that the renal failure was functional in origin, and was caused by a toxin generated as a result of the intestinal bypass. We suspect that the toxin originated from bacteria within the blind bowel loop. Its delivery to the renal circulation was probably facilitated by increased absorption from the ulcerated large intestine and by impaired clearance by the diseased liver. When the bacterial flora were returned toward normal by take-down of the bypassed intestine, the quantity of circulating toxins probably decreased, which allowed renal function to improve.
A Monte Carlo simulation was used to investigate the potential of Marker Assisted Selection (MAS) in a multiple-trait situation. Only additive effects were considered. The base population was assumed to be in linkage equilibrium and, next, the population was managed over 15 discrete generations, 10 males and 50 females were chosen out of the 100 candidates of each sex. Performance for two traits was simulated with an overall heritability of a given trait equal to 0.25 or 0.10 and the overall genetic correlation between traits was generally equal to -0.4 except in one case where it was equal to 0. The model involved one biallelic QTL, accounting for 10 or 20% of the genetic variance of a given trait, plus polygenes. Initial allelic frequencies at the QTL, were generally equal to 0.5 but in one case were equal to 0.1 and 0.9. A marker with 120 different alleles in the 60 founder parents was simulated in the vicinity of the QTL. Two values of the recombination rate between these two loci were considered, 0.10 and 0.02. The genetic evaluation was based on a multiple-trait BLUP animal model, accounting (MAS) or not (conventional BLUP) for marker information. Two sets of simulations were run: (1) a "missing data" case, with males having no record for one of the traits, and (2) a "secondary trait" case, with one trait having a weight in the aggregate genotype 4 times less than the other trait and the QTL acting only on this secondary trait. In the first set, evaluation methods were found to mainly affect the accuracy of overall genetic values prediction for the trait with missing data. In comparison with BLUP, MAS led to an extra overall genetic response for the trait with missing data, which was strongly penalised under the conventional BLUP, and to a deficit in response for the other trait. This more balanced evolution of the two traits was obtained, however, at the expense of the long-term overall cumulated response for the aggregate genotype, which was 1 to 2.5% lower than the one obtained under the conventional BLUP. In the second set of simulation, in the case of low initial frequency (0.1) of the QTL allele favourable to the secondary trait, MAS was found to be substantially more efficient to avoid losing this allele than BLUP only when the QTL had a large effect and the marker was close. More benefits should be expected from MAS with more specific applications,such as early selection of animals, or by applying dynamic procedures i.e. letting the respective weights to QTL and polygenic values in the selection criterion vary across generation.
Simulations were used to study the influence of model adequacy and data structure on the estimation of genetic parameters for traits governed by direct and maternal effects. To test model adequacy, several data sets were simulated according to different underlying genetic assumptions and analysed by comparing the correct and incorrect models. Results showed that omission of one of the random effects leads to an incorrect decomposition of the other components. If maternal genetic effects exist but are neglected, direct heritability is overestimated, and sometimes more than double. The bias depends on the value of the genetic correlation between direct and maternal effects. To study the influence of data structure on the estimation of genetic parameters, several populations were simulated, with different degrees of known paternity and different levels of genetic connectedness between flocks. Results showed that the lack of connectedness affects estimates when flocks have different genetic means because no distinction can be made between genetic and environmental differences between flocks. In this case, direct and maternal heritabilities are under-estimated, whereas maternal environmental effects are overestimated. The insufficiency of pedigree leads to biased estimates of genetic parameters.