Biomedical subjects
Publications and source records attributed to Jean-Jacques Lehot.
Cardiac resynchronization therapy improves symptoms and survival in chronic heart failure patients, but has been poorly studied in the acute heart failure setting. We report the case of successful cardiac resynchronization therapy in the early postoperative period after cardiac surgery in a patient with left bundle branch block and proven ventricular dyssynchrony.
BACKGROUND: Left ventricular stroke area by transoesophageal echocardiographic automated border detection has been shown to be strongly correlated to left ventricular stroke volume. Respiratory variations in left ventricular stroke volume or its surrogates are good predictors of fluid responsiveness in mechanically ventilated patients. We hypothesised that respiratory variations in left ventricular stroke area (DeltaSA) can predict fluid responsiveness. METHODS: Eighteen mechanically ventilated patients undergoing coronary artery bypass grafting were studied immediately after induction of anaesthesia. Stroke area was measured on a beat-to-beat basis using transoesophageal echocardiographic automated border detection. Haemodynamic and echocardiographic data were measured at baseline and after volume expansion induced by a passive leg raising manoeuvre. Responders to passive leg raising manoeuvre were defined as patients presenting a more than 15% increase in cardiac output. RESULTS: Cardiac output increased significantly in response to volume expansion induced by passive leg raising (from 2.16 +/- 0.79 litres per minute to 2.78 +/- 1.08 litres per minute; p < 0.01). DeltaSA decreased significantly in response to volume expansion (from 17% +/- 7% to 8% +/- 6%; p < 0.01). DeltaSA was higher in responders than in non-responders (20% +/- 5% versus 10% +/- 5%; p < 0.01). A cutoff DeltaSA value of 16% allowed fluid responsiveness prediction with a sensitivity of 92% and a specificity of 83%. DeltaSA at baseline was related to the percentage increase in cardiac output in response to volume expansion (r = 0.53, p < 0.01). CONCLUSION: DeltaSA by transoesophageal echocardiographic automated border detection is sensitive to changes in preload, can predict fluid responsiveness, and can quantify the effects of volume expansion on cardiac output. It has potential clinical applications.
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OBJECTIVE: Many changes have occurred in the natural history and the management of active infectious endocarditis (AIE) in recent years. Therefore, the records of patients admitted in a tertiary care specialized hospital presenting with the Duke criteria were reviewed. METHODS: Adults operated on to treat AIE were included during a 3-year period. Patients presenting with AIE associated with a pacemaker were not included. Bacteriologic investigations included blood cultures, intraoperative samplings (including polymerase chain reaction), and serologies. Clinical and bacteriologic factors associated with hospital mortality were studied by univariate regression analysis (p < 0.05). RESULTS: Ninety-eight of 164 patients (60%) admitted with the diagnosis of AIE underwent valvular surgery. The duration between the beginning of AIE and surgery was 23 +/- 16 (mean +/- standard deviation) days. Only 45 patients had a previous history of valvular disease. Seventy-two patients presented with aortic and 41 with mitral valve AIE. Fifty suffered from embolic events. Streptococcus species were responsible in 64 cases (23 were Streptococcus bovis) and Staphylococcus species in 24 cases. Death occurred postoperatively in 19 patients. The factors associated with fatal outcome were preoperative hemodynamic instability, age, Parsonnet and Simplified Acute Physiology Score II scores, diabetes mellitus, preexisting valvulopathy, antiarrhythmic treatment, hypoalbuminemia, renal dysfunction, duration of extracorporeal circulation, and red cell allogeneic transfusions. The type of bacteria did not influence mortality. The mean intensive care unit and hospital stays were 10 and 39 days, respectively. Eleven patients suffered from neurologic sequelae; 2 years later, 2 of them presented with severe deficit and 1 had died. CONCLUSIONS: AIE necessitating cardiac surgery should be considered as a severe and resource-consuming disease.
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BACKGROUND: Recent investigations have focused on the pivotal role of the mitochondria in the underlying mechanisms volatile anesthetic-induced myocardial preconditioning. This study aimed at examining the effect of anesthetic preconditioning on mitochondrial permeability transition (MPT) pore opening. METHODS: Anesthetized open chest rabbits were randomized to one of four groups and underwent 10 min of ischemia, except for the sham 1 group (n = 12). Before this, they underwent a treatment period consisting of (1) no intervention (ischemic group; n = 12), (2) 30 min of desflurane inhalation (8.9% end-tidal concentration) followed by a 15-min washout period (desflurane group; n = 12), or (3) ischemic preconditioning (IPC group; n = 12). A second set of experiments was performed to evaluate the effect of a putative mitochondrial adenosine triphosphate-sensitive potassium channel antagonist, 5-hydroxydecanoate (5-HD). The animals underwent the same protocol as previously, plus pretreatment with 5 mg/kg 5-HD. They were randomized to one of five groups: the sham 2 group, receiving no 5-HD (n = 12); the sham 5-HD group (n = 12); the ischemic 5-HD group (n = 12), the desflurane 5-HD group (n = 12), and the IPC 5-HD group (n = 12). At the end of the protocol, the hearts were excised, and mitochondria were isolated. MPT pore opening was assessed by measuring the amount of calcium required to trigger a massive calcium release indicative of MPT pore opening. RESULTS: Desflurane and IPC group mitochondria needed a higher calcium load than ischemic group mitochondria (362 +/- 84, 372 +/- 74, and 268 +/- 110 microM calcium, respectively; P < 0.05) to induce MPT pore opening. The sham 1 and sham 2 groups needed a similar amount of calcium to trigger mitochondrial calcium release (472 +/- 70 and 458 +/- 90 microM calcium, respectively). 5-HD preadministration had no effect on sham animals (458 +/- 90 and 440 +/- 128 microM calcium without and with 5-HD, respectively) and ischemic group animals (268 +/- 110 and 292 +/- 102 microM calcium without and with 5-HD, respectively) but abolished the effects of desflurane on calcium-induced MPT pore opening (362 +/- 84 microM calcium without 5-HD vs. 238 +/- 96 microM calcium with 5-HD; P < 0.05) and IPC (372 +/- 74 microM calcium without 5-HD vs. 270 +/- 104 microM calcium with 5-HD; P < 0.05). CONCLUSION: Like ischemic preconditioning, desflurane improved the resistance of the transition pore to calcium-induced opening. This effect was inhibited by 5-HD, suggesting a link between mitochondrial adenosine triphosphate-sensitive potassium and MPT.
This study investigated patients undergoing elective cardiac surgery to evaluate the effects of cardiopulmonary bypass (CPB) on the spontaneous variability of mean arterial pressure (MAP) and heart rate (HR). Forty-one adult patients receiving different cardiovascular system drugs were included in the study. Patients were divided into three groups: no preoperative pharmacological cardiovascular treatment (n = 12), beta-blocker (BB) (n = 13), and angiotensin-converting enzyme inhibition (ACEI) (n = 16). MAP was recorded before anaesthesia until the end of surgery. MAP and HR variability was analysed in very low- (VLF), low- (LF) and high-frequency bands. The LF spectral component of MAP was observed to decrease in patients under ACEI (-92%) or BB (-87%) following induction of anaesthesia. In addition, during CPB, VLF power decreased in BB group (-67%), and LF power decreased in ACEI group (-77%). Concerning HR, VLF spectral power decreased following anaesthesia in BB group (-74%). In addition, after CPB, VLF power reached lower value in ACEI group than in BB group (P < 0.05). LF spectral power of HR showed a large decrease after CPB in ACEI group (-89%). This study showed that MAP variability did not change during CPB in patients with no preoperative pharmacological cardiovascular treatment, suggesting an unaltered vascular control of MAP. Moreover, the change in LF spectral power of MAP in ACEI and BB groups, suggests that both the renin-angiotensin and sympathetic systems participate to the genesis of LF variability of MAP.
The instant centre frequency (ICF) of RR interval has been proposed as a global index to analyse the sympathovagal interaction in the heart. The aim of this study was to assess the ICF during anaesthesia to test if it can reliably capture the neural control of the cardiovascular system. Twenty-four ASA II or III patients scheduled for cardiac surgery were included in the study. They were allocated in two groups: control, no treatment (group 1, n = 12), and beta-adrenergic blockade by atenolol (group 2, n = 12). Spectra of pulse interval series were computed with a time-frequency method and they were divided into: very low frequency (VLF, 0.000-0.040 Hz), low frequency (LF, 0.050-0.150 Hz) and high frequency (HF, 0.160-0.500 Hz). Normalized power was obtained by dividing the cumulative power within each frequency band (LF or HF) by the sum of LF and HF; the ratio of LF/HF was also calculated. Instant centre frequency is a time-varying parameter that the evolution along time of the gravity centrum of a local spectrum. All spectral indexes were recorded at the following time points: before induction, after induction and before intubation, during intubation, and after intubation. The atenolol group had lower normalized LF and the LF/HF ratio (P < 0.05) higher HF before induction; and lower LF/HF ratio after induction and before intubation (P < 0.05). The ICF was higher in atenolol group at all times. The ICF shifted towards HF frequency after induction and before intubation and shifted towards LF during intubation in both groups. The autonomic nervous system control on the heart through the interaction of sympathetic and parasympathetic reflex mechanisms could be studied by the ICF. The ICF may assess the autonomic cardiac modulation and may provide useful information for anaesthetic management.
OBJECTIVES: To compare the efficacy and safety of 3 doses of remifentanil as part of a total intravenous anesthesia technique with low-dose propofol in patients undergoing coronary artery bypass graft (CABG) surgery. DESIGN: Multicenter, multinational, double-blind, randomized, dose comparison study. SETTING: Nine hospitals in 5 countries. PARTICIPANTS: One hundred forty-one patients undergoing first-time elective CABG surgery. INTERVENTIONS: Patients were premedicated with a short-acting oral benzodiazepine up to 2 h before surgery and randomized to receive continuous infusions of remifentanil 1.0 microg/kg/min (n = 45), 1.5 microg/kg/min (n = 44), or 2.0 microg/kg/min (n = 43), in combination with propofol 3 mg/kg/h. Nine patients received remifentanil 1.0 microg/kg/min on an open-label basis. Three different induction sequences (IS) were used. In IS 1 (n = 31), induction was started with remifentanil infusion followed 5 minutes later by propofol 0.5 mg/kg bolus and infusion at 3 mg/kg/h. Further bolus doses of propofol (10 mg) were given if loss of consciousness (LOC) was not attained after 5 minutes; pancuronium, 0.04 to 0.1 mg/kg, was administered at LOC. In IS 2 (n = 68), a priming dose of pancuronium, 0.015 mg/kg, was administered just before starting remifentanil. In IS 3 (n = 42), bolus doses of propofol, 10 mg every 10 seconds, were given until LOC, followed by pancuronium, 0.04 to 0.1 mg/kg, and the remifentanil and propofol infusions were started. MEASUREMENTS AND MAIN RESULTS: There were no significant differences among the remifentanil dose groups with regard to the primary outcome measure, responses to sternotomy/sternal spread/maximal sternal spread. Responses to these stimuli were recorded in 11%, 11%, and 14% of patients in the remifentanil 1.0, 1.5, and 2.0 microg/kg/min dose groups, respectively. Similarly, there were no significant differences in the responses to other surgical stimuli. There was a high incidence of muscle rigidity when remifentanil was used to induce anesthesia. CONCLUSIONS: All 3 remifentanil dose regimens provided profound suppression of responses to surgical stimuli in the majority of patients. There was no apparent advantage in starting the remifentanil infusion rate above 1.0 microg/kg/min. Remifentanil is not suitable for use as a sole induction agent.
OBJECTIVE: Antibiotic prophylaxis is recommended in pediatric cardiac surgery, but no data concerning the current antibiotic regimen were available. DESIGN: Prospective study from April to June 2000. SETTING: University hospital operating room and postoperative intensive care unit. PARTICIPANTS: Nineteen consecutive infants less than 10 kg with normal renal function undergoing cardiac surgery with cardiopulmonary bypass longer than 30 minutes. INTERVENTIONS: Intravenous administration of cefazolin, 40 mg/kg, and gentamicin, 5 mg/kg, at induction of anesthesia; followed by cefazolin, 35 mg/kg every 8 hours, and gentamicin, 2 mg/kg every 12 hours, over 48 hours. MEASUREMENTS AND MAIN RESULTS: Levels of serum antibiotics were measured: cefazolin (microbiologic) and gentamicin (fluorescence immunoassay) with 8 intraoperative and 5 postoperative samplings. Intraoperatively, cefazolin levels decreased from 166 +/- 44 (mean +/- standard deviation) down to 54 +/- 16 microg/mL and gentamicin from 20.8 +/- 9.5 down to 5.9 +/- 1.5 microg/mL. The postoperative trough levels were 12 +/- 7, 15 +/- 10, and 19 +/- 22 microg/mL for cefazolin and 1.1 +/- 0.5, 0.8 +/- 0.4, and 0.8 +/- 0.9 microg/mL for gentamicin. CONCLUSIONS: Antibiotic serum levels are consistent with satisfactory efficacy, but intraoperative gentamicin peak levels appeared too high.
BACKGROUND: To provide anesthesia for cardiac surgery, hypnotics and opioids are frequently titrated on variables such as mean arterial pressure and heart rate. In this study conducted in patients scheduled to undergo coronary artery bypass grafting, propofol and sufentanil, both administered by computer-controlled infusion, were titrated on the Bispectral Index (BIS) values using a predefined algorithm. METHODS: After written informed consent, 110 patients, 95 men and 15 women aged 61 (9) yr [mean (SD)], were randomly allocated to receive predicted sufentanil effect site concentrations (Ce) of 0.5, 0.75, 1, 1.25, and 1.5 ng/ml, decreased by a third after sternotomy (groups 1-5). Target induction propofol concentration was 1.5 microg/ml and subsequently adjusted on BIS values. The following parameters were recorded: BIS values, predicted propofol Ce, the number of changes of propofol target, mean arterial pressure, heart rate, the number of bolus injection and doses of vasoconstrictor and vasodilator drugs, time to tracheal extubation, postoperative awareness and satisfaction scores, and cumulative morphine doses for the first postoperative day. RESULTS: One patient randomized to group 1 required 0.75 ng/ml sufentanil Ce instead of 0.5 ng/ml for increased BIS values on tracheal intubation. BIS values were similar in the five groups. The predicted propofol Ce values were different (P < 0.05; analysis of variance) among the five groups: 1.59 (0.47) to 1.23 (0.25) microg/ml in group 1 and group 4, respectively. Significantly fewer changes of propofol target were required in group 4 as compared to group 1. There were no differences among the five groups for mean arterial pressure, heart rate, time to tracheal extubation, awareness, satisfaction scores, and morphine requirements. CONCLUSION: These results suggest the BIS, as part of an algorithm that uses both the absolute BIS value and its increase following tracheal intubation, can be used to effectively titrate both propofol and sufentanil. A predicted sufentanil Ce of 1.25 ng/ml before and 0.8 ng/ml after sternotomy was associated with the lowest predicted propofol Ce and fewer changes of propofol target. Lower sufentanil concentrations required higher propofol concentrations and more frequent changes of the target propofol concentration and were associated with similar hemodynamic tolerance.
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We sought to determine whether brain death-induced catecholamine release preconditions the heart, and if not, whether it precludes further protection by repetitive ischemia or isoflurane. Anesthetized rabbits underwent 30 min of coronary occlusion and 4 h of reperfusion. The effect on infarct size of either no intervention (controls), ischemic preconditioning (IPC), or isoflurane inhalation (Iso) was evaluated with or without previous brain death (BD) induced by subdural balloon inflation. Plasma catecholamine levels were measured at several time points. Although it dramatically increase plasma catecholamine levels, BD failed to reduce infarct size that averaged 0.49 +/- 0.34 without BD versus 0.45 +/- 0.27 g with BD. IPC and Iso, alone as well as after BD, significantly reduced infarct size that averaged 0.11 +/- 0.04, 0.21 +/- 0.15, 0.10 +/- 0.09, and 0.22 +/- 0.10 g in IPC, Iso, BD + IPC, and BD + Iso groups, respectively (means +/- SD, P < 0.05 vs. controls). BD-induced catecholamines "storm" does not precondition the rabbit heart that however retains the ability to be protected by repetition of brief ischemia or isoflurane inhalation.