Cardiac troponin I assessment and late cardiac complications after carotid stenting or endarterectomy

PurposeWhen compared with carotid endarterectomy (CEA), percutaneous carotid angioplasty with stent replacement (CAS) is a less invasive technique in the treatment of carotid stenosis. However, periprocedural hemodynamic instability still remains a challenge. This instability might lead to myocardial damage, which is now measured accurately by using cardiac troponin I (CTnI).MethodsThis study was designed to compare the periprocedural variation of CTnI in 150 consecutive patients scheduled to undergo CEA (n = 75) or CAS (n = 75). The levels of CTnI were measured until the third postoperative day in all patients. Short-term (1 month) and long-term (up to 5 years) postoperative cardiac outcome were assessed by means of chart review, regular follow-ups, and telephone calls.ResultsThere was not any statistically significant difference between the 2 groups regarding the demographic characteristics and preprocedural medical status. The incidence of increase of CTnI (>0.5 ng/mL) was significantly higher in the CEA group (13%) compared with that in the CAS group (1%; P = .001). During the acute postprocedural period, the CAS group was significantly more prone to hypotension, requiring vasopressor therapy, whereas the CEA group had more hypertension, necessitating hypotensive medications (P < .001). At 5 years, the overall incidence of major cardiac complications (nonfatal myocardial infarction and death related to cardiac origin) was significantly more frequent in the CEA group (20% vs 5%, P < .01).ConclusionThe results of our study suggest that CAS yielded less myocardial damage in the short and long term when compared with CEA. Larger randomized multicenter trials with long-term outcomes are necessary to confirm our findings

Intracuff Pressure and Tracheal Morbidity Influence of Filling Cuff with Saline during Nitrous Oxide Anesthesia

Background: Diffusion of nitrous oxide into the cuff of the endotracheal tube results in an increase in cuff pressure. Excessive endotracheal tube cuff pressure may impair tracheal mucosal perfusion and cause tracheal damage and sore throat. Filling the cuff of the endotracheal tube with saline instead of air prevents the increase in cuff pressure due to nitrous oxide diffusion. This method was used to test whether tracheal morbidity is related to excess in tracheal cuff pressure during balanced anesthesia. Methods: Fifty patients with American Society of Anesthesiologists physical status I or II were randomly allocated to two groups with endotracheal tube cuffs initially inflated to 20 -30 cm H 2 O with either air (group A) or saline (group S). Anesthesia was maintained with isoflurane and nitrous oxide. At the time of extubation, a fiberoptic examination of the trachea was performed by an independent observer, and abnormalities of tracheal mucosa at the level of the cuff contact area were scored. Patients assessed their symptoms (sore throat, dysphagia, and hoarseness) at the time of discharge from the postanesthesia care unit and 24 h after extubation on a 101-point numerical rating scale. Results: Cuff pressure increased gradually during anesthesia in group A but remained stable in group S. The incidence of sore throat was greater in group A than in group S in the postanesthesia care unit (76 vs. 20%) and 24 h after extubation (42 vs. 12%; P &lt; 0.05). Tracheal lesions at time of extubation were seen in all patients of group A and in eight patients (32%) of group S (P &lt; 0.05). Conclusion: Excess in endotracheal tube cuff pressure during balanced anesthesia due to nitrous oxide diffusion into this closed gas space causes sore throat that is related to tracheal mucosal erosion

Comparative effect of intraoperative propacetamol versus placebo on morphine consumption after elective reduction mammoplasty under remifentanil-based anesthesia: a randomized control trial [ISRCTN71723173]

BACKGROUND: Postoperative administration of paracetamol or its prodrug propacetamol has been shown to decrease pain with a morphine sparing effect. However, the effect of propacetamol administered intra-operatively on post-operative pain and early postoperative morphine consumption has not been clearly evaluated. In order to evaluate the effectiveness of analgesic protocols in the management of post-operative pain, a standardized anesthesia protocol without long-acting opioids is crucial. Thus, for ethical reasons, the surgical procedure under general anesthesia with remifentanil as the only intraoperative analgesic must be associated with a moderate predictable postoperative pain. METHODS: We were interested in determining the postoperative effect of propacetamol administered intraoperatively after intraoperative remifentanil. Thirty-six adult women undergoing mammoplasty with remifentanil-based anesthesia were randomly assigned to receive propacetamol 2 g or placebo one hour before the end of surgery. After remifentanil interruption and tracheal extubation in recovery room, pain was assessed and intravenous titrated morphine was given. The primary end-point was the cumulative dose of morphine administered in the recovery room. The secondary end-points were the pain score after tracheal extubation and one hour after, the delay for obtaining a Simplified Numerical Pain Scale (SNPS) less than 4, and the incidence of morphine side effects in the recovery room. For intergroup comparisons, categorical variables were compared using the chi-squared test and continuous variables were compared using the Student t test or Mann-Whitney U test, as appropriate. A p value less than 0.05 was considered as significant. RESULTS: In recovery room, morphine consumption was lower in the propacetamol group than in the placebo group (p = 0.01). Pain scores were similar in both groups after tracheal extubation and lower in the propacetamol group (p = 0.003) one hour after tracheal extubation. The time to reach a SNPS < 4 was significantly shorter in the propacetamol group (p = 0.02). The incidence of morphine related side effects did not differ between the two groups. CONCLUSIONS: Intraoperative propacetamol administration with remifentanil based-anesthesia improved significantly early postoperative pain by sparing morphine and shortening the delay to achieve pain relief

Quantitative assessment of fibrinogen cross-linking by εaminocaproic acid in patients with end-stage liver disease

Analysis of the effectiveness of antifibrinolytic therapy for liver transplant recipients is hampered by lack of quantitative assays for assessing drug effects. We adapted chemical engineering tools used in polymerization studies to quantify fibrinogen cross-linking by plasma from liver transplant patients obtained before and after εaminocaproic acid (EACA) therapy. A target fluorescein isothiocyanate–fibrinogen (FITC—fibrinogen) molecule was constructed; it fluoresces in a quantifiable pattern when in solution, and undergoes cross-linking in the presence of plasmin inhibitors. Cross-linking quenches the fluorescent signal, and the quenching is a quantifiable endpoint. Thus fluorescence from this reporter molecule can be used to assess functional improvement in fibrinogen cross-linking as a result of antifibrinolytic therapies, and it is sensitive to picomolar amounts of plasmin inhibitors and activators. Cross-linking of FITC-fibrinogen by patient plasma, before and after EACA therapy, was assessed using fluorescence spectrometry. Fluorescence patterns from FITC-fibrinogen indicated no significant cross-linking of the target fibrinogen as a consequence of EACA in posttreatment plasma. When the fibrinogen-FITC target was assayed without plasma in the presence of EACA at concentrations that bracket therapeutic levels (100 and 400 Μg/ml), significant fluorescence quenching (target FITC-fibrinogen cross-linking) was achieved. These results suggest that fibrinogen-FITC fluorescence is sensitive enough to detect EACA activity in clinically relevant ranges, but that EACA given in usual doses is insufficient to promote fibrinogen cross-linking in patients with end-stage liver disease. (Liver Transpl 2004;10:123–128.)Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/35285/1/20011_ftp.pd