POSTOPERATIVE ANALGESIA WITH EXTRADURAL CLONIDINE

The analgesic effect of extradural clonidine was evaluated ina double-blind study. In the recovery room, following orthopaedicor perineal surgery 20 ASA I and II patients were allocatedrandomly to two groups. The extradural clonidine (EC) groupreceived clonidine 2 µg kg^–1 in isotonic salinesolution 15 µg ml^–1. The extradural saline (ES)group received the equivalent volume of plain isotonic salinesolution. Pain was evaluated by a visual analogue scale (VAS)at 15-min intervals for the first 2 h and subsequently at 30-minintervals for the following 4 h. Morphine 5 mg was given s.c.when patients complained of pain after extradural saline orclonidine. In the EC group, the mean (SD) maximum pain reliefwas 68.2 (24.1)% of the initial VAS score, but it was only 14.7(25.2)% in the ES group. The mean duration of analgesia, beforeinjection of morphine, was significantly longer in the EC group(210 (87) min) compared with the ES group (45 (27) min) (P <0.001). Drowsiness and moderate hypotension were observed inthe EC group.     

Isolation,structure determination and synthesis of a novel tryptophan-containing heptapeptide (basic tryptophyllin) from the skin of Phyllomedusa rohdei

A novel tryptophyllin has been isolated from the methanol extracts of the skin of the South American frog Phyllomedusa rohdei. Its primary structure, as determined by chemical/enzymatic methods and by FAB mass spectrometry, is the following: Lys-Pro-Hyp-Ser-Trp-Ile-Pro-NH₂. This basic tryptophyllin has been synthesized in solid phase, in order to allow its complete pharmacological characterization.     

Relationship Between Catheter Forces, Lesion Characteristics, "Popping," and Char Formation: Experience with Robotic Navigation System

Introduction: Popping, char and perforation are complications that can occur following catheter ablation. We measured the amount of grams (g) applied to the endocardium during ablation using a sensor incorporated in the long sheath of a robotic system. We evaluated the relationship between lesion formation, pressure, and the development of complications.
Methods: Using a robotic navigation system, lesions were placed in the left atrium (LA) at six settings, using a constant duration (40 seconds) and flow rate of either 17 cc/min or 30 cc/min with an open irrigated catheter (OIC). Evidence of complications was noted and lesion location recorded for later analysis at necropsy.
Results: Lesions using 30 Watts (W) were more likely to be transmural at higher (>40 g) than lower (<30 g) pressures (75% vs 25%, P < 0.001). Significantly higher number of lesions using >40 g of pressure demonstrated "popping" and crater formation as compared with lesions with 20–30 g of pressure (41% vs 15%, P = 0.008). A majority of lesions placed using higher power (45 W) with higher pressures (>40 g) were associated with char and crater formation (66.7%). No lesions using 10 g of pressure were transmural, regardless of the power. Lesions placed with a power setting less than 35 W were more likely to result in "relative" sparing of the endocardial surface than lesions at a power setting higher than 35 W (62% vs 33.3%, P = 0.02) regardless of the pressure.
Conclusions: When using an OIC, lower power settings (≤35 W) and lower/medium contact pressure were more likely to show a "relative" spared endocardial surface. Overall, contact pressure between 20 g and 30 g and a power setting of 40 W appeared to achieve transmurality by preserving safety.     

Silent Cerebral Events/Lesions Related to Atrial Fibrillation Ablation: A Clinical Review

Brain magnetic resonance imaging (MRI) has identified a high incidence of cerebral ischemia in asymptomatic patients after atrial fibrillation (AF) ablation (silent). Detection of cerebral ischemic events on MRI is based on acute hyperintense lesions on diffusion‐weighted imaging. In the literature, the incidence is related to specifications of MRI and depends on the definition applied. In comparative studies, silent cerebral events (SCE, diffusion‐weighted MRI [DWI] positive only) appear to be approximately 3 times more common compared to using a definition of silent cerebral lesions (SCL; without fluid attenuated inverse recovery sequence [FLAIR] positivity). Whereas the FLAIR sequence may turn positive within days after the ischemic event, SCE definition is highly sensitive for early phases of ischemic brain damage. SCE/SCL appear to represent cerebral ischemic infarcts and determine the “embolic fingerprint” of a specific ablation technology and strategy used. The optimum time point for detecting SCE is early after AF ablation (24–72 hours), whereas detection of SCL can only be performed within the first 2–7 days (due to delay of FLAIR positivity). Different technology‐, procedure‐, and patient‐related parameters have been identified to play a role in the multifactorial genesis of SCE/SCL. In recent years, evidence has been gathered that there may be differences of SCE/SCL rates depending upon the ablation technology used, but small patient numbers and a large number of potential confounders hamper all studies. As major findings of recent studies, mode of periprocedural and intraprocedural anticoagulation has been identified as a major predictor for incidences of SCE/SCL. Whereas procedural characteristics related to higher SCE/SCL‐rates may be modified, unchangeable patient‐related factors should be taken into account for future individualized risk assessment. Novel ablation devices introduced into the market should be tested for their potential embolic fingerprint and refinements of ablation procedures to reduce their embolic potential should be prompted. The knowledge of “best practice” in terms of low SCE/SCL rates has prompted changes in work‐flow, which have been implemented into ablation procedures using novel ablation devices. So far, no study has linked SCE/SCL to neuropsychological decline and the low number of AF‐ablation‐associated events needs to be weighted against the multitude of preexisting asymptomatic MRI‐detected brain lesions related to the course of AF itself. Future studies are needed to evaluate if more white matter hyperintensities due to AF may be prevented by AF ablation (producing only a small number of SCE/SCL).     

Interleukin-6 and Outcomes in Acute Heart Failure: An ASCEND-HF Substudy

BackgroundThe inflammatory cytokine IL-6 has been previously implicated in the pathophysiology of acute decompensated heart failure (HF). Prior observations in acute HF patients have suggested that IL-6 may be associated with outcomes and modulated by nesiritide. We aimed to evaluate the associations between serial IL-6 measurements, mortality and rehospitalization in acute HF.Methods and ResultsWe analyzed the associations between IL-6 in acute HF, readmission, and mortality (30 and 180 days) using a cohort of 883 hospitalized patients from the ASCEND-HF trial (nesiritide vs placebo). Plasma IL-6 was measured at randomization (baseline), 48–72 hours, and 30 days. The median IL-6 was highest at baseline (14.1 pg/mL) and decreased at subsequent time points (7.6 pg/mL at 30 days). In a univariable Cox regression analysis, the baseline IL-6 was associated with 30- and 180-day mortality (hazard ratio per log 1.74, 95% confidence interval 1.09–2.78, P = .021; hazard ratio 3.23, confidence interval 1.18–8.86, P = .022, respectively). However, there was no association after multivariable adjustment. IL-6 at 48–72 hours was found to be independently associated with 30-day mortality (hazard ratio 8.2, confidence interval 1.2–57.5, P= .03), but not 180-day mortality in multivariable analysis that included the ASCEND-HF risk model and amino terminal pro-B-type natriuretic peptide as covariates. In comparison with placebo, nesiritide therapy was not associated with differences in serial IL-6 levels.ConclusionsAlthough elevated IL-6 levels were associated with higher all-cause mortality in acute HF, no independent association with this outcome was identified at baseline or 30-day measurements. In contrast with prior reports, we did not observe any impact of nesiritide over placebo on serial IL-6 levels.