Electroencephalographic features in patients undergoing extracorporeal membrane oxygenation.

BACKGROUND: Neurologic injury is one of the most frequent causes of death in patients undergoing extracorporeal membrane oxygenation (ECMO). As neurological examination is often unreliable in sedated patients, additional neuromonitoring is needed. However, the value of electroencephalogram (EEG) in adult ECMO patients has not been well assessed. Therefore, the aim of this study was to assess the occurrence of electroencephalographic abnormalities in patients treated with extracorporeal membrane oxygenation (ECMO) and their association with 3-month neurologic outcome. METHODS: Retrospective analysis of all patients undergoing venous-venous (V-V) or venous-arterial (V-A) ECMO with a concomitant EEG recording (April 2009-December 2018), either recorded intermittently or continuously. EEG background was classified into four categories: mild/moderate encephalopathy (i.e., mostly defined by the presence of reactivity), severe encephalopathy (mostly defined by the absence of reactivity), burst-suppression (BS) and suppressed background. Epileptiform activity (i.e., ictal EEG pattern, sporadic epileptiform discharges or periodic discharges) and asymmetry were also reported. EEG findings were analyzed according to unfavorable neurological outcome (UO, defined as Glasgow Outcome Scale < 4) at 3 months after discharge. RESULTS: A total of 139 patients (54 [41-62] years; 60 (43%) male gender) out of 596 met the inclusion criteria and were analyzed. Veno-arterial (V-A) ECMO was used in 98 (71%); UO occurred in 99 (71%) patients. Continuous EEG was performed in 113 (81%) patients. The analysis of EEG background showed that 29 (21%) patients had severe encephalopathy, 4 (3%) had BS and 19 (14%) a suppressed background. In addition, 11 (8%) of patients had seizures or status epilepticus, 10 (7%) had generalized periodic discharges or lateralized periodic discharges, and 27 (19%) had asymmetry on EEG. In the multivariate analysis, the occurrence of ischemic stroke or intracranial hemorrhage (OR 4.57 [1.25-16.74]; p = 0.02) and a suppressed background (OR 10.08 [1.24-82.20]; p = 0.03) were independently associated with UO. After an adjustment for covariates, an increasing probability for UO was observed with more severe EEG background categories. CONCLUSIONS: In adult patients treated with ECMO, EEG can identify patients with a high likelihood of poor outcome. In particular, suppressed background was independently associated with unfavorable neurological outcome.

Homocysteine and P wave dispersion in patients with heart transplantation.

BACKGROUND: Hyperhomocysteinemia (HHcy), a putative independent risk factor for the development of atherotrombosis in the general population, represents a very common finding in orthotopic heart transplantation (OHT) patients. Starting from previous studies suggesting a pro-arrhythmogenic activity of homocysteine (Hcy), we evaluated the possible correlation among Hcy plasma levels and P wave dispersion (PWD), corrected QT interval (QTc), and QTc dispersion (QTcD) as parameters of electric instability of the myocardium in patients undergone OHT whose hearts are therefore completely denervated, thus unresponsive to autonomic influences. METHODS AND RESULTS: Homocysteine plasma levels, PWD, QTc, QTcD, and QTc dynamics were measured in 32 patients, who underwent OHT, and in 20 control subjects. In OHT patients, PWD (39.5 ± 11 vs. 34 ± 6 ms, p = 0.04) and QTc interval (438 ± 20 vs. 410 ± 10 ms, p < 0.001) were significantly higher in comparison with control subjects. Moreover, OHT subjects with HHcy had higher PWD values than those with normal Hcy plasma levels (44.1 ± 10.7 vs. 33.9 ± 8.8 ms, p = 0.007), but no difference was found between this latter OHT group and controls. Accordingly, in OHT patients, plasma Hcy level correlated significantly with PWD (Spearman r = 0.70; p < 0.0001), whereas no correlation was found with QTc, QTcD, and QTc circadian dynamics. CONCLUSION: HHcy seems associated with an alteration in the electrical atrial conduction, possibly contributing, at least in part, to the increased risk of cardiac arrhythmias in the denervated hearts of OHT patients.

Cyclosporin and tacrolimus increase plasma levels of adenosine in kidney transplanted patients.

The immunosuppressive agents, cyclosporin (CsA) and tacrolimus (FK506), display cardioprotective activities. The mechanism would consist on the inhibition of the enzyme, adenosine kinase (AK), leading to an increase in adenosine (ADO) levels. ADO, inosine (INO) and nucleotide plasma levels were measured in kidney transplant recipients before and 1, 2, 4, 6 and 8 h after the administration of CsA or FK506. After CsA and FK506 administration, ADO plasma levels significantly increased, reaching a peak level after 2 h (483 +/- 124 and 429 +/- 96 nm, respectively), and then progressively declined. Calculated peak values (t(max)) of ADO were slightly delayed with respect to those of CsA and FK506. Treatment with rapamycin did not influence the phenomenon. The dynamic profile of plasma changes of ADO, nucleotides and INO were consistent with the inhibition of the enzyme, AK. ADO increase may be clinically relevant in terms of anti-ischaemic, tissue protecting, and immunosuppressive activities as well as in terms of nephrotoxicity.