Characterization of Benign Myocarditis Using Quantitative Delayed-Enhancement Imaging Based on Molli T1 Mapping

Delayed contrast enhancement after injection of a gadolinium-chelate (Gd-chelate) is a reference imaging method to detect myocardial tissue changes. Its localization within the thickness of the myocardial wall allows differentiating various pathological processes such as myocardial infarction (MI), inflammatory myocarditis, and cardiomyopathies. The aim of the study was first to characterize benign myocarditis using quantitative delayed-enhancement imaging and then to investigate whether the measure of the extracellular volume fraction (ECV) can be used to discriminate between MI and myocarditis.In 6 patients with acute benign myocarditis (32.2 ± 13.8 year-old, subepicardial late gadolinium enhancement [LGE]) and 18 patients with MI (52.3 ± 10.9 year-old, subendocardial/transmural LGE), myocardial T1 was determined using the Modified Look-Locker Imaging (MOLLI) sequence at 3 Tesla before and after Gd-chelate injection. T1 values were compared in LGE and normal regions of the myocardium. The myocardial T1 values were normalized to the T1 of blood, and the ECV was calculated from T1 values of myocardium and blood pre- and post-Gd injection.In both myocarditis and MI, the T1 was lower in LGE regions than in normal regions of the left ventricle. T1 of LGE areas was significantly higher in myocarditis than in MI (446.8 ± 45.8 vs 360.5 ± 66.9 ms, P = 0.003) and ECV was lower in myocarditis than in MI (34.5 ± 3.3 vs 53.8 ± 13.0 %, P = 0.004).Both inflammatory process and chronic fibrosis induce LGE (subepicardial in myocarditis and subendocardial in MI). The present study demonstrates that the determination of T1 and ECV is able to differentiate the 2 histological patterns.Further investigation will indicate whether the severity of ECV changes might help refine the predictive risk of LGE in myocarditis.     

Beta-adrenergic receptor changes during coronary artery bypass grafting

To evaluate whether the function of beta-adrenergic receptors, essential to the biologic activity of catecholamines, is altered during coronary artery bypass grafting, we measured, in 16 patients undergoing myocardial revascularization, the density and the affinity of lymphocyte beta-adrenergic receptors before anesthesia induction (control) and at the end of cardiopulmonary bypass. Variations in the density and affinity of beta-adrenergic receptors were determined in vitro. Repeated determinations of plasma epinephrine and norepinephrine concentrations were also performed. Overall, no significant modification was observed in mean density and affinity of beta-adrenergic receptors at the end of cardiopulmonary bypass when compared with control values. However, a significant decrease (p less than 0.05) in affinity for isoproterenol was found in the six patients who had high catecholamine levels during cardiopulmonary bypass. In contrast, no significant modification of beta-adrenoreceptor affinity for isoproterenol was observed in the 10 patients who did not have this degree of adrenergic activation. In addition, beta-adrenoreceptor affinity for isoproterenol was decreased in the three patients in whom intraaortic balloon pumping was mandatory after discontinuation of cardiopulmonary bypass. We suggest that this decreased affinity of lymphocyte beta-adrenergic receptors could be related, at least in part, to a sustained adrenergic activation occurring in some patients during cardiopulmonary bypass.     

Direct determination of benzalkonium chloride in ophthalmic systems by reversed-phase high-performance liquid chromatography

High-performance liquid chromatography has been used to quantitate benzalkonium chloride (alkylbenzyldimethylammonium chloride) in complex ophthalmic formulations at or below concentration levels of 50 ppm. The method involves a one-step dilution for sample preparation and direct injection; therefore, recovery and/or conversion problems are nonexistent. The assay is quick, specific, reproducible, and simple. This new approach makes routine determinations far simpler than previous methods and is especially useful for product stability studies and quality control procedures.     

Glial changes following an excitotoxic lesion in the CNS--I. Microglia/macrophages.

When an area of the adult rat CNS is depleted of neurons by an in situ excitotoxic injection, afferent axons to the area exhibit morphological alterations reminiscent of growth cones. These morphological changes are likely to be related to the deprivation of target cells. In addition, however, the area of neuronal loss is itself the site of profound changes in glial cell content, and altered axon-glial interactions may play a role in the axonal changes. In an attempt to define these interactions, we have undertaken a systemic study of glial populations in excitotoxically lesioned CNS over time. The microglial/macrophagic response is analysed in this paper; the astrocytic response is described in the companion paper [Dusart et al. (1991) Neuroscience 45, 541-549]. The microglial/macrophagic response was studied following kainic acid-induced neuronal loss in the thalamus of the adult rat. These microglial/macrophagic cells were labeled with the B4 isolectin from Griffonia simplicifolia, and the time-course of their response was studied between one day and one year post-lesion. This time-course study revealed different stages in the evolution of the response. At one day post-lesion, cell counts indicated that there was no increase in the number of non-neuronal cells in the neuron-depleted area. However, activated labeled cells were present in the entire thalamus on the side of the lesion, neuron-depleted or not. They were characterized by both increased lectin-binding and altered morphology when compared to quiescent microglia. In the absence of recruitment and/or proliferation, this result indicates that the early response consisted solely of the activation of resident microglia. By contrast, we observed a progressive increase in the number of non-neuronal cells in the lesion from four to 15 days post-lesion. A recruitment of blood-borne monocytes was apparent, and the observation of mitotic labeled cells indicated a proliferation of microglial/macrophagic cells in situ. There was a progressive decrease in the microglial/macrophagic reaction that began one month after lesion. In a thin band of parenchyma surrounding the neuron-depleted area, activated microglial/macrophagic cells were seen contacting neurons, and clusters of glial cells were observed around neurons up to one year post-lesion. These results suggest that neurons around the lesion site itself may be injured, secondarily, from a long term deleterious effect of the inflammatory process. This study allows us to conclude that activated microglia/macrophages are the predominant glial cell type in the excitotoxically lesioned CNS over the first weeks.(ABSTRACT TRUNCATED AT 400 WORDS)