Infarction quantifying

Metabolic information of infarcted tissue can be retrieved by selecting a single cuboid volume of the pathological area for the spectroscopic examination using one of the above described SVS spectroscopy sequences. Results from an SVS MRS examination at 1.5 T with the PRESS sequence applying a TE of 144 ms are shown in Fig. 11.2. As expected, the infarcted area shows lactate which is visible as two inverted peaks (doublet) around 1.33 ppm while the contralateral tissue exhibits the spectrum of a healthy white matter. To achieve sufficient S/N for quantifiable SVS data from a 3 ml volume (approximately 1.5x1.5x1.5 cm3), the data acquisition time will take approximately 4 min. This leads to a rather... 

Upregulation of adhesion molecules has been documented in human stroke patients [7]. It was demonstrated that leukocytes from patients suffering an ischemic stroke or transient ischemic attack showed increased CDl la expression within 72 hours of the onset of symptoms [123]. Increased ICAM-1 expression on the surface of vessels fi om cerebral cortical infarcts was detected in four patients [124]. In some studies, soluble isoforms of adhesion molecules shed fi om the surfaces of activated cells were quantified in serum. Serum endothelial-leukocyte adhesion molecule-1 (ELAM-1, E-selectin) levels increased up to 24 hours after stroke. Similar increases were observed in serum vascular cell adhesion molecule-1 (VCAM-1) levels and these increases were sustained up to 5 days [125]. In contrast, serum ICAM-1 levels in acute ischemic stroke patients have been found to be lower than or the same as those of asymptomatic control subjects matched for age, sex, and vascular risk factors [125,126]. The reason not to detect an increase in serum levels of adhesion molecules might be due to the late enrolling of patients. Once adhesion molecules bind to leukocytes and endothelial cells, they can no longer be detected in serum [7]. 

To measure and quantify the mass ofthe infarcted area, a score system has been developed by Selvester, Wagner and Hindman (1985), although currently CMR is the gold-standard technique for quantification of infarcted mass (see Quantification of the infarcted area p. 285). 

Myocardial damage and viability may be approximately quantified in the chronic phase of a Q-wave infarction. Different scores have been described, to know with a greater or lesser accuracy the amount of myocardium involved and, indirectly, the LV function (EF) (Palmeri et al., 1982). Selvester, Wagner and Hindman (1985) described a 31-point scoring system, on the basis of 50 criteria (presence of Q wave in different leads, R wave in V1-V2 as mirror pattern, etc.). This score quantifies the amount of infarcted tissue (3% of the left-ventricular mass for each point). Also, the reduction of the EF due to the infarction may be... 

However, at the individual level, the standard error of myocardial damage quantification using this score is large, such that its clinical usefulness is limited. The most important cause of errors of this score is produced by the method s inability to quantify basal infarcted areas, mainly the septal and lateral areas. 

Wilkins ML, Pryor AD, Maynard C et al. An electrocardiographic acuteness score for quantifying the timing of a myocardial infarction to guide decisions regarding reperfusion therapy. Am J Cardiol 1995 75(8) 617-20. 

Spertus JA, Radford MJ, Every NJ, et al. Challenges and opportunities in quantifying die quality of care for acute myocardial infarction Summary from die Acute Myocardial Infarction Working Group of die American Heart Association/American College of Cardiology First Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke. Circulation 2003 107 1681-1691. 

In addition to simply quantifying the extent of myocardial infarcts, DE-CMR can provide other potentially useful anatomic findings to help risk-stratify patients. Yan et al. (13) evaluated 144 patients with CAD and abnormal DE-CMR findings and determined that the extent of the peri-infarct zone was superior to EF in predicting mortality over a median follow-up period of 2.4 years. Even after adjustment for age and ejection fraction, the size of the peri-infarct zone maintained strong and independent associations with all-cause and cardiovascular-related mortality. 

In additional experiments, adult male rats previously implanted with lateral cerebral ventricular guide cannula were subjected to ischemia with the permanent occlusion of the medial cerebral artery (MCAO), and the resulting brain lesion was visualized and quantified 24 h later. Animals that had received a single intracerebroventricular injection of the IGFBP ligand inhibitor (50 p,g) at the time of the MCAO had much smaller total lesion volumes than those injected with vehicle, primarily because of a reduction of the cerebral cortical infarct volume, although some protection was also evident in the striatum (Loddick et al.,... 

Hypoxia can now be detected and quantified by microelectrodes and the binding of reactive, reduced metabolites of nitroimidazoles, which reflect oxygen levels (because the radical-anion reduction intermediate is oxygen reactive) [30]. A new fibre-optic probe for tissue oxygenation, now available commercially, relies on measurements of emission from a ruthenium probe, which has an oxygen-dependent excited-state lifetime [31]. Acute or fluctuating hypoxia, which has features in common with ischaemia/reperfusion and therefore with myocardial infarction and stroke, can be detected by vascular stains such as bisbenzimidazole intercalators with different fluorescent characteristics. These can be administered intravenously a few minutes apart ... 

We have also quantified the effect of specific conjugate accumulation in the target area by comparing the quantity of radioactivity accumulated in normal and infarcted myocardium tissue after 5 hours and calculating an infarct-to-normal radioactivity ratio. This ratio depends on the degree of necrotization in each tissue sample and can vary between 5 and 50 for the labeled DTPA-PLL-Fab. At the same time, in case of routine DTPA-Fab preparations (direct labeling), the ratio even in the most necrotized samples is usually not higher than 1.5 to 3. 

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