OBJECTIVE

Previous studies have associated low serum albumin levels with poor outcome in ischemic stroke. Animal studies also demonstrated neuroprotective effects of serum albumin in focal ischemia. However, there are very limited studies on the association of serum albumin levels with stroke outcome in ischemic stroke divided into subtypes. The present study was carried out to investigate the association of serum albumin levels with outcome in ischemic stroke and its subtypes.

METHODS

The study involved 560 patients. Serum albumin levels were estimated and follow-up interviews were conducted at 3 mo postevent to determine stroke outcome. The association between serum albumin levels and stroke outcome was evaluated by multiple logistic regression analysis after adjustment for potential confounders.

RESULTS

Low levels of albumin associated significantly with poor outcome (score of >3 on the modified Rankin Scale). The adjusted odds ratio was 1.972 (95% confidence interval, 1.103-4.001; P < 0.001). The recurrence of stroke and death rate also was high in patients with low levels of albumin compared with patients with elevated levels of albumin. The reduced level of serum albumin associated significantly with poor outcome in all the stroke subtypes classified according to TOAST (Trial of ORG 10172 in Acute Stroke Treatment).

CONCLUSIONS

Relatively high serum albumin levels in acute stroke decrease poor outcome.

OBJECTIVE

This study examined the effectiveness of dexmedetomidine in preventing lung injury resulting from pneumoperitoneum in a ventilated rat model.

METHODS

Animals (n=18) were allocated randomly into 3 groups: control group, no pneumoperitoneum; sham group, pneumoperitoneum with intra-abdominal pressure of 12 mm Hg for 60 minutes; and dexmedetomidine group, dexmedetomidine administration 30 minutes before pneumoperitoneum. The rats were rested for 30 minutes after abdominal deflation. Then, blood samples were obtained for plasma malondialdehyde and ischemia-modified albumin (IMA) analyses. Tissue samples were taken for histopathologic examination and malondialdehyde analysis.

RESULTS

Compared with the control group, the sham group had a significantly higher level of plasma IMA. Pretreatment with dexmedetomidine significantly reduced the IMA level. Histopathologically, tissues from sham rats exhibited moderate or severe tissue damage, compared with control tissues. Dexmedetomidine-treated rats showed significantly less tissue damage than sham rats.

CONCLUSIONS

Dexmedetomidine prophylaxis resulted in significantly less IMA production and significantly less neutrophil infiltration, thereby helping to protect the lungs from injury after pneumoperitoneum.

OBJECTIVE

The purpose of this study was to identify changes taking place in the rat testis at the 24th hour of reperfusion following testicular torsion and to evaluate the effects of resveratrol (RSV), a powerful antioxidant, in preventing these changes using novel biochemical parameters and histopathology.

METHODS

Eighteen adult male rats were divided into three groups: Sham-operated (S), torsion/detorsion (T/D), and T/D+RSV groups. In the T/D group, testicular ischemia was achieved by rotating the left testis 720° clockwise for 4h. In the T/D+RSV group, 20mg/kg RSV was administered intraperitoneally 30 min before detorsion. All rats were sacrificed 24h after detorsion. Serum and tissue malondialdehyde (MDA) concentrations, ischemia modified albumin (IMA), total oxidative status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and histopathological damage score were analyzed.

RESULTS

Serum MDA, IMA, TOS, and OSI levels rose significantly in the T/D group. Serum MDA and IMA values were lower in the T/D+RES groups, but not significantly. OSI and TOS values were lower in the T/D+RES group, and the difference was significant. TAS values decreased significantly in the T/D group and rose in the T/D+RSV group, but not significantly. Ipsilateral tissue MDA values were significantly elevated in the T/D group and decreased in the T/D+RSV group, but not significantly. Apoptosis and histopathological damage increased significantly in the T/D group and decreased significantly in the T/D+RSV group. In the contralateral testis, apoptosis increased significantly in the T/D group. It decreased significantly in the T/D+RSV group.

CONCLUSIONS

Our findings show that RSV had a protective effect against oxidative damage induced with a testicular T/D model, especially at the antiapoptotic and histopathological level. OSI may be a good guide to the clinical status of testicular T/D.

OBJECTIVE

Knowledge about the role of oxidative stress in human diseases, including cardiovascular system disorders, emphasizes the need for reliable markers of oxidative stress. Here, we evaluated the levels of the novel marker ischemia-modified albumin (IMA), albumin-adjusted IMA (adj-IMA), and the IMA/serum albumin ratio (IMAR) in patients with chronic ischemic heart failure (CIHF).

METHODS

A total of 55 patients with CIHF and 40 age- and sex-matched healthy individuals were included in the study. Serum levels of IMA, total antioxidant status, and total oxidant status were analyzed, and the adj-IMA level, IMAR, and oxidative stress index were calculated.

RESULTS

Serum IMA, IMAR, total oxidant status levels, and oxidative stress index were significantly higher in patients with CIHF than in the controls (all P < 0.0001), whereas albumin and total antioxidant status levels were significantly lower in the CIHF patients (P < 0.0001 and P = 0.0004, respectively). However, there was no significant difference in serum adj-IMA levels between the groups (P = 0.8).

CONCLUSIONS

We observed impaired oxidant/antioxidant status in favor of oxidative stress in CIHF patients. Oxidative stress may be a key factor in the development of hypoalbuminemia in CIHF. Further studies are needed to establish the relationships among IMA, albumin, and redox balance in CIHF.

BACKGROUND

Existing cardiac markers are not sensitive for reversible myocardial ischemia. Ischemia modified albumin (IMA) has recently been shown to be an early and sensitive marker of myocardial ischemia. We established a newly standardized, albumin-adjusted IMA index that was more sensitive and accurate than the conventional IMA value.

METHODS

We enrolled 413 consecutive patients with symptoms suggestive of acute coronary syndrome (ACS). All patients were classified to either the ACS group (n=129) or 4 other groups (n=284). The ideal cutoff value of IMA was calculated by the receiver operating characteristic (ROC) curve analysis. The albumin-adjusted IMA index was calculated from the results of correlation assay between serum albumin concentration and IMA value and re-applied.

RESULTS

The sensitivity and specificity of IMA for ACS were 93.0% and 35.6%, respectively, at 85.0 U/ml. IMA had a negative linear relationship with serum albumin and albumin-adjusted IMA index was calculated by using the following equation [IMA index=serum albumin conc. (g/dl) x 23+IMA (U/ml)-100]. The sensitivity and specificity were 98.4% and 34.5%, respectively, at IMA index of 83.4.

CONCLUSIONS

The use of the calculated albumin-adjusted IMA index is recommended to increase the sensitivity of the ACS diagnosis although IMA is a sensitive marker for the identification of ACS.

OBJECTIVE

The objective of this study was to determine ischemia modified albumin (IMA) and oxidant status in Alzheimer's disease (AD). Therefore, we evaluated the IMA and oxidant status by measuring serum uric acid, albumin and gamma-glutamyltransferase (GGT) in AD.

METHODS

The plasma albumin, uric acid, GGT and IMA levels were measured by spectrophotometric methods in 32 AD patients and 32 healthy controls. The Mini Mental Status Examination and Clinical Dementia Rating Scale were used to evaluate the cognitive functions of AD patients.

RESULTS

AD patients had significantly higher IMA levels as compared to those of the controls respectively. Uric acid concentrations were significantly decreased and GGT values were significantly increased in AD when compared with control group. Albumin levels of the patients were also compared and no significant difference was detected.

CONCLUSIONS

Oxidative stress and IMA levels rise in AD. However, large prospective studies are required to understand the mechanisms leading to increased IMA levels during AD, whether preceded or not by AD.

BACKGROUND

Chronic obstructive pulmonary disease (COPD) has been associated with increased oxidative stress or reduced antioxidant resources. The main goal of this study was to evaluate the levels of serum ischemia-modified albumin (IMA), oxidized low-density lipoprotein (ox-LDL), total oxidant status (TOS), and total antioxidant status in patients with stable COPD, compared with a control group.

METHODS

This study was performed on 51 patients with stable COPD (42 men and 9 women; mean age 56.92 ± 3.0 years) and 45 healthy control participants (32 men and 13 women; 54.8 ± 3.8 years). The levels of serum lipids, IMA, total antioxidant status, TOS, and ox-LDL were measured in all participants.

RESULTS

The levels of serum IMA, ox-LDL, and TOS were significantly higher in patients with COPD than those in control individuals. There was no difference between the levels of serum total antioxidant status, triglycerides, total cholesterol, and low-density lipoprotein cholesterol (LDL-C) of patients with COPD and those of control individuals. Serum high-density lipoprotein cholesterol levels were significantly lower in patients with COPD than in control individuals.

CONCLUSIONS

Our study indicated that serum IMA, ox-LDL, and TOS may be increased as a result of chronic hypoxia, inflammation, and oxidative stress in patients with severe and very severe stable COPD. Our findings also revealed that IMA is higher in patients with Global Initiative for Chronic Obstructive Lung Disease Stages II, III, and IV, while TOS and ox-LDL are higher in patients with Global Initiative for Chronic Obstructive Lung Disease Stage IV. Measurements of serum IMA, TOS, and ox-LDL levels may be useful markers in the evaluation of stable COPD.

BACKGROUND

Circulating xanthine oxidase activity and the generated oxidants have been linked to lung reperfusion injury from no flow-reflow conditions in other organs after organ transplantation or surgery. N-acetyl-1-cysteine (NAC), an oxidant scavenger, promotes glutathione in its reduced form (GSH) that is depleted during ischemia. We have recently demonstrated its efficacy in protecting lungs from reperfusion injury if administered during reperfusion of postischemic liver. We now investigated whether preconditioning of lungs with NAC could attenuate lung respiratory or vascular derangement after no flow-reflow (ischemia-reperfusion, IR) and if this depends on lung GSH levels.

METHODS

Rat isolated livers were stabilized and perfused with modified Krebs-Henseleit solution (KH) (control, n=12) or made ischemic (no flow, IR-0, n=12) for 2 hr. Meanwhile, lungs were isolated, ventilated, and stabilized (KH+bovine albumin 5%). Serial perfusion (15 min) of liver+lung pairs took place followed by lung only recirculation (45 min) with the accumulated solution. Another three controls and three ischemic groups included lungs treated during stabilization with NAC at 100 mg x kg(-1), 150 or 225 mg x kg(-1) (in 2.5, 3.7 or 5.5 mmol solutions, respectively). Results. Ischemic liver damage, expressed by circulating hepatocellular constituents, was associated with pulmonary artery and ventilatory pressure increases by 70-100% of baseline, abnormal wet-to-dry weight ratio, and abnormal bronchoalveolar lavage volume and content in the IR-0 (nontreated) and the IR-100 and IR-225 pretreated lungs. NAC-150 pretreatment afforded preservation for most parameters. GSH content in the IR-150 lung tissue was only 11% higher than that of IR-225, but 2-fold that in IR-0 and IR-100 GSH lungs.

CONCLUSIONS

Lung preconditioning with NAC prevents reperfusion injury but not in a dose-related manner. Although enhanced GSH tissue content explains lung protection, GSH-independent NAC activity is another possibility.

BACKGROUND

Behçet's disease (BD) is a chronic inflammatory vasculitis characterized by endothelial dysfunction, elevated reactive oxygen species (ROS), and neutrophil hyperfunction production including acute attacks and remission periods. Ischemia modified albumin (IMA), advanced oxidation protein products (AOPP), prooxidants-antioxidants balance (PAB), and ferric reducing antioxidant power (FRAP) were evaluated in regard to their role in the pathogenesis of BD as well as their relation to clinical presentation, uveitis attacks and remission periods, and healthy volunteers.

METHODS

The study included 28 BD cases and 27 healthy volunteers as the control group. Blood samples were taken twice from each patient; first during an attack and second about three months after an attack, during remission period.

RESULTS

AOPP, IMA and PAB levels were significantly increased in active periods of patients with BD compared with healthy control and remission periods of patients with BD (p < 0.0001, p < 0.0001, p < 0.0001, respectively). FRABP levels were found to be lower in active periods of patients with than healthy controls and remission periods of patients with BD (p < 0.001, p < 0.05, respectively). The AOPP levels were negatively correlated with the levels of FRAB in patients (r = -0.468, p = 0.012; r = -0.394, p = 0.038, respectively). The PAB levels were positively correlated with the levels of CRP in patients (r = -0.606, p = 0.001).

CONCLUSIONS

Our results show that these parameters play a major role in the inflammatory reactions observed in BD. Increased levels of IMA and PAB are likely to be a result of inflammation-induced oxidative stress and hence its potential significance as a new marker of oxidative stress in BD.

OBJECTIVE

Familial Mediterranean fever (FMF) is an autoinflammatory, autosomal recessive, inherited disease characterized by recurrent self-limiting attacks of serosal surfaces. The imbalance of oxidants/antioxidants may play a role in such attacks. In this study, we aimed to evaluate the relationship between serum paraoxonase (PON1) activity, PON1 phenotype, and other parameters in patients with FMF and healthy controls.

METHODS

A total of 120 FMF patients with an attack-free period (AFP) and 65 healthy subjects were included in this study. The serum PON1 activity, stimulated paraoxonase (SPON) activity, PON1 phenotype (representing Q192R polymorphism; QQ, QR, RR), arylesterase activity, total oxidant status (TOS), total antioxidant capacity (TAC), oxidative stress index (OSI), advanced oxidative protein products (AOPP), total thiols (TTL), and ischemia-modified albumin (IMA) and cystatin-c (CYS-C) levels were measured.

RESULTS

For the QQ phenotype, the median TTL and AOPP levels of the control group were 264.50 (57.75) mol/L and 21.26 (21.17) mmol/L, respectively, whereas the median TTL, AOPP levels of the patients were 309.00 (47.00) mol/L and 12.98 (6.96) mmol/L, respectively. There was a statistically significant difference between the patients and controls with the QQ phenotype in terms of TTL and AOPP (p< 0.001 and p= 0.004, respectively). However, there were no statistically significant differences between the QQ and QR+RR phenotypes with respect to TAC, TOS, OSI, or the other parameters.

CONCLUSIONS

The FMF patients with AFP had higher TTL and lower AOPP levels than the controls. However, other oxidant and antioxidant parameters were similar among the patients during AFP and the controls.

BACKGROUND

The relationship between ischemia-modified albumin (IMA) and thyroid dysfunction remains uncertain. This study aimed to investigate the influence of overt hypothyroidism (Oho), overt hyperthyroidism (Ohe), and their treatments on serum IMA levels.

METHODS

A total of 35 untreated patients with Ohe, 35 untreated patients with Oho, and 35 control subjects were enrolled in the study. C-reactive protein (CRP), homocysteine (Hcy), IMA, and lipid profiles were measured and evaluated before and after treatment.

RESULTS

CRP, Hcy, and IMA levels and lipid profiles were higher in patients with Oho than in euthyroid or Ohe subjects (p<0.05). Basal IMA levels were reduced after treatments in all patients (p<0.05). In Ohe patients, serum IMA levels were positively correlated with free triiodothyronine (r=0.424, p=0.011) and free thyroxine (r=0.567, p<0.001) levels. In Oho patients, serum IMA levels were inversely correlated with free triiodothyronine (r=-0.555, p=0.001) and free thyroxine (r=-0.457, p=0.006) but positively correlated with anti-thyroid peroxidase antibody, C-reactive protein, and homocysteine levels (p<0.05). Linear regression analyses showed that free triiodothyronine was the most important factor affecting serum IMA levels in Ohe (β=0.694, p=0.019) and in Oho (β=-0.512, p=0.025).

CONCLUSIONS

IMA levels are increased in patients with thyroid dysfunction, particularly in overt hypothyroidism. Thyroid dysfunction has a significant impact on the oxidative stress status.

BACKGROUND

Ischemia-modified albumin, a new marker of myocardial ischemia, is known to elevate during ischemia induced by percutaneous coronary intervention. It is, however, not known whether ischemia-modified albumin also elevates during transient coronary vasospasm.

METHODS

We evaluated ischemia-modified albumin in patients undergoing intracoronary ergonovine spasm provocation test (n=26). For additional comparison, ischemia-modified albumin was also evaluated in elective percutaneous coronary intervention patients (n=18) and in patients with normal coronary angiography (n=10). Blood samples were taken from the arterial sheath before the procedure, just after procedural completion, or balloon inflation.

RESULTS

Median ischemia-modified albumin level elevated significantly in patients with positive provocation test compared with baseline [n=16, 106.0 (interquartile range 96.5, 115.5) versus 128.5 (114.8, 171.8) U/ml, P<0.001], whereas it did not change in patients with negative provocation test [n=10, 109.5 (103.3, 115.0) versus 113.5 (104.0, 118.3) U/ml, P=0.108]. Ischemia-modified albumin was also higher after percutaneous coronary intervention [113.5 (101.0, 131.5) versus 151.0 (129.3, 231.0) U/ml, P<0.0001] and did not change in patients with normal coronary angiography [108.5 (99.3, 114.0) versus 110.0 (108.0, 114.0) U/ml, P=0.085]. Ischemia-modified albumin elevation higher than 9 U/ml after provocation test could detect the presence of coronary vasospasm, with an area under the receiver operating characteristic curve of 0.975 (95% confidence interval 0.921-1.000), with a sensitivity of 94% and a specificity of 99%. Serum albumin levels were within reference range for all patients and there was no significant relationship between albumin and baseline ischemia-modified albumin or postischemic ischemia-modified albumin.

CONCLUSIONS

Thus, ischemia-modified albumin may have a role as a biochemical marker for transient myocardial ischemia induced by coronary vasospasm.

This study compared ischemia-modified albumin levels, a marker of ischemia in patients undergoing percutaneous coronary intervention. Ischemia-modified albumin levels were significantly lower in patients with collateral circulation compared with those without collateral circulation.

OBJECTIVE

Heart fatty acid-binding protein (h-FABP) and ischemia-modified albumin (IMA) have recently been evaluated, but to the best of our knowledge, no study has reported an analysis of these two markers for the detection of early myocardial infarction and myocardial ischemia in a large cohort of consecutive patients presenting to an emergency department (ED). This study evaluates the diagnostic accuracy and the clinical utility of h-FABP and IMA for non-ST-segment elevation acute coronary syndrome (ACS) diagnosis in the first hour of management in an ED.

METHODS

In a prospective 11-month study, 677 patients admitted to the ED with chest pain and suspected non-ST-segment elevation ACS were enrolled. On presentation, blood samples were obtained for the measurement of the biomarkers h-FABP (immunodetection with CardioDetect) and IMA (albumin cobalt-binding test). Two physicians, blinded to the results of the markers, independently categorized patients as having or not having non-ST-segment elevation ACS.

RESULTS

Of the 677 patients who were prospectively recruited, non-ST-segment elevation ACS was diagnosed in 185 (27.3%). While IMA was not predictive of the ACS diagnosis (odds ratio [OR] = 1.23; 95% CI = 0.87 to 1.81), h-FABP was predictive of ACS diagnosis (OR = 4.65; 95% CI = 2.39 to 9.04) with specificity at 96.8% (95% CI = 95.4% to 98.1%) and sensitivity at 13.5% (95% CI = 10.9% to 16.1%). However, h-FABP did not add significant additional information to a predictive model that included the usual diagnostic tools for non-ST-elevation ACS management (p = 0.40).

CONCLUSIONS

In this study on a large cohort of patients admitted to an ED for chest pain, IMA and h-FABP did not provide valuable information for ACS diagnosis.

OBJECTIVE

To assess the value of an intravascular, albumin-targeted contrast agent, MS-325, in visualizing myocardial ischemia with magnetic resonance imaging (MRI).

METHODS

Left anterior descending coronary artery (LAD) stenosis was created in 19 pigs using a closed-chest modified angioplasty technique. Myocardial ischemia was detected by first-pass, contrast-enhanced MRI at peak dipyridamole stress and was compared to Technetium-99m (Tc-99m) sestamibi single photon emission computed tomography (SPECT). Regional coronary blood flow was determined using microspheres.

RESULTS

Inducible myocardial ischemia with >40% reduction in stress myocardial blood flow was created in eight animals. An MRI defect, classified as>> or=75% reduction in peak myocardial signal intensity in the affected territory, was detected in 92.3% of these animals. In the presence of mild coronary stenosis, there was uniform enhancement with MRI and tracer uptake by SPECT. Concordance of MRI and SPECT for detecting perfusion defects was 85%.

CONCLUSIONS

The pattern of prolonged and persistent MR hypoenhancement of the ischemic myocardial bed using MS-325, which is retained primarily in the vascular bed due to its albumin-binding properties, facilitates the detection of myocardial perfusion defects.

Recently a new biological marker, Ischemia Modified Albumin (IMA), measured by the Albumin Cobalt Binding (ACB) test, was introduced for detection of myocardial ischemia. During ischemia, the metal binding capacity of albumin for certain transition metals like cobalt is reduced. The precise mechanism of action for producing IMA is not known but appears to be related to the production of reactive oxygen species that modify the metal binding sites. The ACB test is a quantitative assay that detects IMA by measuring the cobalt binding capacity of albumin in human serum. We evaluated the analytical characteristics of the ACB test, and reagent and specimen stability, using the Cobas MIRA Plus instrument. Coefficients of variation for within-run and between-run assays were <4%. No significant interference was observed for concentrations of triglycerides and hemoglobin up to 7 mmol/l and 3.8 g/l, respectively. No interference was apparent with bilirubin. Measures from paired samples of heparinized plasma and serum were not equivalent. The assay is validated for commercial use with serum, therefore our study reported results for serum specimens only. All assays were completed within 5 hours after blood withdrawal. The one-sided upper 95th percentile, calculated for the ACB test in 150 healthy subjects, was 87.00 U/ml. There was no observed difference between men and women or with age. We conclude that the ACB test adapted on the Cobas MIRA Plus analyzer is satisfactory, but strict attention to sample handling procedures is necessary to maintain stability of the analyte.

Ischemia modified albumin (IMA) is a new biochemical marker of ischemia. IMA levels rise in patients who develop ischemia during percutaneous coronary intervention (PCI). It is unclear whether IMA elevations correlate with PCI variables. The possible prognostic value of post-PCI IMA elevation has not yet to be studied.

METHODS

We studied 60 patients (mean age 61 years; 51 male) who underwent successful elective single-vessel PCI for the management of stable angina pectoris. IMA levels were measured and compared with PCI variables and target lesion revascularization rate. The median post-PCI follow up is 46 months (CI 44.6 to 47.7).

RESULTS

We found that the only variable related to post-PCI IMA levels was periprocedural dissection of target vessel (147.6 vs. 141.1 kU/l, p=0.035). No correlation between high and low balloon inflation pressure (143.6 vs. 141.6 kU/l, p=0.64), short and long inflation pressure (141.5 vs. 143.6 kU/l, p=0.17), with and without stent placement (143.7 vs. 141.3 kU/l, p=0.93) was found. IMA level more then 130 kU/l was associated with higher frequency of target lesion revascularization at nearly 4-years follow-up (p=0.026).

CONCLUSIONS

Post-PCI IMA elevation is associated with higher target lesion revascularization.

BACKGROUND

Early and accurate prediction of survival to hospital discharge following resuscitation after cardiac arrest (CA) is a major challenge. Our aim was to investigate the levels of ischemia-modified albumin (IMA) and malondialdehyde (MDA) in CA patients and whether IMA levels are valuable early marker of post-cardiopulmonary resuscitation prognosis in CA patients.

METHODS

We enrolled 52 in- or out-of-hospital CA patients, with 47 healthy volunteers as the control group (CG). Blood samples were taken for IMA and MDA measurement at the beginning or within 5 min of commencement of CPR. The patients were classified according to the Glasgow Outcome Score (GOS) into a poor outcome group (POG) and a good outcome group (GOG).

RESULTS

Mean IMA levels were higher in POG (0.25+/-0.07 ABSU) than in GOG (0.19+/-0.07 ABSU, p=0.002) and also than CG (0.16+/-0.04 ABSU, p=0.0001). The IMA levels were not significantly higher in GOG than in CG (p=0.32). The mean MDA levels in POG (0.77+/-0.27 nmol/ml) were comparable to the levels in GOG (0.75+/-0.18 nmol/ml, p>0.05), but were significantly higher than in CG (0.60+/-0.15 nmol/ml, p=0.001). MDA levels were not significantly higher in GOG than in CG (p=0.06). The optimum cut-off point for IMA maximizing sensitivity and specificity was 0.235 ABSU, with sensitivity of 65.8% and specificity of 78.6%. The corresponding +PV and -PV were 85.3% and 45.8%, respectively.

CONCLUSIONS

In conclusion, though the result may not be applied clinically in every patient, the ischemia-modified albumin may be a valuable prognostic marker in cardiac arrest patients following CPR.

OBJECTIVE

To investigate whether ischemia-modified albumin (IMA) is reliable for early diagnosing symptomatic lacunar infarction (SLI) in type 2 diabetics.

METHODS

Ninety-seven consecutive diabetic patients, 47 with SLI, and 45 healthy controls were enrolled. Serum IMA and plasma total homocysteine (tHcy) were measured on an autoanalyzer and evaluated in distinguishing SLI.

RESULTS

Serum IMA levels were 97.35 ± 5.25 U/L in the healthy control group, 103.26 ± 7.43 U/L in the non-SLI group, and 139.84 ± 20.00 U/L in the SLI group. Plasma tHcy levels were 8.08 ± 1.82 μmol/L, 11.31 ± 3.03 μmol/L, and 13.10 ± 3.67 μmol/L, respectively. The differences in IMA and tHcy levels were statistically significant for all groups (p<0.05). Receiver operating characteristic curve analyses revealed the areas under curve were 0.866 for IMA and 0.352 for tHcy.

CONCLUSIONS

This study indicates that IMA was significantly elevated in the acute phase of SLI and more sensitive than tHcy in distinguishing SLI.

The present study employed novel echocardiographic tools and cardiac markers to obtain a greater understanding of the aetiology and time course of altered cardiac function and cardiac damage following prolonged exercise and, in particular, the possible role of transient ischaemia within these phenomena. Fourteen runners in the 2004 London Marathon were assessed pre-, immediately post-, 1 h post- and 24 h postcompletion of the race. Left ventricular function was examined echocardiographically using 2-D, M-mode, tissue Doppler imaging and flow propagation velocity (Vp). Venous blood samples were analysed for N-terminal pro-B-type natriuretic peptide (proBNP), cardiac troponin T (cTnT) and ischaemia-modified albumin (IMA). Left ventricular (LV) diastolic filling was altered on completion of the race, as indicated by significant decreases in mean early to late diastolic myocardial wave (E':A') ratio and Vp (from 1.82 +/- 0.9 to 1.32 +/- 0.32, and from 67.5 +/- 9.3 to 60.2 +/- 8.2 cm s(-1), respectively, P < 0.05), accompanied by an increase in proBNP (from 21.6 +/- 11 to 47.08 +/- 19.5 pg l(-1), P < 0.05). The observed reduction in LV diastolic filling following completion of a marathon, unrelated to changes in heart rate or loading parameters, indicates an intrinsically mediated change in diastolic filling. Exercise-induced elevations in cTnT in nine individuals (range, 0.023-0.37 microg l(-1)) were indicative of minor cardiac damage. A significant reduction in IMA was observed after the marathon (from 63.68 +/- 9.83 to 44.94 +/- 16.13 Um l(-1), P < 0.05), unrelated to the alterations in cardiac function, proBNP or cTnT. The absence of an elevation in IMA suggests that exercise-induced myocardial ischaemia did not occur and therefore could not explain the changes in cardiac function or biomarkers. Future studies in this area should investigate alternative diagnostic tools for the detection of transient ischaemia, and other potential mechanisms, in order to extend the understanding of this phenomenon.

OBJECTIVE

To assess if the combination of cardiac troponin (cTn) and Ischemia Modified Albumin (IMA) can be used for early exclusion of acute myocardial infarction (AMI).

METHODS

Prospective consecutive admissions to the emergency department (ED) with undifferentiated chest pain were assessed clinically and by electrocardiography. A total of 539 patients (335 men, 204 women; median age 51.9 years) considered at low risk of AMI had blood drawn on admission. If the first sample was less than 12 hours from onset of chest pain, a second sample was drawn two hours later, at least six hours from onset of chest pain. Creatine kinase MB isoenzyme (CKMB) mass was measured on the first sample and CKMB mass and cTnT on the second sample. An aliquot from the first available sample was frozen and subsequently analysed for IMA. If cTnT had not been measured on the original sample cTnI was measured (n = 189).

RESULTS

Complete data were available for 538/539 patients. IMA or cTn was elevated in the admission sample of all patients with a final diagnosis of AMI (n = 37) with IMA alone elevated in 2/37, cTn alone in 19/37, and both in 16/37. In 173/501 patients in whom AMI was excluded both tests were negative. In the non-AMI group 22 patients had elevation of both IMA and cTn in the initial sample, suggesting ischaemic disease.

CONCLUSIONS

Admission measurement of cardiac troponin plus IMA can be used for early classification of patients presenting to the ED to assist in patient triage.

The investigation of oxygen radical-induced lipid peroxidative neuronal damage in the context of acute and chronic neurodegenerative disorders has been largely limited to the use of ex vivo analytical methodologies. These are often fraught with sensitivity or specificity problems, or they are indirect. Furthermore, none of the analytical methods allow precise anatomical identification of the cells that are undergoing peroxidative injury. This paper describes an immunocytochemical method for localization of central nervous system (CNS) lipid peroxidation (LP) that employs a rabbit-derived antibody raised against malondialdehyde (MDA)-modified rabbit serum albumin (RSA). MDA is a breakdown product of peroxidized membrane polyunsaturated fatty acids that avidly binds to cellular proteins. Using the anti-MDA-RSA, we herein illustrate increased MDA-derived immunostaining: (1) in the spinal cord of transgenic familial amyotrophic lateral sclerosis (ALS) mice; and (2) in the selectively vulnerable gerbil hippocampal CA1 region after a 5 min episode of forebrain ischemia and its relationship to the time course of neuronal degeneration.