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Association of Serum Calcium Levels with Infarct Size in Acute Ischemic Stroke: Observations from Northeast India

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      Abstract

      Background:Calcium is known to be major mediator in ischemic neuronal cell death. Recent studies have shown that elevated serum calcium levels at admission in patients with stroke have been associated with less severe clinical deficits and with better outcomes.Aim:The aim of this to determine the correlation between serum calcium (total, corrected, and ionized) and infarct size (IS) in patients with acute ischemic stroke.Materials and Methods:Data were collected from 61 patients presenting with acute ischemic stroke from May 2015 to April 2016 at a tertiary care institute in Northeast India. Only patients aged ≥40 years and diagnosed as having acute ischemic cerebrovascular stroke with clinical examination and confirmed by a computed tomography scan were included in the study. Serum calcium levels (total, albumin corrected, and ionized) were collapsed into quartiles, and these quartile versions were used for calculating correlation. Pearson's correlation coefficient was used for comparing calcium levels with IS.Results:Total calcium, albumin-corrected calcium, and ionized calcium had a statistically significant negative correlation with IS with r = −0.578, −0.5396, and −0.5335, respectively. Total and ionized calcium showed a significant negative correlation with IS across all four quartiles. Albumin-corrected calcium levels showed a significant negative correlation with IS only across the lowest and highest quartiles.Conclusion:The findings in our study suggest that serum calcium can be used as a prognostic indicator in ischemic stroke as its levels directly correlates with the IS.

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      Most cited references 25

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      Cardiovascular disease in non-Western countries.

       Ashvini Reddy (2004)
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        Calcium in ischemic cell death.

         B Siesjo,  T Kristian (1998)
        This review article deals with the role of calcium in ischemic cell death. A calcium-related mechanism was proposed more than two decades ago to explain cell necrosis incurred in cardiac ischemia and muscular dystrophy. In fact, an excitotoxic hypothesis was advanced to explain the acetylcholine-related death of muscle end plates. A similar hypothesis was proposed to explain selective neuronal damage in the brain in ischemia, hypoglycemic coma, and status epilepticus. The original concepts encompass the hypothesis that cell damage in ischemia-reperfusion is due to enhanced activity of phospholipases and proteases, leading to release of free fatty acids and their breakdown products and to degradation of cytoskeletal proteins. It is equally clear that a coupling exists between influx of calcium into cells and their production of reactive oxygen species, such as .O2, H2O2, and .OH. Recent results have underscored the role of calcium in ischemic cell death. A coupling has been demonstrated among glutamate release, calcium influx, and enhanced production of reactive metabolites such as .O2-, .OH, and nitric oxide. It has become equally clear that the combination of .O2- and nitric oxide can yield peroxynitrate, a metabolite with potentially devastating effects. The mitochondria have again come into the focus of interest. This is because certain conditions, notably mitochondrial calcium accumulation and oxidative stress, can trigger the assembly (opening) of a high-conductance pore in the inner mitochondrial membrane. The mitochondrial permeability transition (MPT) pore leads to a collapse of the electrochemical potential for H+, thereby arresting ATP production and triggering production of reactive oxygen species. The occurrence of an MPT in vivo is suggested by the dramatic anti-ischemic effect of cyclosporin A, a virtually specific blocker of the MPT in vitro in transient forebrain ischemia. However, cyclosporin A has limited effect on the cell damage incurred as a result of 2 hours of focal cerebral ischemia, suggesting that factors other than MPT play a role. It is discussed whether this could reflect the operation of phospholipase A2 activity and degradation of the lipid skeleton of the inner mitochondrial membrane. Calcium is one of the triggers involved in ischemic cell death, whatever the mechanism.
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          ABC/2 for rapid clinical estimate of infarct, perfusion, and mismatch volumes.

          Rapid and easy clinical assessments for volumes of infarction and perfusion mismatch are needed. We tested whether simple geometric models generated accurate estimates of these volumes. Acute diffusion-weighted image (DWI) and perfusion (mean transit time [MTT]) in 63 strokes and established infarct volumes in 50 subacute strokes were measured by computerized planimetry. Mismatch was defined as MTT/DWI > or = 1.2. Observers, blinded to planimetric values, measured lesions in three perpendicular axes A, B, and C. Geometric estimates of sphere, ellipsoid, bicone, and cylinder were compared to planimetric volume by least-squares linear regression. The ABC/2 formula (ellipsoid) was superior to other geometries for estimating volume of DWI (slope 1.16, 95% confidence interval [CI] 0.94 to 1.38; R(2) = 0.91, p = 0.001) and MTT (slope 1.11, 95% CI 0.99 to 1.23; R(2) = 0.89, p = 0.001). The intrarater and interrater reliability for ABC/2 was high for both DWI (0.992 and 0.965) and MTT (0.881 and 0.712). For subacute infarct, the ABC/2 formula also best estimated planimetric volume (slope 1.00, 95% CI 0.98 to 1.19; R(2) = 0.74, p = 0.001). In general, sphere and cylinder geometries overestimated all volumes and bicone underestimated all volumes. The positive predictive value for mismatch was 92% and negative predictive value was 33%. Of the models tested, ABC/2 is reproducible, is accurate, and provides the best simple geometric estimate of infarction and mean transit time volumes. ABC/2 has a high positive predictive value for identifying mismatch greater than 20% and might be a useful tool for rapid determination of acute stroke treatment.
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            Author and article information

            Affiliations
            Department of Biochemistry, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, Meghalaya, India
            [1 ]Department of Radiology, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, Meghalaya, India
            [2 ]Department of Pharmacology, Assam Medical College and Hospital, Dibrugarh, Assam, India
            Author notes
            Address for correspondence: Dr. Alice Abraham Ruram, Department of Biochemistry, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, Meghalaya, India. E-mail: ruramalice9@ 123456gmail.com
            Journal
            J Neurosci Rural Pract
            J Neurosci Rural Pract
            JNRP
            Journal of Neurosciences in Rural Practice
            Medknow Publications & Media Pvt Ltd (India )
            0976-3147
            0976-3155
            December 2016
            : 7
            : Suppl 1
            : S41-S45
            5244059
            JNRP-7-41
            10.4103/0976-3147.196461
            Copyright: © Journal of Neurosciences in Rural Practice

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