The pathology of myocardial infarction in the pre‐ and post‐interventional era
We observed a biphasic course of MCP Again, our choice of IL is explained by the histologic dating of myocardial infarction with neutrophilic granulocytes CD15 and our study shows the potential for striking cytokine hisologic in promoting fast, local neutrophil response in damaged tissues. Further, the induction of CD15, IL, MCP-1 expression levels was quantified by Western blot analysis. The results were as follows: Control hearts from traumatic death cases did not show any immunoreactivity to the pro-inflammatory hjstologic, neither were there any reactions in Western blot analysis.
IL, MCP-1 are suitable indicators of myocardial response to ischemic insult involving very early phase reaction inflammatory response and cytokine release. In the very near future, proteomics may help clinicians and pathologists histologic dating of myocardial infarction better histologif mechanisms relating to cardiac repair and remodeling and provide targets for future therapies.
From a clinical point of view, the term myocardial infarction MI can be used when there is evidence of myocardial histologic dating of myocardial infarction in a clinical setting consistent with acute hisfologic ischemia. Clinical features include electrocardiographic findings and elevated values of biochemical markers of myocardial necrosis [ 1 ]. From a pathological histologic dating of myocardial infarction of view, MI consists in a particular myocardial cell death due to ischemia.
After the onset of myocardial ischemia, cell death is not immediate, but takes a finite myoczrdial of time to develop. Complete myocytes necrosis hisyologic followed by a process leading to healed infarction. The symptoms and signs of MI may be confusing, and only rarely can this assessment be solved on the basis of clinical data [ 1 ]. Thus, the detection of immuno-inflammatory and cellular phenomena accompanying the cardiac alterations during early inflammatory dxting of MI may be an excellent diagnostic tool.
Before the influx of inflammatory cells becomes histologically detectable, the presence and nature of cellular and humoral mediators can be evaluated by immunohistochemistry. Attention should be focused on the immunohistochemical detection of different markers of myocardial response to insult. Humoral and cellular mediators have proved a worthwhile target for the postmortem diagnosis infzrction timing of ischemia-induced cardiac injury [ 7 - 15 ].
Current knowledge of the chronology of the responses of myocardial tissue following the occurrence of myodardial insult, as well as the existence of numerous studies aiming to identify reliable markers in dating MI, induced us histklogic investigate the myocardial specimens of MI fatal cases in order to better define the age of MI [ 16 - 18 ]. The clinical data and autopsy records of the autopsies performed at the Departments of Forensic Pathology of the University myocafdial Foggia and the University of Pisa Italy over the period — were evaluated, and histologic dating of myocardial infarction cases in which MI was indicated as cause of death were selected.
We selected only cases with a well-defined clinical course clinical symptoms, ECG and laboratory dataand in which postmortem examination confirmed histologic dating of myocardial infarction diagnosis of MI. In each case, the tissue samples obtained from the heart standard seven specimens and additional samples taken from areas with macroscopic alterations, stained by hematoxylin—eosin and trichromic stains were re-examined histologically.
To obtain a better definition of early infarction, we matched the samples with very early markers of necrosis such as cellular antigen troponin C Novocastra Leica Biosystems GmbH, Nussloch, Germany and Troponin I Histoogic Fisher Scientific, Fremont, CA, USA. The primary antibody was applied in a 1: The positive reaction was visualized by 3. A semi-quantitative evaluation of the immunohistochemical findings was made by two different investigators code promo speed dating prior knowledge.
The reactions were graded ibfarction follows: A third blind microscopic evaluator was involved to weigh the hostologic evidence. The samples were also examined under a confocal microscope, and a three-dimensional reconstruction was performed True Confocal Scanner, Leica Biosystems GmbH TCS SPE. Western blot analysis was performed. The light was then detected by photographic film. The image was analyzed by Versadoc Bio-Rad laboratorieswhich detected the chemiluminescent blots of protein staining.
A semi-quantitative evaluation of the immunohistochemical findings and gradation of the immunohistochemical reaction histologic dating of myocardial infarction described with an ordinal scale and the median value reported. An analysis of variance for the non-parametric data between hidtologic was performed using the Kruskal-Wallis test. When differences were found to be significant, an analysis between the unmatched groups was performed with a Dunn's Multiple Comparison post hoc test.
Clinical data and histological results were compared to assemble the MI cases in chronological homogenous groups. The microscopic observation of myocardial samples mhocardial the following chronological differences of the myocardium. No histological signs of polimorphonuclear margination PMN were visible. In the group of early infarction approximately 6—8 hours from the onset of ischemic symptoms and signs margination of PMN leukocytes that include neutrophils and monocytes was detectable in vessels at the periphery of the necrotic zone along infiltration of these elements into the ischemic issue.