Myocardial infarction - Wikipedia
Myocardial infarct size is a major determinant of prognosis in IHD patients, and development of a novel strategy to limit infarction is of great. short-term and long-term prognosis!5"8!. Data con- cerning the relationship between infarct size, and cardiac arrhythmias are, however, fewf IO1. Despite. variation of myocardial infarction size and in-hospital mortality in a large multicenter registry. as a prognosis factor in patients with myocardial infarction. We analyzed the relationship between peak CK and STEMI onset.
All patients manifested delayed hyperenhancement observed with MRI; in Mean infarct size relative to heart weight was Ventricular function evaluated by MRI revealed a mean ejection fraction of The median absolute value for infarct size was Open in new tab Figure 1.
The slope coefficients Rho are indicated for each time point B. These data indicate that clinicians can rely on values on days 1—4 to provide an approximation to MRI-determined reperfused infarct size.
Importantly, the slopes of the correlation curves are different for each day Fig.
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It is also likely that there will be differences with and without reperfusion. The use of imaging techniques such as positron-emission tomography and contrast-enhanced MRI 4 to enable determination of infarct size are currently impeded owing to limited availability and high cost. Small infarcts may escape visualization because of inadequate resolution.
We now show with MRI that single-point values of cTnI between 24 and 96h, as with sestamibi measurements 5correlate well. Troponin measurements are not only cheaper and more available but provide an estimate of the size of infarction not confounded by prior infarction.
This investigation shows that for patients with reperfused STEMI, early as well as later measurements of cTnI are reliable estimates of infarct size.
The fact that cTnI measurement at time-points earlier than 96 h correlate well with MRI-determined infarct size should allow for an earlier evaluation of prognosis in of these patients. Larger prospective and controlled studies are needed to confirm our results.
He has received research support from Roche Diagnostics. He is a consultant to Ortho Diagnostics and has consulted over time for most of the major diagnostic companies. Briefly, animals were anesthetized with 2. The fractional shortening FS and ejection fraction EF were estimated based on the M-mode or a two-dimensional analysis, respectively.
The hearts were cut with a razor blade into 2- or 1-mm sections from the rats and mice, respectively: Each section was embedded in paraffin using a standard histological procedure. Bersoft Image Analysis software Bersoft Technology and Software; Lunenburg, Canada was used to measure the scar thickness in the middle of the infarct, septum thickness, left ventricle LV cavity area, infarct area, and LV tissue area.
The measurements were performed on one slice of each heart section and averaged according to Takagawa et al. Linear regression analyses were performed using Prism software. The non-parametric Spearman test was computed in a two-tailed manner. The non-parametric Wilcoxon matched pairs test was used to compare two paired groups. Results Myocardial Infarction A total of 28 rats and 23 mice were included in the study.
Peri-operative mortalities were low no rat, one mice. Each of the sham and healthy groups comprised three rats and three mice. The LAD ligations resulted in a reduction in heart function, and there was a significant difference between the LAD-ligated groups and the healthy and sham groups. The ligations were performed at a random site on the coronary artery. Accordingly, an assessment of the heart function showed large variability on the echocardiogram at the 2-week follow-up.
Longitudinal echocardiographic assessments of heart function performed at 2 weeks black bars and 6 weeks white bars after the time of surgery are represented for mice above and rats below. The fractional shortening FS was calculated using the M-mode and ejection fraction EF from the two-dimensional imaging mode. After 6 weeks, the average EF and FS remained stable in both the mice and rats in all of the groups compared with the measurements performed at 2 weeks post-ligation.
The relationship of myocardial infarct size and prognosis. - Semantic Scholar
As illustrated in Figure 2Athe histological measurements showed a wide panel of myocardial injury, with large to small infarcts within the MI group. The lesions increased from base to apex. The sham group did not display any infarcts. A Representative sections with Masson-Goldner trichome staining showing healthy myocardia in red and fibrotic tissues in green.
Scale bars indicate 1. The sections were from a healthy control and LAD ligated animal, respectively.
- The relationship of myocardial infarct size and prognosis. Discussion.
- The relationship of myocardial infarct size and prognosis
- Myocardial infarction
B Myocardial injury was assessed as the percentage of the infarcted area of the left ventricle and the infarct expansion index in mice and rats at 6 weeks post LAD ligation. In ligated rats, the EI varied from of 0. When expressed as a percentage of the LV, the estimation of the infarct size may be biased. Indeed, thinning of the LV wall from remodeling-induced transmural infarct is not included in the calculation. The EI showed higher accuracy for infarct size variability estimation.
The cTnI concentration peaked between 24 and 48 h in the infarcted mice, and it varied between the individual animals. Representative individual kinetics of plasma cTnI for mice A and rats B: Y-axis scales have been individually optimized for each graph. The FS recorded 6 weeks post-MI is also reported. For mice, we observed significant correlations between the EI and plasma troponin levels at 24 and 48 h, mean value between 24 and 48 h, and AUC.
Relationship between the expansion index EI and cTnI level: The cTnI concentrations are presented at 24 and 48 h, as the mean of the 24—48 h time period, and as the AUC.
The r2 and p-values from the regression and correlation analyses are shown for each graph. For mice, the selected value for the cTnI level was the mean of the 24 and 48 h plasma concentrations; the peak level at 24 h was used for rats.
As shown in Figure 5Ain mice, a significant correlation was found between cTnI and heart function, with a maximum r2 of 0. The relationship between heart function FS and EF at 2 and 6 weeks after surgery and cTnI levels are represented as the mean value at 24—48 h for mice A and the level at 24 h for rats B.
Discussion Monitoring troponin levels in the body is an important tool for clinicians Babuin and Jaffe, ; Thygesen et al. However, the use of cardiac biomarkers in preclinical models is almost only used in toxicology following administration of cardiotoxic drugs O'Brien et al. Discrepancies have been found between preclinical and clinical studies of MI, which have emphasized the need for improved small animal models. To assess the therapeutic efficacy of a treatment, preclinical investigations often use MI size as an end-point outcome without evaluating the infarct size before treatment or using a biomarker-guided prediction of myocardial injury.
Therefore, the resulting high inter-animal variability impairs the comparison between the treated and non-treated groups and the accuracy of the therapeutic efficacy. In this study, we demonstrated that the plasma level of cTnI can be easily quantified in a sensitive manner in mice and rats.
Furthermore, we validated the use of plasma cTnI as an early maker of myocardial injury and, importantly, provided evidence of its predictive value for myocardial injury in small animal models. Numerous studies have validated the plasma level of cTnI in animals using a model of cardiac toxicity induced by isoproterenol O'Brien et al. Indeed, it has been shown that commercially available immunoassays for human cTn provide sensitive and reproducible measurements of cTn levels in various laboratory animals, including rats and mice O'Brien et al.
Absolute values are specific to the assay used. Nevertheless, the kinetics of cTnI appearance and clearance were similar with all assays. The detection of cTnI required either one measurement at 24 h for rats and two measurements at 24 and 48 h for mice, making it appropriate for small animal models. Importantly, we did not observe any cTnI in animals that received a sham operation, suggesting that general muscle injury from surgery does not interfere with cTnI detection.
We obtained a wide representation of infarct sizes by varying the sites of ligation. The EI and percentage of infarcted LV varied accordingly. In agreement with a study from Takagawa et al. Indeed, the EI calculation includes more measured parameters, such as infarct thickness relative to septum thickness.
This parameter is critical for chronic models of MI that present large inter-individual variability in remodeling and transmural MI such as the rat LAD ligation model. By contrast, the mouse model appeared less prone to inter-individual variability in remodeling and wall thinning. Previously, in acute MI, Vietta et al. Additionally, the cTnT level assessed at 24 h after LAD ligation has also been correlated with the size of the infarct in mice Metzler et al.
In addition, the plasma concentration of cTnI measured 1 day post MI as marker of infarct size has been recently used in mice and validated by the classic triphenyltetrazolium-chloride assay performed 2 days post MI Santulli et al.
Indeed, to the best of our knowledge, this study provides the first evidence that the cTnI level can predict the size of a 6-week-old infarct in both mice and rats. Taken together, our results indicate that the cTnI plasma level can predict MI development within the first 24—48 h.