Background Cardiac troponin T (cTnT) and troponin I (cTnI) are expressed as an obligate 1:1 complex in the myocardium. However, blood levels of cTnI often rise much higher than cTnT in myocardial infarction (MI), whereas cTnT is often higher in patients with stable conditions such as atrial fibrillation. Here we examine hs-cTnI and hs-cTnT after different durations of experimental cardiac ischemia. Methods hs-cTnI, hs-cTnT, and the hs-cTnT/hs-cTnI ratio were measured in plasma samples from rats before and at 30 and 120 minutes after 5, 10, 15, and 30 minutes of myocardial ischemia. The animals were killed after 120 minutes of reperfusion, and the infarct volume and volume at risk were measured. hs-cTnI, hs-cTnT, and the hs-cTnT/hs-cTnI ratio were also measured in plasma samples collected from patients with ST-elevation myocardial infarction. Results hs-cTnT and hs-cTnI increased over ten-fold in all rats subjected to ischemia. The increase of hs-cTnI and hs-cTnT after 30 minutes was similar, resulting in a hs-cTnI/hs-cTnT ratio around 1. The hs-cTnI/hs-cTnT ratio was also around 1 in blood samples collected at 120 minutes in rats subjected to 5 or 10 minutes of ischemia where no localized necrosis was observed. In contrast, the hs-cTnI/hs-cTnT ratio at 2 hours was 3.6-5.5 after longer ischemia that induced cardiac necrosis. The large hs-cTnI/hs-cTnT ratio was confirmed in patients with anterior STEMI. Conclusion Both hs-cTnI and hs-cTnT increased similarly after brief periods of ischemia that did not cause overt necrosis, whereas the hs-cTnI/hs-cTnT ratio tended to increase following longer ischemia that induced substantial necrosis. A low hs-cTnI/hs-cTnT ratio around 1 may signify non-necrotic cTn release.

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Introduction and Objectives Using existing transthoracic echocardiographic indices to quantify left ventricular wall motion abnormalities (WMAs) can be difficult due to the variations in the location of the abnormalities within the left ventricle, the quality of examinations, and the inter‐/intra‐observer variability of available indices. This study aimed to evaluate a new approach for measuring the extent of WMA by calculating the percentage of abnormal wall motion and comparing it to the wall motion score index (WMSI). The study also sought to assess inter‐ and intra‐observer variability. Methods The study included 140 echocardiograms from 54 patients presenting with ST‐elevation myocardial infarction or Takotsubo syndrome. All patients underwent an echocardiographic examination according to a standard protocol and the images were used to measure the extent of akinesia (proportion akinesia, PrA), akinesia and hypokinesia (proportion akinesia/hypokinesia, PrAH), and WMSI. The inter‐observer variability between the two operators was analyzed. The intra‐observer analysis was performed by one observer using the same images at least 1 month after the first measurement. The agreement was analyzed using the Pearson correlation coefficient and Bland‐Altman plots. Results Inter‐ and intra‐observer variability for PrA and PrAH were low and comparable to those for WMSI. Conclusion PrA and PrAH are reliable and reproducible echocardiographic methods for the evaluation of left ventricular wall motion.