Differences between cardiac troponin I vs. T according to the duration of myocardial ischaemia

Abstract

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.

Ischemic preconditioning affects phosphosites and accentuates myocardial stunning while reducing infarction size in rats

“…Rats were anesthetized with an intraperitoneal injection of Ketamine (120 mg/kg) and Xylazine (5 mg/kg) (9,10). They were intubated endotracheally and ventilated with a small-animal ventilator (SAR-1000: CWE Inc, PA, USA).…”

“…The rationale behind conducting an acute experiment lies in the demonstrated optimal efficacy of TTC staining when employed shortly after the event, rather than an extended period thereafter (12). Myocardial infarction size was determined using Evans blue/TTC double staining as described in prior studies (9). Two hours after reperfusion, the LAD was re-ligated, and 5% Evans blue dye was injected via the lateral tail vein to label the nonischemic region.…”