Abstract
Abstract Background Circulating levels of cardiac troponin I (cTnI) after STEMI were considered prognostic factors for predicting MACE. ΔcTnI is the difference between peak cTnI post-primary PCI and cTnIon initial admission. Purpose Study aimed to assess the relationship between ΔcTnI, the ratio of ΔcTnI to cTnI on initial admission and MACE during the follow-up period. Methods A total of 2596 patients with cTnI measured upon admission and one-time measurement of cTnI during hospitalization were enrolled. Results In the adjusted models of the survival ROC curve, ΔcTnI and the ratio of ΔcTnI to cTnI on initial admission have stronger discrimination power of MACE [AUC 0.730 and 0.717] compared with peak cTnI post-PPCI and cTnI at admission (AUC 0.590, 0.546). Multivariate Cox regression analysis identified ΔcTnI [HR 1.018, 95% CI 1.001 to 1.035] as a relevant factor for MACE during follow-up. On the K-M survival curves,the incidence of MACE, mortality and angina pectoris were significantly higher in the group with maximum ΔcTnI (p=0.035, 0.049, 0.026). Conclusion ΔcTnI level and the ratio have stronger discrimination power of MACE. The group with maximum ΔcTnI has higher incidence of MACE, mortality and angina pectoris during the follow-up period. Flow chart + survival ROC curve + K-M curve Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): This study was supported by the Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences
Highlights
Cardiac troponin I is a highly specific and sensitive biomarker of cardiac injury and a regulatory protein with cytosolic and structural compartments within the cardiac myocytes [1]. cTnI is a heart-specific protein released in the circulation upon myocardial injury and plays a significant role in the regulation of muscle contraction and cardiac troponins [2]
Conventional assay measurements of cTnI levels are routinely used to rule out acute myocardial infarction (AMI) and to assess the 30-day and 90-day prognoses of patients presenting with acute coronary syndrome (ACS) [3, 4]
The relationship of the cTnI level difference between the pre- and post-primary percutaneous coronary intervention (PPCI) is not well defined. To address this knowledge gap, this study aimed to explore the prognostic value of the cTnI level difference between PPCI peak cTnI and first admission cTnI to major adverse cardiovascular events (MACE) during follow-up in a contemporary, homogeneous, and well-defined cohort of patients with segment elevation myocardial infarction (STEMI) undergoing PPCI
Summary
Cardiac troponin I (cTnI) is a highly specific and sensitive biomarker of cardiac injury and a regulatory protein with cytosolic and structural compartments within the cardiac myocytes [1]. cTnI is a heart-specific protein released in the circulation upon myocardial injury and plays a significant role in the regulation of muscle contraction and cardiac troponins [2]. The relationship of the cTnI level difference between the pre- and post-primary percutaneous coronary intervention (PPCI) is not well defined To address this knowledge gap, this study aimed to explore the prognostic value of the cTnI level difference between PPCI peak cTnI and first admission cTnI to MACE during follow-up in a contemporary, homogeneous, and well-defined cohort of patients with STEMI undergoing PPCI. Circulating levels of cardiac troponin I (cTnI) after ST-segment elevation myocardial infarction (STEMI) were considered as prognostic factors for predicting the incidence of major adverse cardiovascular events (MACE). △cTnI is the difference between peak cTnI after primary percutaneous coronary intervention (PPCI) and cTnI on initial admission. Is study aimed to assess the relationship between △cTnI, the ratio of △cTnI to cTnI on initial admission, and the incidence of MACE during the follow-up period. Conclusion. e △cTnI level and the ratio of △cTnI have stronger discrimination power of predicting the incidence of MACE. e group with maximum △cTnI has higher incidence of MACE, mortality, and angina pectoris during the follow-up period
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