심장 특이 단백질, 트로포닌, What is troponin

트로포닌 I와 트로포닌 T는 액틴과 마이오신의 calcium-mediated interaction을 조절하는 cardiac regulatory proteins입니다. 이 단백질들은 특정 유전자의 생성물이어서 심장에 특이적입니다. 트로포닌 I의 연구에서 신생아 발달 어느 단계에서도 심장 이외의 부위에서 cTnI를 발견하지 못했습니다. 반대로 cTnT는 골격근에서 소량 표현됩니다. 이것은 일부 환자에서 골격근이 증가된 cTnT의 원인이 될 수 있음을 나타냅니다. 만일 같은 환자에서 cTnI 수치가 정상임에도 cTnT가 증가되어 있다면 원인으로서 chronic skeletal muscle disease가 의심되어야 합니다.

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대부분 임상에서 트로포닌 T와 I는 동등한 유용성을 갖지만 트로포닌 I보다 T가 더 상승되는 신부전 환자는 예외입니다. 높은 민감도 검사를 할 때, 투석 환자의 거의 100 %는 증가된 트로포닌 T를 갖습니다. 트로포닌 I는 비율이 더 낮습니다.

WHAT IS TROPONIN ​ Cardiac troponin I (cTnI) and T (cTnT) are cardiac regulatory proteins that control the calcium-mediated interaction of actin and myosin. Both have early releasable and structural pools, with most troponin being present in the structural pool.   These proteins are products of specific genes and therefore have the potential to be unique to the heart (ie, specific cardiac isoforms). Studies performed with cTnI have failed to find any cTnI outside of the heart at any stage of neonatal development. In contrast, cTnT is expressed to a minor extent in skeletal muscle. Data indicate that there are at least some patients with chronic skeletal muscle disease who have proteins that are detected by the antibodies in the cTnT and high sensitivity cTnT assay. This implies that skeletal muscle can, in some patients, be the source for elevations of cTnT detected in the blood. Data suggest this may be more common than was originally thought. In most (but not all) of these patients, the typical rise and fall of cTnT with myocardial infarction is not seen. In addition, chronic skeletal muscle disease should be suspected as a cause for the cTnT increase if a cTnI measurement for the same patient is within the normal range. For most clinical purposes, it appears that cTnT and cTnI have equal utility except in patients with renal failure where there are more elevations of cTnT than of cTnI. With high sensitivity assays, almost 100 percent of dialysis patients will have an increased cTnT; a lesser percentage will have increases in cTnI. Such increases are associated with an adverse clinical prognosis.

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증가된 cTnI가 CVD outcome과 좀 더 강한 관련성이 있고, 반면 cTnT는 non-CVD death 위험과 더 강한 관련성이 있음을 나타내는 연구도 있었습니다.

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Abstract Background: There is great interest in widening the use of high-sensitivity cardiac troponins for population cardiovascular disease (CVD) and heart failure screening. However, it is not clear whether cardiac troponin T (cTnT) and troponin I (cTnI) are equivalent measures of risk in this setting. We aimed to compare and contrast (1) the association of cTnT and cTnI with CVD and non-CVD outcomes, and (2) their determinants in a genome-wide association study. ​ Methods: High-sensitivity cTnT and cTnI were measured in serum from 19 501 individuals in Generation Scotland Scottish Family Health Study. Median follow-up was 7.8 years (quartile 1 to quartile 3, 7.1–9.2). Associations of each troponin with a composite CVD outcome (1177 events), CVD death (n=266), non-CVD death (n=374), and heart failure (n=216) were determined by using Cox models. A genome-wide association study was conducted using a standard approach developed for the cohort. ​ Results: Both cTnI and cTnT were strongly associated with CVD risk in unadjusted models. After adjusting for classical risk factors, the hazard ratio for a 1 SD increase in log transformed troponin was 1.24 (95% CI, 1.17–1.32) and 1.11 (1.04–1.19) for cTnI and cTnT, respectively; ratio of hazard ratios 1.12 (1.04–1.21). cTnI, but not cTnT, was associated with myocardial infarction and coronary heart disease. Both cTnI and cTnT had strong associations with CVD death and heart failure. By contrast, cTnT, but not cTnI, was associated with non-CVD death; ratio of hazard ratios 0.77 (0.67–0.88). We identified 5 loci (53 individual single-nucleotide polymorphisms) that had genome-wide significant associations with cTnI, and a different set of 4 loci (4 single-nucleotide polymorphisms) for cTnT. ​ Conclusions: The upstream genetic causes of low-grade elevations in cTnI and cTnT appear distinct, and their associations with outcomes also differ. Elevations in cTnI are more strongly associated with some CVD outcomes, whereas cTnT is more strongly associated with the risk of non-CVD death. These findings help inform the selection of an optimal troponin assay for future clinical care and research in this setting.

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cTnT보다는 cTnI가 더 심장 특이적이다.

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Ref. UpToDate 2020.09.09