Abstract
Introduction:
The role of high sensitivity troponin (HsTn) is clear in patients with acute coronary syndrome (ACS), however, its role in non-ACS positive HsTn is not. Accordingly, we studied the heterogeneity of outcomes as related to cardiac and non-cardiac causes of positive HsTn.
Methods and Results:
Retrospectively, 288 consecutive patients [60±17 years, 143 (49%) females, EF:59±14%] who had HsTn measured to exclude ACS were included and followed for a median of 4.9 months. Compared to negative HsTn, patients with positive HsTn were older (64±15 vs 57±16 year), with worse EF (55±16 vs 65±8%), left atrial volume index (43±15 vs 26±11 ml/m
2
, all p<0.001), E/e’ ratio (11.6±5.5 vs 9.4±2.7, p=0.002) Tricuspid regurgitation velocity (TRV, 2.8±0.5 vs 2.6±0.4, p=0.015). and pro-BNP (4625±12657 vs 166±228 pg/ml, p=0.003). Survival curves (figure 1) showed that composite of mortality and rehospitalization were not different between both groups at follow-up (p=0.789). Patients with positive HsTn were classified according to the cause of HsTn rise non-cardiac, cardiac non-coronary, coronary non-ACS, and ACS, figure 1). Admission and follow-up HsTn were highest in the non-cardiac group and comparable to the ACS group. Furthermore, the worst EF and diastolic dysfunction were found in ACS and cardiac non-coronary groups, while. Survival curves suggested that the composite outcomes were worst in non-cardiac and cardiac non coronary groups, best in coronary non-ACS group and intermediate in the ACS groups (p=0.05).
Conclusion:
Stratifying causes of HsTn elevation differentiated phenotypes of cardiac function and risk. Patients with non-cardiac or cardiac non-coronary causes had worse outcomes than ACS, while patients with non-ACS coronary causes approach the negative HsTn in terms of outcomes which may explain the lack of significant difference in composite outcomes between positive and negative admission HsTn.