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Prognosis of Troponin-Positive Patients with Non-Obstructive Coronary Artery Disease
Nancy Z K Wassef1, Javed Ehtisham2, Neeta Petal3
1Cardiology Department, New Cross Hospital, Wolverhampton, UK. nancy.wassef@gmail.com.
Insights
Troponin elevation in patients with non-obstructive coronary artery disease (CAD) and an identified cause carries a similar mortality risk as obstructive CAD. Unidentified causes in non-obstructive CAD patients present a low-risk profile.
Area of Science:
- Cardiology
- Internal Medicine
- Clinical Research
Background:
- Troponin elevation is a known mortality risk factor.
- Prognosis for patients with troponin elevation and non-obstructive coronary artery disease (CAD) is not well-defined.
- Emerging data suggest increased mortality risk in this population.
Purpose of the Study:
- To investigate the outcomes of troponin-positive patients with both obstructive and non-obstructive CAD.
- To compare mortality and major adverse cardiac and cerebrovascular event (MACCE) rates between these groups.
Main Methods:
- Retrospective cohort analysis of 1,351 troponin-positive patients.
- Stratification into obstructive CAD (O-CAD) and non-obstructive CAD (NO-CAD) groups based on angiogram results (≤50% stenosis).
- Sub-analysis of O-CAD by management strategy and NO-CAD by identified (NO-CAD-I) or unidentified (NO-CAD-U) cause of troponin elevation.
Main Results:
- Non-obstructive CAD group showed a higher prevalence of hypertension and severe renal impairment.
- NO-CAD-U patients had a 1-year MACCE rate of 0%.
- NO-CAD-I patients exhibited similar 30-day and 1-year MACCE and mortality rates compared to O-CAD patients, with higher rates than the emergency re-vascularized subgroup, driven by non-cardiac deaths.
Conclusions:
- Patients with identified causes for troponin elevation and non-obstructive CAD face risks equivalent to those with obstructive CAD.
- This finding highlights the importance of identifying the cause of troponin elevation in non-obstructive CAD.
- Risk stratification and management should consider non-cardiac causes of death in NO-CAD-I patients.
Introduction:
Troponin elevation is an independent risk factor for mortality, but the prognosis of patients with troponin elevation and non-obstructive coronary artery disease (CAD) is unknown. Recent data have suggested an increased risk of mortality. This study was performed to further investigate the outcomes of troponin-positive patients with obstructive and non-obstructive CAD.
Methods:
A retrospective cohort analysis was performed of all patients with raised troponin presenting to Kettering General Hospital (January 2010 to December 2011, n = 1,351). The patients who had angiograms were stratified anatomically into obstructive CAD and non-obstructive CAD (≤50% stenosis). The obstructive CAD group (O-CAD) was sub-analyzed by management strategy: emergency re-vascularization (<12 h), urgent, delayed, and medically managed. Patients with non-obstructive CAD were grouped by the cause of the raised troponin if this could be identified (NO-CAD-I) or cause remained unidentified (NO-CAD-U). The major adverse cardiac and cerebrovascular event (MACCE) and mortality rates were calculated at 30 days and 1-year follow-up.
Results:
There was a preponderance of hypertension and severe renal impairment in the non-obstructive CAD group. The patients with NO-CAD-U were a low-risk group (MACCE at 1-year follow-up = 0). The remaining NO-CAD-I group had a similar risk to the O-CAD group for MACCE and mortality at 30 days and 1-year follow-up. In fact, at 1-year follow-up, the NO-CAD-I patients when compared with the subgroups of O-CAD, had higher MACCE rates and mortality compared with the emergency re-vascularized group [MACCE: relative risk (RR) (95% CI) = 2.27 (1.29-3.40), P = 0.0047; mortality: RR (95% CI) = 2.08 (1.10-3.93), P = 0.024]. This was driven by higher risk non-cardiac death [RR (95% CI) = 4.10 (1.53-10.99), P = 0.005].
Conclusion:
Patients with identified cause for raised troponin and non-obstructive CAD are at equivalent risk of MACCE and mortality at 30 days and 1-year follow-up compared to those with obstructive CAD.
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