Mechanism of Elevated Cardiac Troponin in Acute Ischemic Stroke
What is the coronary vessel status in acute ischemic stroke (AIS) patients with elevated cardiac troponin (cTn), compared to patients presenting with non-ST-elevation acute coronary syndrome (NSTE-ACS)?
TRELAS (TRoponin ELevation in Acute ischemic Stroke) was a prospective, observational study with blinded endpoint assessment of AIS patients presenting within 72 hours after symptom onset. AIS was defined as a sudden neurological deficit caused by cerebral ischemia, as confirmed by neuroimaging. Patients with elevated cTn levels (>50 ng/L) on presentation or during the following day underwent diagnostic coronary angiography within 72 hours. Patients with impaired kidney function (creatinine >1.20 mg/dl) were excluded. Twenty-nine AIS patients underwent conventional angiography and were compared to age- and gender-matched patients with NSTE-ACS. The primary outcome was the presence of a coronary culprit lesion on diagnostic coronary angiography.
Median cTn on presentation did not differ between patients with AIS or NSTE-ACS. Compared to patients with NSTE-ACS, AIS patients were less likely to have coronary culprit lesions (7/29 vs. 23/29, p < 0.001) or any obstructive coronary artery disease (15/29 vs. 25/29, p = 0.02). Angioplasty with stenting of the culprit lesion was performed in the same session in three AIS patients. In three other AIS patients, a staged intervention after neurological rehabilitation was recommended. In contrast, 20 patients with NSTE-ACS received immediate revascularization and three underwent coronary artery bypass graft surgery.
Despite similar baseline cTn levels, coronary culprit lesions are significantly less frequent in AIS patients compared to age- and gender-matched patients with NSTE-ACS.
This is an important study, albeit limited by a small sample size of 29 AIS patients compared to age- and gender-matched patients with NSTE-ACS, that helps clarify coronary vessel status in AIS patients with elevated cTn. Indeed, elevation of cTn in AIS is a common finding and often presents a dilemma. The majority of AIS patients with elevated cTn do not have coincident ACS and about 50% of patients do not have evidence of obstructive coronary artery disease. As the authors opine, ‘Clinical conditions provoking coronary demand ischemia (i.e., Type 2 MI) and non-coronary causes are more likely to be the source of cTn release in the majority of AIS patients.’
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