Key result
Lnc-MALAT1 levels were significantly higher in AMI patients compared to controls (median 2.245 vs. 0.996, p=0.004) and high levels were associated with an elevated MACE accumulation rate (p=0.035).
Why the study?
Long noncoding RNA MALAT1 modulates atherosclerosis, myocardial ischemia, and inflammation, but its relationship to AMI risk, clinical features, cytokines, and prognostication remained to be explored.
Does circulating lnc-MALAT1 correlate with disease risk, inflammation, and MACE in patients with acute myocardial infarction?
Case-Control (n=210)
Yes
Does circulating lnc-MALAT1 correlate with disease risk, inflammation, and MACE in patients with acute myocardial infarction?
Absolute Event Rate: 2.245% vs 0.996%
p-value: p=0.004
Circulating lnc-MALAT1 is a potential biomarker for diagnosing acute myocardial infarction and predicting infarct size, systemic inflammation, and subsequent MACE risk.
May support lnc-MALAT1 evaluation as AMI biomarker; leaves open incremental MACE value pending validation.
OBJECTIVE: Long noncoding RNA MALAT1 (lnc-MALAT1) modulates atherosclerotic progression, myocardial ischemia injury, and systematic inflammation, which may be closely involved in acute myocardial infarction (AMI) pathogenesis. Thus, the current study intended to explore the relationship of lnc-MALAT1 to disease risk, features, cytokines, and prognostication in AMI patients. METHODS: This multicenter study consecutively enrolled 160 newly diagnosed AMI patients and 50 controls (angina pectoris patients). Their peripheral blood mononuclear cells were obtained to measure lnc-MALAT1 by RT-qPCR. Serum cytokines in AMI patients were detected by ELISA. In addition, AMI patients were followed up for major adverse cardiovascular event (MACE) risk evaluation. RESULTS: Lnc-MALAT1 was higher in AMI patients than in controls (median: 2.245 vs. 0.996, p = 0.004), and it also presented a good capacity for differentiating AMI patients from controls with an area under the curve of 0.823. Lnc-MALAT1 was positively related to C-reactive protein (p = 0.005), low-density lipoprotein cholesterol (p = 0.022), cardiac troponin I (p = 0.021), and infarct size (p = 0.007), but not other biochemical indexes in AMI patients. Meanwhile, lnc-MALAT1 was positively associated with tumor necrosis factor-alpha (p = 0.001), interleukin (IL)-6 (p = 0.031), IL-17A (p = 0.042), vascular cell adhesion molecule-1 (p = 0.004), and intercellular adhesion molecule-1 (p = 0.021) among AMI patients. Importantly, after categorization, lnc-MALAT1 high (vs. low) was related to an elevated MACE accumulation rate (p = 0.035); furthermore, a higher lnc-MALAT1 quartile showed a trend to be linked with an increased MACE accumulation rate (p = 0.092). CONCLUSION: Lnc-MALAT1 may serve as a biomarker for AMI risk, infarct size, inflammation and prognosis, but further validation by large-scale studies is needed.
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Li et al. (2022) conducted a case-control in Acute myocardial infarction (n=210). lnc-MALAT1 vs. Controls (angina pectoris patients) was evaluated on lnc-MALAT1 level (p=0.004). Lnc-MALAT1 levels were significantly higher in AMI patients compared to controls (median 2.245 vs. 0.996, p=0.004) and high levels were associated with an elevated MACE accumulation rate (p=0.035).
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