Patients or experimental models | Major results | References |
---|---|---|
MPO diagnostic value | ||
Chest pain patients | 1. MPO was a more efficient marker than CK-MB and cTn I within 0–6 h after the onset of AMI 2. A combination of MPO, CK-MB, and Tn I could discriminate 91% of the AMI patients as high as a specificity of 76% | [40] |
MI patients | MPO as a valid test detection of MI yielded a specificity of 0.85 | [41] |
AMI patients | 1. MPO levels increased in patients finally diagnosed with AMI even when Tn I exhibited a negative result at an early stage 2. MPO is more efficient than Tn I in AMI patients with a symptom onset of less than 2 h | [43] |
Chest pain patients | Patients with a negative test by a higher sTn I assay, the value of MPO was most notable | [44] |
Chest pain patients | 1. MPO was inferior to the highly sensitive TnI in predicting AMI at 3 h and 6 h after admission of patients with chest pain 2. Both of the sensitivity and specificity were lower 3. MPO failed to provide incremental information when added to sTNI | [45] |
MPO prognosis value | ||
ACS patients | MPO and Tn I were markedly associated with adverse cardiovascular events during hospitalization | [41] |
MI patients | Higher MPO prospectively forecasts the outcome of MACE | [42] |
ACS patients | MPO exhibited a strong prognosis value for MACE in serial sensitive cTnI negative patients | [44] |
ACS patients | MPO was a predictive marker of increased risk of adverse events and mortality at 30 days and 6-month | [45] |
AMI patients | Higher MPO predicted adverse cardiac outcome and lower ejection fraction | |
AMI patients | MPO is a risk factor for long-term mortality | [48] |
MI patients | MPO was an independent predictor of 6-month mortality and major adverse cardiac events | [49] |
STEMI patients | Plasma MPO levels are correlated with plaque erosion | [50] |
AMI patients | 1. A high MPO level associated with more severe MO and IS 2. Higher MPO in the culprit artery indicated an exacerbated cardiac remodeling and infarct area at 6 months | [51] |
ACS patients | 1. Plasma MPO was significantly higher in STEMI patients than in NSTE-ACS patients 2. MPO failed to predict the short-term or long-term outcomes | [52] |
Azurocidin diagnostic value | ||
STEMI patients | 1. Azurocidin levels were significantly upregulated 2. Azurocidin was closely associated with thrombolysis 3. Azurocidin might be necessary for patients with STEMI | [71] |
NGAL diagnostic value | ||
Post-MI patients | 1. Plasma NGAL levels in STEMI patients were higher than those in the stable angina pectoris patients and control subjects 2. Plasma NGAL showed a better ability in discriminating severe coronary disease than MMP-9, hs-CRP, and IL-1β | [85] |
MI patients | 1. Plasma NGAL levels were markedly higher in death patients with STEMI than survivors 2. Plasma NGAL levels were increased in patients with acute and chronic heart failure as a complication of MI | [86] |
NGAL prognosis value | ||
MI patients | Higher baseline NGAL and a more significant increase in serum NGAL level were correlated with lower 6-month LV ejection fraction recovery | [76] |
AMI patients | 1. Plasma NGAL level was significantly higher in death patients than in survived patients of AMI 2. Predict cardiovascular mortality in STEMI patients | [86] |
STEMI patients | 1. Plasm NGAL on day 12 could predict combined adverse outcomes 2. A marker of MI severity | [87] |
STEMI patients | Plasm NGAL level of more than 1.25 ng/mL on the 12th–14th day was associated with a higher risk of a combined endpoint of cardiovascular death or any cardiovascular complication | [88] |
ACS patients | NGAL concentration could predict long-term mortality | [89] |
STEMI patients | Plasm NGAL level above 2.6 ng/ml on day 12 after onsetting STEMI was related to a fourfold increase of all-cause mortality | [90] |
STEMI patients | STEMI patients in the higher NGAL group presented greater risk of MACEs and all-cause mortality | [91] |
Cathelicidin diagnostic value | ||
Patients or MI mice | 1. CRAMP was reduced from I/R mice and oxygen glucose treated cardiomyocytes 2. CRAMP was significantly reduced in MI patients | [97] |
I/R mice | CRAMP might be detrimental in ischemia-associated cardiovascular disease | [102] |
MMP8 prognosis value | ||
AMI patients | 1. MMP-8 and MMP9 have a significant positive correlation with malignant cardiac remodeling and left end-diastolic volume post-MI 2. MMP8 presented a significant association with adverse cardiovascular death or hospitalization | [104] |
AMI patients | The plasma MMP-8 level was still higher in MI patients during 20 ± 3 months follow-up | [108] |
MMP9 diagnostic value | ||
MI patients | The higher early level of MMP9 was associated with worsened left remodeling | [116] |
MI rats | 1. MMP-9 accumulated in the damaged rat myocardium after an ischemic injury | [117] |
MI mice | Transgenic overexpression of MMP-9 specifically in macrophages could significantly restrict extracellular matrix synthesis and attenuate MI-induced left ventricular function | [118] |
AMI patients | 1. MMP-9 serum activity is increased in AMI, but markedly suppressed in cardiogenic shock 2. Maintaining MMP-9 activity could be a therapeutic target to limit Receptor for advanced glycation end products-induced deleterious inflammation in cardiogenic shock | [119] |
STEMI patients | The MMP-9 expression might indicate the early clinical presentation in STMI patients | [120] |
STEMI patients | MMP-9 is considered a potential biomarker for the diagnosis of acute STEMI | [121] |
AMI patients | MMP-9 could discriminate AMI patients from healthy subjects with a mean area under the receiver operating characteristic (ROC) curves of 0.81 and with diagnostic cut-off points of 690.066 ng/mL | [123] |
AMI patients | The serum level of MMP-9 was associated with the risk of suffering AMI, and MMP-9 polymorphism and its level might be useful clinical biomarkers for predicting the outcome of AMI | [123] |
Arginase | ||
MI patients | 1. Arginase concentrations be significantly up-regulated in MI patients 2. The increased arginase in MI patients was markedly negatively associated with left ventricular ejection fraction | [136] |