Table 2.

Diagnostic and prognostic value of granules in ischemic heart disease

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	[46, 47]
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]

MPO myeloperoxidase, pro-MPO pro-myeloperoxidase, CK creatine kinase, cTn I troponin I, STEMI ST-segment elevation MI, ACS acute coronary syndromes, sTn I sensitive cardiac troponin I, MO microvascular obstruction, IS infarct size, AKI acute kidney injury, MMPs matrix metalloproteinases, ROS reactive oxygen species, MACE major adverse cardiovascular events