Abstract
Background: Whether the role of plasma heat shock protein 70 (HSP70) in acute myocardial infarction (AMI) is protective or detrimental remains debated, and the relationship between HSP70 and total occlusion remains elusive.Methods: A total of 112 patients with primary diagnosis of AMI and 52 patients with chronic coronary syndrome (CCS) were enrolled into the study. Plasma HSP70 level was determined by ELISA on day 1 and day 7 after the onset of AMI and was examined before angiography in patients with CCS. Peak NT-proBNP, high-sensitivity C-reactive protein (CRP), troponin T (cTnT), and left ventricular ejection fraction were measured.Results: Plasma HSP70 was significantly higher in CCS than AMI (P < 0.0001), and it showed a significant decrease from day 1 to day 7 after AMI (P < 0.01). Elevated HSP70 was associated with decreased levels of LDL-C (P < 0.05), peak cTnT (R = −0.3578, P < 0.0001), peak NT-proBNP (R = −0.3583, P < 0.0001), and peak CRP (R = −0.3539, P < 0.0001) and a lower diagnosis of AMI (R = −0.4016, P < 0.0001) and STEMI (R = −0.3675, P < 0.0001), but a higher diagnosis of total occlusion in target vessels (R = 0.1702, P < 0.05). HSP70 may provide certain predictive value for the diagnosis of AMI, STEMI, and total occlusion in target vessels, and the area under the receiver operating characteristic curves were 0.7660, 0.7152, and 0.5984, respectively. HSP70 was also negatively associated with in-hospital stay (P < 0.001) and positively correlated with left ventricular ejection fraction (LVEF) at 1-year follow-up (P < 0.05), despite no association with in-hospital major adverse cardiovascular events (MACE).Conclusion: Plasma HSP70 level was found to decrease from day 1 to day 7 post-AMI, but the overall level of patients with AMI was lower than that of patients with CCS. However, the ability of HSP70 to identify clinically significant AMI and STEMI was moderate, and the predictive value to total occlusion was slight.
Highlights
Heat shock proteins (HSPs) are known as molecular chaperones that function in protein folding [1], usually induced by hyperthermia, which may indicate other forms of cellular stress such as lipopolysaccharide, high blood pressure, infection [2], and ischemic injury [1]
It is demonstrated that the plasma levels of Heat shock protein 70 (HSP70), age, history of previous myocardial infarction (MI), administration of statins, total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), D-dimer, peak cardiac troponin T (cTnT) level, peak NT-proBNP, peak Creactive protein (CRP), and left ventricular ejection fraction (LVEF) were different among the four subgroups
Considering the pathologic disparity between acute occlusion and chronic occlusion, a detailed comparison was conducted among the three subgroups, MI1d, MI7d, and chronic coronary syndrome (CCS)-NCTO, and it was found that only plasma HSP70 (P = 0.0015), statin use (P = 0.0342), TC (P = 0.0013), LDL-C (P = 0.0004), D-dimer (P < 0.0001), p-cTnT (P < 0.0001), pNT-proBNP (P < 0.0001), p-CRP (P < 0.0001), and LVEF (P < 0.0001) were significantly different
Summary
Heat shock proteins (HSPs) are known as molecular chaperones that function in protein folding [1], usually induced by hyperthermia, which may indicate other forms of cellular stress such as lipopolysaccharide, high blood pressure, infection [2], and ischemic injury [1]. Despite the view that HSPs may act as damage-associated molecular patterns (DAMPs) during the ischemic damage to interact with pattern recognition receptors (PRRs) and induce a strong immune response in acute myocardial infarction (AMI), HSPs are not bona fide intracellular molecules that normally are not exposed to an extracellular environment [3], and they are detectable in normal circulation. In vivo studies found that overexpression of HSP72, which refers to HSP70, could improve functional recovery of hearts and decrease infarct size after myocardial ischemia and reperfusion (IR) [7]. Whether the role of plasma heat shock protein 70 (HSP70) in acute myocardial infarction (AMI) is protective or detrimental remains debated, and the relationship between HSP70 and total occlusion remains elusive
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