SHA 101. Peak CRP levels are higher in patients with ST elevation than non-ST elevation acute coronary syndrome

Value of pentraxin-3 and galectin-3 in acute coronary syndrome: a short-term prospective cohort study

“…CRP and pentraxin-3 belong to the same family of proteins. An earlier study found that CRP was markedly elevated in STEMI patients compared with NSTEMI patients [Habib et al 2011] It was also observed that LVEF, diabetic and hypertension status significantly differed between the two groups divided based on pentraxin-3 levels. A greater percentage of patients with higher levels of pentraxin were found to be hypertensive, diabetic and having a lower LVEF.…”

Increased Levels of Inflammatory Marker hsCRP, MDA and Lipid Profile in Non-obese Hypertension Subjects

“…Currently, anti-inflammatory drugs (methotrexate and IL-1b inhibitorcanakinumab), which do not affect CRP or LDL cholesterol concentration, are being investigated. And if they proved to be effective, it would support the theory that atherosclerosis has an inflammatory Origin [20]. Thus a practical definition ohypertension is 'the level of BP at which the benefits of treatment towards the significance of the costs anhazards' [21] Oxidative stress because of excessive production of ROS outstripping antioxidant defense mechanism has been implicated in many pathophysiological conditions that affect the cardiovascular system, such as hypercholesterolemia, diabetes, and hypertension [22,23].…”

Serum Low Density Lipoprotein and Serum High Sensitive C - Reactive Protein as a Diagnostic Markers for Acute Coronary Syndrome

“…CRP levels are higher in patients with STEMI than those with NSTEMI with further and significant decrease of CRP in patients with UAP when compared to STEMI and NSTEMI [21] , [22] . Therefore, the observed variation in CRP concentrations among the types of ACS might be at least partially attributed to the differences in the area of the infracted myocardium [23] . This can be explained by CRP which has been found in atherosclerotic lesions and binds to LDL then taken up by macrophages without the need for modification of it [24] and promote inflammation by disrupt thromboregulation via suppresses prostacyclin synthase expression while potentially augmenting thromboxane A2 bioactivity which present in atherosclerotic lesions then elicits platelet aggregation and smooth muscle contraction that are prone to plaque rupture and thrombosis and development of ACS [14], [25] .…”