Abstract
Adipose tissue-derived serine protease inhibitor (vaspin), which has endocrine and local roles in atherosclerosis growth, is also synthesized by adipose tissue; it was found that vaspin was negatively correlated with blood pressure in obese patients, while vaspin levels were decreased in endothelial dysfunction. The aim of the present study was to determine rosuvastatin modulation effects on serum vaspin levels in acute coronary syndrome (ACS) with class I obesity. A total number of seventy patients with acute coronary syndrome previously and currently treated with rosuvastatin was compared to 40 patients with IHD not treated by rosuvastatin as a control. Vaspin serum levels were higher in rosuvastatin-treated patients with acute coronary syndrome compared to the patients with acute coronary syndrome not treated by rosuvastatin, p < 0.01. Additionally, in the rosuvastatin-treated group, patients with STEMI showed higher vaspin serum levels compared to NSTEMI p < 0.01. Conclusion: Rosuvastatin significantly increases vaspin serum levels in acute coronary syndrome.
Highlights
Acute coronary syndrome (ACS) is a cluster of pathological conditions due to a reduction in coronary blood flow caused by coronary thrombosis and/or atherosclerosis, leading to myocardial ischemia and necrosis [1]
Acute coronary syndrome includes ST-elevation myocardial infarction (STEMI) 30%, non-ST elevation myocardial infarction (NSTEMI) 25%, and unstable angina 38%; these are classified according to electrocardiographic changes in ST-segment [2]
Acute myocardial infarction (MI) is known as myocardial cell death because of prolonged myocardial ischemia, STEMI occurs when the coronary artery thrombus is initiated rapidly at coronary vascular wall injury, which can be triggered by many factors, including hypertension, cigarette smoking and dyslipidemia [4]
Summary
Acute coronary syndrome (ACS) is a cluster of pathological conditions due to a reduction in coronary blood flow caused by coronary thrombosis and/or atherosclerosis, leading to myocardial ischemia and necrosis [1]. Acute coronary syndrome includes ST-elevation myocardial infarction (STEMI) 30%, non-ST elevation myocardial infarction (NSTEMI) 25%, and unstable angina 38%; these are classified according to electrocardiographic changes in ST-segment [2]. Acute myocardial infarction (MI) is known as myocardial cell death (necrosis) because of prolonged myocardial ischemia, STEMI occurs when the coronary artery thrombus is initiated rapidly at coronary vascular wall injury, which can be triggered by many factors, including hypertension, cigarette smoking and dyslipidemia [4]. MI patients usually have numerous vulnerable plaques at risk of disruption and rupture, so platelet aggregation in acute coronary syndromes (ACS) leads to unstable plaque [5]. The damage to the full thickness of the heart muscle is an indicator of increased damage percentage, while the partial thickness of the heart muscle damage is called NSTEMI [6]
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