Abstract
To analyze lipid profile in patients with ACS, and to study the pattern of the involvement and complication in ACS. Hundred and eight consecutive cases of ACS, attending the CCU of Tribhuvan University Teaching Hospital fulfilling the criteria, were taken for the present study. Patient from age 30 and older were studied. All cases were scrutinized to detail serial 12 lead EKG, serial cardiac biochemical markers, laboratory test, echocardiographic study. Design of the study was carried out in prospective, cross sectional study. Hyperlipidemia was present in 61% of the patients. Only 27% of them were on statins. Most of them had high cholesterol level 68%, high Tgl level 75%, Ldl 50%, where as <40 Hdl (93%) patient were found to be low. 40% was found to have UAP. In addition patient with hypertension (76%) diabetes (65%) also had comorbidity for obesity 35%, and lipid abnormalities 75% for triglycerides, 66% for TC, 50% for LDL-C, 93% for low HDL-C, and a family history of CAD in 57%. The outcome of this study showed that the majority are male, relatively younger as compared to Western population. USA and STEMI were the dominant types of ACS. Strong correlations between TC, LDL-C, and low HDL-C in patient with ACS were noted. Majority of patients had hypertension, IHD in their families and Hyperlipidemia diabetes, smoking as the major risk factors. Better control of risk factors and the awareness of preventive strategies are needed.
Highlights
To analyze lipid profile in patients with ACS, and to study the pattern of the involvement and complication in ACS
Developing and implementing effective population-based intervention strategies focusing on diabetes are warranted to lower the CHD risk for patient with
This research shows that patients who developed chest pain due to cardiac event as confirmed by positive Troponin test had lipid parameters in the risk levels as suggested by ATP III
Summary
To analyze lipid profile in patients with ACS, and to study the pattern of the involvement and complication in ACS. Atherosclerosis is a chronic, multifocal immuno inflammatory; fibroproliferative disease of mediumsized and large arteries mainly driven by lipid accumulation.[1] The fundamental etiologic mechanism shared by all the forms of ACS is an imbalance between myocardial oxygen supply and demand. The most common cause of ACS is thrombus formation over a preexisting atherosclerotic plaque that has undergone disruption or erosion. Plaques vulnerable to disruption and thrombosis formation commonly have a large lipid core with elevated tissue factor content, a thin fibrous cap, and enhanced inflammatory activity within the plaque. When endothelial erosion of a plaque occurs, the subendothelial connective tissue is exposed, allowing platelets to adhere and eventual thrombus to form at the plaque surface.[2] Alternatively, during plaque disruption, the fibrous cap tears or fissures to expose t_h_e__hi_g_h_ly__th_r_om__b_og_e_n_ic__li_p_id__c_or_e__to__a_rt_e_ri_al__bl_o_o_d, Correspondence: Dr Bikash Dali, Department of Internal
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
