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العنوان
Heart fatty acid binding protein and CD40 ligand as well as its allelic polymorphism in patients with acute coronary syndrome /
المؤلف
El-Beyali, Yara Mohamed Mohamed Mostafa.
هيئة الاعداد
باحث / يارا محمد محمد مصطفى البيلي
مشرف / حمدي فؤاد علي ابراھيم
مشرف / عبير مصباح عبدالحميد
مشرف / احمد حسني العدوي
مشرف / نانسي محسوب سعيد احمد
مناقش / محمد على عطوة بركات
مناقش / اسامة سعد الشاعر
الموضوع
Coronary heart disease. Myocardial infarction. Cardiology. Cardiovascular Diseases - therapy. Heart - Diseases - Treatment.
تاريخ النشر
2022.
عدد الصفحات
online resource (201 pages) :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الطب
تاريخ الإجازة
1/1/2022
مكان الإجازة
جامعة المنصورة - كلية الطب - قسم الباثولوجيا الاكلينيكية
الفهرس
Only 14 pages are availabe for public view

from 201

from 201

Abstract

Acute coronary syndrome (ACS) refers to a group of conditions that include ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina. It is a type of coronary heart disease (CHD), which is responsible for one-third of total deaths in people older than 35. Some forms of CHD can be asymptomatic, but ACS is always symptomatic. It is thought that most acute coronary syndromes (ACS) are the result of luminal thrombosis, although not all are associated with occlusive diseases. There are three main causes of coronary thrombosis such as plaque rupture, erosion, and calcified nodule. Based on the autopsy studies, the majority of thrombosis occurs from plaque rupture (55–65%), followed by erosion (30–35%) and, least frequent, calcified nodule (2–7%). Early diagnosis of ACS is essential because of improvement in prognosis following timely interventions. Currently, the diagnosis of ACS is based on elevation of (high-sensitive) cardiac troponin I or T (cTnI or cTnT), in the context of clinical and ECG findings. Unfortunately, these biomarkers are not consistently elevated within the first hours after symptom onset, requiring repetitive measurements and hindering early diagnosis. cTns cannot be detected until 6 to 12 h after coronary occlusion, even high-sensitive Tn can only be detected until 3 h after MI. H-FABP is 20 times more specific to cardiac muscle than myoglobin it is found at 10-fold lower levels in skeletal muscle than heart muscle and the amounts in the kidney, liver and small intestine are even lower again.