الفهرس 
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Abstract
HF is a complex progressive condition involving numerous pathways and pathological mechanisms either destroys the heart muscle, leading to loss of functioning cardiac myocytes, or disrupts the myocardium’s capability to contract and/or relax normally. Because of the diminished heart function, it cannot pump blood to the body at a rate commensurate with its needs, or can do so only at the cost of high filling pressures.
There are several compensatory mechanisms that occur as the failing heart attempts to maintain adequate function. These include increasing cardiac output, increasing ventricular volume and wall thickness through ventricular remodeling, and maintaining tissue perfusion with augmented mean arterial pressure through activation of neurohormonal systems.
Although initially beneficial, adaptive and compensatory in the early stages of HF, all of these compensatory mechanisms when sustained eventually lead to a vicious cycle of worsening HF.
There is no single diagnostic test serving as gold standard for HF, since it is largely a clinical diagnosis based upon a careful history, physical examination, laboratory and imaging data. Most patients with suspected HF don’t require invasive testing for diagnosis, so there a persistent need to construct studies shed the light on new noninvasive reliable tools for diagnosis of HF.
Circulatory biomarkers can fulfill the aforementioned needs, since HF involves numerous pathways and pathological mechanisms that can manifest as biomarkers in the blood and tracking blood levels of them can help clinicians to diagnose and predict future events.
Since the fibrosis and inflammation are the hallmark processes in HF, the current study was designed to measure the serum concentration of group of novel cardiac biomarkers related to cardiac fibrosis, and remodeling such as Galectin-3 (Gal-3) and Suppression of tumorigenicity-2 (ST2); beside markers related to inflammation including several interleukins such as IL-33, IL-18, IL-37 and IL 1-1ß in HF patients and patients belonging to different stages of cardiac disorders but without HF to eventually assess the effectiveness of certain cardiac biomarkers to diagnose HF.
The present study was carried out on blood samples from 120 individuals, 74 males and 46 females, with ages ranged from 40 – 75 years old. They are divided into four groups as follow:
group I (Normal control): Includes 20 clinically healthy subjects of both sexes (10 males &10 females) were aged from 44 -74 years old.
group II (HR group): Includes 50 patients with risk factors to develop MI of both sexes (22 females & 28 males), aged from (42-74) years old. They were defined as those with high risk for cardiovascular events, which include those with known coronary artery disease (CAD) diagnosed by coronary catheterization, positive stress or nuclear study, but no previous MI, age range should be (40-75) years old.
group III (MI group): Includes 25 patients exposed to MI of both sexes (6 females & 19 males), aged from (40-75) years old. They were patients with MI within first 72 hours, and proven by 2 of those 3 criteria which are: typical chest pain, ST elevation and elevated cardiac enzymes.
group IV (HF group): Include 25 patients having HF of both sexes (17 males & 8 females), aged from (42 -72) years old. The patients had a diagnosis of chronic HF of ischemic or nonischemic etiology for at least six months before the initiation of screening procedures, with NYHA functional class II or functional class III symptoms. They were with a history of coronary artery disease.
A volume of 5 ml of blood samples were collected from median cubital vein under aseptic precautions into tubes, allowed to clot for 30 minutes and centrifuged for 15 minutes at 1000 rpm. Serum was separated and assayed for the following: Gal-3, ST2, IL-33, IL-37, IL-18 and IL-1β using ELISA technique. hs-cTn, CK-MB, BNP, hs-CRP and lipid profile were assayed using Advia centaur XPT, ARCHITECT i1000SR, COBAS c 501 and Beckman Coulter AU680 analyzer respectively.
The results demonstrated that:
In HR group patients, IL-18, IL-37 and Gal-3 levels revealed significant elevation in about 50% of patients, while ST2, IL-33 and IL-1β showed normal results in all patients.
In MI group patients, both of IL-37 and IL-18 levels were elevated significantly in 52% of MI patients, while Gal-3 levels were raised in 36% of patient, and IL-33 was elevated in 20% of patients, whereas IL-1β levels were increased in only 8% of patients, regarding ST2 results, they showed normal results in all patients.
In HF group patients, serum Gal-3 showed significant elevation in all patients, while IL-37 results revealed an elevation in 52% of patients, ST2 was elevated in 32% of patients meanwhile serum IL-18 and IL-1β showed mild elevation in only 16% patients. IL-33 showed normal results in all HF group patients.