The document discusses biomarkers for ischemic heart disease. It describes traditional and recent molecular biomarkers that can be detected through blood tests to diagnose conditions caused by reduced blood flow to the heart, such as myocardial infarction and angina. Some highlighted biomarkers mentioned include malondialdehyde low density lipoprotein, whole blood choline, ischemia modified albumin, and certain microRNAs. Genetic factors like single nucleotide polymorphisms that may influence the risk of ischemic heart disease are also discussed.

1. American Heart Association. (2004) Heart disease and stroke statistics – 2004 update. Dallas, Texas: American Heart Association
Antithrom- botic
Recent Molecular and traditional Diagnostic Biomarkers for
Ischemic Heart Disease
Abanoub Moawad; Ahmed Ibrahim; Ahmed Ramadan; Ahmed Ismael; Ahmed Salem; Ahmed Said; Ahmed Osma; Ahmed Fouad; Ahmed Fathi; Ahmed Magdi; Ahmed Fouad;
Ahmed Nagib; Ahmed Mahmoud; Ahmed Mukhtar; Ahmed Moatamed; Ahmed Mousa; Osama Kamel; Esraa Hassan
Ischemic heart disease (IHD) is a condition
which results from reduced blood supply to
the heart muscle. This usually involves
impairment of blood flow through the
coronary arteries, most commonly caused by
atherosclerotic narrowing, but occasionally
due to arterial spasm.(1)
1. Myocardial infarction .
2.Angina pectoris.
3. Chronic IHD with heart failure.
4.Sudden cardiac death.(3)
Causes
Bio markers
Genetics
Atherosclerosis may start when certain factors
damage the inner layers of the arteries. These factors in-
clude:
•Smoking
•High amounts of certain fats and cholesterol in the blood
•High blood pressure
•High amounts of sugar in the blood due to insulin
resistance or diabetes (2)
Syndromes
1.Malondialdehyde low density lipoprotein (MDA-lDl)
MDA is a candidate compound which causes oxidative modification of
LDL and not only serves as an oxidative stress marker but as a marker of
plaque destabilization.
i) Traditional
ii)Recent
2. Whole blood choline.
Whole blood (WBCHO) and plasma choline concentrations increase after
stimulation of phospholipase D and the activation of coronary plaque cell
surface receptors or ischemia. Phospholipase D activation in coronary
plaques causes stimulation of macrophage by oxidized LDL, secretion of
matrix metalloproteinase enzymes and activation of platelets..
3. Ischemia modified albumin (IMA)
Ischemia Modified Albumin generation:mainly start from hypoxia from anaerobic metabolism reduces ATP and
causes a [2]lower localized pH inducing acidosis. [3]Cu+2
ions are released from plasma proteins such as
caeruloplasmin. In the presence of ascorbic acid, [4]Cu+2
is converted to Cu+.
reacts with O2 to form [5]O2
•
dismutase
dismutates the O2 •–
to [6]H2O2, which in presence of Cu++
or Fe+
, undergoes the Fenton reaction forming [7]OH•
hydroxyl radicals. Free Cu++
is scavenged by [8]HSA, where it binds tightly to the N-terminus. OH •
radicals alter the
amino acid N-terminus of [9]HSA rendering it incapable of binding Cu++
. These two altered forms are known as
IMA. altereforms are known as IMA.
DNA polymorphism (5)
1) Rs2296545
 Present in Renalase gene which expressed to produce
renalase enzyme which decreases ambulatory blood pres-
sure and that prevent the development of cardiac hypertro-
phy, which present on position on chromosome (10).
C allele was found to be associated with down regulation of
renalase enzyme and lead to increase in BP and elevated
 circulated catecholamine so C allele may be predisposing
factor for IHD
2) RS 2241766
Present in adipopectin gene (ADIPQ) which expressed to ADIPQ protein act
as protective protein against IHD working by inhibiting binding LDL to
biglycan so decrease atherosclerosis plaque formation . Result from C to G
variant at position 11.377 in promoter region of gene lead to down regulation
of protein so it present a risk factor for IHD
Micro RNA (6)
MiR-1231
MiR-1231 was abnormally over expressed in human MI hearts, MiR-1231
suppresses CACNA2D2 gene (calcium channel gene) expression by target-
ing its mRNA. which exacerbates arrhythmia in myocardial infarcted heart.
References
1/American Heart Association. (2004) Heart disease and stroke statistics – 2004 update. Dallas, Texas: American Heart As-
sociation
2/Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for pre-
vention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324:71-86 as cited by BMJ Best Practice
(2009) ‘Non-ST-elevation myocardial infarction’ accessed at http://bestpractice.bmj.com/best-practice/monograph/151/
treatment/step-by-step.html November 2009
3/Baxter, P., Petch, M., (2000) ‘Cardiovascular Disorders’ in Cox, R. Edwards, F. Palmer, K. (Eds.) (2000) ‘Fitness for Work:
3rd Edition’ pp349-70 Oxford University Press, Oxford
4/Benowitz NL. (1992) ‘Cardiotoxicity in the workplace’ in Occupational Medicine 1992;7:465-78 as cited by British Heart
Foundation (2005) ‘Factfile – returning to work’ accessed at www.bhf.org October 2009
5/Best Practice ‘Unstable Angina’ accessed at http://bestpractice.bmj.com/best-practice/monograph/149/highlights.html No-
vember 2009
6/ BMJ Clinical Evidence (2009) ‘Angina (Chronic Stable) accessed at http://clinicalevidence.bmj.com/ceweb/conditions/
Under supervision
There are different proteins released in blood after heart
injury by different time intervals and used as traditional
biomarkers for MI as summarized in figure 2 (3)
(1)
Figure 1
Figure 2
(4)
FIGURE 3
(4)
Prof. Zeinab A. Hassan Dr. Heba T. Sharf Dr. Hanaa B .atya Dr. Doaa Abdel-mohsen