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Ischaemia-modified albumin in dilated cardiomyopathy
Eftihia Sbarouni1, Panagiota Georgiadou, Maria Koutelou
12nd Department of Cardiology, Onassis Cardiac Surgery Center, Athens 176 74, Greece. esbarouni@yahoo.gr
Insights
Ischaemia-modified albumin (IMA) levels do not differ in stable dilated cardiomyopathy (DCM) patients compared to healthy individuals. However, IMA levels vary with heart failure severity in DCM patients.
Area of Science:
- Cardiology
- Biomarker Research
- Heart Failure Studies
Background:
- Myocardial necrosis biomarkers can elevate in chronic heart failure.
- Investigating ischaemia-modified albumin (IMA) in compensated heart failure due to dilated cardiomyopathy (DCM).
Purpose of the Study:
- To determine if IMA levels are elevated in patients with compensated heart failure from DCM.
- To assess the relationship between IMA and disease severity in DCM.
Main Methods:
- Studied 42 DCM patients and 42 age-matched healthy volunteers.
- Assessed serum IMA levels using the albumin cobalt binding test.
Main Results:
- No significant difference in IMA levels between DCM patients and controls (P = 0.11).
- IMA levels significantly differed by New York Heart Association classification (P = 0.003).
- IMA showed a negative correlation with left ventricular ejection fraction (r = -0.40, P = 0.014).
Conclusions:
- IMA does not differ in clinically stable DCM patients versus controls.
- IMA levels significantly correlate with the severity of DCM and heart failure.
Background:
Biomarkers of myocardial necrosis may be increased in patients with chronic heart failure. We investigated whether ischaemia-modified albumin (IMA), a marker of ischaemia, is also elevated in patients with compensated heart failure, due to dilated cardiomyopathy (DCM).
Methods:
We studied 42 patients with DCM and an equal number of age-matched normal volunteers. We assessed IMA serum levels with the albumin cobalt binding test.
Results:
IMA was 89.9 +/- 13.1 (71-117) KU/L in the patient group and 93.9 +/- 9.9 (76-122) KU/L in the control group, with no significant difference between the two (P = 0.11). However, IMA differed significantly according to the New York Heart Association classification (P = 0.003) and was negatively correlated with the left ventricular ejection fraction (r = -0.40, P = 0.014).
Conclusions:
We conclude that IMA, a marker of ischaemia, does not differ in patients with clinically stable DCM compared with normal subjects, but varies significantly in relation to the severity of the disease.
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