Author + information
- Yüksel Çavuşoğlu1,
- Sule Korkmaz2,
- Selda Demirtaş2,
- Erkan Gencer3,
- Hatice Sasmaz4,
- Fezan Mutlu1 and
- Mehmet Birhan Yilmaz5
Ischemia-modified albumin (IMA) is a very sensitive biomarker of myocardial ischemia before necrosis. IMA has also been found to be elevated in the setting of oxidative stress, acidosis, hypoxia, inflammatory state and sodium and calcium pump disruptions which are also involved in the pathophysiologic process of heart failure (HF). However, data about IMA levels specifically in patients with HF are still lacking. Dobutamine (DOB) is known to increase myocardial contractility and oxygen consumption, and thereby may precipitate myocardial ischemia and myocyte damage. In contrast to DOB, levosimendan (LEVO) does not increase myocardial oxygen demand and therefore is thought to have cardio protective properties. So, we aimed to evaluate 1-) serum IMA concentrations in acute decompensated HF and 2-) the effects of DOB and LEVO treatments on IMA levels.
This prospective multicenter study was performed at the five independent sites. Fifty-nine patients admitted to participating centers with clinical signs and symptoms of NYHA III-IV acute decompensated HF and LVEF <35% were enrolled in this study. Blood samples for IMA measurements were obtained from all patients at baseline and 24 h after the initiation of HF therapy. 18 patients were treated with guidelines-recommended HF therapy with oxygen, diuretic, vasodilators (control group), 18 received an additional 24-h infusion of LEVO with a loading dose of 12 μg/kg over 10 min followed by a continuous infusion of 0.2 μg/kg/min (LEVO group) and 23 had DOB treatment with a continuous infusion of 10 μg/kg/min for 24-h in addition to optimal pharmacologic therapy (DOB group). A single serum specimen was also collected from 32 apparently healthy individuals. IMA concentrations were measured by albumin cobalt binding colorimetric assay and results were given as absorbance units (AU).
In patients with acute decompensated HF, mean serum concentration of IMA was found to be significantly higher than those of apparently healthy population (0.894±0.23 AU vs 0.379±0.08 AU, p<0.0001). Overall, IMA levels significantly decreased after 24-h of the initiation of appropriate HF therapy (0.894±0.23 AU and 0.832±0.18 AU, p <0.013). Furthermore, IMA levels were also found to significantly decrease in control group (1.041±0.28 vs 0.884±0.15 AU, p<0.041), in LEVO group (0.771±0.18 vs 0.728±0.18 AU, p<0.046) and also in DOB group (0.892±0.18 vs 0.820±0.13 AU, p<0.035).
This study suggested for the first time that patients with acute decompensated HF had elevated levels of IMA when compared to healthy controls and appropriate HF therapy significantly reduced serum IMA levels. The findings of this study also demonstrated that both DOB and LEVO treatments did not increase in IMA levels, suggesting lower potential in inducing myocardial ischemia when used in recommended doses.