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Peripheral plasma adenosine release in patients with chronic heart failure
F Franceschi1, J-C Deharo, R Giorgi
1Department of Cardiology, CHU Timone, Marseille, France.
Insights
In chronic heart failure (CHF), adenosine release occurs peripherally, not from the myocardium. Peripheral adenosine plasma levels (APLs) correlate with tissue ischemia markers like ischaemia-modified albumin (IMA).
Area of Science:
- Cardiovascular Physiology
- Biochemistry of Heart Failure
Background:
- Chronic heart failure (CHF) is associated with elevated adenosine plasma levels (APLs).
- The specific origin of adenosine release in CHF—peripheral versus myocardial—remains unclear.
Purpose of the Study:
- To determine if adenosine release in CHF patients originates from the periphery or the myocardium.
- To investigate correlations between APLs, ischaemia-modified albumin (IMA), and brain natriutretic peptide (BNP).
Main Methods:
- Prospective study including 26 patients with CHF undergoing resynchronization.
- Simultaneous blood sampling for APLs from the brachial vein (peripheral) and coronary sinus (myocardial).
- Measurement of IMA and BNP from peripheral blood samples.
Main Results:
- Peripheral APLs were significantly higher than coronary sinus APLs (1.69 vs 0.75 μM, p<0.01).
- Peripheral APLs showed significant correlations with IMA (r=0.59, p<0.01) and BNP (r=0.73, p<0.001).
- BNP correlated with IMA (r=0.71, p<0.001) but not with myocardial APLs (r=0.38, p>0.05).
Conclusions:
- Adenosine release in CHF patients primarily occurs at the peripheral level.
- The myocardium is not the main source of adenosine release in this context.
- Peripheral APLs are linked to markers of tissue ischemia and cardiac strain in CHF.
Objective:
Chronic heart failure (CHF) is accompanied by increased adenosine plasma levels (APLs). It is unknown whether adenosine release occurs at the peripheral level or whether the myocardium itself is the source of adenosine release. To answer this question, we evaluated APLs in the coronary sinus of CHF patients during a resynchronisation procedure and compared the values with those at the peripheral level. We also investigated a possible correlation between APLs and ischaemia-modified albumin (IMA) levels, a useful marker of tissue ischaemia.
Methods:
19 men and seven women were prospectively included. Blood samples for APLs were collected simultaneously from a brachial vein (peripheral) and from the coronary sinus. Blood samples for brain natriutretic peptide (BNP) and IMA were collected from a brachial vein.
Results:
APLs from the brachial vein were higher than those from the coronary sinus (1.69 vs 0.75 muM p<0.01). IMA levels were correlated with APLs from the brachial vein (r = 0.59, p<0.01). BNP concentrations were correlated with APLs from the brachial vein (r = 0.73, p<0.001) but not with APLs from the coronary sinus (r = 0.38, p>0.05). BNP concentrations and IMA levels were correlated (r = 0.71, p<0.001).
Conclusions:
In CHF patients, adenosine release occurs at a peripheral level and not at the myocardium level.
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