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Inotropic stimulation by dobutamine increases left ventricular regional function at the expense of metabolism in
C Indolfi1, F Piscione, P Perrone-Filardi
1Department of Medicine, Federico II University. Napoli, Italy.
Insights
Dobutamine enhances heart muscle contraction in patients with hibernating myocardium. However, this stimulation may paradoxically activate anaerobic glycolysis, suggesting a potential perfusion-contraction mismatch.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Myocardial Metabolism
Background:
- The precise mechanisms by which dobutamine improves contractility in chronically dysfunctional myocardium remain unclear.
- Investigating dobutamine's metabolic effects on hibernating myocardium is crucial for understanding its therapeutic potential.
Purpose of the Study:
- To evaluate regional myocardial metabolism at rest and during dobutamine infusion in patients with hibernating myocardium.
- To assess the impact of dobutamine on lactate and free fatty acid metabolism in dysfunctional heart muscle.
Main Methods:
- Prospective study of 11 patients with left anterior descending coronary artery stenosis and left ventricular dysfunction.
- Assessment of regional left ventricular function via 2D echocardiography and perfusion using thallium-201 SPECT.
- Measurement of lactate and free fatty acid (FFA) concentrations in great cardiac vein and aortic blood samples.
Main Results:
- Intracoronary dobutamine infusion improved regional left ventricular function.
- The arteriovenous lactate difference was negligible at rest and decreased significantly during dobutamine infusion (p < 0.05).
- Hibernating myocardium did not produce lactate at rest but showed evidence of anaerobic glycolysis activation upon dobutamine stimulation.
Conclusions:
- Hibernating myocardium exhibits altered metabolic activity during dobutamine-induced inotropic stimulation.
- Dobutamine may induce a perfusion-contraction mismatch, leading to anaerobic glycolysis activation in dysfunctional myocardial regions.
- Further research is needed to elucidate the full metabolic consequences of dobutamine in heart failure.
Abstract:
The mechanism by which dobutamine increases the contraction of chronically dysfunctional myocardium and its effects on metabolism are still unknown. The aim of this study was to assess regional myocardial metabolism at rest and during an intracoronary dobutamine infusion in patients with hibernating myocardium. Eleven asymptomatic patients with single proximal stenosis of the left anterior descending coronary artery and persistent left ventricular dysfunction at rest (undergoing percutaneous transluminal coronary angioplasty [PTCA]) were studied prospectively. Regional left ventricular function was assessed by two-dimensional (2D) echocardiography and regional perfusion by thallium-201 single-proton-emission computed tomography. Great cardiac vein and aortic blood samples were obtained for measurements of lactate and plasma free fatty acid (FFA) concentrations. Inotropic challenge, obtained by using intracoronary dobutamine infusion, increases regional left ventricular function. However, the arteriovenous AV lactate difference was 0.206 = 0.070 mmol/L at rest, and it decreased to 0.018 = 0.069 mmol/L (p < 0.05 vs baseline) and 0.066 = 0.068 mmol/L (p < 0.05 vs baseline) at 4 and 10 minutes of dobutamine infusion, respectively. Thus the hibernating myocardium does not produce lactate at rest. However, when regional contraction is stimulated, dobutamine-induced inotropic challenge may cause a perfusion-contraction mismatch with an activation of anaerobic glycolysis.