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Alteration in energetics in patients with left ventricular dysfunction after myocardial infarction: increased oxygen
Y Hayashi1, M Takeuchi, H Takaoka
11st Department of Internal Medicine, Kobe University School of Medicine, Japan.
Insights
Patients with severe left ventricular dysfunction after heart attack have increased oxygen costs for heart contractility. This suggests issues with excitation-contraction coupling, not energy conversion efficiency.
Area of Science:
- Cardiology
- Physiology
- Biomedical Engineering
Background:
- Inotropic agents improve hemodynamics in heart failure but not long-term survival.
- Myocardial infarction alters cardiac energetics, yet mechanoenergetics in left ventricular (LV) dysfunction remain unclear.
Purpose of the Study:
- To compare the oxygen cost of contractility in patients with varying degrees of LV dysfunction.
- To investigate the relationship between oxygen consumption (Vo2) and pressure-volume area (PVA) in different LV dysfunction groups.
Main Methods:
- Assessed Emax, Vo2, and PVA using conductance and Webster catheters in 30 coronary artery disease patients.
- Patients were categorized into three groups based on LV ejection fraction (EF): normal (>=60%), mild (40-60%), and severe (<40%).
- Dobutamine infusion was used to assess responses under varying contractility conditions.
Main Results:
- The Vo2-PVA relationship was linear in all groups, with comparable contractile efficiency.
- The oxygen cost of contractility was significantly higher in the severe LV dysfunction group (0.022 mL O2/mL/mm Hg/beat) compared to mild (0.0012) and normal (0.005) groups.
- This indicates an elevated energy demand for maintaining contractility in severe dysfunction.
Conclusions:
- Altered cardiac mechanoenergetics in severe LV dysfunction may stem from increased oxygen cost of excitation-contraction coupling.
- Reduced efficiency of chemomechanical energy transduction is less likely the primary cause.
- Findings highlight potential targets for improving cardiac energy metabolism in heart failure.
Background:
Although the use of inotropic agents to treat congestive heart failure (CHF) in patients with coronary artery disease has yielded short-term hemodynamic improvement, long-term mortality has shown less improvement. The loss of cardiac muscle as a result of infarction not only decreases the pumping ability of the heart but also leads to some dramatic changes in myocardial energetics. However, little is known about the mechanoenergetics of the heart in patients with left ventricular (LV) dysfunction after myocardial infarction.
Methods And Results:
The present study was designed to compare by means of the Vo2-pressure-volume area relation (PVA, a measure of total mechanical energy) and Emax (LV contractility index), the incremental oxygen cost of contractility measured as nonmechanical energy per unit increment in contractility in patients with various kinds of LV dysfunction. We assessed Emax, Vo2, and PVA using conductance and Webster catheters under control conditions and during different rates of dobutamine infusion (3 and 6 micrograms x kg-1 x min-1) in 30 patients with coronary artery disease. Patients were divided into three groups according to LV ejection fraction (EF): 10 without LV dysfunction (EF>/= 60%), 10 with mild LV dysfunction (40% = EF < 60%), and 10 with severe LV dysfunction (EF < 40%). Under control conditions, the Vo2-PVA relation was linear in each group. Contractile efficiency, the reciprocal of the slope of this relation, was comparable among the three groups. The oxygen cost of contractility in the severe LV dysfunction group was significantly greater than in the groups without and with mild LV dysfunction (0.022 +/- 0.014 versus 0.005 +/- 0.002 and 0.0012 +/- 0.005 mL O2 x mL x mm Hg-1 per beat, P <.05).
Conclusions:
These findings suggest that the alteration in mechanoenergetics in patients with severe LV dysfunction after myocardial infarction may result from the increased oxygen cost of excitation-contraction coupling rather than from a reduction in the efficiency of chemomechanical energy transduction.