Alteration in energetics in patients with left ventricular dysfunction after myocardial infarction: Increased oxygen cost of contractility

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 Vo(2)-pressure-volume area relation (PVA, a measure of total mechanical energy) and E(max) (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 E(max), Vo(2), and PVA using conductance and Webster catheters under control conditions and during different rates of dobutamine infusion (3 and 6 mu g . kg(-1). min(-1)) in 30 patients with coronary artery disease. Patients were divided into three groups according to LV ejection faction (EF): 10 without LV dysfunction (EF greater than or equal to 60%), 10 with mild LV dysfunction (40%less than or equal to EF<60%), and 10 with severe LV dysfunction (EF <40%). Under control conditions, the Vo(2)-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 O-2 . mL . 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.