Cardiovascular research · 1994
Depressed contractile state and increased myocardial consumption for non-mechanical work in patients with heart failure due to old myocardial infarction.
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Takaoka H, Takeuchi M, Odake M, Hata K, Hayashi Y, Mori M, Yokoyama M
Аннотация
OBJECTIVE: The aim was to characterise the impaired myocardial mechanoenergetics in patients with heart failure due to old myocardial infarction by using the oxygen consumption versus left ventricular pressure--volume area (PVA) relationship.
METHODS: The VO2-PVA relationship was assessed in 15 patients: group N consisted of seven patients with vasospastic angina pectoris whose left ventricular ejection fractions were normal [72 (SD 8)%], and group F consisted of eight patients with old myocardial infarction whose left ventricular ejection fractions were reduced [45(11)%]. Left ventricular volume and pressure were measured by the conductance catheter method. VO2 was measured by thermodilution.
RESULTS: Linear VO2-PVA relationships with dextran infusions were obtained in both groups (median r = 0.92 v 0.90). There was no difference in the slope between the two groups. There was a positive correlation between Emax and VO2 at median PVA (VO2,PVA0.8) in group N. Emax, an index of left ventricular contractility, was significantly smaller in group F than in group N, at 5.1(2.1) v 3.2(1.1) mm Hg.ml-1.m2; p < 0.05). On the other hand, the VO2 intercept in group F was comparable to that in group N, at 0.71(0.63) v 0.40(0.29) J x beat-1.100 g LV-1; NS). In addition, the ratio of VO2,PVA0.8 to Emax was significantly larger in group F than in group N: 0.55(0.14) v 0.89(0.37) J x beat-1.100 g LV-1.mm Hg-1.ml.m-2 (p < 0.05).
CONCLUSIONS: These results suggest that the VO2 for non-mechanical work in group F is disproportionately high relative to the reduced contractility. An abnormality of excitation-contraction coupling rather than of crossbridge cycling may be responsible for the impaired mechanoenergetics in patients with heart failure due to old myocardial infarction.
METHODS: The VO2-PVA relationship was assessed in 15 patients: group N consisted of seven patients with vasospastic angina pectoris whose left ventricular ejection fractions were normal [72 (SD 8)%], and group F consisted of eight patients with old myocardial infarction whose left ventricular ejection fractions were reduced [45(11)%]. Left ventricular volume and pressure were measured by the conductance catheter method. VO2 was measured by thermodilution.
RESULTS: Linear VO2-PVA relationships with dextran infusions were obtained in both groups (median r = 0.92 v 0.90). There was no difference in the slope between the two groups. There was a positive correlation between Emax and VO2 at median PVA (VO2,PVA0.8) in group N. Emax, an index of left ventricular contractility, was significantly smaller in group F than in group N, at 5.1(2.1) v 3.2(1.1) mm Hg.ml-1.m2; p < 0.05). On the other hand, the VO2 intercept in group F was comparable to that in group N, at 0.71(0.63) v 0.40(0.29) J x beat-1.100 g LV-1; NS). In addition, the ratio of VO2,PVA0.8 to Emax was significantly larger in group F than in group N: 0.55(0.14) v 0.89(0.37) J x beat-1.100 g LV-1.mm Hg-1.ml.m-2 (p < 0.05).
CONCLUSIONS: These results suggest that the VO2 for non-mechanical work in group F is disproportionately high relative to the reduced contractility. An abnormality of excitation-contraction coupling rather than of crossbridge cycling may be responsible for the impaired mechanoenergetics in patients with heart failure due to old myocardial infarction.