Matching of myocardial oxygen consumption to mechanical load in human left ventricular hypertrophy and dysfunction

The coupling of myocardial oxygen consumption (MVO2) with its determinants in left ventricular hypertrophy in human beings is poorly understood. Therefore, ther-modilution-derived coronary blood flow, MVO2and left ventricular wall stress, obtained from simultaneous left ventricular M-mode echogram and pressure, were compared in 32 patients with various degrees of left ventricular hypertrophy. Patients were studied at rest and after mechanical load alteration with nitroglycerin or phenylephrine. Decreases in MVO2(−5.7 ± 0.8 ml/min; p < 0.001) and the time integral of meridional ejection stress or shortening load (− 1,297 ± 152 × 103dyness/cm2; p < 0.001) were observed after nitroglycerin administration while increases in MVO2(+ 5.5 ± 0.7 ml/min; p < 0.001) and shortening load (+1,412 ± 137 × 103dyness/cm2; p < 0.001) were noted after phenylephrine. An index relating the change in MVO2to the corresponding change in shortening load (SL), % ΔMVO2/% ΔSL, was significantly different in patients without (Group 1) and with (Group 2) clinical left ventricular failure. Left ventricular mass was similar in both groups. The mean % ΔMVO2/% ΔSL with phenylephrine in Group 1 (79.6 ± 9.6) was greater than the index for Group 2 (35.5 ± 6.1; p < 0.005). With nitroglycerin, Group 2 patients exhibited a greater reduction in %ΔMVO2/%ΔSL (110.5 ± 17.8) than Group 1 (54.0 ± 9.4; p < 0.01).In conclusion, in patients with left ventricular hypertrophy and dysfunction there appears to be a state of diminished coronary flow response to load augmentation. However, load reduction in patients with clinical left ventricular failure results in a more balanced relation between oxygen uptake and ejection stress