In a subgroup of patients with noninfarcted collateral-dependent myocardium, immature or insufficiently developed collaterals do not provide adequate flow reserve. Despite nearly normal resting flow and oxygen consumption, these collateral-dependent segments exhibit chronically depressed wall motion and demonstrate marked ultrastructural alterations on morphological analysis. We propose that these alterations result from repeated episodes of ischemia as opposed to chronic hypoperfusion and represent the flow, metabolic, and morphological correlates of myocardial "hibernation."

Previous studies have established that most of the heterogeneity in exercise capacity seen with sedentariness, aging, or physical training can be accounted for by individual differences in the maximal rate of total body oxygen consumption (VO2 max) during dynamic exercise. However, the factors that limit VO2 max in normal subjects remain disputed. To test the hypothesis that differences in left ventricular diastolic performance contribute to the heterogeneity of VO2 max seen in healthy subjects, 57 normal sedentary volunteers (36 +/- 13 yr, range 20-76 yr) and 9 endurance athletes (37 +/- 8 yr, range 26-51 yr) were studied. Aerobic capacity was estimated as VO2 max during a multistage dynamic cycle exercise protocol, whereas resting left ventricular systolic and diastolic function was assessed by two-dimensional and Doppler echocardiography. The relationship of the left ventricular functional indexes with VO2 max was investigated by stepwise multiple regression analysis. VO2 max ranged from 25 to 58 ml.kg-1 x min-1 in sedentary subjects and from 44 to 60 ml.kg-1 x min-1 in athletes. With univariate analysis, significant correlations were observed between VO2 max and age (r = -0.60), maximal heart rate (r = 0.48), maximal work load (r = 0.80), left ventricular volumes at both end diastole (r = 0.51) and end systole (r = 0.62), peak early transmitral filling velocities (r = 0.80), and the ratio of early to late transmitral filling velocities (r = 0.87).(ABSTRACT TRUNCATED AT 250 WORDS)

The relationship of myocardial O2 consumption (MVO2) to its potential hemodynamic and mechanical determinants was investigated in eight healthy normal volunteers at rest and during infusion of dobutamine (5-10 micrograms.kg-1.min-1). MVO2 was calculated from the monoexponential myocardial clearance of [1-11C]acetate with positron emission tomography, and left ventricular mechanical function was assessed by two-dimensional echocardiography. Infusion of dobutamine increased heart rate by 53%, the tension-time index by 31%, and the rate-pressure product by 116%. Cardiac output (+70%), left ventricular ejection fraction (+24%), total mechanical energy [systolic pressure-volume area, (PVA) +84%], and left ventricular pressure-work index (+100%) also increased during infusion of dobutamine. During infusion of dobutamine, MVO2 increased from 96 +/- 17 to 233 +/- 19 J.min-1.100 g left ventricle-1, while myocardial efficiency (the ratio of PVA to MVO2) decreased from 46 +/- 8 to 35 +/- 4% (P < 0.001 each). MVO2 was best correlated (P < 0.001) with the PVA (r = 0.92) and the pressure-work index (r = 0.92). Infusion of dobutamine also resulted in a significant parallel upward shift of the PVA-MVO2 relationship, indicative of an increase in PVA-independent MVO2. Our data indicate that, in human subjects, MVO2 is mainly related to systolic PVA and that inotropic stimulation with dobutamine results in decreased efficiency of contraction, such as that previously described in isolated hearts.

No abstract

No abstract