Background-Early stages of coronary atherosclerosis are characterized by a mainly functional impairment of coronary vasodilator capacity under the impact of such risk factors as hypercholesterolemia. The goal of this study was to determine whether 6-month cholesterol-lowering therapy improves coronary flow reserve in patients with angina, reduced flow reserve despite minimally diseased coronary vessels or even normal angiogram, and mild to moderately elevated LDL levels on average. Methods and Results-We noninvasively investigated 23 consecutive patients (18 men, 5 women; mean age, 56Ϯ7.6 years) with a mean LDL level of 165Ϯ34 mg/dL at baseline by PET for myocardial blood flow measurement with [

CRT induces changes of MVO2 and MBF on a regional level with a more uniform distribution between the myocardial walls and improved ventricular efficiency in NICM. Based on the investigated parameters, CRT appears to be more effective in NICM than in ICM.

SummaryMyocardial oxygen consumption indices that are frequently applied to man such as tension-time index (TTI), pressure-rate product (P 9 HR) and triple product (TP) have not been fully validated so far. These easily obtainable indices and a modified TTI (P -x/H--R), therefore, were examined in I0 closed-chest dogs with very broad variations of hernodynarnics and oxygen consumption (3-36 rnl/rnin -100 g) analyzing 162 steady states. Myocardial blood flow was directly measured by a differential pressure coronary sinus catheter. I~O 2 was varied by administration of catecholamines and other inotropic drugs, atropine, beta-blocking agents and hypoand hypervolernia. Over a wide range of hernodynarnic states, correlations with directly measured MVO 2 of TTI (r = 0.63), P 9 HR (r = 0.87), TP (r = 0.65) and P 9 %/HR (r = 0.80) are not satisfactory due to neglect of contractility and cardiac volumes by these terms. Better correlations are obtained when relating these indices to IV[Vo2 under different inotropic states. At normal and moderately increased contractility, correlations with M~O2 rose as follows: TTI (r = 0.96), P 9 HR (r = 0.91), TP (r = 0.96) and P 9 ~ (r = 0.94). Significant rises in correlation are due to the close relationship between peak pressure and dP/dtma x at only moderately increased contraction velocity. Correlation differences within this inotropic range must be related to incorporation or neglect of ejection time as a partial determinant of MVO 2. At markedly increased contractility, results for these indices, however, are in part very poor: TTI (r = 0.40), P -HR (r = 0.81), TP (r = 0.38) and P 9 ~/HR (r = 0.76). Within this inotropic state neglect of dP/dtma x as a rna]or determinant of MVO 2 and the inverse relationship between ejection time and dP/dtma x mainly account for these correlation shifts. It is concluded that non-invasively obtainable indices, currently in use, are no reliable predictors of actual overall MVO2 of the left ventricle if the contractile state of the rnyocardium is not checked invasively before. The broad variability of the relation of the energy demand of velocity of tension development to rnaintenance of systolic wall tension is not sufficiently considered by these terms. Appropriate caution, therefore, is necessary when applying those indirect indices of M'~rO2 to humans.

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As the impact of cardiac pacing on myocardial energetics has not yet been established, this laboratory investigation was undertaken to evaluate the effects of right atrial (AP), right ventricular apex (VP) and atrioventricular sequential pacing (AVP) on cardiac energetics in a closed-chest model. Ninety-two pacing interventions were performed in ten anesthetized mongrel dogs with normal loading conditions and contractile states. The energetic effects of pacing were assessed in terms of myocardial oxygen consumption (MVO2), its hemodynamic determinants and cardiac efficiency. Efficiency was calculated as the ratio of O2-equivalent of external cardiac work to MVO2, using standard definitions. In the first series of experiments 36 intra-individual comparisons were made between AP and VP at identical rates (95-210 beats/min). In the second series AVP was compared to VP in 10 intra-individual comparisons at identical rates (109-190 beats/min). MVO2 was lower (p less than 0.001) during AP (8.30 +/- 2.14 ml O2/min.100 g) compared to VP (10.16 +/- 3.15 ml O2/min.100 g) at the same rate (158 +/- 32 beats/min). Efficiency (p less than 0.001) was considerably higher during AP (21.6 +/- 5.7%) compared to VP (12.8 +/- 5.9%). During AVP, MVO2 (10.85 +/- 1.76 ml O2/min.100 g) was not significantly different from VP (10.57 +/- 1.34 ml O2/min.100 g) at the same rate (146 +/- 25 beats/min). Hemodynamics were superior with AVP compared to VP. Efficiency was significantly higher (p less than 0.01) with sequential (15.4 +/- 3.9%) as compared to ventricular pacing (12.0 +/- 3.2%). In conclusion, this study indicated that VP exerts disadvantageous effects on MVO2 and cardiac efficiency. AP has beneficial effects on cardiac energetics because it improves the relationship between mechanical performance of the heart and its energy requirements. AVP results in a higher efficiency than VP due to superior hemodynamics, despite MVO2 levels comparable to those of VP. The mechanism of energy waste with right ventricular apex pacing is probably related to an asynchronous contraction in the ventricular myocardium due to a nonphysiological spread of excitation.

The purpose of this study was to examine any reported indices for estimating myocardial oxygen consumption (MVO2) under uniform experimental conditions at maximal variation of hemodynamics and MVO2. One hundred sixty-two steady states were analyzed in 10 closed-chest dog experiments. Myocardial blood flow was directly measured by a different pressure catheter in the coronary sinus. The indirect values of MVO2 calculated from 24 indices were compared with directly measured MVO2. Throughout a wide range of hemodynamic states, the best correlate with MVO2 was found to be the additive parameter Et (r = 0.96). Any indices that do not incorporate potentially important changes of MVO2 related to both myocardial contractility and ventricular dimensions show unsatisfactory correlations with MVO2 at extreme changes of hemodynamics. Tension-time index (TTI) correlates poorly with MVO2 (r = 0.63). This result is due to the neglect of contractility. Pressure-heart rate product (P X HR) correlates with MVO2 with r = 0.86. Better results for TTI and P X HR, as reported in previous works, are reproducible by dividing our data into two groups of different inotropic states. At normal and moderate inotropic stimulation the correlation for TTI rises to r = 0.96, and for P X HR to r = 0.91. This augmentation is to be referred to the close relationship (r = 0.92) of peak ventricular pressure to maximum rate of pressure rise in this group. The additive parameter E1 is the best, both at moderate (r = 0.97) and at maximal inotropic stimulation (r = 0.87), and is to be preferred for indirect estimation of MVO2. Results are discussed with regard to the clinical application of MVO2 indices.

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