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.

For indicator-dilution studies, complete thermal recovery after passage of heat through the pulmonary circulation would be desirable. However, the results in the literature obtained by extrapolation techniques are inconsistent. To overcome problems of the extrapolation approach, transport functions of the pulmonary circulation (including the left heart) were computed by deconvolution of pulmonary arterial and aortic pairs of thermodilution curves after central venous indicator injection (10 ml of an ice-cold blood indocyanine green dye mixture). Thermal recovery was determined as the finite integral of the transport function. Thirteen mongrel dogs under piritramid-N2O anesthesia were examined under base-line conditions, in orthostasis to alter the distribution of pulmonary blood flow (9 dogs), and in oleic acid edema (8 dogs). Using the deconvolution approach, thermal recovery was 0.97 +/- 0.04 under base-line conditions, 0.96 +/- 0.03 in orthostasis, and 0.96 +/- 0.05 in pulmonary edema. Thermal recovery determined from extrapolated dilution curves was greater than 100% in all groups, a physically impossible finding. It is concluded that thermal recovery is incomplete but insensitive with respect to the distribution of blood flow and to the size of the extravascular compartment. Monoexponential extrapolation is unsuited for the determination of thermal recovery.

This method of estimating efficiency is feasible and may represent a unique noninvasive approach for the evaluation of cardiac performance and responses to therapy.

No abstract

CAS using the right transradial approach for left CAS in bovine-type aortic arch or the right transradial approach in type-III aortic arch for right CAS appears to be safe and technically feasible.

The effects of ventricular pacing (90-330 beats/min) and atrial pacing (120-210 beats/min) on myocardial oxygen consumption (MVO2) and its hemodynamic determinants and on myocardial pumping efficiency were studied systematically on intact dogs. In six closed-chest experiments 158 steady states were analyzed. Myocardial blood flow was measured with a differential pressure sinus catheter, oxygen consumption (5-30 ml/min . 100g) was determined simultaneously by the Fick principle and the additive hemodynamic parameter Et. Ventricular and atrial pacing were compared with both methods at identical heart rates. Additionally, the coincidence between both methods of determining MVO2 was examined at sinus rhythm with sympathetic stimulation (norepinephrine, atropine) within each experiment. Ventricular pacing increased MVO2 overproportionally up to 50% in relation to the hemodynamic determinants. Consequently, myocardial pumping efficiency markedly decreased with increasing ventricular rate. The close relation between directly measured MVO2 and Et, found in previous studies, was maintained under sympathetic stimulation. Atrial pacing, as compared to ventricular pacing at identical rates, resulted in a decrease of MVO2 up to 25% although the expected mVO2 according to its hemodynamic determinants rather increased. The hemodynamic and metabolic mechanisms probably responsible for the energetic difference between ventricular and atrial pacing at equal heart rates are discussed.

After myocardial infarction, quantitative indexes of perfusion and oxidative metabolism from acetate PET indicate a critical threshold beyond which tissue is irreversibly injured. Findings support the use of blood flow as a marker of myocardial viability in chronic postinfarct patients with modestly reduced ejection fractions.

No abstract