Unfavorable effects of ventricular pacing on myocardial energetics

Baller, D.; Wolpers, H. G.; Zipfel, J.; Hoeft, Andreas; Hellige, G.

doi:10.1007/bf01907950

Cited by 43 publications

(17 citation statements)

References 15 publications

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“…This type of contraction is characterized by waste of myocardial work as energy is lost in shifting blood within the heart itself instead of contributing to ejection. 55 Left bundle-branch block therefore renders the already failing heart even more inefficient. Recently, in an attempt to counteract the detrimental impact of mechanical dyssynchrony, cardiac resynchronization therapy has emerged as a new treatment for a subgroup of patients with drug-refractory symptomatic dilated cardiomyopathy and mechanical dyssynchrony.…”

Section: Mechanical Dyssynchronymentioning

confidence: 99%

Myocardial Energetics and Efficiency

et al. 2007

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T he heart is an aerobic organ that relies almost exclusively on the aerobic oxidation of substrates for generation of energy. Consequently, there is close coupling between myocardial oxygen consumption (MV O 2 ) and the main determinants of systolic function: heart rate, contractile state, and wall stress. 1 As in any mechanical pump, only part of the energy invested is converted to external power. In the case of the heart, the ratio of useful energy produced (ie, stroke work [SW]) to oxygen consumed is defined as mechanical efficiency, as originally proposed by Bing et al. 2 Under normal conditions this ratio is Ϸ25%, and the residual energy mainly dissipates as heat. 3 In pathophysiological disease states, such as heart failure, mechanical efficiency is reduced, and it has been hypothesized that the increased energy expenditure relative to work contributes to progression of the disease. 4,5 Moreover, therapeutic interventions that enhance mechanical efficiency have proven to be beneficial with respect to outcome. 6 It is therefore desirable to quantify efficiency of the heart to study disease processes and monitor interventions.Both cardiac oxidative metabolism and mechanical work, and thus efficiency, can be quantified through invasive measurements. Although these measurements are accurate and currently considered the gold standard, in clinical practice they are limited because of the need for dual-sided heart catheterization and selective catheterization of the coronary sinus. Recent advances in imaging techniques, however, offer the possibility to noninvasively estimate MV O 2 and mechanical work by positron emission tomography and echocardiography or by magnetic resonance imaging, respectively. This review discusses the principles of mechanical efficiency, together with its invasive and noninvasive assessment, as well as their strengths and pitfalls. Finally, results from clinical pathophysiological studies are discussed. Invasive Measurement of Mechanical EfficiencyTo calculate the efficiency of the heart, input and output energy must be obtained. The first can be derived from MV O 2 (mL O2 · min Ϫ1 ) measurements according to the Fickprinciple by multiplying coronary sinus blood flow (mL · min Ϫ1 ) by the arteriovenous oxygen content difference. 7Blood flow can be estimated with the use of thermodilution or Doppler (electromagnetic flowmeter) methods after accessing the coronary sinus through right-sided heart catheterization. As oxygen dissolved in blood is negligible and hemoglobin concentrations in arterial and venous blood are similar, arteriovenous oxygen content difference can be obtained by determination of the differences in oxygen saturation levels between arterial and coronary sinus blood. This method to determine oxygen utilization is currently considered the gold standard, although it should be noted that it is limited by its invasive nature, susceptibility to sampling errors, and the fact that only global MV O 2 can be assessed, which also includes oxidative metabolism of the right ventricl...

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Section: Mechanical Dyssynchronymentioning

confidence: 99%

Myocardial Energetics and Efficiency

et al. 2007

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“…Rapid ventricular pacing increases left ventricular diastolic pressure in relation to ventricular volume and shows unfavorable effects on myocardial energetics whereas atrial pacing surprisingly performs beneficial effects on myocardial oxygen balance as demonstrated recently in an experimental study (15). Increased MVO2-values over E, during ventricular pacing have been attributed to increased energy requirements due to inhomogeneous contraction, active diastolic wall tension and metabolically related effects of augmented catecholamine release.…”

Section: Discussionmentioning

confidence: 94%

“…Statistical comparison of directly measured myocardial oxygen consumption (MVO2) with indirectly calculated energy demand from its hemodynamic determinants in situations with high mean left ventricular diastolic pressure (PLvD). E t = total energy demand of the left ventricle E0 = basal energy demand of the artificially arrested heart in normothermia E~ = energy demand of electrophysiological processes E2 = energy demand of maintenance of tension during systolic ejection time E3 = energy demand of tension development during isovolumic contraction E4 = energy demand of inactivation of the contractile system E5 = energy demand of maintenance of active diastolic wall tension The detailed formulas of the individual components have been described in previous papers (12,15 Values expressed as mean and standard error of the mean; *** = p < 0.001; ** = p < 0.01; * = p < 0.05 markedly lower significance (p < 0.05) compared to group I and II. Calculation of an additional energy demand E5 (1.64 + 0.14 ml O2/min 9 100 g) due to high ventricular diastolic pressures (25.6 + 1.9 mm Hg) leads to a significant (p < 0.05) overcompensation of E~ (16.33 +__ 1.57 ml OJmin 9 100 g), but a slight decrease of the t-value from -2,740 to 2,353.…”

Section: Resultsmentioning

confidence: 99%

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Increase of myocardial oxygen consumption due to active diastolic wall tension

et al. 1984

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A marked increase in left ventricular diastolic pressure ( PLVD ) relative to volume is regularly observed during angina pectoris and may contribute to further deteriorations of myocardial perfusion in the ischemic myocardium and to pulmonary congestion as well. A possible simultaneous increase in myocardial oxygen consumption (MVO2) due to a reversible diastolic tone during transient ischemia has not been taken into consideration in previous studies on alterations in ventricular diastolic properties. 13 closed-chest experiments were carried out in clinical catheterization technique with situations of high PLVD (18-50 mm Hg) relative to volume induced by right ventricular pacing (n = 19; 172 +/- 5 beats/min) and catecholamine-induced reversible diastolic tone (n = 17) in moderate hypothermia (31 degrees C). MVO2 was directly measured and indirectly calculated from its hemodynamic determinants using Bretschneider's equation (Et) that does not consider ventricular diastolic pressure. In addition, an energy demand for maintenance of active diastolic wall tension (E5) was calculated from PLVD , mean ventricular diastolic volume estimated from endsystolic and stroke volume, diastolic time and heart rate in ml O2/min X 100 g. During pacing tachycardia with high PLVD (27.4 +/- 1.8 mm Hg) the MVO2 (12.49 +/- 0.50 ml O2/min X 100 g) exceeds Et (10.11 +/- 0.25 ml O2/min X 100 g) (p less than 0.001), partly due to neglect of E5 (1.39 +/- 0.11 ml O2/min X 100 g). During catecholamine-induced high PLVD (31.1 +/- 2.5 mm Hg) the MVO2 (12.29 +/- 0.83 ml O2/min X 100 g) increases significantly (p less than 0.001) over Et (10.43 +/- 0.81 ml O2/min X 100 g). Addition of E5 (1.76 +/- 0.14 ml O2/min X 100g) to Et abolishes the differences between MVO2 and Et yielding non-significantly different values. Results indicate by means of indirect energetic evidence the occurrence of a diastolic tone of the heart under unphysiologic conditions. Acute increases in PLVD during angina pectoris are supposed to increase MVO2 markedly due to an additional energy demand for maintenance of reversible active diastolic wall tension.

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“…Although coronary blood flow and myocardial oxygen consumption are both related to the tension-time index (5), it should be noted that during ventricular pacing the TTI significantly underestimates myocardial oxygen consumption due to impaired myocardial pumping efficiency (2). The TrI may, therefore, provide only an indirect parameter for directional changes of myocardial nutritional demand.…”

Section: Discussionmentioning

confidence: 99%

Effect of brief periods of paced ventricular tachycardia on coronary blood flow in dogs before and after graded coronary stenosis

et al. 1983

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The effect of short bouts (1 min) of electrically induced ventricular tachycardias (VT) of increasing rates (160-240/min) was studied in 8 anesthetized dogs before and after graded constrictions of the left anterior descending (LAD) and the circumflex (CCA) coronary arteries. In the absence of coronary stenosis, paroxysmal VT caused a significant decrease in tension-time index (TTI), coronary blood flow (CBF) and coronary vascular resistance (CVR). Single and combined coronary stenosis caused relatively small alterations of the VT-induced depression of the systemic hemodynamics but reversed the effect of paroxysmal VT on the CVR. In the presence of single 90% LAD stenosis, VT resulted in an increase in CVR-LAD and a decrease in F-LAD associated with a fall in CVR-CCA and a rise in F-CCA. Combination of 90% LAD plus 70% CCA stenosis abolished the compensatory fall of CVR-CCA resulting in a pronounced reduction of F-CCA during VT. The results support the concept that in the presence of severe coronary stenosis brief paroxysmal ventricular tachycardias do increase myocardial nutritional demand but rather decrease nutritional supply.

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Unfavorable effects of ventricular pacing on myocardial energetics

Cited by 43 publications

References 15 publications

Myocardial Energetics and Efficiency

Myocardial Energetics and Efficiency

Increase of myocardial oxygen consumption due to active diastolic wall tension

Effect of brief periods of paced ventricular tachycardia on coronary blood flow in dogs before and after graded coronary stenosis

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