A critical look at currently used indirect indices of myocardial oxygen consumption

Baller, D.; Bretschneider, H. J.; Hellige, G.

doi:10.1007/bf01907955

Cited by 133 publications

(81 citation statements)

References 26 publications

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“…Therefore, ST segment changes are widely used as an index of myocardial injury resulting from ischemia in experimental animals (52, 57-59, 64, 86). Indirect indexes of myocardial oxygen consumption, (tension-time index, double product, and triple product) are also used in clinical and experimental studies (2). These indirect indexes are highly correlated with direct measurements of myocardial oxygen consumption.…”

Section: Discussionmentioning

confidence: 99%

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

Lujan

Britton²,

Koch

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity. Am J Physiol Heart Circ Physiol 291: H2933-H2941, 2006. First published August 4, 2006 doi:10.1152/ajpheart.00514.2006.-Reperfusion after a brief period of cardiac ischemia can lead to potentially lethal arrhythmias. Human epidemiological studies and experimental work with animals indicate that regular physical activity is associated with reductions in cardiovascular disease (CVD) risk factors and sudden cardiac death. Similarly, artificial selection of rats for high aerobic treadmill-running capacity (high-capacity runners; HCR) has been shown to reduce CVD risk factors relative to rats selected as lowcapacity runners (LCR). Therefore, we tested the hypothesis that HCR, relative to LCR rats, would be less susceptible to ischemiareperfusion-mediated ventricular tachyarrhythmias. To test this hypothesis, we measured the susceptibility to ventricular tachyarrhythmias produced by 3 min of occlusion and reperfusion of the left main coronary artery in conscious LCR and HCR rats. Results document a significantly lower incidence of ventricular tachyarrhythmias in HCR (3 of 11, 27.3%) relative to LCR (6 of 7, 85.6%) rats. The decreased susceptibility to tachyarrhythmias in HCR rats was associated with a reduced cardiac metabolic demand during ischemia (lower rate-pressure product and ST segment elevation) as well as a wider range for the autonomic control of heart rate. The HCR and LCR represent a unique substrate for evaluation of the mechanisms underlying ischemia-mediated cardiac arrhythmogenesis. artificial selection; cardiovascular risks; arrhythmia; exercise TEMPORARY OCCLUSION of the coronary arteries can lead to potentially lethal arrhythmias (66,82). Coronary artery occlusion-induced arrhythmias are triggered by the ischemic insult directly or on relief of the ischemic insult during the reperfusion phase. The mechanisms underlying the ventricular arrhythmias during ischemia and reperfusion are related but distinct (5,56,75,82). Although ischemia is a more common trigger of sudden death than is reperfusion, life-threatening reperfusion arrhythmias are observed during relief of coronary spasm, during angioplasty or thrombolysis, and after cardiac surgery with ischemic arrest (24).

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Section: Discussionmentioning

confidence: 99%

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

Lujan

Britton²,

Koch

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Methodsmentioning

confidence: 99%

“…[13][14][15][16][17] As an estimate of left ventricular efficiency (E), we calculated useful work (ie, CO ϫ P Ao ) and divided that product by an estimate of myocardial oxygen demand (ie, HR ϫ P Ao ϫ dP/dt max ). 21 E ഡ (CO ϫ P Ao )/(HR ϫ P Ao ϫ dP/dt max )…”

Section: Methodsmentioning

confidence: 99%

“…Myocardial oxygen consumption (MVO 2 ) was not measured directly but was estimated by the product of heart rate (HR) and mean systemic arterial pressure (P Ao ), termed the rate-pressure-product (RPP). [13][14][15][16][17] MVO 2 ഡ HR ϫ P AoAlthough the prime determinants of myocardial oxygen consumption are HR, 18 myocardial contractility, 19 and peak tension, 20 RPP is commonly used for clinical studies. [13][14][15][16][17] As an estimate of left ventricular efficiency (E), we calculated useful work (ie, CO ϫ P Ao ) and divided that product by an estimate of myocardial oxygen demand (ie, HR ϫ P Ao ϫ dP/dt max ).…”

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confidence: 99%

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Cardiovascular Effects of Intravenous Diltiazem in Dogs with Iatrogenic Atrial Fibrillation

Miyamoto

Nishijima

Nakayama

et al. 2000

Veterinary Internal Medicne

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Atrial fibrillation (AF) was induced in anesthetized Beagle hounds to determine the dose of diltiazem (D) that resulted in hemodynamic function similar to that observed during sinus rhythm (SR). Dogs were instrumented to record hemodynamic and electrophysiological parameters. Six dogs were given D, IV at cumulative doses of 0.063, 0.188, 0.438, 0.938, and 1.938 mg/kg, whereas 6 other dogs received vehicle in equivalent volumes. Plasma concentrations (PC) of D were measured. A cumulative dose of D between 0.438 and 0.938 mg/kg produced PC of 67.8 to 117.4 ng/mL and resulted in a heart rate (HR) closest to that observed during SR. At doses up to 0.938 mg/kg, no parameter of systolic function fell below that obtained during SR. At a dose of 0.938 mg/kg, the left ventricular end-diastolic and right atrial pressures exceeded those during SR. The rate-pressure product did not differ from that during SR at a dose of 0.938 mg/kg and fell below that during SR at the dose of 1.938 mg/kg. Left ventricular efficiency decreased from SR to AF, returned to values not different from those during SR at a dose of 0.938 mg/kg, and increased to values above those observed during SR at a dose of 1.938 mg/kg. In AF, slowing the HR with 0.438-0.938 mg/kg of D with resultant PC of 67.8-117.4 ng/mL results in cardiovascular function not different from that observed during SR.Key words: Cardiac efficiency; Heart rate.blocks L-type calcium channels, 1 and has proven useful in both humans 1-8 and dogs 9-12 for slowing the ventricular response in patients with atrial fibrillation (AF). Because of the dose-response relationship, it is possible to slow the ventricular rate (ie, response) to almost any degree, even to rates too low to sustain life. Although it is agreed that a ventricular rate of 250/min in a patient with AF is too fast, there is little agreement on what range of ventricular rates minimizes myocardial oxygen consumption and right atrial pressure but sustains cardiac output and systemic arterial pressure at levels appropriate for optimal performance.The purpose of this study is to report the effects of graded doses of D on parameters of cardiovascular function in dogs with AF produced by rapid atrial pacing. Our hypothesis was that D could produce a ventricular pressure (termed optimal) at which the pressure-rate product (the prime determinant of myocardial oxygen consumption) and right atrial pressure are low and systemic arterial pressure is sustained at nearly normal levels (ie, near values obtained during sinus rhythm [SR]). Such a result should optimize ventricular efficiency (ie, the ratio of useful work to myocardial oxygen consumption). Materials and MethodsTwelve, young adult, healthy Beagles of both sexes were anesthetized with thiopental (12 mg/kg IV) and ␣-chloralose a (100 mg/kg IV), and anesthesia was maintained with ␣-chloralose (30 mg/kg/h IV). Dogs were intubated and ventilated with a tidal volume of 12.5 mL/ kg (room air) and at a frequency of 12-15 breaths per minute to sustain PaCO 2 35-45 mmHg. Dogs were pl...

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“…Inhibition of stressorinduced blood pressure increases may be another reason; the sympathetic feedback gain in the baroreflex efferent limb to the peripheral vasculature may predominantly cause this effect. Both effects could help to inhibit a stressor-induced raise of myocardial oxygen consumption, which is proportional to the product of heart rate and systolic blood pressure (3,29).…”

Section: Limitations Of the Modelmentioning

confidence: 99%

Baroreflex sensitivity, blood pressure buffering, and resonance: what are the links? Computer simulation of healthy subjects and heart failure patients

Vooren

Gademan²,

Swenne

et al. 2007

Journal of Applied Physiology

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Van de Vooren H, Gademan MG, Swenne CA, TenVoorde BJ, Schalij MJ, Van der Wall EE. Baroreflex sensitivity, blood pressure buffering, and resonance: what are the links? Computer simulation of healthy subjects and heart failure patients. J Appl Physiol 102: 1348 -1356, 2007. First published December 21, 2006; doi:10.1152/japplphysiol.00158.2006.-The arterial baroreflex buffers slow (Ͻ0.05 Hz) blood pressure (BP) fluctuations, mainly by controlling peripheral resistance. Baroreflex sensitivity (BRS), an important characteristic of baroreflex control, is often noninvasively assessed by relating heart rate (HR) fluctuations to BP fluctuations; more specifically, spectral BRS assessment techniques focus on the BP-to-HR transfer function around 0.1 Hz. Skepticism about the relevance of BRS to characterize baroreflex-mediated BP buffering is based on two considerations: 1) baroreflex-modulated peripheral vasomotor function is not necessarily related to baroreflex-HR transfer; and 2) although BP fluctuations around 0.1 Hz (Mayer waves) might be related to baroreflex BP buffering, they are merely a not-intended side effect of a closed-loop control system. To further investigate the relationship between BRS and baroreflex-mediated BP buffering, we set up a computer model of baroreflex BP control to simulate normal subjects and heart failure patients. Output variables for various randomly chosen combinations of feedback gains in the baroreflex arms were BP resonance, BP-buffering capacity, and BRS. Our results show that BP buffering and BP resonance are related expressions of baroreflex BP control and depend strongly on the sympathetic gain to the peripheral resistance. BRS is almost uniquely determined by the vagal baroreflex gain to the sinus node. In conclusion, BP buffering and BRS are unrelated unless coupled gains in all baroreflex limbs are assumed. Hence, the clinical benefit of a high BRS is most likely to be attributed to vagal effects on the heart instead of to effective BP buffering. autonomic nervous system; cardiovascular variability; Mayer waves; spectral analysis; transfer function IN DAILY LIFE, multiple processes perturb blood pressure. The duration of these challenges varies widely. For example, respiration makes blood pressure fluctuate with every breath (13), while physical or mental stress elevates blood pressure for minutes or even longer. The arterial baroreflex is a negativefeedback mechanism that effectively buffers such incidental blood pressure fluctuations (11,20,21,23). In negativefeedback systems, feedback delay often causes resonance in a given frequency band; this is the price to be paid for effective buffering at other frequencies. Resonance in blood pressure (5,8,12,31,49) manifests in the form of the well-known Mayer (22, 33) waves (beat-to-beat blood pressure oscillations with a frequency of ϳ0.1 Hz/period of ϳ10 s). Effective baroreflex blood pressure buffering occurs below the Mayer frequency (10, 16).Besides a sympathetic limb that modulates peripheral resistance, the baroreflex has ...

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A critical look at currently used indirect indices of myocardial oxygen consumption

Cited by 133 publications

References 26 publications

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

Cardiovascular Effects of Intravenous Diltiazem in Dogs with Iatrogenic Atrial Fibrillation

Baroreflex sensitivity, blood pressure buffering, and resonance: what are the links? Computer simulation of healthy subjects and heart failure patients

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