Post-extrasystolic potentiation and the force-frequency relationship: Differential augmentation of myocardial contractility in working myocardium from patients with end-stage heart failure

Phillips, Preston; Gwathmey, Judith K.; Feldman, Marc D.; Schoen, Frederick J.; Grossman, William; Morgan, James P.

doi:10.1016/0022-2828(90)90975-8

Cited by 55 publications

(26 citation statements)

References 21 publications

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“…However, there was no direct relationship between frequency-behavior and post-rest behavior. This is in line with findings of Phillips et al (64), who showed a dissociation of frequency-potentiation and postextrasystolic potentiation of force in failing human myocardium. These findings may indicate that the contribution of the various intracellular Ca 2ϩ handling mechanisms are different in frequency-dependent and rest-dependent modulation of contractile force.…”

Section: Discussionsupporting

confidence: 93%

Diminished post-rest potentiation of contractile force in human dilated cardiomyopathy. Functional evidence for alterations in intracellular Ca2+ handling.

et al. 1996

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Section: Discussionsupporting

confidence: 93%

Diminished post-rest potentiation of contractile force in human dilated cardiomyopathy. Functional evidence for alterations in intracellular Ca2+ handling.

et al. 1996

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“…Assuming calcium sensitivity of the myofilaments,'7 Ca2+-release channels,20 and specific Ca21 uptake by sarcoplasmic reticulum vesicles2' are normal, other possibilities for the mechanism of altered tension-frequency relation are: 1) a reduced number of sarcoplasmic reticulum Ca21 pumps22; 2) a reduced production of cyclic AMP23; and 3) intracellular acidosis or metabolite buildup because of increased diffusion distances in hypertrophied myocytes. 19 We were concerned that the 30-mmol/1-BDM exposure of all myocardial tissue used in the present experiments might have introduced an artifactual component in the results obtained. Although there is presently no evidence that BDM has any significant irreversible effect on any aspect of muscle function, control experiments for the possibility that BDM pretreatment alters the tension-frequency relation in human myocardium would be desirable.…”

Section: Discussionmentioning

confidence: 99%

Altered myocardial force-frequency relation in human heart failure.

et al. 1992

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“…Details of the blood-perfused isolated canine heart preparation have been previously reported.9 Briefly, a support dog (weight, [25][26][27][28][29][30] kg) was anesthetized with pentobarbital sodium (30 mg/kg i.v. ), heparinized (5,000 units i.v.…”

Section: Isolated Heart Preparationmentioning

confidence: 99%

Alterations in left ventricular mechanics, energetics, and contractile reserve in experimental heart failure.

Wolff

Tombe

Harasawa

et al. 1992

Circulation Research

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The contributions of changes in primary systolic and diastolic properties, limitations of contractile reserve, and alterations in energy efficiency to the left ventricular dysfunction seen with chronic pacing tachycardia were investigated. Seven dogs (heart failure group) were ventricularly paced at 250 beats per minute for 26.3 ±2.9 days and compared with a separate control group (n =8). Studies were performed with isolated, metabolically supported hearts coupled to a computer-controlled loading system. Pressurevolume relations and myocardial oxygen consumption (MVo2) were measured to assess chamber systolic and diastolic properties and efficiency (relation between MVo2 and pressure-volume area [PVA] significantly larger (33.3±3.9 versus 21.9±7.6 ml,p<0.01). Inotropic response to increased heart rate and exogenous ,-adrenergic stimulation (dobutamine HCI) was significantly impaired in failure compared with control hearts. Most interestingly, failure hearts had a lowered slope of the MVo2-PVA relation (2.1±1.1 versus 2.9±1.4 ml 02 mm Hg-' * ml-l * 100 g left ventricle-', p<0.001), indicating increased effliciency of chemomechanical energy conversion. The y intercept of the MVo2-PVA relation, which reflects oxygen costs of basal metabolism and excitation-contraction coupling, was unchanged in the two groups despite decreased contractility of the heart failure hearts. These results demonstrate reduced chamber and myocardial contractility, dilatation without alteration of passive myocardial properties, impaired contractile reserve, and novel alterations in cardiac efficiency in this model of heart failure. (Circulation Research 1992;70:516- performance from chronic rapid pacing, the mechanisms underlying this dysfunction remain poorly characterized. There are several mechanisms definable at a chamber level that could contribute to reduced net pump function. These include 1) primary reductions in chamber and/or myocardial contractility, 2) abnormal diastolic chamber and/or myocardial stiffness, 3) reduced inotropic reserve caused by blunting of the positive force-frequency relation or decreased response to 83-adrenergic stimulation, and 4) a reduced ability to convert consumed oxygen to mechanical work (decreased metabolic efficiency). The purpose of the present study was to determine the contribution of each of these factors to the cardiac failure induced by chronic rapid pacing.To elucidate the role of each of these mechanisms, studies were performed using isolated, metabolically supported canine hearts coupled to a computer-simulated vascular loading system. This preparation offers the advantages of rigid control of chamber load, heart rate, and coronary perfusion and precise measurements of ventricular volume and myocardial oxygen consumption (MVo2). The results demonstrate reductions in chamber and myocardial contractility, ventricular dilaby guest on

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Post-extrasystolic potentiation and the force-frequency relationship: Differential augmentation of myocardial contractility in working myocardium from patients with end-stage heart failure

Cited by 55 publications

References 21 publications

Diminished post-rest potentiation of contractile force in human dilated cardiomyopathy. Functional evidence for alterations in intracellular Ca2+ handling.

Diminished post-rest potentiation of contractile force in human dilated cardiomyopathy. Functional evidence for alterations in intracellular Ca2+ handling.

Altered myocardial force-frequency relation in human heart failure.

Alterations in left ventricular mechanics, energetics, and contractile reserve in experimental heart failure.

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