Potentiation of Myocardial Contractility by Continual Premature Extra-activations

Koch‐Weser, Jan

doi:10.1161/01.res.18.3.330

Cited by 35 publications

(16 citation statements)

References 16 publications

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“…As a consequence, it is suggested that mechanical alternans, in addition to the observed "postextrasystolic" contractile phenomenon, accounts in great part for the complex variation in inotropic state during the ventricular response to atrial fibrillation. Such interval-dependent contractile alterations appear to reflect an intrinsic property of myocardial tissue common to most mammalian species, for other studies (11) have shown that postextrasystolic potentiation is not dependent upon catecholamine stores or adrenergic innervation.…”

Section: Discussionmentioning

confidence: 81%

The role of inotropic variation in ventricular function during atrial fibrillation

Edmands¹,

Greenspan²,

Fisch³

1970

J. Clin. Invest.

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A B S T R A C T A series of experiments were performed upon intact anesthetized dogs to determine the relevance of a variety of hemodynamic variables to the irregular ventricular performance associated with atrial fibrillation. During experimentally induced atrial fibrillation central aortic pulse pressure was measured in relation to the duration of the preceding diastolic interval, the relative degree of cycle-length change, the magnitude of the preceding aortic end-diastolic pressure, the rate of ventricular tension development (at a fixed diastolic tension), and to ventricular end-diastolic pressure. While all of the latter variables bore a significant relation to the chosen parameters of ventricular function, the most linear correlation lay with the rate of ventricular tension development. It has been suggested, as a consequence, that the irregular ventricular performance observed during atrial fibrillation under these experimental conditions, may be more directly related to variation in the inotropic state of the ventricular myocardium than to an expression of the Frank-Starling concept, resulting from variable ventricular filling. The lability of the inotropic or contractile state has in turn been attributed to abrupt cycle-length change effecting inotropic alteration analogous to postextrasystolic potentiation of contractility and, at rapid rates, effecting an alternation of the contractile state.

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Section: Discussionmentioning

confidence: 81%

The role of inotropic variation in ventricular function during atrial fibrillation

Edmands¹,

Greenspan²,

Fisch³

1970

J. Clin. Invest.

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“…A fundamental interval-strength relation, common to all varieties of potentiation produced by abrupt rate change, has been observed in several studies (4,5); it is constituted by the relative prolongation of the cycle-length (i.e., prolongation relative to the previous cycle-length) preceding the potentiated contraction. The physiologic mechanism of such enhancement has not been further clarified, however.…”

Section: Greenspan Edmands Fischmentioning

confidence: 89%

The Relation of Contractile Enhancement to Action Potential Change in Canine Myocardium

Greenspan

Edmands

Fisch

1967

Circulation Research

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Simultaneous recordings of contractile tension and transmembrane potentials from canine ventricular tissue yielded a consistent correlation of action potential (AP) alteration with contractile change associated with abrupt rate change. The AP terminating a relative prolongation of the cycle-length manifested shortening of phase 2 with lengthening of phase 3 and was associated with potentiation of contractile force. Conversely, the AP terminating a relative abbreviation of cycle-length displayed a broader phase 2 with a more precipitous phase 3, while the associated contraction was less forceful than the control. In each circumstance, the relative magnitude of cycle-length change correlated with the extent of both AP change and contractile alteration. Changes in AP configuration may reflect changes in transmembrane flux of K + during repolarization consistent with the findings of prior workers who have related K* efflux to increased contractility. Mechanical altemans, in addition, was frequently observed in association with abrupt rate change and was consistently associated with an electrical altemans manifested by action potentials with alternately wide and narrow plateaus (phase 2). As above, the more forceful contractions were associated with action potentials which displayed a narrower "phase 2. Mechanical altemans initiated by abrupt fate change may represent an adaptive phenomenon prior to the establishment of a stable contractile state, as reflected by a stable AP configuration. ADDITIONAL KEY WORDScardiac repolarization and contractility cardiac contractility cardiac action potentials post-extrasystolic potentiation compensatory pause and repolarization mechanical and electrical altemans rest potentiation cycle-length, repolarization and contractility• Augmentation of cardiac contraction associated with abrupt rate change has been noted repeatedly in a variety of mammals (1) as well as the human (2) since first described by Langendorff in 1875. The mechanism by which such a phenomenon occurs has, nevertheless, remained obscure and of little more than academic concern until recently. With

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“…A second stimulus was introduced at decreasing intervals after the initial stimulus. The interstimulus interval was shortened in a stepwise fashion from 400 to 80 ms. A second mechanical event was defined as either a discrete second twitch, which if present was easily discernable from the dF/dt tracing, or as an increase in RTI following the second stimulus (20).…”

Section: Methodsmentioning

confidence: 99%

Prolonged contraction duration in aged myocardium.

Lakatta¹,

Gerstenblith²,

Angell³

et al. 1975

J. Clin. Invest.

190

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A B S T R A C T Isometric performance at 29'C was measured in left ventricular trabeculae carneae from young adult (6-mo) and aged (25-mo) rats (n = 18 in each group). Active tension and maximal rate of tension development did not differ with age, but contraction duration was 255±6 ms in the young adult and 283±6 ms in the aged group (P < 0.001). Although catecholamine content per gram heart weight was less in the aged myocardium, additional experiments showed that neither 1 X 10' M propranolol nor pretreatment with 6-hydroxydopamine eliminated the age difference in contraction duration. To determine if this age difference resulted from a prolonged active state, electromechanical dissociation and the overshoot of contraction duration during recovery from hypoxia were measured. During paired stimulation greater mechanical refractoriness was found in aged muscles (P < 0.01), but intracellular action potential recordings showed no age difference in the electrical refractory period. On recovery from hypoxia, contraction duration overshoot was 117±4% of control in the young and 138±4% of control in the aged muscles (P < 0.01). The greater electromechanical dissociation and greater overshoot in contraction duration following hypoxia in aged myocardium suggests that prolonged contraction duration in aged myocardium results from a prolonged active state rather than changes in passive properties or myocardial catecholamine content.

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Potentiation of Myocardial Contractility by Continual Premature Extra-activations

Cited by 35 publications

References 16 publications

The role of inotropic variation in ventricular function during atrial fibrillation

The role of inotropic variation in ventricular function during atrial fibrillation

The Relation of Contractile Enhancement to Action Potential Change in Canine Myocardium

Prolonged contraction duration in aged myocardium.

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