The Initial Electrophysiologic Disturbance in Experimental Myocardial Infarction.

Gambetta, Miguel

doi:10.7326/0003-4819-70-5-1076_1

Cited by 24 publications

(9 citation statements)

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“…"- 12 For studies of cat ventricular muscle, right ventricular papillary muscles were removed from cats (2-5 kg) anesthetized with pentobarbital (30 mg/kg, ip). The muscles were mounted and superfused as described for guinea pig tissue.…”

Section: Methodsmentioning

confidence: 99%

“…If the initial decrease in excitability threshold during ischemia (Fig. 1) is due to a mild increase in extracellular potassium concentration as potassium is released from ischemic cells, 12 …”

Section: Figure 1 Excitability Changes Expressed As Change In Threshmentioning

confidence: 99%

“…At this time LAD occlusion resulted in little or no decrease in excitability threshold because extracellular potassium levels, already elevated by intravenous infusion, rose further following ischemia and achieved concentrations which increased excitability threshold. Preventing the ischemia-induced increase in excitability threshold by "washing out" the ischemic zone with nonoxygenated solutions 12 suggests that accumulation of metabolic by-products of ischemia accounts for the excitability changes, but naturally cannot point to potassium as the cause.…”

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confidence: 99%

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Alterations in canine myocardial excitability during ischemia.

Elharrar

Foster

Jirak

et al. 1977

Circulation Research

150

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The effect of the cardiac membrane potential on the rapid availability of the sodium-carrying system. J Physiol (Lond) 127: 213-224, 1955 20 Alterations in Canine Myocardial Excitability during Ischemia VICTOR ELHARRAR, PETER R. FOSTER, THOMAS L. JIRAK, WINSTON E. GAUM, AND DOUGLAS P. ZIPES SUMMARY Changes in the ventricular diastolic excitability threshold following occlusion of the left anterior descending coronary artery (LAD)were studied in open-chest anesthetized dogs by using a new automatic threshold-following pacemaker (ATFP). The ATFP measures the diastolic excitability threshold by successively decreasing the duration of regularly occurring pacing stimuli until the ventricle fails to respond. Under control conditions, the threshold stimulus duration was 60 ± 4 (mean ± SEM) /Lisec. In the first 1-3 minutes following occlusion of the LAD, the diastolic excitability threshold in the ischemic zone (IZ) decreased to 51 ± 5 fisec and then rapidly increased to 600 pisec at 5 minutes. The initial decrease in excitability threshold at IZ could be abolished by elevating the serum K + concentration prior to the LAD occlusion. These changes in excitability threshold at IZ could be prevented by infusing nonoxygenated solutions into the LAD at a site distal to the occlusion. As the excitability threshold increased in IZ during ischemia, the earliest time at which IZ could be reactivated by a stimulus with a voltage equal to twice the preligation diastolic voltage threshold was increased. In nine of 16 dogs, after 5 minutes of LAD ligation, the IZ to normal zone (NZ) activation time (when stimulating at IZ) exceeded the NZ to IZ activation time (when stimulating at NZ) by an average of 9 msec. We also found that in four dogs the NZ to IZ activation time exceeded the IZ to NZ activation time by an average of 10 msec. We conclude from these findings that a gradient of increasing excitability threshold exists as one moves from normally perfused toward more ischemic tissue, passing through a heterogeneous border zone that manifests some areas which have a decreased excitability threshold and other areas which have an increased excitability threshold, and that these changes in excitability importantly influence the determination of refractory period durations and conduction times.SEVERAL investigators have examined changes in refractory period duration and conduction that accompany

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Section: Methodsmentioning

confidence: 99%

Section: Figure 1 Excitability Changes Expressed As Change In Threshmentioning

confidence: 99%

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confidence: 99%

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Alterations in canine myocardial excitability during ischemia.

Elharrar

Foster

Jirak

et al. 1977

Circulation Research

150

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“…With release of the occlusion and reperfusion there is very rapid return to control levels. The observed changes in activation time indicate that the conduction velocity in the ischemic myocardium is initially accelerated (before Tc) and then later depressed (after Tc) by the ischemic process (18). In addition, the corresponding and near simultaneous change in V suggests that it also is in some manner related to the alterations in the conduction velocity of the depolarizing wave as it travels through the ischemic myocardium.…”

Section: Discussionmentioning

confidence: 78%

The QRS complex during myocardial ischemia. An experimental analysis in the porcine heart.

Holland¹,

Brooks²

1976

J. Clin. Invest.

169

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A B S T R A C T Although ST segment deflections have been widely utilized as a means of assessing the degree of underlying ischemic injury, the relationship of QRS complex alterations to the ischemic process is poorly understood. In this study we made a beat-to-beat analysis of the QRS complex in terms of ventricular activation time (CT) and R wave voltage (V) in the acutely ischemic porcine myocardium and analyzed the relationship of these responses to changes in the area of ischemic involvement, altered myocardial energy demands, and plasma [K+]o levels.With the onset of ischemia the QRS complex underwent a specific and reproducible biphasic sequence with an initial decrease in CT and V indicating a transient increase in the conduction velocity of the ischemic tissue. Subsequently both CT and V returned briefly to control and then increased dramatically, now indicating a marked decrease in conduction velocity. The time when CT first began to increase (Tc) was shortened by enlarging the area of ischemia or after an inotropic intervention and was lengthened by decreasing the area of ischemia or with administration of propranolol. Moreover Tc was found to be inversely proportional to plasma [K+]o in the range 3.4-8.8 mM, above which the initial decrease in CT and V was no longer present.We conclude that this biphasic sequence of QRS alterations in early myocardial ischemia is attributable to a progressive leakage of potassium out of the ischemic cells which in turn alters both the time-course and transmural pathway of the activation process through the ischemic tissue. These changes are related to both inotropic state and the area of ischemic involvement. INTRODUCTIONAlthough ST segment deflections have been widely utilized as a means of assessing the degree of underlying ischemic injury (1, 2) the relationship of QRS complex alterations to the ischemic process is poorly understood. The casual observations of changes in R wave amplitude noticed by some ST segment investigators after coronary artery occlusion in the dog (3-5) as well as the more specific studies of , Scher (9), and Durrer and van der Tweel (10) in the dog and goat suggest that ischemic QRS complex alterations may bear characteristic temporal and/or spatial relationships to the underlying ischemic process.In the present study we have characterized the temporal sequence of QRS complex alterations during early myocardial ischemia in the intact porcine heart, their modification by changes in the area of ischemic involvement, and altered myocardial energy demands, as well as the important role of potassium in their genesis.

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“…These results, therefore, should not be construed to mean that a 75% flow reduction will consistently result in an increase ERP due to a temperature decrease. In fact, four of nine dogs in table 3 showed a slight decrease in ERP. Apparently, the magnitude and direction of change in conduction and refractoriness is not a simple function of ischemia alone.…”

Section: Electrophysiologymentioning

confidence: 99%

Electrophysiologic effects of partial coronary flow reduction in the exposed canine heart. Effects of ischemia and ischemic-induced regional hypothermia on refractoriness and conduction delay.

Daniel¹,

Svenson²,

Masters³

et al. 1978

Circulation

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SUMMARY In the open-chested dog, coronary flow reduction results in a decrease of regional myocardial temperature (T). We assessed the contribution of T decrease to changes in refractoriness and conduction delay attributed to ischemia. The independent effect of regional hypothermia on effective refractory period (ERP) was a linear function of the temperature (ERP =-b T + a) with a F = 0.97 ± 0.02 in 11 dogs. The effect on conduction time of a ventricular premature beat was a linear function of the log T at both endocardium (f = 0.95 ± 0.02) and epicardium (F = 0.96 ± 0.01). A 75% reduction in coronary flow resulted in a mean T decrease of 1.9 ± 0.30 C. The T decrease was sufficient to mask the effects of ischemia on shortening of the ERP. Furthermore, the conduction delay of ventricular premature beats during 75% coronary flow reduction could be accounted for by the decrease in T alone in five of seven dogs. We We hypothesized that a drop in regional temperature caused by a regional decrease in coronary blood flow in the exposed heart would contribute to measured changes in refractoriness and intramyocardial conduction. To test this hypothesis, the independent effect of graded regional hypothermia on ventricular effective refractory period (ERP) and intramyocardial conduction were analyzed and compared to the effects of 75% coronary flow reduction. The accompanying temperature changes were taken into account and its contribution to refractoriness and conduction was judged from the known effects of temperature change alone. Finally, the effects of ischemia alone on ERP were "unmasked" by maintaining myocardial environmental temperature. We chose a level of 75% coronary flow reduction to gain further insight into the electrophysiologic effect of partial coronary artery occlusion. Materials and MethodsMongrel dogs weighing 18-32 kg (23 ± 1) were anesthetized with intravenous pentobarbital (30 mg/kg). The heart was exposed through a left lateral thoracotomy and suspended in a pericardial cradle. The left anterior descending (LAD) coronary artery was isolated proximally before the first large diagonal branch. The sinus node was crushed and left atrial pacing was instituted at a cycle length of 300 msec.

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The Initial Electrophysiologic Disturbance in Experimental Myocardial Infarction.

Cited by 24 publications

References 0 publications

Alterations in canine myocardial excitability during ischemia.

Alterations in canine myocardial excitability during ischemia.

The QRS complex during myocardial ischemia. An experimental analysis in the porcine heart.

Electrophysiologic effects of partial coronary flow reduction in the exposed canine heart. Effects of ischemia and ischemic-induced regional hypothermia on refractoriness and conduction delay.

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