Electrophysiologic characteristics of human ventricular and Purkinje fibers.

Dangman, Kenneth H.; Danilo, Peter; Hordof, Allan J.; Mary-Rabine, L; Reder, Robert F.; Rosen, M R

doi:10.1161/01.cir.65.2.362

Cited by 85 publications

(45 citation statements)

References 14 publications

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“…The loss of cells and cell-to-cell connection that occurs in chronic infarction has been associated with both generalized and local abnormalities of activation in other preparations.20 22 The changes in P layer activation noted in the present study, specifically generalized slowing, local conduction block, and fragmentation as well as electrotonic distortion of action potentials, are strikingly similar qualitatively to abnormalities noted in canine epicardial muscle overlying a chronic infarction20-22 and in isolated human tissue. 23,[36][37][38] It seems clear from our late studies of P and VM activation that the P layer in ischemic regions remains quite viable electrophysiologically, despite complete loss of the underlying VM layer. Despite rather modest generalized slowing, 1:1 conduction was routinely maintained even to sites deep within the ischemic zone.…”

Section: Discussionmentioning

confidence: 99%

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Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction.

et al. 1987

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Permanent coronary occlusion produces time-dependent changes in surviving subendocardial cellular properties. We compared the functional alterations in Purkinje (P) and ventricular muscle (VM) activation early (24 hr) and late (4 weeks or greater) after permanent coronary occlusion in an in vitro preparation of canine papillary muscle. High-density extracellular (1 to 2 mm resolution) and selected intracellular recordings were made in five animals early and seven animals late during stimulation of a free-running P strand. Activation patterns of P and VM layers from ischemic and unaffected papillary muscles were compared in the same animal. Average P layer conduction velocity was determined in normal and ischemic regions with the use of a linear array of recording and stimulating electrodes. Purkinje activation was altered little in the early phase of infarction, while healing was associated with a generalized 25% reduction in P layer conduction velocity and localized block and fragmentation of P waveforms. Intracellular recordings at sites of nonsynchronous P activation revealed electrotonic interaction between cell groups. At 24 hr, small groups of VM were present but with abnormal activation patterns in regions of necrosis with fragmented and delayed extracellular waveforms produced by partially uncoupled groups of cells. Local delay and block could be modulated by rate and site of stimulation. After healing, VM activation abruptly stopped at the visual infarct border, marked by a characteristic "end potential." These studies demonstrate important differences in the functional attributes of the P and VM layers studied early and late after coronary occlusion. Alterations in cell-to-cell relationships are likely very important in determining abnormalities of activation in both settings.

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Section: Discussionmentioning

confidence: 99%

“…Microelectrode studies of human subendocardium have 37 also documented the persistence of viable P activity.…”

Section: Circulation Laboratory Investigation-electrophysiologymentioning

confidence: 99%

Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction.

et al. 1987

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“…The extracelhlar potassium concentration is the primary determinant of resting membrane potential in human cardiac muscle; decreased extracellular potassium will prolong action potential duration; i.e., prolonged QT interval, as well as increase the rate of spontaneous phase 4 depolarization (increase automaticity), and hyperpolarize the resting membrane potential. 16,17 In the potassium deficient state, extraceUular potassium decreases more than intracellular 7 and, as described by the Nernst equation, IS results in membrane hyper-polarization. Isolated chronic hypokalaemia is known to induce Tp,2.1s but this is the first report demonstrating that a rapid onset extracellular hypokalaemia may also induce TP.…”

Section: Discussionmentioning

confidence: 99%

Diuretic-induced hypokalaemia inducing torsades de pointes

1995

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Torsades de pointes (TP),Case report A four-yr-old 18 kg caucasian boy was scheduled for orthotopic liver and small bowel transplantation because of cirrhosis secondary to short bowel syndrome. No symptoms of central nervous system dysfunction were observed. Preoperative laboratory values included a serum potassium of 3.9 mFxl-L -l (3.5-4.7 normal) and magnesium of 2.3 rag. dl -I (1.7-3.0 normal). There was no history of arrhythmia or prolonged QT interval, or family history of sudden death. A corrected QT interval (QTc) of 370 msec was measured preoperatively ( Figure A). After uneventful induction and maintenance of anaesthesia with isoflurane and muscle relaxation with pancuronium, the native fiver was excised and the donor liver placed. During the anhepatic phase, the urine output was noted to be minimal, so furosemide, 15 mg/v, was given. During donor graR placement, the aorta was crossclamped above the renal arteries for a total of 40 rain. Following unclamping, anuria was noted. Furosemide, 180 nag,/v in divided doses was given over three hours with no effect. At that point, the Foley catheter was found to be occluded. Upon recatheterization, 2.7 1 urine were measured over the ensuing 21A hr. Over the same time, serum potassium concentration decreased from 3.9 to 2.9 mEq. L -~, while serum magnesium concentration remained unchanged at 2.3 nag. dl -~. Serum ionized calcium concentrations during this time were 1.17 to 1.18 retool. L -~ (1.18 to 1.30, normal), and arterial blood pH CAN J ANAESTH 1995 / 42:12 / pp 1137-9

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“…Although the data on this is scarce, there have in fact been a few studies performed on ventricular tissues removed from subjects with chronic heart disease during cardiac surgery Singer 1981b;Dangman 1982;Gilmour 1983a In some of the samples of depressed human ventricular tissue the slow response is abolished by the fast Na + channel blocker tetrodotoxin, in others by the slow channel blocker verapamil. This implies that the tissues have different levels of fast and slow current involvement.…”

Section: Relevance To Diseased Human Mocardiummentioning

confidence: 99%

“…There are several studies which have examined the properties of ventricular myocardium and PurkinJe tissue excised from patients undergoing heart surgery Singer 1981b;Dangman 1982;Gilmour 1983). The electrophysiological properties of these tissues appear to be quite similar -90 -to injured preparations derived from animal hearts.…”

Section: Vea In Chronic Heart Diseasementioning

confidence: 99%

A stochastic characterization of chronic ventricular ectopic activity

Albrecht

Cohen

Mark

1988

IEEE Trans. Biomed. Eng.

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Ventricular ectopic beats are clinically important because of their association with the problem of sudden cardiac death. Ventricular ectopic activity (VEA) is most commonly evaluated using long-term ambulatory electrocardiographic (ECG) recordings. The results of these recordings are usually summarized in the form of hourly counts of VEA events.Although such hourly counts are useful, they are a nonspecific measure which, in effect, treats VEA generation as an unpredictable process.This thesis develops a new means for characterizing the activity of the VEA-generating mechanism using the beat type and timing information of the long-term ECG. The approach is founded on the hypothesis that the VEA mechanism is often stable over time, although its activity may be modulated by physiologic influences and by the timing of the sino-atrial node impulses.This hypothesis implies that there should be some relationship between the beat type and timing of preceding beats and the subsequent generation of ectopic beats.The VEA generation was characterized by a multi-dimensional conditional distribution which gives the probability that an ectopic beat will follow a specific conditioning sequence of beat types and intervals. Using this approach a three part study was performed. The first step examined the conditional distributions and tested the null hypothesis that the generation of ectopic beats is unpredictable.Using a database of half-hour ECG tapes from 66 patients, the null hypothesis was rejected at p=0.005 in 80% of the tapes.The second step developed a means of displaying the multidimensional distributions. By an appropriate transformation of the conditioning variables, the distributions could be represented as one-dimensional distributions. The resulting distributions were useful for. separating patients into groups and for finding characteristic, VEA-related events in the ECG data.The third step examined the reproducibility of the onedimensional distributions over time. Using ten-hour ECG tapes, it was found that in 7 of 10 patients the patient-specific distribution, although modulated in amplitude, maintained a similar shape over the ten hours.The VEA characterization which has been developed goes significantly beyond the simple counting of ectopic beats. The distributions can be considered a kind of "fingerprint" of the VEA-generating mechanism -a "fingerprint" which may be useful in the selection and evaluation of therapy.

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Electrophysiologic characteristics of human ventricular and Purkinje fibers.

Cited by 85 publications

References 14 publications

Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction.

Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction.

Diuretic-induced hypokalaemia inducing torsades de pointes

A stochastic characterization of chronic ventricular ectopic activity

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