dc.contributor.author |
Trew, Mark L |
|
dc.contributor.author |
Engelman, Zoar J |
|
dc.contributor.author |
Caldwell, Bryan J |
|
dc.contributor.author |
Lever, Nigel A |
|
dc.contributor.author |
LeGrice, Ian J |
|
dc.contributor.author |
Smaill, Bruce H |
|
dc.coverage.spatial |
United States |
|
dc.date.accessioned |
2021-08-20T01:24:38Z |
|
dc.date.available |
2021-08-20T01:24:38Z |
|
dc.date.issued |
2019-10 |
|
dc.identifier.citation |
American journal of physiology. Heart and circulatory physiology 317(4):H743-H753 Oct 2019 |
|
dc.identifier.issn |
0363-6135 |
|
dc.identifier.uri |
https://hdl.handle.net/2292/56102 |
|
dc.description.abstract |
Altered electrical behavior alongside healed myocardial infarcts (MIs) is associated with increased risk of sudden cardiac death. However, the multidimensional mechanisms are poorly understood and described. This study characterizes, for the first time, the intramural spread of electrical activation in the peri-infarct region of chronic reperfusion MIs. Four sheep were studied 13 wk after antero-apical reperfusion infarction. Extracellular potentials (ECPs) were recorded in a ~20 × 20-mm<sup>2</sup> region adjacent to the infarct boundary (25 plunge needles <0.5-mm diameter with 15 electrodes at 1-mm centers) during multisite stimulation. Infarct geometry and electrode locations were reconstructed from magnetic resonance images. Three-dimensional activation spread was characterized by local activation times and interpolated ECP fields (<i>n</i> = 191 records). Control data were acquired in 4 non-infarcted sheep (<i>n</i> = 96 records). Electrodes were distributed uniformly around 15 ± 5% of the intramural infarct boundary. There were marked changes in pacing success and ECP morphology across a functional border zone (BZ) ±2 mm from the boundary. Stimulation adjacent to the infarct boundary was associated with low-amplitude electrical activity within the BZ and delayed activation of surrounding myocardium. Bulk tissue depolarization occurred 3.5-14.6 mm from the pacing site for 39% of stimuli with delays of 4-37 ms, both significantly greater than control (<i>P</i> < 0.0001). Conduction velocity (CV) adjacent to the infarct was not reduced compared with control, consistent with structure-only computer model results. Insignificant CV slowing, irregular stimulus-site specific activation delays, and obvious indirect activation pathways strongly suggest that the substrate for conduction abnormalities in chronic MI is predominantly structural in nature.<b>NEW & NOTEWORTHY</b> Intramural in vivo measurements of peri-infarct electrical activity were not available before this study. We use pace-mapping in a three-dimensional electrode array to show that a subset of stimuli in the peri-infarct region initiates coordinated myocardial activation some distance from the stimulus site with substantial associated time delays. This is site dependent and heterogeneous and occurs for <50% of ectopic stimuli in the border zone. Furthermore, once coordinated activation is initiated, conduction velocity adjacent to the infarct boundary is not significantly different from control. These results give new insights to peri-infarct electrical activity and do not support the widespread view of uniform electrical remodeling in the border zone of chronic myocardial infarcts, with depressed conduction velocity throughout. |
|
dc.format.medium |
Print-Electronic |
|
dc.language |
eng |
|
dc.publisher |
American Physiological Society |
|
dc.relation.ispartofseries |
American journal of physiology. Heart and circulatory physiology |
|
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. |
|
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
|
dc.subject |
Myocardium |
|
dc.subject |
Heart Conduction System |
|
dc.subject |
Animals |
|
dc.subject |
Sheep, Domestic |
|
dc.subject |
Myocardial Reperfusion Injury |
|
dc.subject |
Myocardial Infarction |
|
dc.subject |
Disease Models, Animal |
|
dc.subject |
Electrophysiologic Techniques, Cardiac |
|
dc.subject |
Cardiac Pacing, Artificial |
|
dc.subject |
Predictive Value of Tests |
|
dc.subject |
Action Potentials |
|
dc.subject |
Time Factors |
|
dc.subject |
Female |
|
dc.subject |
border zone |
|
dc.subject |
conduction |
|
dc.subject |
intramural mapping |
|
dc.subject |
myocardial infarction |
|
dc.subject |
Action Potentials |
|
dc.subject |
Animals |
|
dc.subject |
Cardiac Pacing, Artificial |
|
dc.subject |
Disease Models, Animal |
|
dc.subject |
Electrophysiologic Techniques, Cardiac |
|
dc.subject |
Female |
|
dc.subject |
Heart Conduction System |
|
dc.subject |
Myocardial Infarction |
|
dc.subject |
Myocardial Reperfusion Injury |
|
dc.subject |
Myocardium |
|
dc.subject |
Predictive Value of Tests |
|
dc.subject |
Sheep, Domestic |
|
dc.subject |
Time Factors |
|
dc.subject |
Science & Technology |
|
dc.subject |
Life Sciences & Biomedicine |
|
dc.subject |
Cardiac & Cardiovascular Systems |
|
dc.subject |
Physiology |
|
dc.subject |
Peripheral Vascular Disease |
|
dc.subject |
Cardiovascular System & Cardiology |
|
dc.subject |
border zone |
|
dc.subject |
conduction |
|
dc.subject |
intramural mapping |
|
dc.subject |
myocardial infarction |
|
dc.subject |
EPICARDIAL BORDER ZONE |
|
dc.subject |
REENTRANT VENTRICULAR-TACHYCARDIA |
|
dc.subject |
ISCHEMIC-HEART-DISEASE |
|
dc.subject |
MAGNETIC-RESONANCE |
|
dc.subject |
MYOCARDIAL-INFARCTION |
|
dc.subject |
RISK STRATIFICATION |
|
dc.subject |
MECHANISMS |
|
dc.subject |
SUBSTRATE |
|
dc.subject |
SCAR |
|
dc.subject |
RECONSTRUCTION |
|
dc.subject |
1102 Cardiorespiratory Medicine and Haematology |
|
dc.subject |
Clinical Medicine and Science |
|
dc.subject |
Cardiovascular |
|
dc.subject |
Heart Disease |
|
dc.subject |
Heart Disease - Coronary Heart Disease |
|
dc.subject |
Cardiovascular |
|
dc.subject |
0606 Physiology |
|
dc.subject |
1116 Medical Physiology |
|
dc.title |
Cardiac intramural electrical mapping reveals focal delays but no conduction velocity slowing in the peri-infarct region. |
|
dc.type |
Journal Article |
|
dc.identifier.doi |
10.1152/ajpheart.00154.2019 |
|
pubs.issue |
4 |
|
pubs.begin-page |
H743 |
|
pubs.volume |
317 |
|
dc.date.updated |
2021-07-27T03:01:55Z |
|
dc.rights.holder |
Copyright: 2019 American Physiological Society. |
en |
pubs.author-url |
https://www.ncbi.nlm.nih.gov/pubmed/31419152 |
|
pubs.end-page |
H753 |
|
pubs.publication-status |
Published |
|
dc.rights.accessrights |
http://purl.org/eprint/accessRights/RestrictedAccess |
en |
pubs.subtype |
Research Support, Non-U.S. Gov't |
|
pubs.subtype |
Journal Article |
|
pubs.elements-id |
784221 |
|
dc.identifier.eissn |
1522-1539 |
|