Use of Atrial Fibrillation Electrograms and T1/T2 Magnetic Resonance Imaging to Define the Progressive Nature of Molecular and Structural Remodeling : A New Paradigm Underlying the Emergence of Persistent Atrial Fibrillation
BACKGROUND: The temporal progression states of the molecular and structural substrate in atrial fibrillation (AF) are not well understood. We hypothesized that these can be detected by AF electrograms and magnetic resonance imaging parametric mapping.
METHODS AND RESULTS: AF was induced in 43 dogs (25-35 kg, ≥1 year) by rapid atrial pacing (RAP) (3-33 weeks, 600 beats/min), and 4 controls were used. We performed high-resolution epicardial mapping (UnEmap, 6 atrial regions, both atria, 130 electrodes, distance 2.5 mm) and analyzed electrogram cycle length, dominant frequency, organization index, and peak-to-peak bipolar voltage. Implantable telemetry recordings were used to quantify parasympathetic nerve activity over RAP time. Magnetic resonance imaging native T1, postcontrast T1, T2 mapping, and extracellular volume fraction were assessed (1.5T, Siemens) at baseline and AF. In explanted atrial tissue, DNA oxidative damage (8-hydroxy-2'-deoxyguanosine staining) and percentage of fibrofatty tissue were quantified. Cycle length and organization index decreased (R=0.5, P<0.05; and R=0.5, P<0.05; respectively), and dominant frequency increased (R=0.3, P n.s.) until 80 days of RAP but not thereafter. In contrast, voltage continued to decrease throughout the duration of RAP (R=0.6, P<0.05). Parasympathetic nerve activity increased following RAP and plateaued at 80 days. Magnetic resonance imaging native T1 and T2 times increased with RAP days (R=0.5, P<0.05; R=0.6, P<0.05) in the posterior left atrium throughout RAP. Increased RAP days correlated with increasing 8-hydroxy-2'-deoxyguanosine levels and with fibrosis percentage (R=0.5, P<0.05 for both).
CONCLUSIONS: A combination of AF electrogram characteristics and T1/T2 magnetic resonance imaging can detect early-stage AF remodeling (autonomic remodeling, oxidative stress) and advanced AF remodeling due to oxidative stress and fibrosis.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2024 |
---|---|
Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:13 |
---|---|
Enthalten in: |
Journal of the American Heart Association - 13(2024), 5 vom: 05. März, Seite e032514 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Rottmann, Markus [VerfasserIn] |
---|
Links: |
---|
Themen: |
8-Hydroxy-2'-Deoxyguanosine |
---|
Anmerkungen: |
Date Completed 11.03.2024 Date Revised 18.03.2024 published: Print-Electronic Citation Status MEDLINE |
---|
doi: |
10.1161/JAHA.123.032514 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM364219211 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | NLM364219211 | ||
003 | DE-627 | ||
005 | 20240318233806.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231226s2024 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1161/JAHA.123.032514 |2 doi | |
028 | 5 | 2 | |a pubmed24n1334.xml |
035 | |a (DE-627)NLM364219211 | ||
035 | |a (NLM)37930082 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Rottmann, Markus |e verfasserin |4 aut | |
245 | 1 | 0 | |a Use of Atrial Fibrillation Electrograms and T1/T2 Magnetic Resonance Imaging to Define the Progressive Nature of Molecular and Structural Remodeling |b A New Paradigm Underlying the Emergence of Persistent Atrial Fibrillation |
264 | 1 | |c 2024 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 11.03.2024 | ||
500 | |a Date Revised 18.03.2024 | ||
500 | |a published: Print-Electronic | ||
500 | |a Citation Status MEDLINE | ||
520 | |a BACKGROUND: The temporal progression states of the molecular and structural substrate in atrial fibrillation (AF) are not well understood. We hypothesized that these can be detected by AF electrograms and magnetic resonance imaging parametric mapping | ||
520 | |a METHODS AND RESULTS: AF was induced in 43 dogs (25-35 kg, ≥1 year) by rapid atrial pacing (RAP) (3-33 weeks, 600 beats/min), and 4 controls were used. We performed high-resolution epicardial mapping (UnEmap, 6 atrial regions, both atria, 130 electrodes, distance 2.5 mm) and analyzed electrogram cycle length, dominant frequency, organization index, and peak-to-peak bipolar voltage. Implantable telemetry recordings were used to quantify parasympathetic nerve activity over RAP time. Magnetic resonance imaging native T1, postcontrast T1, T2 mapping, and extracellular volume fraction were assessed (1.5T, Siemens) at baseline and AF. In explanted atrial tissue, DNA oxidative damage (8-hydroxy-2'-deoxyguanosine staining) and percentage of fibrofatty tissue were quantified. Cycle length and organization index decreased (R=0.5, P<0.05; and R=0.5, P<0.05; respectively), and dominant frequency increased (R=0.3, P n.s.) until 80 days of RAP but not thereafter. In contrast, voltage continued to decrease throughout the duration of RAP (R=0.6, P<0.05). Parasympathetic nerve activity increased following RAP and plateaued at 80 days. Magnetic resonance imaging native T1 and T2 times increased with RAP days (R=0.5, P<0.05; R=0.6, P<0.05) in the posterior left atrium throughout RAP. Increased RAP days correlated with increasing 8-hydroxy-2'-deoxyguanosine levels and with fibrosis percentage (R=0.5, P<0.05 for both) | ||
520 | |a CONCLUSIONS: A combination of AF electrogram characteristics and T1/T2 magnetic resonance imaging can detect early-stage AF remodeling (autonomic remodeling, oxidative stress) and advanced AF remodeling due to oxidative stress and fibrosis | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a MRI | |
650 | 4 | |a arrhythmias | |
650 | 4 | |a atrial fibrillation | |
650 | 4 | |a fibrosis | |
650 | 4 | |a mapping | |
650 | 4 | |a reactive oxygen species | |
650 | 7 | |a 8-Hydroxy-2'-Deoxyguanosine |2 NLM | |
650 | 7 | |a 88847-89-6 |2 NLM | |
700 | 1 | |a Yoo, Shin |e verfasserin |4 aut | |
700 | 1 | |a Pfenniger, Anna |e verfasserin |4 aut | |
700 | 1 | |a Mikhailov, Aleksei |e verfasserin |4 aut | |
700 | 1 | |a Benefield, Brandon |e verfasserin |4 aut | |
700 | 1 | |a Johnson, David A |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Wenwei |e verfasserin |4 aut | |
700 | 1 | |a Ghosh, Asish K |e verfasserin |4 aut | |
700 | 1 | |a Kim, Daniel |e verfasserin |4 aut | |
700 | 1 | |a Passman, Rod |e verfasserin |4 aut | |
700 | 1 | |a Knight, Bradley P |e verfasserin |4 aut | |
700 | 1 | |a Lee, Daniel C |e verfasserin |4 aut | |
700 | 1 | |a Arora, Rishi |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Journal of the American Heart Association |d 2012 |g 13(2024), 5 vom: 05. März, Seite e032514 |w (DE-627)NLM222412712 |x 2047-9980 |7 nnns |
773 | 1 | 8 | |g volume:13 |g year:2024 |g number:5 |g day:05 |g month:03 |g pages:e032514 |
856 | 4 | 0 | |u http://dx.doi.org/10.1161/JAHA.123.032514 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 13 |j 2024 |e 5 |b 05 |c 03 |h e032514 |