Abnormal initiation and conduction of slow-wave activity in gastroparesis, defined by high-resolution electrical mapping.
OBJECTIVE
Interstitial cells of Cajal (ICC) generate slow waves. Disrupted ICC networks and gastric dysrhythmias are each associated with gastroparesis. However, there are no data on the initiation and propagation of slow waves in gastroparesis because research tools have lacked spatial resolution. We applied high-resolution electrical mapping to quantify and classify gastroparesis slow-wave abnormalities in spatiotemporal detail.


METHODS
Serosal high-resolution mapping was performed using flexible arrays (256 electrodes; 36 cm(2)) at stimulator implantation in 12 patients with diabetic or idiopathic gastroparesis. Data were analyzed by isochronal mapping, velocity and amplitude field mapping, and propagation animation. ICC numbers were determined from gastric biopsy specimens.


RESULTS
Mean ICC counts were reduced in patients with gastroparesis (2.3 vs 5.4 bodies/field; P < .001). Slow-wave abnormalities were detected by high-resolution mapping in 11 of 12 patients. Several new patterns were observed and classified as abnormal initiation (10/12; stable ectopic pacemakers or diffuse focal events; median, 3.3 cycles/min; range, 2.1-5.7 cycles/min) or abnormal conduction (7/10; reduced velocities or conduction blocks; median, 2.9 cycles/min; range, 2.1-3.6 cycles/min). Circumferential conduction emerged during aberrant initiation or incomplete block and was associated with velocity elevation (7.3 vs 2.9 mm s(-1); P = .002) and increased amplitudes beyond a low base value (415 vs 170 μV; P = .002).


CONCLUSIONS
High-resolution mapping revealed new categories of abnormal human slow-wave activity. Abnormalities of slow-wave initiation and conduction occur in gastroparesis, often at normal frequency, which could be missed by tests that lack spatial resolution. Irregular initiation, aberrant conduction, and low amplitude activity could contribute to the pathogenesis of gastroparesis.
Department of Surgery, University of Auckland, Auckland, New Zealand; Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand. Electronic address: gog@ps.gen.nz.
Gregory
G
O'Grady
Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Timothy R
TR
Angeli
Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Peng
P
Du
Division of Gastroenterology, University of Mississippi Medical Center, Jackson, Mississippi.
Chris
C
Lahr
Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand; Department of Physiology, UAE University, United Arab Emirates.
Wim J E P
WJEP
Lammers
Department of Surgery, University of Auckland, Auckland, New Zealand.
John A
JA
Windsor
Division of Gastroenterology, University of Mississippi Medical Center, Jackson, Mississippi.
Thomas L
TL
Abell
Division of Enteric Neurosciences, Mayo Clinic, Rochester, Minnesota.
Gianrico
G
Farrugia
Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand; Department of Surgery, Vanderbilt University, Nashville, Tennessee.
Andrew J
AJ
Pullan
Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand; Department of Surgery, Vanderbilt University, Nashville, Tennessee.
Leo K
LK
Cheng
D000328:Adult; D001683:Biological Clocks; D001706:Biopsy; D004599:Electric Stimulation Therapy; D004568:Electrodiagnosis / Q000379:methods*; D005260:Female; D005746:Gastric Emptying; D018589:Gastroparesis / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D056885:Interstitial Cells of Cajal / Q000473:pathology*; D008297:Male; D008564:Membrane Potentials; D008875:Middle Aged; D012815:Signal Processing, Computer-Assisted; D013997:Time Factors