Variability in fibrosis in tissue samples obtained during diaphragmatic and apical LVAD implantation.
BACKGROUND
Histopathologic study of left ventricular (LV) tissue can provide structural data on the heart at the time of left ventricular assist device (LVAD) implantation. We assessed the effect of cannula placement site (apical/diaphragmatic) and cardiomyopathy etiology (ischemic/nonischemic) on cardiac histopathologic changes.


METHODS
In 77 heart failure patients, tissue was obtained from the standard apical cannula insertion site or the diaphragmatic surface site during implantation of the HeartMate II (n=53) or HeartWare (n=24) LVAD. Fibrosis and hypertrophy (cytoplasmic and nuclear diameter) were evaluated by computerized morphometry.


RESULTS
Thirty-two patients (27 men, 5 women; age, 57±15 years) underwent diaphragmatic implantation, and 45 (32 men, 13 women; age, 53±12 years) underwent apical implantation. The incidence of ischemic cardiomyopathy in the diaphragmatic and apical groups was 11/32 (34%) vs. 25/45 (56%) (P=.104). Overall, diaphragmatic tissue had less fibrosis than apical tissue (15.7±11.7% vs. 22.0±17.4%, P=.033), but both showed similar hypertrophic changes (cytoplasmic diameter, 39.0±10.3μm vs. 36.3±8.7μm, P=.141; nuclear diameter, 15.5±2.5μm vs. 14.8±3.0μm, P=.171). Likewise, in ischemic cardiomyopathy, apical samples showed more fibrosis than diaphragmatic samples (26.54±19.0% vs. 15.86±11.08%, P=.046) but similar hypertrophic changes (cytoplasmic diameter, 34.95±6.12μm vs. 37.48±12.07μm, P=.288; nuclear diameter, 14.66±2.69μm vs. 14.78±1.31μm, P=.451).


CONCLUSIONS
Myocardial histology results at the time of LVAD placement and their prognostic implications may be affected by inlet placement site and cardiomyopathy etiology. In this study, LV samples from apical implantation in ischemic cardiomyopathy patients were the most fibrotic. Thus, sampling site and cardiomyopathy etiology should be considered when interpreting LV samples obtained during LVAD implantation.
Cardiovascular Pathology Research, Texas Heart Institute, Houston, TX 77030, USA. Electronic address: asegura@texasheart.org.
Ana Maria
AM
Segura
Center for Advanced Heart Failure, The University of Texas Health Science Center, Houston, TX 77030, USA.
Rajko
R
Radovancevic
Cardiopulmonary Transplantation, Texas Heart Institute, Houston, TX 77030, USA.
Alberto
A
Aguayo
Cardiopulmonary Transplantation, Texas Heart Institute, Houston, TX 77030, USA.
O H
OH
Frazier
Cardiovascular Pathology Research, Texas Heart Institute, Houston, TX 77030, USA; Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center, Houston, TX 77030, USA.
L Maximilian
LM
Buja
D000328:Adult; D000368:Aged; D006348:Cardiac Surgical Procedures / Q000295:instrumentation*; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology*; D006353:Heart-Assist Devices; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D019919:Prosthesis Implantation / Q000295:instrumentation* / Q000379:methods; D012189:Retrospective Studies; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
Fibrosis; Heart-assist devices; Hypertrophy