Pseudointima in inflow and outflow conduits of a left ventricular assist system: possible role in clinical outcome.
Activation of blood coagulation and thromboemboli have been shown to present significant clinical risks in patients supported with an left ventricular assist system (LVAS). The interaction of pseudointima (PI) with blood in the conduits of the device could be involved in these clinical complications. Our aim was to study the morphology of the PI versus duration of circulatory support. Novacor N 100 PC LVASs were explanted from 10 men and 2 women after a mean of 209 days (range 23-560 days) of circulatory assistance. PI in the inflow and outflow conduits were investigated with immunohistochemical assays. In the inflow conduits, a loosely adherent PI had built up from collagen type I and III fibers growing into and between fibrin deposits. Disorganized collagenous matrix and longitudinally oriented collagen fibers included alpha-smooth muscle actin positive cells with random orientation. Macrophages were concentrated in the fibrin and were dispersed throughout the extracellular matrix. In the outflow conduits, a thin, adherent PI was composed of regular collagen type I and III layers. Collagen type I fibers had grown into the woven Dacron and alpha-smooth muscle actin positive cells were oriented in the axis of the blood flow. Macrophages were concentrated in the Dacron and reached the inner collagen layers. Venous blood flow in the inflow conduits allows the development of a non endothelialized irregular collagenous matrix intermingled with fibrin and invaded by macrophages. These persistent structural features progress with duration of circulatory assistance and reflect matrix degradation and remodeling. The potential to release thromboembolic fragments from the non stable, thrombogenic PI may be involved in the thromboembolic or neurologic complications sustained by 5 of 12 patients who were on circulatory support for as long as 200 days.
Houël
R
R
Service de Chirurgie Thoracique et Cardiovasculaire CNRS UPRES-A 7054, Association Claude Bernard, H pital Henri Mondor, France.
Moczar
M
M
Ginat
M
M
Loisance
D
D
D000199:Actins / Q000032:analysis; D000328:Adult; D003094:Collagen / Q000032:analysis; D005260:Female; D005337:Fibrin / Q000032:analysis; D006333:Heart Failure / Q000401:mortality* / Q000473:pathology / Q000628:therapy*; D006353:Heart-Assist Devices / Q000009:adverse effects*; D006801:Humans; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011475:Prosthesis Failure; D013923:Thromboembolism / Q000401:mortality / Q000473:pathology*; D017539:Tunica Intima
D000199:Actins; D005337:Fibrin; D003094:Collagen