Determination of cardiovascular mechanics evolution in the presence of the arteriovenous fistula.
Uremic patients are prone to heart damage as a consequence of arteriovenous fistula (AVF) presence and hemodialysis treatment. Arteriovenous fistula induces hand ischemic syndrome and cardiac work increase, thus determining cardiac insufficiency in the medium to long term. This work investigates the cardiovascular mechanics evolution induced by the fistula presence. Twenty patients were enrolled; blood pressure, heart rate (HR), cardiac dimensions, and fistula flow were measured at scheduled intervals. A mathematical model of the cardiocirculatory system was implemented to simulate cardiovascular evolution. Input parameters were heart and vessel features; output of the model were cardiac performances indicators, partly reproducing measurable data and partly quantifiable only by using the model. Input and output variability and their long-term variations were analyzed. Blood pressure and peripheral resistance were found to be higher in uremic than in healthy subjects. Fistula tailoring showed increased cardiac fiber contractility and decreased peripheral resistances. Moreover, between 10 days and 3 months, an increased blood flow at the vascular access determined an increment in fiber contractility. In the same period, the 85% of the patients showed an increase in cardiac fiber stiffness. Similar but less pronounced trends were observed between 3 months and 1 year. The developed model reproduces the cardiovascular system in physiologic and pathologic conditions and allows description of the cardiovascular evolution for a uremic patient.
Casagrande
Giustina
G
Department of Structural Engineering, Laboratory of Biological Structure Mechanics (LaBS), Politecnico di Milano, Milan, Italy. giustina.casagrande@polimi.it
Lanzarone
Ettore
E
Miglietta
Ferruccio
F
Remuzzi
Andrea
A
Fumero
Roberto
R
Costantino
Maria Laura
ML
D000368:Aged; D001166:Arteriovenous Shunt, Surgical / Q000009:adverse effects*; D002319:Cardiovascular System / Q000503:physiopathology; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000628:therapy; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D008962:Models, Theoretical; D006435:Renal Dialysis