A Microsurgical Arteriovenous Malformation Model on Saphenous Vessels in the Rat

Abstract

Arteriovenous malformation (AVM) is an anomaly of blood vessel formation. Numerous models have been established to understand the nature of AVM. These models have limitations in terms of the diameter of the vessels used and the impact on the circulatory system. Our goal was to establish an AVM model that does not cause prompt and significant hemodynamic and cardiac alterations but is feasible for follow-up of the AVM's progression. Sixteen female rats were randomly divided into sham-operated and AVM groups. In the AVM group, the saphenous vein and artery were interconnected using microsurgical techniques. The animals were followed up for 12 weeks. Anastomosis patency and the structural and hemodynamic changes of the heart were monitored. The hearts and vessels were histologically analyzed. During the follow-up period, shunts remained unobstructed. Systolic, diastolic, mean arterial pressure, and heart rate values slightly and non-significantly decreased in the AVM group. Echocardiogram results indicated minor systolic function impact, with slight and insignificant changes in aortic pressure and blood velocity, and minimal left ventricular wall enlargement. The small-caliber saphenous AVM model does not cause acute hemodynamic changes. Moderate but progressive alterations and venous dilatation confirmed AVM-like features. The model seems to be suitable for studying further the progression, enlargement, or destabilization of AVM.

Keywords: arteriovenous malformation; arteriovenous shunt; hemodynamics; microsurgical model; vascular remodelling.

Figure 1

Intraoperative photos of the intact vessels (A), schematic drawing of the affected vessels (B), and the localization of the anastomoses (C).

Figure 2

Intraoperative view (captured from video recording) of the freshly performed shunt (A), and the picture on the 12th postoperative week (B).

Figure 3

Representative echocardiography recordings of the control and the AVM groups.

Figure 4

Parameters obtained from the echocardiography recordings preoperatively and on the 3rd, 7th, and 12th postoperative weeks: thickness of the left ventricle posterior wall in systole (LVPWs [mm]) (A) and in diastole (LVPWd [mm]) (B), the left ventricular mass (LV mass [mg]) (C), the thickness of the left ventricle anterior wall in systole (LVAWs [mm]) (D) and in diastole (LVAWd [mm]) (E), and the aorta diameter (AO diam. [mm]) (F). Means ± S.D.

Figure 5

Parameters obtained from the echocardiography recordings preoperatively and on the 3rd, 7th, and 12th postoperative weeks: heart rate (HR [bpm]) (A), ejection fraction (EF [%]) (B), stroke volume (SV [μL]) (C), ratio of the early and atrial peak mitral inflow velocities (E/A ratio) (D), and the size of the left atrium normalized to the aortic diameter aorta diameter (LA/Ao ratio) (E). Means ± S.D. * p < 0.05 vs. Base.

Figure 6

Parameters obtained from the echocardiography recordings preoperatively and on the 3rd, 7th, and 12th postoperative weeks: peak gradient [mmHg]) (A), deceleration time (DecT [ms]) (B), and aortic mean velocity [mm/s] (C). Means ± S.D. * p < 0.05 vs. base, # p < 0.05 vs. control.

Figure 7

Representative H&E stained histological pictures of the left ventricle (A) and the saphenous vessels (C) in samples taken on the 12th postoperative week, as well as the thickness of the left ventricle wall layer and cardiomyocytes (B) and the vessel wall layers (D). H&E staining. Means ± S.D. * p < 0.05 vs. control.

Figure 8

Representative Van Gieson stained histological pictures of the left ventricle in control (A,B) and AVM group (C,D).