Developing a novel AVM model using saphenous vessels in rats constitutes a significant advancement in the study of these complex vascular anomalies. This research aimed to create a non-congenital, small-caliber AVM model, distinct from existing models that typically employ artificial arteriovenous shunts of varying sizes in different locations. The methodology involved the meticulous construction of arteriovenous shunts on the saphenous vessels of 8 female Sprague Dawley rats, a process requiring advanced microsurgical skills and comparing the alterations to other 8 control female Sprague Dawley rats. This approach was chosen to minimize the risk of acute systemic hemodynamic changes often seen in other AVM models. Over a 12-week period, the model was closely monitored to evaluate any changes in cardiac and vascular histomorphology and micro-rheological parameters. A key finding from this research was that the saphenous vessel AVM model did not induce the acute hemodynamic changes typically observed in other arteriovenous shunt models. However, significant alterations in certain cardiac and vascular histomorphology parameters were noted by the end of the 12-week follow-up. This included the dilatation of shunted vessels, a characteristic feature of AVMs. Interestingly, cardiomyocytes in the AVM group exhibited notable hypertrophy, characterized by an abundance of eosinophilic cytoplasm and box-like nuclei. Furthermore, the architectural layout of the myocardium appeared disordered, indicative of myocardial disarray. Despite these alterations, there was no significant evidence of myocardial fibrosis due to microvascular ischemia in any group. Additionally, the model did not result in significant micro-rheological changes. The observed changes were likely a result of acute phase reactions rather than the presence of the shunt itself. The saphenous vessel AVM model emerges as a promising tool for studying the progression, enlargement, or destabilization of AVMs under various experimental conditions, including altered angiogenesis and vascular remodeling. Its lack of acute hemodynamic and significant micro-rheological changes positions it as an ideal model for investigating AVM presence and treatment's long-term effects. This study recommends that investigations into AVM progression, especially under varying conditions such as hypertensive or diabetic models, should begin after at least a 12- week maturation period in this model. In conclusion, this novel rat model offers a valuable pathway for enhancing our understanding of AVM pathogenesis and the effects of various interventions, while minimizing systemic circulatory impacts.