Recent applications of computational fluid dynamics (CFD) applied to the cardiovascular system have demonstrated its power in investigating the impact of hemodynamics on disease initiation, progression, and treatment outcomes. Flow metrics such as pressure distributions, wall shear stresses (WSS), and blood velocity profiles can be quantified to provide insight into observed pathologies, assist with surgical planning, or even predict disease progression. While numerous studies have performed simulations on clinical human patient data, it often lacks prediagnosis information and can be subject to large intersubject variability, limiting the generalizability of findings. Thus, animal models are often used to identify and manipulate specific factors contributing to vascular disease because they provide a more controlled environment. In this review, we explore the use of CFD in animal models in recent studies to investigate the initiating mechanisms, progression, and intervention effects of various vascular diseases. The first section provides a brief overview of the CFD theory and tools that are commonly used to study blood flow. The following sections are separated by anatomical region, with the abdominal, thoracic, and cerebral areas specifically highlighted. We discuss the associated benefits and obstacles to performing CFD modeling in each location. Finally, we highlight animal CFD studies focusing on common surgical treatments, including arteriovenous fistulas (AVF) and pulmonary artery grafts. The studies included in this review demonstrate the value of combining CFD with animal imaging and should encourage further research to optimize and expand upon these techniques for the study of vascular disease.

The effect of diastolic dysfunction (DD) on the timing of left ventricular (LV) diastolic longitudinal and circumferential expansion and their load dependence is not known. This study evaluated the timing of the peak early diastolic LV inflow velocity (E), mitral annular velocity (e′), and longitudinal and circumferential global strain rates (SRE) in 161 patients in sinus rhythm. The intraventricular pressure difference (IVPD) from the left atrium to the LV apex was obtained using color M‐mode Doppler data to integrate the Euler equation. The diastolic function was graded according to the guidelines. In normals ( N = 57), E, e′, longitudinal SRE, and circumferential SRE occurred nearly simultaneously during the IVPD. With DD ( N = 104), e′ and longitudinal SRE were delayed occurring after the IVPD (e′: 18 ± 23 msec, longitudinal SRE: 13 ± 21 msec from the IVPD), whereas circumferential SRE (−8 ± 28 msec) and E (−2 ± 13 msec) were not delayed. The normal dependence of e′ and longitudinal SRE on IVPD was reduced in DD; while the relation of circumferential SRE and E to IVPD were unchanged in DD. Thus, normally, the LV expands symmetrically during early diastole and both longitudinal and circumferential expansions are related to the IVPD. With DD, early diastolic longitudinal LV expansion is delayed, occurring after the IVPD and LV filling, resulting in their relative independence from the IVPD. In contrast, with DD, circumferential SRE and mitral inflow are not delayed and their normal relation to the IVPD is unchanged.