The left atrial appendage (LAA) is a small pouch located in the left atrium (LA). It is the most common thrombosis site due to its tendency to accumulate stagnant blood, especially when endocardial motion is impaired (e.g., due to fibrotic tissue or atrial fibrillation). The resulting blood stasis leads to an increased risk of blood clot formation and ischemic stroke. Although the underlying mechanisms of coagulation and thrombogenesis are complex, the residence time (RT) of blood inside the cavity is often used as a surrogate marker for stasis and a risk index for thrombosis. Previous studies employed computational fluid dynamics (CFD) analysis to investigate how deranged atrial wall motion impacts flow and LAA stasis. However, most of these works used simplified models for atrial wall motion. There is thus a paucity of mechanistic studies resolving the effect of tissue fibrosis. To bridge this gap, we perform high-resolution, patient-specific electro-mechanical (EM) simulations of the cardiac tissue. The EM model gives us the possibility to apply several different fibrosis patterns to the same underlying LA anatomy. In addition to the fibrosis pattern, we can separately vary the amount of fibrotic tissue (i.e., fibrosis burden). Based on the resulting set of distinct motion profiles for the same baseline LA geometry, we perform CFD simulations. This allows us to independently investigate the effects of fibrosis burden and pattern on the CFD results, in particular, the LA and LAA blood RTs. The results suggest that the changes of RT inside the LA are mainly determined by the amount of fibrosis and only marginally sensitive to the specific pattern. In contrast, the RT inside the LAA is influenced by non-trivial changes in the global flow dynamics and is sensitive to both fibrosis pattern and burden.