Cardiac fibrosis occurs in many forms of heart disease. It is well established that the spatial pattern of fibrosis, its texture, substantially affects the onset of arrhythmia. However, in most modelling studies fibrosis is represented by multiple randomly distributed short obstacles that mimic only one possible texture, diffuse fibrosis. An important characteristic feature of other fibrosis textures, such as interstitial and patchy textures, is that fibrotic inclusions have substantial length, which is suggested to have a pronounced effect on wave propagation. In this paper, we study the effect of the elongation of inexcitable inclusions (obstacles) on wave propagation in a 2D model of cardiac tissue described by the TP06 model for human ventricular cells. We study in detail how the elongation of obstacles affects various characteristics of the waves. We quantify the anisotropy induced by the textures, its dependency on the obstacle length and the effects of the texture on the shape of the propagating wave. Because such anisotropy is a result of zig-zag propagation we show, for the first time, quantification of the effects of geometry and source-sink relationship, on the zig-zag nature of the pathway of electrical conduction. We also study the effect of fibrosis in the case of pre-existing anisotropy and introduce a procedure for scaling of the fibrosis texture. We show that fibrosis can decrease or increase the preexisting anisotropy depending on its scaled texture.