In the PI group, 440 pulmonary artery emboli (PE) were identified, with an average of 14.2 emboli per patient. The most common emboli were found in the right lower lobe artery (61.29%), the right segmental arteries of segments 9 and 10 (74.19%), and the left segmental artery of segment 8 (70.97%). Notably, no PI occurred in the absence of a subsegmental embolus (SSE), indicating that SSEs are a necessary prerequisite for infarct development. Nevertheless, not all SSEs led to infarction, as 21 cases of SSE were observed without subsequent infarction, suggesting potential compensatory perfusion mechanisms.

Analysis of peripheral iodine concentration revealed significant differences depending on the level of embolic occlusion. In segments with isolated SSE, the iodine concentration was lowest, with a ratio of 0.27 (SD ± 0.19). In contrast, in segments with segmental emboli (SE), the ratio was 0.84 (SD ± 0.33), with lobar emboli (LE) it was 1.01 (SD ± 0.15), and with central emboli (CE) it was 0.85 (SD ± 0.08), all significantly higher (p < 0.0001 and p = 0.004, respectively; see Figure 2). A comparison between segments with SSE (ratio 0.27 ± 0.19) and more centrally located emboli (SE + LE + CE, ratio 0.80 ± 0.33) also demonstrated a significant difference (p < 0.0001; see Figure 3).

Iodine concentration in infarcted segments did not differ significantly between early and manifest infarcts. In segments without infarction, the ratio was 0.21 (SD ± 0.17), while in segments with early infarction, it was 0.16 (SD ± 0.12), and in those with manifest infarction, it was 0.16 (SD ± 0.13) (H = 3.59; p = 0.17) (see Figure 4). This indicates that the perfusion deficit is already maximally pronounced in the early stages of infarction and does not worsen over time.