## 4 Results  
### Baseline Cardiac Function in PHD1\({}^{-/-}\) Mice  
Echocardiography was performed on the WT mice and PHD1\({}^{-/-}\) mice at baseline, and various parameters were analyzed. When compared to the WT mice, the PHD1\({}^{-/-}\) mice showed no significant difference in mean HR (446.8 \(\pm\) 28.46 vs. 447 \(\pm\) 22 beats per minute), ejection fraction (67.54 \(\pm\) 3.36% vs. 69 \(\pm\) 3.11%), and fractional shortening (36.99 \(\pm\) 2.542% vs. 38.15 \(\pm\) 2.595%). There was no significant difference in the left ventricular diastolic interventricular diameter (LVIDd) between the two groups at baseline (3.558 \(\pm\) 0.1465 mm vs. 3.534 \(\pm\) 0.007 mm) as well as left ventricle interventricular diameter at systole (LVIDs) (2.242 \(\pm\) 0.135 mm vs. 2.182 \(\pm\) 0.093 mm) (n = 9-12) [21]. PHD1\({}^{-/-}\) Mice Show Increased Capillary Density and Arteriolar Density Compared to WT Mice After MI  
Cardiac tissue samples were taken from the at-risk areas of each group of mice on postoperative day seven to determine capillary and arteriolar density via immunohistochemistry. No significant difference was found between the capillary density of WTS mice and PHD1\({}^{-/-}\) S mice (3209 vs. 2975 counts/mm\({}^{2}\), \(p\) = 0.4673). Our results demonstrate the preservation of capillary density in the cardiac tissue in PHD1\({}^{-/-}\) MI mice compared to PHD1\({}^{-/-}\) S mice (3066 \(\pm\) 182 vs. 2975 \(\pm\) 36.6, \(p\) = 0.9856). In contrast, there was a significant reduction in capillary density in the WTMI mice compared to the WTS mice (2415 \(\pm\) 41.2 vs. 3209 \(\pm\) 87.26, \(p\) = 0.0002). Notably, although there was no significant difference between the WT mice and PHD1\({}^{-/-}\) mice after undergoing a sham procedure, there was a significant difference in capillary density following MI in the two groups, with the PHD1\({}^{-/-}\) MI mice showing maintenance of the capillary density in the at-risk area. In contrast, the capillary density in the WTMI myocardium was significantly decreased (3066 \(\pm\) 182 vs. 2415 \(\pm\) 41.2, \(p\) = 0.0014) (n = 4-5) (Figure 2A,B). Figure 2: (**A**) Representative microphotographs of immunohistochemistry analysis demonstrating capillary density in cardiac tissue for each group of mice. There is a significant increase in capillary density in PHD1\({}^{-/-}\) MI mice compared to WTMI mice. (**B**) The capillary density in each group of murine cardiac tissue is represented in bar graph form (n = 4–5). ns represents no difference in capillary density between the groups, while asterisks represent the degree of significance between the two groups. (**C**) Representative microphotographs of immunofluorescence study demonstrating capillary density in cardiac tissue for each group of mice. There is a significant increase in arteriolar density in PHD1\({}^{-/-}\) MI mice compared to WTMI mice. (**D**) Arterial density in murine cardiac tissue of each group is represented in bar graph form (n = 4). Values are mean \(\pm\) SEM. ns represents  
no difference in capillary density between the groups, while asterisks represent the degree of significance between the two groups (**\(p<0.01\);***\(p<0.001\)). Yellow arrow denotes capillaries and white arrow denotes arterioles. Similarly, we analyzed the arteriolar density in the at-risk area of the myocardial tissues and found results correlating to capillary density. We found no significant difference between the arteriolar density of the WTS mice and PHD1\({}^{-/-}\) S mice (27.75 \(\pm\) 1.594 vs. 28.41 \(\pm\) 1.008 counts/mm\({}^{2}\), \(p\) = 0.9998). Our results again demonstrate the preservation of arteriolar density in the cardiac tissue in PHD1\({}^{-/-}\) MI mice when compared to PHD1\({}^{-/-}\) S mice (29.41 \(\pm\) 1.726 vs. 28.41 \(\pm\) 1.008, \(p\) = 0.9975). Conversely, there was a significant reduction in arteriolar density in the WTMI mice when compared to the WTS mice (19.51 \(\pm\) 1.329 vs. 27.75 \(\pm\) 1.594, \(p\) = 0.0097).