LVH-related changes in the myocardial tissue and extracellular matrix might be related to both an increased risk of myocardial injury due to several pathophysiological pathways (increased cardiac Ang II, endothelial dysfunction, chronic inflammation, upregulated cardiac DPP4 expression) and an abolished cardiovascular response to the stress related to the infection. Here, DPP4 is linked to endothelial dysfunction.