“…This has prompted the testing of L-type Ca 2+ channel blockers (e.g., diltiazem) (22,23), angiotensin II receptor antagonists (e.g., losartan) (24), antioxidants (e.g., N-acetylcysteine) (21,25,26), and metabolic modulators (perhexiline) (27) with success in preventing hypertrophy, fibrosis, and adverse cardiac remodeling in animal models. However, neither diltiazem (28), nor losartan (29,30), nor perhexiline (31) is able to prevent development of the cardiac phenotype in HCM patients. One possible reason for the difference in outcomes between mouse and human studies could be inclusion of patients with a variety of causal HCM mutations in clinical trials.…”