Atorvastatin (Ator) treatment did not improve systolic cardiac function but increased mortality in cVclKO mice. Echocardiographic analysis was performed in 5-wk-old cVclKO and control animals at baseline (0 wk), followed by 2-wk intervals after the initiation of statin. A) VCF: echocardiogram data were analyzed for all time points (until 18 wk) by a baseline adjusted RM 3-way ANOVA with the factors genotype, treatment, and time. Improved cardiac function (VCF) for pravastatin (Prava)-treated cVclKO mice was noted at the 12-wk timepoint (gray shading, P < 0.05) when compared to cVclKO+Vehicle (Veh). B) Kaplan-Meier survival analysis. After 6 wk survival of cVclKO+Ator was reduced when compared to cVclKO+Veh and cVclKO+Prava (gray shading, 4 deaths of 19 VclKO+A animals, 0 deaths of 16 cVclKO+Veh, and 0 deaths of 18 cVclKO+Prava; P < 0.05). After 16 wk, survival of cVclKO+Ator animals was reduced when compared to cVclKO+Veh and cVclKO+Prava (13 deaths of 19 VclKO+Ator, 9 deaths of 16 cVclKO+Veh, and 7 deaths of 18 cVclKO+Prava). Survival analysis at 44 wk did not show any significant change in cVclKO survival (Ctrl+Veh, n = 28; Ctrl+Ator, n = 21; Ctrl+Prava, n = 29; cVclKO+Veh, n = 16; cVclKO+Ator, n = 19; and cVclKO+Prava, n = 18; Gehan-Breslow-Wilcoxon test, cVclKO+Veh vs. cVclKO+Prava, P = 0.7499; cVclKO+Veh vs. cVclKO+Ator, P = 0.1165; and cVclKO+Ator vs. cVclKO+Prava, P = 0.086).