Valsartan reduced the risk of first morbid event (HR 0.74; 95% CI 0.60-0.91; P=0.005) and heart failure hospitalization in patients with low baseline systolic blood pressure (≤110 mm Hg).
RCT (n=5,010)
Does valsartan improve morbidity and mortality in heart failure patients across different baseline systolic blood pressure quartiles?
Valsartan provides cardiovascular protective effects in heart failure patients regardless of baseline systolic blood pressure, including those with SBP <110 mm Hg, without further lowering blood pressure in this high-risk group.
Effect estimate: HR 0.74 (95% CI 0.60 to 0.91)
p-value: p=0.005
Background— Low systolic blood pressure (SBP) is a risk factor for adverse outcomes in patients with heart failure (HF). Valsartan improved morbidity rates in the Valsartan Heart Failure Trial (Val-HeFT) despite a reduction in SBP. The aim of the present study was to investigate the relationship between the SBP-lowering effects of valsartan and its cardiovascular protective effects in this population. Methods and Results— Baseline measurements and changes in SBP at 4 months were related to mortality and morbidity rates. The effects of valsartan on these end points were compared in quartiles of baseline SBP with multivariable Cox proportional hazards regression models that included a test for interaction between the effects of valsartan treatment and baseline SBP and examined the effects of changes in SBP on the valsartan effect. The mean�SD baseline SBP in all patients (n=5010) was 124�18 mm Hg. Patients in the lowest quartile of SBP (SBP ≤110 mm Hg; mean SBP 102 mm Hg; n=940) had more severe HF and a significantly increased adjusted risk of death (hazard ratio HR, 1.21; 95% confidence interval CI, 1.03 to 1.43; P =0.02), first morbid event (HR, 1.25; 95% CI, 1.10 to 1.40; P =0.001), and hospitalization for HF (HR, 1.45; 95% CI, 1.22 to 1.73; P <0.001) than did patients in the upper 3 quartiles of baseline SBP (mean SBP 130 mm Hg; n=3260). Valsartan reduced SBP in patients in the upper 3 quartiles but not in patients in the lowest quartile who had a baseline SBP <110 mm Hg. Valsartan was associated with decreases in the risks of first morbid event (HR, 0.74; 95% CI, 0.60 to 0.91; P =0.005) and hospitalization for HF (HR, 0.60; 95% CI, 0.45 to 0.79; P <0.001) in the lowest quartile that were not significantly different than the valsartan effects in the other 3 quartiles combined (first morbid event HR, 0.90; 95% CI, 0.79 to 1.02; P =0.10; and HF hospitalization HR, 0.77; 95% CI, 0.64 to 0.93; P =0.006; nonsignificant interactions). The decrease in SBP from baseline to 4 months was an independent risk factor for subsequent events. When changes in SBP were added to the regression model, the effects of valsartan in the lowest quartile and in the other 3 quartiles combined did not change substantially. Conclusion— Baseline SBP and a decrease in SBP over time were risk factors for adverse events in HF. Valsartan reduced SBP but not in the high-risk group of patients who had a baseline SBP <110 mm Hg. The beneficial effects of valsartan did not vary significantly with baseline SBP, and decreases in SBP did not counteract the beneficial effects on HF morbidity rates.
Anand et al. (Thu,) conducted a rct in Heart failure (n=5,010). Valsartan was evaluated on First morbid event in the lowest systolic blood pressure quartile (≤110 mm Hg) (HR 0.74, 95% CI 0.60 to 0.91, p=0.005). Valsartan reduced the risk of first morbid event (HR 0.74; 95% CI 0.60-0.91; P=0.005) and heart failure hospitalization in patients with low baseline systolic blood pressure (≤110 mm Hg).
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