Blood pressure reduction with HMG-CoA reductase inhibitors in renal transplant recipients
- PMID: 12472804
- DOI: 10.1046/j.1523-1755.2003.00742.x
Blood pressure reduction with HMG-CoA reductase inhibitors in renal transplant recipients
Abstract
Background: Besides lowering lipid levels, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) modulate endothelial function and decrease vascular tone. The effect of statin therapy on blood pressure has not been previously examined in renal transplant recipients.
Methods: We identified 113 stable recipients with graft survival>1 year and started on a statin >or=1 year post-transplant with no subsequent alteration in type or dose, as well as >or=6 months' follow-up post-statin introduction along with no changes in antihypertensive medication type or dosage. This "statin" group was compared to a control group matched 1:1 by age, gender, donor source, year of transplant, and time since transplant who met identical criteria but were not begun on a statin. Baseline, 6 months, and 12 months outpatient blood pressure were reviewed and compared along with other possible blood pressure predictors. A multivariate analysis was performed controlling for other influences on blood pressure change.
Results: Blood pressure and baseline characteristics other than lipid levels were similar in the two groups. The systolic, diastolic, and mean arterial blood pressure decreased by 7 mm Hg (P = 0.005), 3 mm Hg (P = 0.05), and 4 mm Hg (P = 0.007), respectively, at 12 months' post-statin introduction, while no blood pressure change was seen in the control group (P = NS). At 12 months, the systolic, diastolic, and mean arterial blood pressures were lower in the statin group compared to the control group (P = 0.05, 0.03, and 0.02, respectively). These changes in blood pressure were independent of changes in serum lipid levels.
Conclusion: Renal transplant recipients exhibit a significant blood pressure reduction associated with statin therapy. This finding has important mechanistic and clinical implications in the management of cardiovascular disease risk factors in this population.
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