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VALsartan In Diastolic Dysfunction - VALIDD – Presented at ACC 2007
Description:
The goal of the trial was to evaluate blood pressure lowering with valsartan compared with blood pressure lowering without an inhibitor of the renin-angiotensin-aldosterone system (RAAS) among patients with diastolic dysfunction.
Study Design
Study Design:
Patients Screened: 482
Patients Enrolled: 384
Mean Follow Up: 9 months
Mean Patient Age: Mean age, 60 years
Female: 51
Patient Populations:
Age >45 years, history of or untreated hypertension, no evidence of heart failure, and evidence of diastolic dysfunction based on low lateral annular relaxation velocities on Doppler assessment
Exclusions:
LVEF ≤50%, hypertension ≥ stage 3, creatinine >2.5 mg/dl, uncontrolled diabetes, or heart failure within the prior year
Primary Endpoints:
Change in myocardial relaxation velocity at 9 months
Drug/Procedures Used:
Following Doppler identification of evidence of diastolic dysfunction, patients were randomized in a double-blind manner to blood pressure lowering with valsartan (320 mg/d; n = 186) or blood pressure lowering without an inhibitor of the RAAS (n = 198) for 38 weeks. Target blood pressure was 135/80 mm Hg in both groups. Both groups were treated with standard blood pressure-lowering therapies, including diuretics, beta-blockers, or calcium channel blockers.
Principal Findings:
Mean blood pressure at baseline was 144/86 mm Hg and mean left ventricular ejection fraction (LVEF) was 57%. Antihypertensive therapy was being used at baseline in 76% of patients. Diabetes was present in 12% of patients. Less than 3% of patients at entry had LV hypertrophy.
Systolic blood pressure was reduced in both treatment groups compared with baseline (by 13 mm Hg in the valsartan group and by 10 mm Hg in the control group), without a difference between groups. Likewise, the primary endpoint of change in myocardial relaxation velocity at 9 months was significantly increased from baseline (by 0.60 cm/s in the valsartan group and by 0.44 cm/s in the control group), without a difference between groups (p = 0.29). LV mass index was reduced by 3.9 in the valsartan group and 3.8 in the control group (p = 0.84 between groups).
Interpretation:
Among patients with diastolic dysfunction, treatment with valsartan was not associated with a difference in change in myocardial relaxation velocity at 38-week follow-up compared with treatment without a RAAS inhibitor.
Both treatment arms showed significant improvements in myocardial relaxation velocity from baseline, without a difference between groups. It should be noted that at study entry, patients had very mild hypertension and very few had LV hypertrophy; the effect of RAAS inhibitors on diastolic dysfunction in patients with more severe hypertension or more prevalent LV hypertrophy is unknown.
References:
Solomon SD, et al. Effect of angiotensin receptor blockade and antihypertensive drugs on diastolic function in patients with hypertension and diastolic dysfunction: a randomised trial. Lancet 2007; 369: 2079–87.
Presented by Dr. Scott D. Solomon at the American College of Cardiology Annual Scientific Session, New Orleans, LA, March 2007.
Keywords: Hypertrophy, Left Ventricular, Follow-Up Studies, Diuretics, Renin-Angiotensin System, Blood Pressure, Valine, Tetrazoles, Calcium Channel Blockers, Angiotensin II Type 1 Receptor Blockers, Heart Failure, Stroke Volume, Diabetes Mellitus, Hypertension
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