Effects of Nifedipine-GITS on Left Ventricular Mass and Left Ventricular Filling

Abstract

Summary: Sixteen patients with initial diastolic blood pressure ≥ 120 mm Hg were treated for 1 year with extendedrelease nifedipine [nifedipine-GITS (gastrointestinal therapeutic system)]. Serial changes in left ventricular mass index and associated alterations in left ventricular systolic function, left ventricular filling, plasma renin activity, atrial natriuretic peptide, and catecholamines were evaluated. Blood pressure was significantly reduced from 200 ± 8/122 ± 3 mm Hg (mean ± SEM) to 144 ± 5/89 ± 2 mm Hg (p < 0.0001) at 1 year. Eleven patients (69%) required only nifedipine-GITS for blood pressure control and 5 (31%) required the addition of chlorthalidone. After 6 months, the left ventricular mass index was significantly reduced by 19% from 121 ± 8 to 96 ± 7 g/² and this reduction was sustained at 1 year. Septal and posterior wall thicknesses were reduced from 13.4 ± 0.1 to 11.2 ± 0.04 mm and from 12.8 ± 0.1 to 10.0 ± 0.03 mm (ρ < 0.001), respectively. Prevalence of left ventricular hypertrophy decreased from 63 to 25%. Left ventricular fractional shortening increased from 34 to 42% (ρ <0.05) and the relationship between fractional shortening and end-systolic stress did not change. Over the year of sustained blood pressure reduction, the peak velocity of early filling increased from 58 to 63 cm/s (ρ = 0.07), the peak velocity of late filling did not change, and the ratio of late to early peak velocity of left ventricular filling significantly decreased (ρ < 0.05). Plasma atrial natriuretic peptide, markedly elevated at entry, decreased from 70 ± 15 to 41 ± 8 pg/ml at 1 year (ρ < 0.05). Plasma renin activity and catecholamines were not altered. Therefore, treatment of subjects with initial diastolic blood pressure ≥ 120 mm Hg for 1 year with nifedipine-GITS is accompanied by left ventricular mass regression, maintenance of left ventricular systolic function, reduction in atrial natriuretic peptide, and no detectable activation of either the sympathetic or renin systems.