These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Regression of hypertrophy following nitrendipine: effect on systolic and diastolic function].
    Author: Vogt M, Kreutz KU, Motz W, Strauer BE.
    Journal: Z Kardiol; 1989 Jul; 78(7):469-77. PubMed ID: 2528245.
    Abstract:
    The purpose of the present study was to determine whether an antihypertensive treatment with the dihydropyridine nitrendipine can induce regression of severe hypertensive hypertrophy and, whether alterations in systolic and diastolic ventricular function do occur. Eleven patients (age 49 +/- 11 years) with hypertensive hypertrophy were treated with nitrendipine (10-40 mg/day) for 12 months. Before and after therapy left ventricular hypertrophy, systolic, and diastolic function were measured by M-mode, two-dimensional- and digitized M-mode echocardiography. Systolic blood pressure dropped from 185.5 +/- 19.8 to 164.1 +/- 15.6 mm Hg (p less than 0.05). Left ventricular muscle mass was reduced from 234.5 +/- 51.2 to 201.5 +/- 37.9 g/m2 (p less than 0.05). Systolic wall stress (257.2 +/- 50.5 vs 245.2 +/- 44.4 x 10(3) dyn/cm2) and fractional shortening (34.9 +/- 6.1 vs 37.1 +/- 5.4%) remained nearly unchanged. The peak rate of left ventricular internal dimension change during diastole (MLVD), as an index of rapid early diastolic filling was increased (13.1 +/- 3.0 vs 16.5 +/- 3.7 cm/s; p less than 0.01), the relaxation time index, as an index of isovolumic relaxation, remained nearly unchanged (76 +/- 35 vs 64 +/- 24 ms; n.s.). A long-term treatment with nitrendipine regressed hypertensive left ventricular hypertrophy in proportion to blood pressure reduction. While systolic function remained unchanged as a consequence of an unaltered systolic wall stress, i.e. afterload, diastolic filling was markedly improved due to changes in left ventricular geometry through reduction in mass to volume ratio. Since relaxation time index remained nearly unchanged, factors contributing to the phase of isovolumic relaxation were not essentially affected by regression of left ventricular hypertrophy.
    [Abstract] [Full Text] [Related] [New Search]