Advertisement

Cardiovascular Drugs and Therapy

, Volume 4, Supplement 5, pp 957–961 | Cite as

Early regression of left ventricular diastolic abnormalities in hypertensive patients treated with nifedipine

  • I. Sheiban
  • G. Covi
  • C. Zenorini
  • G. Arcaro
  • E. Arosio
  • S. Tonni
  • G. Montresor
  • A. Lechi
Nifedipine in Hypertension

Summary

The effects of nifedipine on blood pressure (BP), left ventricular hypertrophy, and diastolic function were evaluated in 14 patients with essential hypertension (EH). All males with a mean age of 44±6 years (range 35–58 years), and in ten normotensive subjects (control group) aged 32–42 years (mean age 36±4). A complete echocardiogram (ECHO) was performed in basal conditions after 1 and 6 months of therapy with nifedipine (20–40 mg/day). Left ventricular echocardiograms (LV ECHO, M-mode, two-dimensional guided) were plotted with a simultaneous ECG tracing by means of a computerized system that allows evaluation of the following parameters: LV end-diastolic and systolic diameters (EDD, ESD); variations in LV diameter and volume during the entire cardiac cycle, and the velocities of such variations; end-diastolic thicknesses of the interventricular septum and posterior wall (ST, PWT); LV mass, mass/volume (M/V) index, end-diastolic diameter/thickness (D/Th) index, and LV ejection fraction (EF). Left ventricular volume curves were obtained and the contributions of rapid filling (RF) and atrial systole (AS) to EDV were evaluated. Filling velocities during RF (vRF) and AS (vAS) were estimated, as well as the isovolumic relaxation period (IR).

No significant changes were observed in the heart rate. After 1 month of therapy, systolic and diastolic BP were significantly decreased (p<0.05). ST and PWT were reduced, with a simultaneous increase in EDD and EDV (p<0.01). LV mass was slightly reduced, as was the M/V index. The D/Th index was increased (p<0.01). The RF contribution to EDV was increased, together with a simultaneous decrease in the AS contribution (p<0.01). The IR period was reduced (p<0.01), while vRF and vAS showed significant increases (p<0.01).

After 6 months of therapy, all the above-mentioned modifications were confirmed.

In conclusion, mild EH induces early modifications in LV geometry, with consequent LV diastolic abnormalities, characterized by prolonged and incomplete diastolic filling. Thus, LV wall thickness may appear increased, with a simultaneous reduction in LV diameter and volume (without any significant changes in LV mass). Antihypertensive treatment with a Ca2+ antagonist (nifedipine) induces early regression of such abnormalities with normalization of LV diastolic function.

Key Words

diastolic function nifedipine hypertension 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Hanrath P, Mathey DG, Siegert R, Bleifeld W. Left ventricular relaxation and filing pattern in different forms of left ventricular hypertrophy: An echocardiographic study.Am J Cardiol 1980;45:15–23.CrossRefPubMedGoogle Scholar
  2. 2.
    Hartford M, Wikstrand J, Wallentin I, et al. Diastolic function of the heart in untreated primary hypertension.Hypertension 1984;6:329–338.PubMedGoogle Scholar
  3. 3.
    Shapiro LM, Mackinnon J, Beevers DG. Echocardiographic features of malignant hypertension.Br Heart J 1981;46:374–379.PubMedCrossRefGoogle Scholar
  4. 4.
    Papademetriou V, Gottdiener JS, Fletcher RD, Freis ED. Echocardiographic assessment by computer-assisted analysis of diastolic left ventricular function and hypertrophy in borderline or mild systemic hypertension.Am J Cardiol 1985;56:546–550.CrossRefPubMedGoogle Scholar
  5. 5.
    Inouye I, Massie B, Loge D, et al. Abnormal left ventricular filling: An early finding in mild systemic hypertension.Am J Cardiol 1984;53:120–126.PubMedCrossRefGoogle Scholar
  6. 6.
    Smith VE, Schulman P, Karimeddini MF, et al. Rapid ventricular filling in left ventricular hypertrophy. II Pathologic hypertrophy.J Am Coll Cardiol 1985;5:869–874.PubMedCrossRefGoogle Scholar
  7. 7.
    Fouad FM, Slominski JM, Tarazi RC. Left ventricular diastolic function in hypertension: Relation to left ventricular mass and systolic function.J Am Coll Cardiol 1984;3:1500–1506.PubMedGoogle Scholar
  8. 8.
    Phillips RA, Coplan NL, Krakoff LR, et al. Doppler echocardiographic analysis of left ventricular filling in treated hypertensive patients.J Am Coll Cardiol 1987;9:317–322.PubMedCrossRefGoogle Scholar
  9. 9.
    Sheiban I, Arcaro G, Covi G, et al. Regression of cardiac hypertrophy after antihypertensive therapy with nifedipine and captopril.J Cardiovasc Pharmacol 1987;10(Suppl. 10): S187-S191.PubMedGoogle Scholar
  10. 10.
    Reicher KM, Franklin BB, Chandler T, et al. Reversal of left ventricular hypertrophy by antihypertensive therapy.Eur Heart J 1982;3(Suppl A):165–169.PubMedGoogle Scholar
  11. 11.
    Hills LS, Monaghan M, Richardson PJ. Regression of left ventricular hypertrophy during treatment with antihypertensive agents.Br J Clin Pharmacol 1979;7(Suppl 2):225–229.Google Scholar
  12. 12.
    Drayer J, Gardin JM, Weber MA, Aronow WS. Change in left ventricular septal thickness during diuretic therapy.Clin Pharmacol Ther 1982;32:283–288.PubMedCrossRefGoogle Scholar
  13. 13.
    Ostman-Smith I Cardiac sympathetic nerves as the final pathway in the induction of cardiac hypertrophy.Clin Sci 1981;61:265–272.PubMedGoogle Scholar
  14. 14.
    Tarazi RC, Aen S, Saragoga M Khairallah P. The multifactorial role of catecholamines in hypertensive cardiac hypertrophy.Eur Heart J 1982;3(Suppl A):103–110.PubMedGoogle Scholar
  15. 15.
    Ferrara LA, De Simone G, Mancini M, et al. Changes in left ventricular mass during a double-blind study with chlorthalidone and slow-release nifedipine.Eur J Clin Pharmacol 1984;27:525–528.CrossRefPubMedGoogle Scholar
  16. 16.
    Nakashima Y, Fouad FM, Tarazi RE. Regression of left ventricular hypertrophy from systemic hypertension by enalapril.Am J Cardiol 1984;53:1044–1049.CrossRefPubMedGoogle Scholar
  17. 17.
    Sen S, Trazi RC. Regression of myocardial hypertrophy and influence of adrenergic system.Am J Physiol 1983;13:H97-H101.Google Scholar
  18. 18.
    Lombardo M, Zaini G, Pastori F, et al. Left ventricular mass and function before and after antihypertensive treatment.J Hypertens 1983;1:215–219.PubMedCrossRefGoogle Scholar
  19. 19.
    Abi-Samra F, Fouad FM, Tarazi RC. Determinants of LV hypertrophy and function in hypertensive patients: An echocardiographic study.Am J Med 1983;75(Suppl 3A):26–33.CrossRefPubMedGoogle Scholar
  20. 20.
    Gaasch WH, Levine HJ, Quinones MA, Alexander JK. Left ventricular compliance: Mechanisms and clinical implications.Am J Cardiol 1976;38:645–653.PubMedCrossRefGoogle Scholar
  21. 21.
    Bing OHL, Keefe JF, Wolk MJ, et al. Tension prolongation during recovery from myocardial hypoxia.J Clin Invest 1971;50:660–666.PubMedCrossRefGoogle Scholar

Copyright information

© Kluwer Academic Publishers 1990

Authors and Affiliations

  • I. Sheiban
    • 1
  • G. Covi
    • 1
  • C. Zenorini
    • 1
  • G. Arcaro
    • 1
  • E. Arosio
    • 1
  • S. Tonni
    • 1
  • G. Montresor
    • 1
  • A. Lechi
    • 1
  1. 1.Centro Cardiopneumologico, Instituto di Clinica MedicaUniversità di Verona, Ospedale PoliclinicoVeronaItaly

Personalised recommendations