Cardiac remodeling in hypertension and following myocardial infarction: effects of arteriolar vasodilators

  • J F Smits*
  • , J P Cleutjens
  • , C van Krimpen
  • , R G Schoemaker
  • , M J Daemen
  • *Corresponding author for this work

Research output: Contribution to journal(Systematic) Review articlepeer-review

Abstract

Cardiac remodeling constitutes a risk factor in cardiovascular disease. It may occur in a variety of circumstances. In hypertension and following myocardial infarction, pharmacological intervention in the remodeling process has been the subject of several studies. But the mechanisms of action of drugs that do contribute to regression of the remodeling response are still a matter of debate. Much of the confusion around the subject comes from the fact that classic arteriolar vasodilators do not result in such regression in hypertensive cardiac hypertrophy. This paper reviews some of the literature to examine whether there is indeed an exceptional position for vasodilators in hypertensive heart disease. Although, conceptually, arteriolar dilatation, and thus afterload reduction, might also have favorable effects on the remodeling response following myocardial infarction, clinical studies suggest the opposite. In the present paper, possible mechanisms are discussed, and evidence is presented that shows that hydralazine has an unexpected effect on the remodeling response at the level of the extracellular matrix.

Original languageEnglish
Pages (from-to)133-139
Number of pages7
JournalBasic Research in Cardiology
Volume86
Issue numberS1
Publication statusPublished - 1991

Keywords

  • Animals
  • Arterioles/drug effects
  • Cardiomegaly/etiology
  • Extracellular Matrix/drug effects
  • Humans
  • Hydralazine/therapeutic use
  • Hypertension/complications
  • Myocardial Infarction/complications
  • Rats
  • Vasodilator Agents/therapeutic use

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