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Systemic vascular resistance during brief withdrawal of angiotensin converting enzyme inhibition in heart failure

A Gabrielsen1, P Bie, N J Christensen

  • 1Department of Aviation Medicine, The Heart Centre, National University Hospital Rigshospitalet, Copenhagen, Denmark. Anders.Garbielsen@cmm.ki.se

Scandinavian Journal of Clinical and Laboratory Investigation
|December 13, 2002
PubMed

Insights

Moderate increases in angiotensin II (Ang II) in heart failure (HF) patients do not worsen systemic vascular resistance (SVR). Angiotensin converting enzyme inhibition withdrawal in HF did not impair SVR control compared to controls.

Area of Science:

  • Cardiovascular Physiology
  • Renal Physiology

Background:

  • Compensated heart failure (HF) patients on chronic medical therapy often have elevated angiotensin II (Ang II) levels.
  • Angiotensin converting enzyme inhibitors (ACE-I) are a cornerstone therapy for HF, modulating the renin-angiotensin-aldosterone system (RAAS).

Purpose of the Study:

  • To test if moderate increases in endogenous Ang II, induced by ACE-I withdrawal in compensated HF patients, increase or impair systemic vascular resistance (SVR).

Main Methods:

  • Systemic vascular resistance (SVR) was measured in supine and seated positions in 12 HF patients and 9 controls.
  • HF patients were studied during high Ang II (ACE-I withdrawal for 24h) and low Ang II (sustained ACE-I therapy) conditions.

Main Results:

  • Withdrawal of ACE-I in HF led to moderately increased Ang II concentrations (30 +/- 5 pg/ml) compared to controls (12 +/- 2 pg/ml).
  • Despite higher Ang II, SVR in HF patients was similar to controls in both supine and seated positions.
  • Sustained ACE-I therapy in HF lowered Ang II (6 +/- 2 pg/ml) with no effect on supine SVR, but attenuated the posture-induced increase in SVR.

Conclusions:

  • Brief, moderate increases in circulating Ang II in compensated HF do not increase SVR compared to controls.
  • Control of SVR in response to postural changes is not significantly impaired by moderate Ang II increases in compensated HF.

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