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Increase in plasma digitalis-like activity during percutaneous transluminal coronary angioplasty in patients with

P Delva1, E Barbieri, M A Devynck

  • 1Department of Clinical Medicine, University of Verona, Italy.

Life Sciences
|January 1, 1990
PubMed

Insights

Plasma from patients showed increased digitalis-like factor after percutaneous transluminal coronary angioplasty (PTCA). This suggests a potential compensatory mechanism in heart disease, impacting Na-K ATPase activity.

Area of Science:

  • Cardiology
  • Biochemistry
  • Physiology

Background:

  • The presence of an endogenous digitalis-like factor in plasma is known in essential hypertension.
  • Limited data exists on this factor in general heart disease, particularly in low cardiac output states.
  • Percutaneous transluminal coronary angioplasty (PTCA) can transiently affect cardiac output and pressures.

Purpose of the Study:

  • To investigate the levels of a digitalis-like factor in plasma of patients with coronary artery disease.
  • To assess changes in this factor before and after percutaneous transluminal coronary angioplasty (PTCA).
  • To evaluate the impact on Na-K ATPase activity and intraerythrocyte electrolyte concentrations.

Main Methods:

  • Plasma was collected from the femoral vein of 6 patients with angina pectoris and severe coronary stenosis.
  • Measurements were taken before and immediately after percutaneous transluminal coronary angioplasty (PTCA).
  • Assayed plasma's ability to inhibit human renal Na(+)-K+ ATPase and measured intraerythrocyte sodium and potassium.

Main Results:

  • Significantly greater inhibition of Na(+)-K+ ATPase was observed after PTCA compared to basal levels (31.5% vs 16.1%).
  • No significant alterations in intraerythrocyte sodium and potassium concentrations were detected post-PTCA.
  • The study indicates an increase in the digitalis-like factor following the procedure.

Conclusions:

  • Percutaneous transluminal coronary angioplasty (PTCA) leads to a significant increase in plasma digitalis-like factor.
  • The mechanism remains unclear, but a rise in cardiac pressures due to reduced cardiac output may stimulate its production.
  • This factor might play a compensatory inotropic role in the context of heart disease and procedural interventions.

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