PROSTACYCLIN: HAEMODYNAMIC AND METABOLIC EFFECTS IN PATIENTS WITH CORONARY ARTERY DISEASE Academic Article Article uri icon

Overview

MeSH Major

  • Cardiac Catheterization
  • Heart Defects, Congenital
  • Heart Valve Diseases
  • Heart Valve Prosthesis Implantation
  • Postoperative Complications
  • Vascular Diseases

abstract

  • The therapeutic potential of prostacyclin was evaluated in 10 patients with angina pectoris and angiographically proved coronary artery disease. Platelet aggregation and coronary and systemic haemodynamic effects were examined before and after intravenous infusions of 2, 4, 6, and 8 ng/kg/min of prostacyclin and were dose related. At 8 ng/kg/min the ADP concentration required to induce 50% of maximum platelet aggregation increased from 1.8 to 4.5 mumol/l (p less than 0.001). Heart rate and cardiac index rose from 77 to 93 beats/min and 2.47 to 3.48 l/min/m2, respectively (p less than 0.01). Mean blood pressure and systemic and pulmonary resistances fell from 107 to 92 mm Hg and 1704 to 1048 and 80 to 45 dyn s cm-5, respectively (p less than 0.01). Coronary vascular resistance also fell from 0.95 to 0.73 units (p less than 0.01). Mean atrial pacing time to angina rose from 142 to 241 s (p less than 0.05), while lactate production during rapid atrial pacing was decreased, lactate extraction ratio rising from -25 to -9% (p less than 0.05). These coronary and systemic vasodilator effects and the prolongation of pacing time to angina indicate an acute beneficial effect of prostacyclin on angina. Since prostacyclin has been shown to prevent platelet accumulation and progression to total occlusion in animals with experimental coronary stenoses, the observed inhibition of platelet aggregation suggests that prostacyclin should be further evaluated in unstable angina.

publication date

  • March 14, 1981

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1016/S0140-6736(81)92028-6

PubMed ID

  • 6110816

Additional Document Info

start page

  • 569

end page

  • 72

volume

  • 317

number

  • 8220