Related Experiment Video
Updated: Mar 16, 2026
Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
Published on: October 15, 2010
Role of endothelin in microvascular dysfunction following percutaneous coronary intervention for non-ST elevation
Raviteja R Guddeti1, Abhiram Prasad2, Yasushi Matsuzawa2
1Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, Minnesota, USA; Division of Internal Medicine, Marshfield Clinic, Marshfield, Wisconsin, USA.
Insights
Adjunctive therapy with an endothelin A receptor antagonist improved coronary microvascular blood flow and reduced cardiac biomarkers after percutaneous coronary intervention (PCI) in non-ST elevation acute coronary syndromes (NSTACS) patients. This suggests endothelin plays a role in microvascular dysfunction during PCI.
Area of Science:
- Cardiology
- Vascular Biology
- Pharmacology
Background:
- Percutaneous coronary intervention (PCI) for acute coronary syndromes (ACS) can lead to impaired myocardial perfusion despite patent epicardial vessels.
- Endothelin-1 (ET-1), a potent vasoconstrictor, is upregulated in atherosclerosis and post-PCI, contributing to microvascular dysfunction.
Purpose of the Study:
- To investigate the role of endothelin in regulating coronary microvascular blood flow and myocardial perfusion following PCI in non-ST elevation acute coronary syndromes (NSTACS).
- To assess if adjunctive therapy with a selective endothelin A (ETA) receptor antagonist acutely improves postprocedural coronary microvascular blood flow.
Main Methods:
- A randomized, double-blinded, placebo-controlled trial involving 23 NSTACS patients.
- Patients received either placebo (n=11) or BQ-123 (n=12), a selective ETA antagonist, via intracoronary infusion before PCI.
- Coronary microvascular blood flow and myocardial perfusion were assessed by Doppler-derived average peak velocity (APV); cardiac biomarkers were quantified.
Main Results:
- Immediately post-PCI, APV was significantly higher in the BQ-123 group compared to placebo (30 vs 19 cm/s; p=0.03).
- While hyperaemic APV was higher in the BQ-123 group, the difference was not statistically significant (p=0.090).
- Per cent change in creatine kinase isoenzyme MB was significantly lower in the BQ-123 group at 8 and 16 hours post-PCI, indicating reduced myocardial injury.
Conclusions:
- Endothelin is implicated as a mediator of microvascular dysfunction during PCI in NSTACS.
- Adjunctive therapy with a selective ETA antagonist shows potential to augment myocardial perfusion post-PCI.
Objectives:
Percutaneous coronary intervention (PCI) for acute coronary syndromes frequently fails to restore myocardial perfusion despite establishing epicardial vessel patency. Endothelin-1 (ET-1) is a potent vasoconstrictor, and its expression is increased in atherosclerosis and after PCI. In this study, we aim to define the role of endothelin in regulating coronary microvascular blood flow and myocardial perfusion following PCI in patients with non-ST elevation acute coronary syndromes (NSTACS), by assessing whether adjunctive therapy with a selective endothelin A (ETA) receptor antagonist acutely improves postprocedural coronary microvascular blood flow.
Methods:
In a randomised, double-blinded, placebo-controlled trial, 23 NSTACS patients were enrolled to receive an intracoronary infusion of placebo (n=11) or BQ-123 (n=12) immediately before PCI. Post-PCI coronary microvascular blood flow and myocardial perfusion were assessed by measuring Doppler-derived average peak velocity (APV), and cardiac biomarker levels were quantified.
Results:
Compared with the placebo group, APV was significantly higher in the drug group immediately after PCI (30 (20, 37) vs 19 (9, 26) cm/s; p=0.03). Hyperaemic APV, measured post-adenosine administration, was higher in the BQ-123 group, but the difference did not achieve statistical significance (56 (48, 72) vs 46 (34, 64) cm/s; p=0.090). Maximum coronary flow reserve postprocedure was not different between the two groups (2.1 (1.6, 2.3) vs 2.5 (1.8, 3.0)). Per cent change in creatine kinase isoenzyme MB from the time of PCI to 8 and 16 hours post-PCI was significantly lower in the drug group compared with the placebo group (-17 (-26, -10) vs 26 (-15, 134); p=0.02 and -17 (-38, 14) vs 107 (2, 446); p=0.007, respectively).
Conclusions:
Endothelin is a mediator of microvascular dysfunction during PCI in NSTACS, and adjunctive selective ETA antagonist may augment myocardial perfusion during PCI.
Trial Registration Number:
NCT00586820; Results.
More Related Videos
Related Concept Videos
01:18Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
01:30Acute Coronary Syndrome I: Introduction
01:26Coronary Artery Disease II: Pathophysiology
01:28Acute Coronary Syndrome IV: Interprofessional Care
01:29Heart Failure II: Pathophysiology