Role of Endothelin in Microvascular Dysfunction Following PCI for NSTEMI
Status:
Completed
Trial end date:
2012-01-01
Target enrollment:
Participant gender:
Summary
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 atherosclerotic
coronary arteries. Our hypothesis is that increased activity of the endogenous endothelin
system contributes to microvascular dysfunction, and adjunctive therapy with an endothelin
receptor antagonist will result in improved microvascular blood flow.
Aims: The aims of the study are to assess in patients with non ST-elevation myocardial
infarction, whether: 1) PCI causes an increase in coronary blood ET-1 level; 2) an endothelin
receptor antagonist acutely improves coronary microvascular blood flow following PCI.
Non-ST segment elevation myocardial infarction (NSTEMI) is one type of heart attack. It is
defined as the development of heart muscle necrosis results from an acute interruption of
blood supply to a part of the heart which is demonstrated by an elevation of cardiac markers
Creatinine Kinase Isoenzyme Muscle/Brain Type (CK-MB) in the blood and the absence of
ST-segment elevation in ECG (electrocardiography). ST-segment is a portion of ECG, its
elevation indicates full thickness damage of heart muscle. Absence of ST-segment elevation in
NSTEMI indicates partial thickness damage of heart muscle occurs. Therefore, NSTEMI is less
severe type of heart attack compared to STEMI (ST-segment elevation myocardial infarction) in
which full thickness damage of heart muscle occurs.