Incidence of high-strain patterns in human coronary arteries:Assessment with three-dimensional intravascular palpography and correlation with clinical presentation

Rupture of thin-cap fibroatheromatous plaques is a major cause of acute myocardial infarction (AMI). Such plaques can be identified in vitro by 3D intravascular palpography with high sensitivity and specificity. We used this technique in patients undergoing percutaneous intervention to assess the in...

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Published in:Circulation (New York, N.Y.) N.Y.), 2004-06, Vol.109 (22), p.2716-2719
Main Authors: SCHAAR, Johannes A, REGAR, Evelyn, MASTIK, Frits, MCFADDEN, Eugene P, SAIA, Francesco, DISCO, Clemens, DE KORTE, Chris L, DE FEYTER, Pim J, VAN DER STEEN, Antonius F. W, SERRUYS, Patrick W
Format: Article
Language:English
Subjects:
Aged
Angina Pectoris - diagnostic imaging
Angina, Unstable - diagnostic imaging
Biological and medical sciences
Blood and lymphatic vessels
C-Reactive Protein - analysis
Cardiology. Vascular system
Coronary heart disease
Coronary Vessels - diagnostic imaging
Cross-Sectional Studies
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Female
Heart
Humans
Male
Medical sciences
Middle Aged
Myocardial Infarction - diagnostic imaging
Myocardial Ischemia - blood
Myocardial Ischemia - diagnostic imaging
Stress, Mechanical
Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases
Surgery of the heart
Ultrasonography, Interventional - methods
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Summary:Rupture of thin-cap fibroatheromatous plaques is a major cause of acute myocardial infarction (AMI). Such plaques can be identified in vitro by 3D intravascular palpography with high sensitivity and specificity. We used this technique in patients undergoing percutaneous intervention to assess the incidence of mechanically deformable regions. We further explored the relation of such regions to clinical presentation and to C-reactive protein levels. Three-dimensional palpograms were derived from continuous intravascular ultrasound pullbacks. Patients (n=55) were classified by clinical presentation as having stable angina, unstable angina, or AMI. In every patient, 1 coronary artery was scanned (culprit vessel in stable and unstable angina, nonculprit vessel in AMI), and the number of deformable plaques assessed. Stable angina patients had significantly fewer deformable plaques per vessel (0.6+/-0.6) than did unstable angina patients (P=0.0019) (1.6+/-0.7) or AMI patients (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.0000131887.65955.3B