The diagnostic performance of adenosine stress cardiovascular magnetic resonance (CMR) for the detection of significant stenosis in infarct-related arteries is widely unknown. Two different types of perfusion defects can be observed: (a) larger than or (b) equal size as scar.
We hypothesized that: (a) defect>scar predicts significant coronary stenosis, and (b) defect=scar predicts an unobstructed infarct-related artery, and (c) angina symptoms might be of additional value in stratification.
Patients with previous myocardial infarction referred for work-up of myocardial ischemia undergoing adenosine stress CMR were included if they had coronary angiography within 4 weeks of CMR.
Two hundred patients with a mean age of 66±11 years, ischemic scars (subendocardial/transmural), and a mean left ventricular ejection fraction of 53% were included. In patients with defect>scar, the positive predictive value was excellent (88%) and typical angina was reported only in the stenosis group (P=0.002). However, patients with defect=scar (with 50% showing subendocardial scar) had a prevalence of 37% for stenosis, yielding a low negative predictive value of 63%. In this group, symptoms of typical angina were independent of stenosis (P=1.0).
A perfusion defect larger than scar is highly predictive for significant stenosis in infarct-related arteries. However, more than a third of the patients with perfusion defect of equal size as scar also showed significant coronary stenosis. As half of these patients showed still viable (subendocardial) scars, there is a high-risk of reinfarction. The addition of angina symptoms seems to increase diagnostic accuracy only in patients with perfusion defects larger than scar.
aDepartment of Cardiology and Cardiovascular Diseases, University of Tübingen, Tübingen
bDivision of Cardiology
cDivision of Radiology, Robert-Bosch-Medical Center, Stuttgart
dDepartment of Internal Medicine III (Cardiology), University of Heidelberg, Heidelberg, Germany
Correspondence to Simon Greulich, MD, Department of Cardiology and Cardiovascular Diseases, University of Tübingen, Otfried-Müller-Strasse 10, 72076 Tübingen, Germany Tel: +49 707 1298 3688; fax: +49 707 129 5749; e-mail: email@example.com
Received September 19, 2018
Accepted December 12, 2018