PT  - JOURNAL ARTICLE
AU  - Marcelo F. Di Carli
AU  - David Charytan
AU  - Graham T. McMahon
AU  - Peter Ganz
AU  - Sharmila Dorbala
AU  - Heinrich R. Schelbert
TI  - Coronary Circulatory Function in Patients with the Metabolic Syndrome
AID  - 10.2967/jnumed.110.082883
DP  - 2011 Sep 01
TA  - Journal of Nuclear Medicine
PG  - 1369--1377
VI  - 52
IP  - 9
4099  - http://jnm.snmjournals.org/content/52/9/1369.short
4100  - http://jnm.snmjournals.org/content/52/9/1369.full
SO  - J Nucl Med2011 Sep 01; 52
AB  - The metabolic syndrome affects 25% of the U.S. population and greatly increases the risk of diabetes and coronary artery disease (CAD). We tested the hypothesis that the metabolic syndrome is associated with impaired coronary vasodilator function, a marker of atherosclerotic disease activity. Methods: Four hundred sixty-two patients at risk for CAD, as defined by a low-density lipoprotein cholesterol ≥ 160 mg/dL with fewer than 2 coronary risk factors, a low-density lipoprotein cholesterol ≥ 130 mg/dL with 2 or more coronary risk factors, or with documented CAD were included. A subset of 234 individuals underwent repeated PET at 1 y. Myocardial blood flow (MBF) and vasodilator reserve were assessed by PET. Modified criteria of the National Cholesterol Education Program, Adult Treatment Panel III were used to characterize the metabolic syndrome. Results: Adenosine- and cold-stimulated MBF were similar in patients with and without metabolic syndrome, whereas baseline MBF showed a stepwise increase with increasing features of the syndrome. Consequently, patients with metabolic syndrome showed a lower coronary flow reserve (CFR) (2.5 ± 1.0) than those without metabolic syndrome (3.0 ± 0.9, P = 0.004). Differences in CFR were no longer present after correcting rest flows for the rate–pressure product. Change in MBF and CFR at 1 y were not different across groups of patients with increasing features of the metabolic syndrome. Conclusion: Patients with metabolic syndrome demonstrate impaired CFR, which is related to the augmentation in resting coronary blood flow caused by hypertension. In high-risk individuals, peak adenosine- and cold-stimulated blood flows are impaired even in the absence of the metabolic syndrome.