Patients with syndrome X have normal transmural myocardial perfusion and oxygenation: a 3-T cardiovascular magnetic resonance imaging study.
BACKGROUND
The pathophysiology of chest pain in patients with cardiac syndrome X remains controversial. Advances in perfusion imaging with cardiovascular magnetic resonance (CMR) now enable absolute quantification of regional myocardial blood flow (MBF). Furthermore, blood oxygen level-dependent (BOLD) or oxygenation-sensitive CMR provides the unprecedented capability to assess regional myocardial oxygenation. We hypothesized that the combined assessment of regional perfusion and oxygenation with CMR could clarify whether patients with syndrome X show evidence of myocardial ischemia (reduced perfusion and oxygenation) during vasodilator stress compared with normal volunteers.


RESULTS
Eighteen patients with syndrome X (chest pain, abnormal exercise treadmill test, normal coronary angiogram without other causes of microvascular dysfunction) and 14 controls underwent CMR scanning at 3 T. Myocardial function, scar, perfusion (2-3 short-axis slices), and oxygenation were assessed. Absolute MBF was measured during adenosine stress (140 μg/kg per minute) and at rest by model-independent deconvolution. For oxygenation, using a T2-prepared BOLD sequence, signal intensity was measured at adenosine stress and rest in the slice matched to the midventricular slice of the perfusion scan. There were no significant differences in MBF at stress (2.35 versus 2.37 mL/min per gram; P=0.91), BOLD signal change (17.3% versus 17.09%; P=0.91), and coronary flow reserve measurements (2.63 versus 2.53; P=0.60) in patients with syndrome X and controls, respectively. Oxygenation and perfusion measurements per coronary territory were also similar between the 2 groups. More patients with syndrome X (17/18 [94%]) developed chest pain during adenosine stress than controls (6/14 [43%]; P=0.004).


CONCLUSIONS
Patients with syndrome X show greater sensitivity to chest pain compared with controls but no evidence of deoxygenation or hypoperfusion during vasodilatory stress.
Department of Cardiovascular Medicine, Centre for Clinical Magnetic Resonance Research, University of Oxford, Oxford, UK. theo.karamitsos@cardiov.ox.ac.uk
Theodoros D
TD
Karamitsos
Jayanth R
JR
Arnold
Tammy J
TJ
Pegg
Jane M
JM
Francis
Jacqueline
J
Birks
Michael
M
Jerosch-Herold
Stefan
S
Neubauer
Joseph B
JB
Selvanayagam
D000241:Adenosine; D000368:Aged; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D003287:Contrast Media; D003326:Coronary Circulation; D004739:England; D005260:Female; D019786:Gadolinium DTPA; D006439:Hemodynamics; D006801:Humans; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D017566:Microvascular Angina / Q000175:diagnosis* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008875:Middle Aged; D055414:Myocardial Perfusion Imaging / Q000379:methods*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010101:Oxygen Consumption; D010147:Pain Measurement; D011237:Predictive Value of Tests; D014665:Vasodilator Agents
D003287:Contrast Media; D014665:Vasodilator Agents; C064925:gadodiamide; D019786:Gadolinium DTPA; D000241:Adenosine