Background/Purpose:

To investigate serial changes in the prevalence of coronary microvascular
dysfunction and coronary artery disease (CAD) by cardiac imaging in a cohort of
SLE patients with chest pain.

Methods:

Twenty female SLE patients with chest pain (CP) underwent stress
cardiac MRI (CMR) and coronary CT angiography (CCTA) at baseline with follow-up
imaging at 5-years in addition to history of major
cardiac or vascular events, CAD risk factors, SLE activity, hormones and
medications.

1.5T CMR was performed with gadolinium
stress and rest 1^st-pass perfusion and delayed
enhancement. Analysis was conducted semi-quantitatively by myocardial perfusion
reserve index (MPRI) and by visual 5-point segmental scoring. 
Patients also underwent 64-slice CCTA. Images were analyzed for coronary artery
calcium score, plaque type, location, and stenosis.  In the absence of
obstructive CAD, patients with abnormal myocardial perfusion or MPRI <1.84
are suspected to have coronary microvascular dysfunction.

Results:

Of 17 subjects re-enrolled for follow-up, 15 (mean age 47, BMI 26)
underwent follow-up imaging: 14 underwent both stress CMR and CCTA and 1
had CCTA alone. Seven of 15 subjects had abnormal imaging at follow-up (Table
1): 4 abnormal CMR with no CAD, 2 normal CMR with nonobstructive CAD, and 1
abnormal CMR with ischemic scar and obstructive CAD. Framingham risk
score and Reynold’s risk score were </= 1% in all patients, yet 11 (73%)
reported CP in the 4 weeks preceding initial study visit. Five of 15 patients (33%)
were hyperlipidemic, 10 (67%) menopausal, 2 (13%) diabetic, 5 (33%) smokers,
and 7 (47%) with current corticosteroid use. The average SLEDAI in patients
that underwent follow-up imaging was 3.6.

In our follow-up cohort, we note a 36%
prevalence of abnormal CMR and 20% abnormal CCTA (1 obstructive, 2
nonobstructive CAD).  Of 8 subjects with baseline abnormal CMR, half had
continued CP and similar or worse CMR on follow-up. Mean MPRI at 5-year
follow-up was 2.19 versus 2.04 (p=0.28) at baseline in the subepicardium and
1.85 versus 1.86 (p=0.70) in the subendocardium. Using Wilcoxon signed-rank
test, results were not significantly different between baseline and follow-up
MPRI.

Conclusion:

Some patients demonstrate reversible hypoperfusion and others progress
to worsening subendocardial disease in the absence of obstructive CAD,
suggesting coronary microvascular dysfunction and challenging the theory of
SLE-related accelerated CAD. Those with abnormal CCTA at follow-up were >/=
55 years of age, suggesting age-related, not accelerated, increase in
coronary atherosclerosis. Abnormal CMR did not correlate with abnormal
CCTA. While duration of follow-up was short, no major cardiac events were
reported, and macrovascular CAD progression is no more than the general
population. Microvascular disease progression and potential cardiac
risk-stratifying interventions merit additional studies.