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Abstract Number: 1810

A Five-Year Follow-up of Microvascular Dysfunction and Coronary Artery Disease in SLE: Results from a Community-Based Lupus Cohort

Vaneet K. Sandhu1, Mariko L. Ishimori1, Janet Wei2, Louise Thomson2, Daniel Berman2, Jay Schapira2, Noel Bairey Merz2, Daniel Wallace3 and Michael Weisman3, 1Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA, 2Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA, 3Cedars-Sinai Medical Center, Los Angeles, CA

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords: MRI, SLE and coronary artery disease

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Session Information

Date: Monday, November 9, 2015

Session Title: Systemic Lupus Erythematosus - Clinical Aspects and Treatment Poster Session II

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

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 1st-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.

 

Table 1: Subjects with abnormal imaging

Subject

Age

Baseline perfusion defect (%) on CMR

Follow-up Perfusion defect (%) on CMR

Baseline CCTA: plaque (yes/no)

Follow-up CCTA: new plaque (yes/no)

Elevated CRP

Obesity (BMI>/=30)

HLD

Menopausal

Diabetes

Depression

Current steroid therapy

Current HRT

Smoking history

2

34

None

9%

No

No

Yes

Yes

No

No

Yes

Yes

Yes

No

Yes

3

56

None

None

 

Yes

Yes

No

Yes

Yes

No

No

No

Yes

Yes

4

52

38%

11%

No

No

Yes

Yes

No

No

Yes

Yes

Yes

No

Yes

5

57

28%

12.5%*

Yes

Yes

No

No

No

Yes

No

Yes

Yes

Yes

Yes

6

59

14%

10%

No

No

No

No

No

Yes

No

Yes

No

Yes

No

11

65

9%

None

Yes

Yes

No

No

Yes

Yes

No

No

No

No

No

12

58

16%

19%

No

No

Yes

Yes

Yes

Yes

No

Yes

No

No

No

BMI: body mass index (kg/m2), HLD: hyperlipidemia, defined by total cholesterol >200mg/dL, HRT: hormone-replacement therapy

* Small subendocardial infarction with significant stenosis

 


Disclosure: V. K. Sandhu, None; M. L. Ishimori, None; J. Wei, None; L. Thomson, None; D. Berman, None; J. Schapira, None; N. Bairey Merz, None; D. Wallace, None; M. Weisman, None.

To cite this abstract in AMA style:

Sandhu VK, Ishimori ML, Wei J, Thomson L, Berman D, Schapira J, Bairey Merz N, Wallace D, Weisman M. A Five-Year Follow-up of Microvascular Dysfunction and Coronary Artery Disease in SLE: Results from a Community-Based Lupus Cohort [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/a-five-year-follow-up-of-microvascular-dysfunction-and-coronary-artery-disease-in-sle-results-from-a-community-based-lupus-cohort/. Accessed March 4, 2021.
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