Coronary Microvascular Dysfunction Proposed as Cause of Persistent Chest Pain in SLE

The presence of coronary microvascular dysfunction (CMD) in patients with systemic lupus erythematosus (SLE) may provide an “alternative explanation” for persistent chest pain in this patient population, according to research published in Arthritis Care and Research.

Authors of previously published research found that 44% of women with SLE and chest pain without obstructive coronary artery disease (CAD) (n=20) demonstrated elevated prevalence of CMD. To further understand these findings, the investigators evaluated 17 patients from the same cohort, monitoring serial changes in chest pain, CMD, and obstructive CAD.

Participants underwent baseline and 5-year follow-up adenosine stress cardiac magnetic resonance imaging (CMRI) that analyzed left ventricular function, volumes, cardiac output, and mass. Participants also underwent baseline and 5-year follow-up coronary computed tomography angiography.

Demographic data revealed the cohort to be relatively young, with a “low prevalence” of traditional cardiac risk factors and demonstrating mildly severe SLE disease activity. Cardiac risk scores, including the 10-year Framingham Risk Score, the Reynolds Risk Score, and the American College of Cardiology/American Heart Association Atherosclerotic Cardiovascular Disease (CVD) Risk Score, were ≤1% for all participants.

In total, 65% of participants presented with persistent anginal chest pain at 5-year follow-up. One participant reported pericarditis, 3 reported hospitalization for acute coronary syndrome/unstable angina, and 1 reported undergoing an intracranial vascular aneurysm clipping procedure. None of the participants reported experiencing a myocardial infarction, stroke, or revascularization procedure.

Within the cohort, 3 participants progressed to nonobstructive or obstructive CAD; 2 of those participants demonstrated markers of nonobstructive CAD at baseline (noncalcified plaque with <50% stenosis). One participant who presented with progressive plaque demonstrated new subepicardial myocardial scarring on CMRI.

At both baseline and follow-up, all participants had normal left ventricular ejection fraction on CMRI, with 36% showing CMD on follow-up. Among these participants, 60% had persistently abnormal myocardial perfusion reserve index, and 40% presented with newly abnormal findings. Overall, mean myocardial perfusion reserve index was “not significantly different” from baseline to follow-up (2.03±0.39 vs 2.12±0.58, respectively).

“These findings propose an alternate explanation for chest pain in [patients with SLE] compared to the traditional concept of SLE-related accelerated obstructive CAD as the primary or major cause for chest pain and adverse CVD events in SLE,” the researchers noted.  

Study limitations include the exclusion of men, as well as the relatively small sample size and the limited analyses of risk factors associated with CMD and obstructive CAD progression.

The researchers concluded, “Our results support that obstructive CAD is not related to persistent chest pain, while persistent/worsened evidence of CMD is associated with persistent chest pain. Advanced imaging allows for a noninvasive evaluation of CVD including CMD, which appears to be prevalent in SLE.”

Reference

Sandhu VK, Wei J, Thompson LEJ, et al. A five-year follow up of coronary microvascular dysfunction and coronary artery disease in SLE: Results from a community-based lupus cohort [published online May 6, 2019]. Arthritis Care Res. doi: 10.1002/acr.23920