Arthritis care & research · 2020
Five-Year Follow-Up of Coronary Microvascular Dysfunction and Coronary Artery Disease in Systemic Lupus Erythematosus: Results From a Community-Based Lupus Cohort.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
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Sandhu Vaneet K, Wei Janet, Thomson Louise E J, Berman Daniel S, Schapira Jay, Wallace Daniel, Weisman Michael H, Bairey Merz C Noel, Ishimori Mariko L
Аннотация
OBJECTIVE: The present study was undertaken to investigate prospective change in the prevalence of coronary microvascular dysfunction (CMD) and obstructive coronary artery disease (CAD) in a cohort of subjects with systemic lupus erythematosus (SLE) initially evaluated for anginal chest pain (CP). Prior work documented a relatively high prevalence of CMD in the absence of obstructive CAD in subjects with SLE.
METHODS: Twenty female SLE subjects with CP who underwent stress cardiac magnetic resonance imaging (CMRI) and coronary computed tomography angiography at baseline were reevaluated at 5 years.
RESULTS: Seventeen subjects (85%) were available and reenrolled, of which 11 (65%) had persistent CP at follow-up. Fourteen subjects had complete follow-up CMRI, of which 36% (n = 5) demonstrated CMD at follow-up. Further, 25% (1 of 4) of the originally abnormal myocardial perfusion reserve index (MPRI) findings at baseline were lower at follow-up, while 2 additional abnormal MPRI findings at follow-up were noted in previously normal MPRI results. The prevalence of CMD and nonobstructive/obstructive CAD both was unchanged between baseline and follow-up, respectively (both P values not significant). During follow-up, 33% of subjects (5 of 15) had adverse cardiac outcomes, including pericarditis, unstable angina, or intracranial aneurysm clipping procedure.
CONCLUSION: At the 5-year follow-up of SLE subjects with CP who were evaluated at baseline and follow-up, a majority had persistent CP, and nearly one-half had similar or worse myocardial perfusion consistent with CMD without obstructive CAD. These findings propose an alternative explanation for CP in SLE subjects compared to the more common SLE-related accelerated obstructive CAD accounting for CP and adverse outcomes. These findings support further studies of CMD as an etiology for cardiac morbidity and mortality in SLE.
METHODS: Twenty female SLE subjects with CP who underwent stress cardiac magnetic resonance imaging (CMRI) and coronary computed tomography angiography at baseline were reevaluated at 5 years.
RESULTS: Seventeen subjects (85%) were available and reenrolled, of which 11 (65%) had persistent CP at follow-up. Fourteen subjects had complete follow-up CMRI, of which 36% (n = 5) demonstrated CMD at follow-up. Further, 25% (1 of 4) of the originally abnormal myocardial perfusion reserve index (MPRI) findings at baseline were lower at follow-up, while 2 additional abnormal MPRI findings at follow-up were noted in previously normal MPRI results. The prevalence of CMD and nonobstructive/obstructive CAD both was unchanged between baseline and follow-up, respectively (both P values not significant). During follow-up, 33% of subjects (5 of 15) had adverse cardiac outcomes, including pericarditis, unstable angina, or intracranial aneurysm clipping procedure.
CONCLUSION: At the 5-year follow-up of SLE subjects with CP who were evaluated at baseline and follow-up, a majority had persistent CP, and nearly one-half had similar or worse myocardial perfusion consistent with CMD without obstructive CAD. These findings propose an alternative explanation for CP in SLE subjects compared to the more common SLE-related accelerated obstructive CAD accounting for CP and adverse outcomes. These findings support further studies of CMD as an etiology for cardiac morbidity and mortality in SLE.