This Article Free upon publication Full Text Full Text (PDF) All Versions of this Article: 116/4/419    most recent CIRCULATIONAHA.106.673319v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pieretti, J. Articles by Salmon, J. E. Search for Related Content PubMed PubMed Citation Articles by Pieretti, J. Articles by Salmon, J. E. Related Collections Hypertrophy Echocardiography

(Circulation. 2007;116:419-426.)
© 2007 American Heart Association, Inc.

Vascular Medicine

Systemic Lupus Erythematosus Predicts Increased Left Ventricular Mass

Janice Pieretti, MD; Mary J. Roman, MD; Richard B. Devereux, MD; Michael D. Lockshin, MD; Mary K. Crow, MD; Stephen A. Paget, MD; Joseph E. Schwartz, PhD; Lisa Sammaritano, MD; Daniel M. Levine, PhD; Jane E. Salmon, MD

From the Divisions of Cardiology (J.P., M.J.R., R.B.D.) and Rheumatology (M.D.L., M.K.C., S.A.P., L.S., J.E.S.) and the Rogosin Institute (D.M.L.), Weill Medical College of Cornell University and the Hospital for Special Surgery, New York, NY; and Department of Psychiatry (J.E.S.), SUNY-Stony Brook, Stony Brook, NY.

Correspondence to Mary J. Roman, Division of Cardiology, 525 E 68th St, New York, NY 10021. E-mail mroman{at}med.cornell.edu

Received October 31, 2006; accepted June 1, 2007.

Background— Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis and vascular stiffening. Whether SLE alters left ventricular (LV) structure and function in the absence of valvular and clinical coronary artery disease is unknown.

Methods and Results— SLE patients without clinical or echocardiographic evidence of valvular or coronary disease were age and gender matched to a reference group (n=173 in both groups). Subjects underwent echocardiography to quantify LV structure and function and carotid ultrasonography to detect atherosclerosis. Disease characteristics and radial applanation tonometry to measure arterial stiffness were evaluated in SLE patients. The 2 groups were similar in subjects’ body size, hypertension and diabetes status, smoking status, and cholesterol levels. LV mass (38.3 versus 32.8 g/m^2.7), ejection fraction (71% versus 67%), and prevalence of LV hypertrophy (17.9% versus 6.4%) were higher in SLE patients than in referent subjects (all P<0.001). The combination of SLE and hypertension further increased LV mass. In multivariable analysis, LV mass was associated with SLE (P<0.001) in addition to body mass index, diabetes mellitus, and hypertension. Among SLE patients, LV mass was associated with arterial stiffness (P<0.001). Carotid atherosclerosis, SLE duration, damage index, serum creatinine, and homocysteine were significantly related to LV mass in univariate but not multivariable analyses.

Conclusions— SLE predicts increased LV mass, possibly because of inflammation-related arterial stiffening. Excess LV hypertrophy may contribute to the increased cardiac morbidity and mortality observed in SLE patients.

---

 

CLINICAL PERSPECTIVE

This article has been cited by other articles:

				G W-K Yip, Q Shang, L-S Tam, Q Zhang, E K-M Li, J W-H Fung, and C-M Yu Disease chronicity and activity predict subclinical left ventricular systolic dysfunction in patients with systemic lupus erythematosus Heart, June 15, 2009; 95(12): 980 - 987. [Abstract] [Full Text] [PDF]

				M. J. Roman and J. E. Salmon Cardiovascular Manifestations of Rheumatologic Diseases Circulation, November 13, 2007; 116(20): 2346 - 2355. [Full Text] [PDF]