Association of N-terminal pro–brain natriuretic peptide with cardiac disease, but not with vascular disease, in systemic lupus erythematosus
✍ Scribed by Diana Goldenberg; Emily Miller; Michelle Perna; Naveed Sattar; Paul Welsh; Mary J. Roman; Jane E. Salmon
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 57 KB
- Volume
- 64
- Category
- Article
- ISSN
- 0004-3591
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✦ Synopsis
Association of N-terminal pro-brain natriuretic peptide with cardiac disease, but not with vascular disease, in systemic lupus erythematosus Accelerated atherosclerosis is an important health threat in patients with systemic lupus erythematosus (SLE). Traditional cardiac risk factors do not appear to adequately identify SLE patients who are at increased risk of atherosclerosis development (1). Additionally, SLE patients are more likely to develop other cardiac and vascular abnormalities such as left ventricular (LV) hypertrophy and other abnormalities of LV structure and function, as well as inflammation-related arterial stiffening (1). As a result, cardiovascular risk is likely underestimated in these patients, and there is a need for reliable biomarkers to identify those who are at increased risk.
N-terminal pro-brain natriuretic peptide (NT-proBNP) is beginning to show promise as a potentially clinically helpful biomarker of cardiovascular risk in the general population, including those without existing heart disease (2). ProBNP is released from cardiac myocytes in response to volume and pressure overload. Once released, it is cleaved into 2 peptides, NT-proBNP and BNP. NT-proBNP has no known activity in vivo, whereas BNP has 2 major effects on the systemic circulation: vasodilation and sodium and water balance through diuresis and natriuresis. While NT-proBNP has no known biologic effects in vivo, both BNP and NT-proBNP have been useful in aiding the diagnosis of congestive heart failure and stratifying risk of cardiovascular disease in the general population (2). NT-proBNP levels are elevated in the settings of congestive heart failure, arterial stiffness, acute coronary syndromes, first cardiovascular events, stroke, renal failure, and death (2,3).
Little is known about NT-proBNP in SLE. It has been suggested that serum NT-proBNP levels are higher in SLE patients than in healthy subjects, but the relationship of this peptide to markers of vascular and myocardial function has received little investigation (4,5). NT-proBNP levels appear to correlate with SLE disease damage and duration, but not with markers of vascular disease such as coronary calcification and augmentation index ( ). An association between BNP levels and echocardiographic left atrial diameter was found in 59 SLE patients (5).
We hypothesized that serum NT-proBNP levels would correlate with markers of both vascular and myocardial function in SLE patients, and we tested this hypothesis in an analysis of 124 patients meeting the American College of Rheumatology (ACR) criteria for SLE (6,7) who were participating in a longitudinal study of cardiovascular disease at the Hospital for Special Surgery. Patients underwent clinical and laboratory assessment and were classified as having atherosclerosis based on the presence of plaque (focal protrusion Ͼ50% of the thickness of the surrounding wall) on carotid ultrasonography (8). Arterial stiffness was estimated with the pressure-independent arterial stiffness index as previously described (8), and echocardiography was performed using standard techniques as previously described (9). The Systemic