Assessment of Arterial Elastance and Ventricular-Arterial Coupling in Patients with Systemic Lupus Erythematosus

Abstract

To the Editor:Patients with systemic lupus erythematosus (SLE) are at in-creased risk of premature atherosclerosis, mediated by endothelialdysfunction and increased arterial stiffness[1]. The latter, mostcommonly assessed using carotid-femoralpulse wave velocity, isincreased in patients with SLE and is associated with cardiovascu-lar risk factors[1]. Recently, a more sensitive measure of arterialstiffness (effective arterial elastance; Ea), and ventricular-arterialcoupling (ratio of arterial and end-systolic ventricular elastance;Ea/Ees) demonstrated incremental prognostic value in patientswith chronic heart failure[2]. We aimed to assess the potential ofEa and Ea/Ees as novel biomarkers of cardiovascular risk in SLEwomen without ischemic heart disease.Women whosatisfiedtherevised American College of Rheumatolo-gy classification criteria for SLE were prospectively recruited from therheumatology clinics, as described previously [3]. Patients with recentactive flares, ischemic heart disease (all patients underwent nuclearstress perfusion imaging as part of the study), cardiomyopathies(including myocarditis) and valvular heart disease of≥ moderateseverity were excluded. Cardiovascular risk was defined as historyof hypertension, hyperlipidemia, diabetes mellitus, current tobacco use,cerebrovascularevents,familyhistoryofcoronaryarterydiseaseandsec-ondary anti-phospholipid syndrome. Age-matched control women wererecruited from the community. Left ventricular mass, diastolic functionand systolic ejection fraction were assessed with echocardiography;Ea was estimated as 0.9 x (arm-cuff systolic pressure/Doppler strokevolume) and Ees was calculated by the well-validated approach ofusing arm-cuff pressures, Doppler stroke volumes, ejection fraction,pre-ejection and systolic periods [4,5]. The study was conducted inaccordance with the Declaration of Helsinki and approved by the localresearch ethics committee. Written informed consent was obtainedfrom all participants.Continuousvariableswerepresentedinmean±SDormedian[inter-quartile range] and compared using either the Student t test or Mann-Whitney U test, as appropriate. The mean differences in Ea and Ea/Eeswere adjusted for age,systolic ejection fraction and systolicblood pres-sure. We assessed associations using the Pearson (r) or Spearman (ρ)correlation, as appropriate. All statistical analyses were performedwiththeSPSSversion19(SPSSInc,Chicago,USA).Atwo-sidedP b0.05 was considered statistically significant.Forty-eight patients with SLE (43±9 years old; disease durationof 14±6 years; 1 [0,2] risk factors) and 20 control women (42±9years old) were recruited. There were no differences in left ventricu-lar mass, diastolic function and Ees between SLE and control women(PN0.50 for all;Table 1). Compared to control individuals, patientswithSLEhadlowersystolicejectionfraction,albeitasmalldifference(71±8 versus 75±7%; P=0.04). Despite similar systolic blood pres-sure compared with control women (116±12 versus 119±16mmHg; P=0.52), patients with SLE had increased Ea (1.77±0.56versus 1.37±0.27 mmHg/mL; adjusted mean difference 0.30mmHg/mL, 95% confidence interval [CI] 0.08 to 0.53 mmHg/mL,Pb0.001) and Ea/Ees (0.61±0.18versus 0.50±0.07; adjusted meandifference 0.06, 95% CI 0.01 to 0.12, P=0.04). Furthermore, Ea wasassociated with increasing cardiovascular risk (ρ=0.35; P=0.02),systolic blood pressure (r=0.55, Pb0.001) and duration of predniso-lone use (ρ=0.33, P=0.03).Over 3 years of follow-up (median 31 [17,37] months), 8% ofpatients with SLE developed cardiovascular events (event rate 3.2 per100 person-years; non-fatal myocardial infarction, n=2; stroke, n=1;