Abstract
BACKGROUND: Antiphospholipid syndrome (APS) is characterized by the combination of recurrent arterial and venous thrombotic events and detection of persistently elevated antiphospholipid antibody titers in the serum or plasma. APS clinical manifestations also include non-thrombotic complications from various organ systems, mainly the CNS, kidneys, and heart. Cardiac manifestations of APS include valvulopathy, myocardial infarction and angina (stable, unstable, and Pritzmental angina). A previously published case series of cardiac magnetic resonance (CMR) in patients with APS has revealed a high rate of asymptomatic myocardial necrosis and scarring, but the prevalence of myocardial ischemia identified as CMR perfusion defects prior to development of necrosis is unknown. AIMS OF THE STUDY: To detect CMR imaging markers of myocardial ischemia in APS patients without symptoms of cardiovascular disease (CVD). METHODS: We will scan fifty APS patients without symptoms of CVD stress-perfusion CMR in a 1.5 Tesla tomographer, after intravenous infusion of adenosine and gadolinium. In addition to markers of cardiac anatomy and function, we will record imaging markers of ischemia and scarring, namely perfusion defects (PDs), and late gadolinium enhancement (LGE). We will perform parametrics using dedicated software in order to derive each patient's myocardial perfusion reserve index (MPRI). Scans will be reviewed independently by two experienced reviewers, with evaluation of inter- and intra-observer reliability. Statistical hypotheses will be examined using Student's test and Pearson's correlation coefficient, or non-parametric equivalents (Kruskall-Wallis and Spearman) for continuous variables, and Fisher's exact test for binary variables. Linear or logistic regression analyses will be used to investigate APS-related determinants of subclinical myocardial ischemia. ANTICIPATED BENEFITS: We expect to identify CMR imaging patterns characteristic of APS, which will allow proactive therapeutic interventions for primary prevention of CVD and guide further research into the pathogenesis of APS cardiac manifestations.