Silent Myocardial Perfusion Abnormalities Detected by Stress Cardiovascular Magnetic Resonance in Antiphospholipid Syndrome: A Case-Control Study.

Sophie I Mavrogeni,Stella Velitsista,Maria G Tektonidou,Dimitrios Apostolou,George Markousis-Mavrogenis,Panagiotis Argyriou,Konstantinos Toutouzas,Olga Karapanagiotou,Petros P Sfikakis,David Hautemann,George Kanoupakis

doi:10.3390/jcm8071084

Abstract

Objective: To examine the prevalence of silent myocardial ischemia and fibrosis in antiphospholipid syndrome (APS), using stress cardiovascular magnetic resonance (CMR). Methods: Forty-four consecutive APS patients without prior cardiac disease (22 primary APS, 22 systemic lupus erythematosus (SLE)/APS, mean age 44 (12.9) years, 64% women) and 44 age/gender-matched controls were evaluated using CMR at 1.5 T. Steady-state free precession imaging for function assessment and adenosine stress-CMR for perfusion-fibrosis evaluation were employed. The myocardial perfusion reserve index (MPRI), and myocardial fibrosis expressed as late gadolinium enhancement (LGE), were evaluated. Coronary angiography was indicated in patients with LGE. Associations with APS characteristics, classic cardiovascular disease (CVD) risk factors, high-sensitivity CRP (hs-CRP) and high-sensitivity Troponin (hs-TnT) levels were tested. All patients were followed up for 12 months. Results: Median MPRI was significantly lower in APS patients versus controls [1.5 (0.9–1.9) vs. 2.7 (2.2–3.2), p < 0.001], independently of any LGE presence. LGE was detected in 16 (36.3%) patients versus none of controls (p < 0.001); 12/16 were subsequently examined with coronary angiography and only two of them had coronary artery lesions. In multivariable analysis, none of the APS-related and classic CVD risk factors, or hs-CRP and hs-TnT covariates, were significant predictors of abnormal MPRI or LGE. At the twelve month follow-up, three (6.8%) patients experienced coronary artery disease, notably those with the lowest MPRI values. Conclusions: Abnormal MPRI and LGE are common in asymptomatic APS patients, independently so of any APS-related and classic CVD risk factors, or coronary angiography findings in cases with LGE. Stress-CMR is a valuable tool to detect silent myocardial ischemia and fibrosis in APS.

Highlights

Antiphospholipid syndrome (APS) is a rare systemic autoimmune disorder characterized by vascular thrombosis of large, medium or small vessels, pregnancy morbidity and persistently positive antiphospholipid antibodies, including lupus anticoagulant, anticardiolipin antibodies and/or anti–β2-glycoprotein I antibodies [1]
Meaningful statistical analyses could not be performed due to small numbers. This is the first study to our knowledge that evaluated the presence of silent myocardial ischemia and fibrosis by stress cardiovascular magnetic resonance (CMR) in patients with antiphospholipid syndrome (APS)
Myocardial fibrosis, expressed as late gadolinium enhancement (LGE), was detected in one third of APS patients, of which only two patients had abnormal coronary angiography findings. These findings demonstrate that even in asymptomatic APS patients without evidence of fibrosis or macrovascular coronary artery disease (CAD) detected by coronary angiography, silent myocardial ischemia may exist

Summary

Introduction

Antiphospholipid syndrome (APS) is a rare systemic autoimmune disorder characterized by vascular thrombosis of large, medium or small vessels, pregnancy morbidity and persistently positive antiphospholipid antibodies (aPL), including lupus anticoagulant, anticardiolipin antibodies and/or anti–β2-glycoprotein I antibodies [1]. These antibodies may be detected individually or in combinations of two or three (double- or triple-positive aPL, respectively). In a multi-center European cohort of 1000 patients with APS, heart valve disease—mostly valve thickening and/or vegetation—was observed in 30% of patients, while ischemic heart disease manifesting mainly as myocardial infarction (MI), was demonstrated in 5.5% of patients [2]. Other types of heart disease have been reported in APS, including coronary vasospasm, known as variant (Prinzmetal’s) angina and syndrome X [6,7], myocardial ischemia associated with thrombotic cardiac microvasculopathy [8], and endomyocardial fibrosis due to coronary microcirculation defects [9]

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Conclusion