Myocardial perfusion imaging using a technetium-99m Sestamibi in asymptomatic and low risk for coronary artery disease patients with diagnosed systemic lupus erythematosus

Abstract

This study's significant finding was that asymptomatic CAD is common in SLE patients, even in those thought to be low risk for CAD and in the absence of cardiac symptoms.

Early Detection of Silent Myocardial Impairment in Drug‐Naive Patients With New‐Onset Systemic Lupus Erythematosus

“…The cause of the elevation might differ from ischemic heart disease; the latter mainly represents myocardial scar and necrosis. Since SLE is possibly a small vessel disease, myocardial involvement in SLE can include myocarditis (inflammation), fibrosis replacement, or myocardial ischemia , all of which can induce increases in T1 values. However, it was not possible to examine the pathologic features of myocardium in our study; it would be ideal in future studies to perform biopsies in animal models of SLE to confirm the components of abnormal myocardium.…”

Myocardial Ischaemia, Coronary Atherosclerosis and Pulmonary Pressure Elevation in Antiphospholipid Syndrome Patients

“…The previous data showing myocardial perfusion defects in autoimmune diseases referred mainly to systemic lupus erythematosus (SLE) [11−13] or rheumatoid arthritis (RA) [14]. There is only a single study referring to PAPS.…”

“…There is only a single study referring to PAPS. In SLE, perfusion defects were detected in 36−38% of asymptomatic patients [14,15], and when assessed globally in autoimmune diseases (such as SLE, RA and PAPS) it was slightly lower, 27% [13], despite normal rest ECG recordings and lack of myocardial ischaemia clinical symptoms. To the best of our knowledge, this is the first study which shows such a high frequency of myocardial perfusion defects in relatively young PAPS patients who were free from classic risk factors and symptoms of ischemic heart disease.…”

“How many times must a man look up before he can really see the sky?” Rheumatic cardiovascular disease in the era of multimodality imaging

“…Pre-contrast T1W and T2W dark blood imaging but also post-gadolinium T1W imaging can reveal presence of inflammation, even when the disease is clinically under remission [60] ; (2) Function, oedema, early, late gadolinium enhancement and stress CMR for RA, SLE, SSc and MTCD. Evidence of myocardial inflammation and/or fibrosis can be identified by STIR T2, early and late gadolinium enhancement, even if the rheumatic disease is under remission [61,62] ; (3) Additionally, it is the gatekeeper for differential diagnosis between various types of scar: scar due to CAD that should motivate coronary artery evaluation (subendocardial or transmural scar following the distribution of coronary arteries in CAD) and scar due to inflammation or vasculitis (subepicardial or intramural scar not following the distribution of coronary arteries in inflammation and diffuse subendocardial fibrosis in case of diffuse subendocardial vasculitis) [61][62][63] ; (4) Function, oedema, early and late gadolinium enhancement in inflammatory myopathies using SSFP, STIR T2, early and late gadolinium enhancement, even if the disease is under remission [64,65] ; (5) Carotid angiography and vessel wall imaging in RA and SLE [60] ; (6) Coronary angiography, oedema, early, late gadolinium enhancement, stress CMR and scar detection for Kawasaki disease [66] ; and (7) Assessment of PAH includes information about low risk for CAD in SLE patients using a technetium99m sestamibi [44] . Finally, in SLE patients with cardiac symptoms an abnormal glucose metabolism of the myocardium was detected, shown as a pathological 18FDG scan, whereas perfusion appeared normal (reversed mismatch) [45] .…”