Nuclear cardiology in the literature: A selection of recent, original research papers

Abstract

Myocardial Microvascular Dysfunction in Rheumatoid Arthritis. Quantitation by 13N-Ammonia Positron Emission Tomography/Computed Tomography Isabelle Amigues, Cesare Russo, Jon T. Giles, Aylin Tugcu, Richard Weinberg, Sabahat Bokhari and Joan M. Bathon New York, NY Circ Cardiovasc Imaging. 2019;12:e007495. http s://doi.org/10.1161/circimaging.117.007495 Context: Patients with rheumatoid arthritis (RA) have a high prevalence of cardiovascular disease. Inflammation in RA could be associated with myocardial microvascular disease and in turn result in cardiac dysfunction. Methods and Results: In order to assess the prevalence of myocardial microvascular dysfunction in patients with RA, the authors prospectively performed rest/vasodilator stress N-13 ammonia positron emission tomography (PET) and echocardiography in 76 patients with RA, but no clinical cardiovascular disease. Data on non-RA controls was retrospectively collected from patients (asymptomatic, n = 14 and symptomatic, n = 34) who had undergone rest/vasodilator stress N-13 ammonia PET. Global myocardial blood flow was quantified at rest and during peak hyperemia, and myocardial flow reserve (MFR) was calculated as the ratio peak stress myocardial blood flow and resting myocardial blood flow. The authors observed that the mean MFR in RA patients was 2.9 ± 0.8, with 29% having reduced MFR (\\ 2.5). Male gender (b-coefficient, p value: 0.54, 0.008) and higher interleukin-6 levels (b-coefficient, p value: 0.33, 0.04) were significantly associated with lower MFR, while the use of tumor necrosis factor (TNF) inhibitors was associated with higher MFR (b-coefficient, p value: 0.43, 0.02). Lower MFR was associated with higher left ventricle mass index and higher left ventricle volumes but not with ejection fraction or diastolic dysfunction. MFR was similar in RA and symptomatic controls (2.9 ± 0.8 versus 2.55 ± 0.6; p = 0.48), while it was higher in the asymptomatic controls (3.25 ± 0.7), though not statistically different. Results of this study indicate that microvascular dysfunction is present in a significant proportion of patient with RA and no clinical cardiovascular disease, and that MFR in RA patients was similar to symptomatic patients referred for a clinically indicated myocardial perfusion PET. Significance: The report of the high prevalence of microvascular dysfunction in RA is a novel finding. The association of microvascular dysfunction with inflammatory markers suggests a pathophysiologic mechanism of cardiac dysfunction in these patients. Whether microvascular dysfunction contributes to heart failure in RA patients needs to be further explored.