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Background: Myocardial flow reserve (MFR) by positron emission tomography (PET) is a validated measure of cardiovascular risk. Elevated resting rate pressure product (RPP = heart rate x systolic blood pressure) can cause high resting myocardial blood flow (MBF), resulting in reduced MFR despite normal/near-normal peak stress MBF. When resting MBF is high, it is not known if RPP-corrected MFR (MFR corrected ) helps reclassify CV risk. We aimed to study this question in patients without obstructive coronary artery disease (CAD)., Methods: We retrospectively studied patients referred for rest/stress cardiac PET at our center from 2006 to 2020. Patients with abnormal perfusion (summed stress score >3) or prior coronary artery bypass grafting (CABG) were excluded. MFR corrected was defined as stress MBF/corrected rest MBF where corrected rest MBF = rest MBF x 10,000/RPP. The primary outcome was major cardiovascular events (MACE): cardiovascular death or myocardial infarction. Associations of MFR and MFR corrected with MACE were assessed using unadjusted and adjusted Cox regression., Results: 3276 patients were followed for a median of 7 (IQR 3-12) years. 1685 patients (51%) had MFR <2.0, and of those 366 (22%) had an MFR ≥2.0 after RPP correction. MFR <2.0 was associated with an increased absolute risk of MACE (HR 2.24 [1.79-2.81], P < 0.0001). Among patients with MFR <2.0, the risk of MACE was not statistically different between patients with an MFR corrected ≥2.0 compared with those with MFR corrected <2.0 (1.9% vs 2.3% MACE/year, HR 0.84 [0.63-1.13], P = 0.26) even after adjustment for confounders (P = 0.66)., Conclusions: In patients without overt obstructive CAD and MFR< 2.0, there was no significant difference in cardiovascular risk between patients with discordant (≥2.0) and concordant (<2) MFR following RPP correction. This suggests that RPP-corrected MFR may not consistently provide accurate risk stratification in patients with normal perfusion and MFR <2.0. Stress MBF and uncorrected MFR should be reported to more reliably convey cardiovascular risk beyond perfusion results., (Copyright © 2024 American Society of Nuclear Cardiology. Published by Elsevier Inc. All rights reserved.)

Objectives: The purpose of this study was to evaluate the prognostic value of quantitative myocardial blood flow (MBF) and myocardial flow reserve (MFR), reflecting the integrated effects of diffuse atherosclerosis and microvascular dysfunction in patients with systemic inflammatory disorders., Background: Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and psoriasis (PsO) are common inflammatory conditions with excess cardiovascular (CV) risk compared to the general population. Systemic inflammation perturbs endothelial function and has been linked to coronary vasomotor dysfunction. However, the prognostic significance of this vascular dysfunction is not known., Methods: This was a retrospective study of patients with RA, SLE, and PsO undergoing clinically indicated rest and stress myocardial perfusion positron emission tomography (PET). Patients with an abnormal myocardial perfusion study or left ventricular dysfunction were excluded. MFR was calculated as the ratio of myocardial blood flow (MBF, ml/min/g) at peak stress compared to that at rest., Results: Among the 198 patients (median age: 65 years; 80% female), 20.7% had SLE, 31.8% had PsO, and 47.5% had RA. There were no differences in mean MFR between these conditions. Over a median follow-up of 7.8 years, there were 51 deaths and 63 major adverse cardiovascular events (MACE). Patients in the lowest tertile (MFR <1.65) had higher all-cause mortality than the highest tertile, which remained significant after adjusting for age, sex, and the pre-test clinical risk score (hazard ratio [HR]: 2.4; 95% confidence interval [CI]: 1.05 to 5.4; p = 0.038). Similarly, compared to the highest MFR tertile, those in the lowest tertile had a lower MACE-free survival after adjusting for age, sex, and the pre-test clinical risk score (HR: 3.6; 95% CI: 1.7 to 7.6; p = 0.001)., Conclusions: In patients with systemic inflammatory disorders, impaired coronary vasodilator reserve was associated with worse cardiovascular outcomes and all-cause mortality., Competing Interests: Funding Support and Author Disclosures Supported by National Heart, Lung, and Blood Institute (NHLBI) grant T32 HL094301 (Drs Weber and Divakaran), grant T32 T32HL007604 (Dr Brown), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) grant K24 AR066109 (Dr Costenbader), National Institutes of Health (NIH) grant K23 HL135438 (Dr Taqueti), and National Heart, Lung, and Blood Institute grant R01HL150342 (Dr Divakaran). Dr Di Carli has received grants from Gilead Sciences and Spectrum Dynamics; and is a consultant for Janssen and Bayer, outside the submitted work. Dr Dorbala has received grants from Pfizer and GE Healthcare; and is a consultant for GE Healthcare and Pfizer, outside the submitted work. Dr Blankstein has received grants from Amgen and Astellas; and is a consultant for Amgen, outside of the submitted work. Dr Merola has received grants from and is a consultant for Merck, Abbvie, Dermavant, Eli Lilly, Novartis, Janssen, Union Chimique Belge (UCB), Celgene, Sanofi, Regeneron, Arena, Sun Pharma, Biogen, Pfizer, EMD Sorono, Avotres, and Leo Pharma. Dr Massarotti has received grants from Bristol-Myers Squibb; and is a consultant for UCB and Exagen; and serves on data safety monitoring board for EMD Serono. Dr Costenbader has received grants from Merck, AstraZeneca, Janssen, and Glaxo Smith Kline; and is a consultant for Merck. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background Systemic lupus erythematosus (SLE) is a systemic autoimmune inflammatory disorder associated with premature atherosclerosis and increased cardiovascular risk. Systemic inflammation is an emerging risk factor for coronary microvascular dysfunction (CMD). We aimed to test whether CMD, defined as abnormal myocardial flow reserve (MFR) by positron emission tomography-computed tomography, would be independently associated with SLE after adjusting for nonobstructive atherosclerotic burden and common cardiovascular risk factors. Methods and Results Consecutive patients with SLE who underwent symptom-prompted stress cardiac positron emission tomography-computed tomography were included (n=42). Obstructive coronary artery disease and systolic dysfunction were excluded. MFR was quantified by positron emission tomography-computed tomography, and CMD was defined as MFR <2. We frequency matched patients who did not have SLE and had symptom-prompted positron emission tomography studies on age, sex, and key cardiovascular risk factors (n=69). The attenuation correction computed tomography scans were reviewed for qualitative assessment of coronary artery calcium. Patients with SLE had a more severe reduction in global MFR compared with controls and a higher prevalence of CMD, despite a similar degree of nonobstructive atherosclerotic burden (1.91±0.5 versus 2.4±0.7, respectively, P <0.0001; CMD, 57.1% versus 33.3%, respectively, P =0.017). Conclusions We demonstrated that patients with SLE with cardiac symptoms without obstructive coronary artery disease have a high prevalence of coronary vasomotor abnormalities. In comparison with symptomatic matched controls, patients with SLE have a more severe reduction in MFR that is not accounted for by common cardiovascular factors or atherosclerotic burden.