Rationale and Objectives
To evaluate the effects of 1 year of medical treatment on myocardial function in active rheumatoid arthritis (RA).
Materials and Methods
Thirty-nine female patients with RA without any known cardiovascular disease underwent a cardiovascular magnetic resonance (CMR) examination before and after 1 year of antirheumatic treatment. The population comprised untreated active early RA (ERA) and chronic RA patients, who were grouped accordingly. The CMR protocol included volumetric determinations, late gadolinium enhancement imaging, myocardial tagging, and native T1 mapping. DAS28-CRP disease activity scores were calculated before and after the treatment.
Results
Results are reported as median (quartile 1–quartile 3). Time to peak diastolic filling rate improved in ERA (495 [443–561] ms vs 441 [340–518] ms, P = .018). Peak diastolic mean mid short-axis circumferential strain rate of all six segments was improved (82 [74–91] %/s vs 91 [77–100] %/s, P = .05), particularly in the anterior segment (82 [63–98] %/s vs 86 [77–109] %/s, P = .013). DAS28-CRP decreased in ERA (3.8 [3.2–4.1] vs 1.6 [1.4–2.2], P < .001). In chronic RA, no statistically significant improvement was detected.
Conclusions
Early treatment of active RA is important, as myocardial function detected with CMR tagging improved in ERA in parallel with decreasing inflammatory activity.
Introduction
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease with common and often subclinical cardiovascular involvement . The mechanisms of myocardial disease in RA are not fully understood, but higher prevalence of myocardial fibrosis, diastolic dysfunction, or heart failure with normal ejection fraction has been documented . The prevalence of heart failure with normal ejection fraction in patients with RA has been reported to be as high as 23% and the prevalence of predominant diastolic dysfunction to be even higher (31%–66%) . Cardiac involvement is assumed to result from a combination of processes, such as chronic inflammation leading to endothelial dysfunction, and increased levels of inflammatory cytokines that lead to the development of myocardial dysfunction . A major contributor to reduced life expectancy in RA patients is coronary heart disease and heart failure . Therefore, early detection of myocardial changes in RA is crucial to ensure early therapeutic intervention.
Global left ventricular ejection fraction and left ventricular filling parameters measured with cardiovascular magnetic resonance (CMR) imaging can be insensitive for the detection and assessment of early changes in myocardial contractility and relaxation . The myocardial contractility and relaxation use strain as a measure of myocardial deformation, and this approach can be assessed with strain echocardiography or CMR tagging. Tagging is considered as the gold standard for noninvasive deformation imaging . Global circumferential strain assessed by CMR can identify myocardial dysfunction for several conditions that are independent of left ventricular ejection fraction . Recently, global circumferential strain has been shown to have an independent prognostic value in both asymptomatic patients and those with heart failure . For noninvasive evaluation of diffuse myocardial inflammation and fibrosis, native T1 mapping has become a promising CMR tool. Decreased native T1 values have been identified in myocardial iron overload states or glycosphingolipid accumulation in Anderson-Fabry disease, whereas high native T1 values have been related to myocardial inflammation, fibrosis, amyloid accumulation, and other conditions . The influence of active RA and the effects of medical treatment with synthetic and biological disease modifying drugs (DMARDs) were our area of interest in this 1-year follow-up study.
Materials and Methods
Study Population
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TABLE 1
Baseline Clinical Features of Patients with RA
Clinical Feature Patients with Early RA
( n = 25) Patients with Chronic RA
( n = 14)P Value ( t test) Age (y) 48 ± 14 49 ± 15 .921 RF positivity; n (%) 22 (88%) 13 (93%) 1.000 ACPA positivity; n (%) 22 (88%) 13 (93%) 1.000 Swollen joints 8 ± 6 6 ± 5 .296 Tender joints 8 ± 8 7 ± 4 .549 DAS28-CRP 3.7 ± 0.9 3.2 ± 1.1 .356 Extra-articular manifestations; n (%) 4 (16%) 7 (50%) .033 Erosions on radiographs; n (%) 3 (13%) 11 (85%) <.001 Duration of RA symptoms (mo) 11 ± 15 207 ± 133 <.001 CRP (mg/L) 12 ± 14 6 ± 6 .058 LDL (mmol/L) 2.9 ± 0.7 3.2 ± 1.0 .434 BMI (kg/m 2 ) 23 ± 4 24 ± 4 .518 Waist circumference (cm) 79 ± 10 81 ± 11 .668 Mean blood pressure (mm Hg) 109 ± 13 111 ± 19 .779
ACPA, anti-citrullinated peptide antibody; BMI, body mass index; CRP, C-reactive protein; DAS28-CRP, disease activity score; LDL, low density lipoprotein; RA, rheumatoid arthritis; RF, rheumatoid factor.
Data expressed as mean ± standard deviation.
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CMR Examination
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Image Analysis
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Statistical Analysis
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Results
Volumetric Findings
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TABLE 2
Volumetric Results for Patients with ERA ( n = 25)
Volumetric Studies Before Treatment After Treatment Change_P_ Value BSA (m 2 ) 1.7 (1.7–1.8) 1.7 (1.7–1.8) 0.0 .742 Mean heart rate (bpm) 70 (66–77) 71 (65–79) 2.0 (−1.5–5.5) .577 LVEDV (mL/m 2 ) 81 (76–90) 83 (76–94) 2.0 (−4.5–4.0) .639 LVESV (mL/m 2 ) 35 (31–40) 33 (30–40) 0.0 (−3.0–2.0) .704 LVEF (%) 57 (56–60) 57 (55–62) 0.0 (−1.0–2.0) .978 LV mass (mg/m 2 ) 51 (46–57) 54 (50–58) 1.0 (−2.5–7.5) .211 PFR (1/s) 1.5 (1.3–1.9) 1.7 (1.5–2.1) 0.1 (0.0–0.2) .646 TPFR (ms) 495 (443–561) 441 (340–518) −64 (−91–(−33)) .018 * DAS28-CRP 3.8 (3.2–4.1) 1.6 (1.4–2.2) −1.7 (−2.4–(−1.2)) <.001 *
BSA, body surface area; DAS28-CRP, RA disease activity score; LVEF, left ventricle ejection fraction; LVESV, left ventricle end-systolic volume; PFR, peak filling rate; TPFR, time to peak filling rate.
Results are expressed as median (Q1–Q3). Statistically significant difference.
TABLE 3
Volumetric Results for Patients with CRA ( n = 14)
Volumetric Studies Before Treatment After Treatment Change_P_ Value BSA (m 2 ) 1.7 (1.6–1.7) 1.7 (1.6–1.7) 0.0 .971 Mean heart rate (bpm) 75 (68–89) 75 (67–81) −2.0 (−9.0–5) .730 LVEDV (mL/m 2 ) 81 (74–92) 77 (72–87) −2.5 (−10.0–0.0) .031 LVESV (mL/m 2 ) 32 (28–40) 32 (25–35) −1.0 (−5.0–0.0) .307 LVEF (%) 60 (58–62) 59 (58–64) 0.0 (−2.0–2.0) .791 LV mass (mg/m 2 ) 52 (45–56) 51 (45–56) 0.0 (−7.0–4.0) .441 PFR (1/s) 1.8 (1.4–2.2) 1.8 (1.5–2.0) −0.1 (−0.4–0.2) .952 TPFR (ms) 433 (326–516) 433 (393–504) 2.8 (−27.8–60.1) .670 DAS28-CRP 3.4 (2.3–4.2) 3.0 (2.3–3.4) −0.2 (−1.3–0.6) .296
BSA, body surface area; DAS28-CRP, RA disease activity score; LVEF, left ventricle ejection fraction; LVESV, left ventricle end-systolic volume; PFR, peak filling rate; TPFR, time to peak filling rate.
Results are expressed as median (Q1–Q3).
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Strain Tagging Findings
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TABLE 4
Results of Strain Tagging Analysis for Patients with ERA ( n = 25)
Segment Before Treatment After Treatment Change_P_ Value Peak systolic SA strain (%) Anterior −21.6 (−24.2–(−19.8)) −22.0 (−24.8–(−19.4)) 0.1 (−2.1–1.6) .775 Anteroseptal −17.0 (−19.8–(−15.4)) −17.6 (−21.1–(−16.5)) −0.2 (−2.6–1.2) .753 Inferoseptal −15.0 (−17.6–(−12.2)) −16.2 (−18.5–(−14.4)) −1.1 (−2.7–1.2) .076 Inferior −18.7 (−19.9–(−16.4)) −17.5 (−22.6–(−15.4)) 0.4 (−2.2–2.2) .886 Inferolateral −20.8 (−23.9–(−18.7)) −21.6 (−23.6–(−15.4)) −0.7 (−2.8–1.0) .391 Anterolateral −19.8 (−20.8–(−17.3)) −20.5 (−21.9–(−17.1)) 0.7 (−0.7–2.1) .932 Mean −18.9 (−20.8–(−16.6)) −19.3 (−21.3–(−17.0)) −0.4 (−1.6–0.8) .199 Peak diastolic SA strain rate (%/s) Anterior 82.2 (63.3–98.4) 85.5 (76.5–109.2) 18.7 (3.1–26.4) .013 \* Anteroseptal 82.0 (75.8–97.0) 95.8 (78.1–102.7) 5.5 (−6.7–22.7) .159 Inferoseptal 71.0 (64.7–81.3) 79.0 (64.6–92.8) 2.2 (−7.8–11.5) .394 Inferior 77.2 (65.9–97.4) 84.7 (67.6–92.8) 2.6 (−13.0–21.4) .434 Inferolateral 89.3 (83.8–120.8) 103.4 (75.6–133.6) 8.0 (−21.9–33.3) .664 Anterolateral 76.6 (61.3–90.6) 88.7 (73.1–105.6) 14.6 (−10.1–36.4) .092 Mean 82.3 (73.9–90.7) 91.1 (77.0–100.1) 7.7 (−8.2–23.4) .050 \* Peak systolic LA strain (%) Mean −15.0 (−16.4–(−13.1)) −14.1 (−15.6–(−12.6)) 0.5 (−0.8–1.6) .549 Peak diastolic LA strain rate (%/s) Mean 42.0 (32.7–49.1) 43.2 (34.9–49.7) −0.1 (−9.1–9.9) .670
LA, long-axis; SA, short-axis.
Results are expressed as median (Q1–Q3).
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TABLE 5
Results of Strain Tagging Analysis for Patients with CRA ( n = 14)
Segment Before Treatment After Treatment Change_P_ Value Peak systolic SA strain (%) Anterior −21.3 (−24.5–(−18.8)) −20.5 (−23.0–(−18.4)) −0.1 (−1.6–4.4) .380 Anteroseptal −16.6 (−18.5–(−13.4)) −17.5 (−19.2–(−15.2)) −1.1 (−3.0–0.7) .204 Inferoseptal −14.1 (−16.9–(−13.1)) −14.7 (−19.6–(−12.2)) −1.4 (−2.5–2.9) .733 Inferior −17.9 (−19.7–(−17.0)) −18.3 (−20.0–(−16.1)) −0.5 (−1.4–1.0) .622 Inferolateral −20.0 (−23.5–(−18.5)) −22.8 (−24.1–(−16.5)) −0.1 (−3.3–1.6) .791 Anterolateral −19.6 (−21.2–(−17.2)) −17.5 (−19.2–(−15.5)) 1.8 (−2.4–5.8) .204 Mean −18.1 (−19.5–(−17.2)) −19.1 (−20.1–(−15.7)) −0.7 (−1.9–2.5) .733 Peak diastolic SA strain rate (%/s) Anterior 87.0 (56.0–104.4) 80.3 (65.2–94.7) −17.7 (−24.9–14.2) .519 Anteroseptal 85.7 (66.6–101.8) 75.2 (63.0–87.7) −15.0 (−32.4–6.5) .266 Inferoseptal 79.5 (66.5–99.7) 84.8 (53.1–96.6) −18.4 (−35.1–11.8) .266 Inferior 91.4 (77.8–97.8) 83.7 (76.8–110.6) −5.8 (−13.6–21.4) .910 Inferolateral 91.1 (72.3–112.8) 77.5 (61.7–92.8) −10.3 (−31.8–7.6) .233 Anterolateral 87.5 (68.0–93.7) 81.5 (50.8–94.7) −5.5 (−24.4–10.8) .622 Mean 86.7 (76.3–94.7) 83.3 (61.1–97.8) −7.2 (−17.3–1.3) .176 Peak systolic LA strain (%) Mean −11.1 (−15.6–(−9.9)) −12.7 (−16.4–(−8.7)) 0.5 (−1.8–1.3) .776 Peak diastolic LA strain rate (%/s) Mean 34.3 (27.5–38.7) 35.2 (28.5–48.3) 2.3 (−6.0–22.9) .380
LA, long-axis; SA, short-axis.
Results are expressed as median (Q1–Q3).
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LGE Findings
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T1 Findings and Correlation
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Correlation with DAS28-CRP
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Correlation of the Changes in Peak Systolic Strain and Peak Diastolic Strain Rate
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Discussion
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Limitations
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Conclusion
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Acknowledgments
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Appendix
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TABLE A1
Results of Mid Short-Axis T1 Analysis for 25 ERA Patients ( n = 7 for 1.5T and n = 18 for 3T). Results are Expressed as Median (Q1–Q3)
Segment Before Treatment After Treatment Change_P_ ValueT1 relaxation (ms) Anterior 1.5T 980 (949–1011) 969 (946–996) −15 (−16–(−14)) 0.844 3T 1126 (1116–1139) 1135 (1109–1196) 7 (−77–35) 0.084 Anteroseptal 1.5T 968 (950–1031) 1019 (966–1033) −11 (−49–28) 0.219 3T 1172 (1161–1175) 1146 (1109–1196) −15 (−82–49) 0.417 Inferoseptal 1.5T 978 (956–1043) 1010 (991–1023) −21 (−66–24) 0.578 3T 1162 (1148–1182) 1147 (1109–1200) −23 (−66–11) 0.815 Inferior 1.5T 971 (938–1038) 1004 (997–1016) 4 (−54–62) 0.469 3T 1160 (1153–1165) 1148 (1112–1198) −16 (−81–29) 0.532 Inferolateral 1.5T 964 (948–1010) 958 (945–992) −9 (−26–9) 1 3T 1165 (1110–1185) 1153 (1140–1179) −53 (−69–(−34)) 0.148 Anterolateral 1.5T 944 (934–983) 991 (985–998) 25 (−25–74) 0.219 3T 1130 (1116–1149) 1137 (1105–1170) 1 (−50–37) 0.833 Mean 1.5T 963 (953–1011) 989 (977–1003) −4 (−39–30) 0.375 3T 1159 (1143–1166) 1147 (1117–1181) −15 (−71–21) 0.669
TABLE A2
Results of Mid Short-Axis T1 Analysis for 14 CRA Patients ( n = 9 for 1.5T and n = 5 for 3T). Results are Expressed as Median (Q1–Q3)
Segment Before Treatment After Treatment Change_P_ ValueT1 relaxation (ms) Anterior 1.5T 1000 (977–1019) 982 (977–1047) −20 (−24–(−2)) 0.906 3T 1164 (1127–1175) 1096 (1084–1108) −47 (−56–(−37)) 0.313 Anteroseptal 1.5T 1005 (970–1042) 1028 (1026–1048) 31 (29–35) 1 3T 1187 (1159–1189) 1163 (1135–1191) −10 (−52–32) 0.813 Inferoseptal 1.5T 1007 (973–1028) 997 (980–1000) −7 (−28–(−6)) 0.570 3T 1148 (1147–1163) 1154 (1138–1171) 7 (−9–23) 0.750 Inferior 1.5T 1001 (996–1010) 1000 (987–1010) −6 (−16–(−3)) 0.382 3T 1178 (1139–1192) 1165 (1116–1213) 6 (−62–74) 1 Inferolateral 1.5T 980 (976–999) 992 (989–995) 33 (−8–48) 0.938 3T 1168 (1147–1197) 1147 (1114–1179) −11 (−33–11) 1 Anterolateral 1.5T 987 (955–996) 999 (989–1011) 24 (14–29) 0.469 3T 1146 (1135–1190) 1108 (1095–1121) −16 (−25–(−7)) 0.813 Mean 1.5T 1000 (991–1008) 990 (989–1014) 6 (−2–12) 0.570 3T 1154 (1147–1184) 1139 (1114–1163) −12 (−33–10) 1
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