Myocardial T1 mapping by cardiac magnetic resonance imaging shows early myocardial changes in treatment-naive patients with active rheumatoid arthritis and positive autoantibodies.

OBJECTIVES: We aimed to study whether myocardial changes are already detectable by cardiac magnetic resonance (CMR) imaging at the time of rheumatoid arthritis (RA) diagnosis. METHODS: This single-centre prospective study included 39 treatment-naive patients with early rheumatoid arthritis (ERA, symptom duration <1 year) without any history of heart disease, and 38 age- and sex-matched healthy volunteers. The disease severity was assessed with clinical evaluation (Disease Activity Score-28 for Rheumatoid Arthritis with CRP (DAS28-CRP) score) and serological testing (rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA)). The ERA patients were classified into group A (DAS28-CRP score ≥3.2, positive RF and ACPA; n=17) and group B (not fulfilling the group A criteria). The ERA patients and healthy controls underwent 1.5T CMR. RESULTS: Group A patients had significantly higher myocardial global T1 relaxation times than the healthy controls, 987 [965, 1003] ms vs. 979 [960, 991] ms (median [IQR]; p=0.041). A significant difference in T1 was found in the basal, mid inferior and mid anterolateral segments. In a multivariate analysis, prolonged global T1 relaxation time was independently associated with female sex (95% CI [5.62, 51.31] ms, p=0.016), and group A status (95% CI [4.65, 39.01] ms p=0.014). CONCLUSIONS: At the time of diagnosis, ERA patients with a higher disease activity (DAS28-CRP score ≥3.2) and both positive RF and ACPA showed prolonged T1 relaxation times in basal myocardial segments. These segments could be most susceptible to the development of myocardial fibrosis, and a segmental reporting style could be useful when estimating the first signs of myocardial fibrosis.

Assessment of myocardial infarct size with body surface potential mapping: validation against contrast-enhanced cardiac magnetic resonance imaging.

BACKGROUND: Assessment of myocardial infarct (MI) size is important for therapeutic and prognostic reasons. We used body surface potential mapping (BSPM) to evaluate whether single-lead electrocardiographic variables can assess MI size. METHODS: We performed BSPM with 120 leads covering the front and back chest (plus limb leads) on 57 patients at different phases of MI: acutely, during healing, and in the chronic phase. Final MI size was determined by contrast-enhanced cardiac magnetic resonance imaging (DE-CMR) and correlated with various computed depolarization- and repolarization-phase BSPM variables. We also calculated correlations between BSPM variables and enzymatic MI size (peak CK-MBm). RESULTS: BSPM variables reflecting the Q- and R wave showed strong correlations with MI size at all stages of MI. R width performed the best, showing its strongest correlation with MI size on the upper right back, there representing the width of the "reciprocal Q wave" (r = 0.64-0.71 for DE-CMR, r = 0.57-0.64 for CK-MBm, P < 0.0001). Repolarization-phase variables showed only weak correlations with MI size in the acute phase, but these correlations improved during MI healing. T-wave variables and the QRSSTT integral showed their best correlations with DE-CMR defined MI size on the precordial area, at best r = -0.57, P < 0.0001 in the chronic phase. The best performing BSPM variables could differentiate between large and small infarcts at all stages of MI. CONCLUSIONS: Computed, single-lead electrocardiographic variables can estimate the final infarct size at all stages of MI, and differentiate large infarcts from small.

Can strain rate imaging predict recovery of contraction after acute myocardial infarction?

AIMS: To assess whether strain rate imaging (SRI) can serve to evaluate myocardial viability in patients with acute coronary syndrome (ACS). METHODS AND RESULTS: In 23 patients with ACS, we measured longitudinal tissue Doppler strain and strain rate values from left ventricular basal, mid, and apical segments (n = 414). These segments were grouped according to their acute end-systolic strain values (S(ES)) into those with normocontraction (S(ES)≤-13%), hypocontraction (S(ES) between -13 and -7%), and severe contraction abnormality (S(ES)>-7%). At 8 months, we evaluated the recovery of contraction: Segments with acutely severe contraction abnormality that improved their strain values to ≤-7% were defined as viable, and those that failed to do so as non-viable. In the acute phase, S(ES), post-systolic strain, as well as systolic, early, and late diastolic strain rate values were significantly better in the viable than in the non-viable segments. Post-systolic strain had the best AUC 0.78, and a cut-off value of -3.8% predicted recovery from severe contraction abnormality with a sensitivity of 85% and specificity of 62%. The transmurality of the infarction, assessed by magnetic resonance imaging with delayed enhancement, was significantly larger in the non-viable than in the viable segments (P = 0.006). Acute global S(ES) and systolic strain rate showed the best correlations with final global S(ES) and global infarction percentage after recovery. CONCLUSION: SRI can serve to evaluate myocardial viability in patients with ACS, and to assess the recovery of segmental as well as global left ventricular function.

Early familial dilated cardiomyopathy: identification with determination of disease state parameter from cine MR image data.

PURPOSE: To characterize early changes in cardiac anatomy and function for lamin A/C gene (LMNA) mutation carriers by using magnetic resonance (MR) imaging and to develop tools to analyze and visualize the findings. MATERIALS AND METHODS: The ethical review board of the institution approved the study, and informed written consent was obtained. The patient group consisted of 12 subjects, seven women (mean age, 36 years; age range, 18-54 years) and five men (mean age, 28 years; age range, 18-39 years) of Finnish origin, who were each heterozygotes with one LMNA mutation that may cause familial dilated cardiomyopathy (DCM). All the subjects were judged to be healthy with transthoracic echocardiography. The control group consisted of 14 healthy subjects, 11 women (mean age, 41 years; range, 23-54 years) and three men (mean age, 45 years; range, 34-57 years), of Finnish origin. Cine steady state free precession MR imaging was performed with a 1.5-T system. The volumes, wall thickness, and wall motion of both left ventricle (LV) and right ventricle were assessed. A method combining multiple MR image parameters was used to generate a global cardiac function index, the disease state parameter (DSP). A visual fingerprint was generated to assess the severity of familial DCM. RESULTS: The mean DSP of the patient group (0.69 +/- 0.15 [standard deviation]) was significantly higher than that of the control group (0.32 +/- 0.13) (P = .00002). One subject had an enlarged LV. CONCLUSION: Subclinical familial DCM was identified by determination of the DSP with MR imaging, and this method might be used to recognize familial DCM at an early stage.

Tissue Doppler strain-mapping in the assessment of the extent of chronic myocardial infarction: validation using magnetic resonance imaging.

AIMS: The distribution of myocardial strain values can be visualized by colour-coded strain images. We examined for the first time if this strain-mapping function can be used to study the extent of prior myocardial infarction. METHODS AND RESULTS: Echocardiography and cardiac magnetic resonance imaging with delayed contrast enhancement were performed in 26 patients with chronic myocardial infarction. Two-dimensional strain images of the left ventricle were obtained in all standard apical views. Myocardial segments (n = 416) were assigned a score ranging from one to four based on the strain-coded colour of the segment, with higher scores representing worse myocardial function. Strain-mapping scores and quantitative strain values averaged, respectively, 1.3 +/- 0.6 and -16.4 +/- 7.6% in segments without infarction, 1.7 +/- 1.0 and -15.0 +/- 8.6% in non-transmural infarctions, and 2.8 +/- 1.2 and -6.5 +/- 8.6% in transmural infarctions. Strain-mapping had a sensitivity of 60% and a specificity of 95% in detecting segments with transmural myocardial infarction. Corresponding values for echocardiographic wall motion analysis were 50 and 96%. Strain-mapping was possible in 80% of the segments and inter-observer agreement was substantial (kappa = 0.63). CONCLUSION: Strain-mapping is a clinically applicable method for the assessment of regional myocardial function in post-myocardial infarction patients. Strain-mapping has reasonable feasibility and is more sensitive in detecting infarction damage than routine wall motion analysis.