Abstract
Ventricular remodeling leads to fibrotic changes in systemic right ventricles (RV). Native T1 mapping provides a quantitative measure in myocardial tissue characterization. The aim of our study was to correlate native T1 values of the systemic RV to function and volumetric data. Native T1 maps were generated with a single breath hold Modified Look-Locker Inversion-recovery pulse (MOLLI) sequence was acquired in the mid-ventricular short axis. Regions of interest (ROI) were drawn in both ventricular free walls, the interventricular septum (IVS), superior insertion point (SIP) and inferior insertion point (IIP) to obtain native T1 values. T1 values were compared to CMR ventricular volumes and function using Spearman correlation. The median age was 36 years (IQR 27–48 years). There were elevated mean native left ventricular (LV) T1 and IIP T1 values at 1122 ± 171 ms and 1117 ± 96 ms, respectively. RV dysfunction was associated with elevated IIP T1 (p = 0.007). Significant moderate negative correlations were seen between RV T1 and LV ejection fraction (LVEF) (r= −0.63, p = 0.01), between RV: IVS T1 ratio and LVEF (r= −0.68, p = 0.006), between LVEF and SIP: IVS T1 ratios (r= −0.54, p = 0.04), and RVEF and IIP T1 (r= −0.59, p = 0.02). Fibrosis measured by native T1 mapping in the systemic RV is most prominent in the LV wall and septal insertion point and correlates with decreased function. T1 values can be used in non-invasive imaging assessment of the RV, but further studies with larger cohorts are needed to assess ability to risk stratify and guide therapy.
Keywords: Transposition of the great arteries, Systemic right ventricle, Cardiac magnetic resonance imaging, Parametric mapping
Introduction
Due to advances in both diagnosis and treatment, there has been an increase in the life expectancy of those born with congenital heart disease (CHD). It is estimated that over 2 million people in the United States live with CHD, greater than half of which are adults [1]. Over 85% of CHD patients born in recent decades survive to adulthood [2, 3]. A unique cohort within the adult congenital population are patients with biventricular circulation and systemic right ventricles (RV). These include congenitally corrected transposition of the great arteries (L-TGA) and dextro-transposition of the great arteries (D-TGA) who have undergone the atrial switch operation with either the Senning or the Mustard technique [4, 5].
Multiple studies have shown that patients with a systemic RV have a significant risk of developing ventricular dysfunction as they age [6–10]. The altered loading conditions these ventricles face cause compensatory changes including dilation and hypertrophy of the RV and atrophy of the left ventricle (LV) (Fig. 1) [11, 12]. Prior studies have found that the LV in this physiology may be subject to diffuse fibrosis, ultimately leading to ventricular dysfunction [13]. Generally, treatment includes intervening on residual lesions, cardiac resynchronization therapy, medical therapy, or heart transplant [14]. There has been paucity of data on the effect to the RV. The underlying myocardial structural changes are certainly related, however not commonly assessed with standard non-invasive techniques. Alternative modalities to risk stratify patients with systemic RV physiology and accurately target medical therapy before progression of ventricular dysfunction are needed.
Fig. 1.
Graphical illustration of fibrotic changes in the systemic RV anatomy associated with decreased ventricular function
Transthoracic echocardiography (TTE) is the first line test to evaluate ventricular function, but multiple limitations prevent accurate functional assessment in this population [15]. The gold standard to assess histological changes (including fibrosis) is endomyocardial biopsy (EMB), however the risks do not justify the benefits and thus non-invasive diagnostic testing is preferred. Late gadolinium enhancement (LGE) by CMR has become an important tool in assessing myocardial fibrosis in a myriad of disease processes, however, diffuse LGE can be difficult to assess and quantify [16]. There are other limitations to consider including contraindications to gadolinium and the risk of gadolinium deposition with repeat doses [17, 18].
Native T1 parametric mapping is a non-invasive method that has been used for quantitative myocardial tissue characterization in the systemic LV [19]. These maps provide a pixel-wise representation of tissue T1 values with increased values in fibrotic regions. In normal anatomy, it is difficult to accurately obtain T1 values of the thin-walled RV due to partial volume averaging that includes blood pool or pericardial adipose contamination. The systemic right ventricle is hypertrophied and therefore can be more reliably measured [13].
Native T1 mapping has proven effective in non-invasive tissue characterization for multiple myocardial pathologies [20–24]. While some preliminary and pilot studies have suggested extracellular volume (ECV) values of systemic right ventricular myocardium may have importance, there has not been extensive research in correlating T1 values to function and volumetric ventricle data in biventricular patients with systemic RVs [25, 26]. The aim of our study was to correlate native T1 values of the systemic right ventricle to functional and volumetric data. We hypothesized that T1 values would be elevated in the systemic RV due to fibrotic changes and correlate to decreased ventricular function along with elevated volume indices of the systemic RV.
Materials and methods
This was an IRB-approved, retrospective single center study that included clinical MRI examinations of fifteen patients with biventricular circulation and a systemic RV between 10/2020 and 12/2022. Along with native T1 values, standard cardiac MRI volumetry, LGE, surgical history, and clinical history were noted.
CMR
Studies were performed on a 1.5T Siemens Sola scanner (Siemens Healthcare, Erlangen, Germany). A single breath held Modified Look-Locker Inversion-recovery pulse sequence was performed in the mid-ventricular short axis slice generating native T1 maps (Fig. 2)25. LGE imaging was performed in six subjects. LGE was acquired in the short axis plane using a T1-weighted inversion recovery spoiled gradient echo sequence 7–8 min after IV bolus of gadobutrol (Gadavist®). Post-processing was performed on cvi42 (Circle Cardiovascular Imaging Inc, Alberta, Canada). Native T1 values were generated by a single observer (SS) manually drawing regions of interest (ROI) in the interventricular septum (IVS), inferior insertion point (IIP), superior insertion point (SIP), RV free wall, and LV lateral wall. Attention was given to ensure that the tracings did not include blood pool or adjacent tissues. The ROIs were individually reviewed and confirmed by a pediatric cardiologist with 6 years of CMR experience (AC). Figure 2 demonstrates a typical T1 map and ROIs.
Fig. 2.
Native T1 heat map images with demonstration of ROI tracings in D-TGA after atrial switch (a) and L-TGA (b) with IVS (1), LV free wall (2), RV free wall (3), SIP (4), IIP (5)
Native T1 ratios among ROIs were used as a method of standardization given a lack of local normal values as well as to make the findings more easily generalizable to other systems regardless of local software or magnetic field inhomogeneities.
Statistical methods.
Data are presented as mean ± standard deviation, unless stated otherwise. Interclass correlation coefficient (ICC) was used to measure interobserver variability. The native T1 values were compared with standard ventricular volumetric and function data using Spearman correlation using SPSS v27.0 (SPSS, Inc., Chicago, IL). P values < 0.05 were considered statistically significant.
Results
Fifteen patients were included, a median age 36 years (IQR 27–48 years) and 60% male, 73% had a prior surgery requiring cardiopulmonary bypass (Table 1). Eight (53%) patients had D-TGA s/p atrial switch operation in infancy, and seven (47%) patients had L-TGA. Three participants with L-TGA underwent interventions: one had left ventricle to pulmonary artery (LV-PA) conduit placement with ventricular septal defect (VSD) closure, one had LV-PA conduit placement with mechanical St. Jude mechanical AV valve replacement, and VSD closure, and the last had resection of subpulmonary stenosis, VSD closure, and RPA stent placement. On average, patients had a mean RV ejection fraction (RVEF) of 45 ± 8% and mean LV ejection fraction (LVEF) of 56 ± 8%. Overall, the patient cohort had elevated mean native LV T1 and IIP T1 values at 1122 ± 171 ms and 1117 ± 96 ms, respectively. Comparatively, the RV T1 (1055 ± 77), Septal T1 (1062 ± 75), and SIP T1 (1041 ± 96) trended high but were within typical normal ranges reported in the literature for adult patients. Interclass correlation coefficient of 20% of cases, with T1 ROIs traced by two independent reviewers, was 0.81 (95% CI 0.51–0.92).
Table 1.
Demographic and CMR findings of systemic RV
| Variable | Median with IQR or Frequency (%) |
|---|---|
| N | 15 |
| Age at CMR (years) | 36.3(27.4–48.1) |
| BSA (m2) | 2 (1.9–2.3) |
| Sex | |
| Female (n) | 6 (40%) |
| Male (n) | 9 (60%) |
| Diagnosis | |
| D-TGA (n) | 8 (53%) |
| L-TGA (n) | 7 (47%) |
| Operation | |
| Total (n) | 11 |
| Senning procedure (n) | 3 (20%) |
| Mustard procedure (n) | 5 (33%) |
| Age of operation (months) | 18 (6–26) |
| NYHA Class | II (I–II) |
| CMR Data | |
| RVEDVi (mL/m2) | 123.3 (100.5–130.7) |
| RVESVi (mL/m2) | 65.9 (61.0–73.3) |
| RVEF (%) | 43.0 (35.7–48.4) |
| LVEDVi (mL/m2) | 69.8 (58.4–88.0) |
| LVESVi (mL/m2) | 26.1 (25.0–41.3) |
| LVEF (%) | 55.7 (53.1–62.4) |
| LV Mass (g) | 70 (51.2–78.8) |
| RV T1 (ms) (mean ± SD) | 1055 ± 77 |
| LV T1 (ms) (mean ± SD) | 1122 ± 171 |
| Septal T1 (ms) (mean ± SD) | 1062 ± 75 |
| SIP T1 (ms) (mean ± SD) | 1041 ± 96 |
| IIP T1 (ms) (mean ± SD) | 1117 ± 96 |
CMR cardiac magnetic resonance imaging, BSA body surface area, TGA transposition of the great arteries, NYHA New York Heart Association, RVEDVi indexed right ventricular end diastolic volume, RVESVi indexed right ventricular end systolic volume, RVEF right ventricular ejection fraction, LVEDVi indexed left ventricular end diastolic volume, LVESVi indexed left ventricular end systolic volume, LVEF left ventricular ejection fraction, LV left ventricle, SIP superior insertion point, IIP inferior insertion point
Elevated IIP T1 values were associated with RV dysfunction (p = 0.007) (Fig. 1). Although not statistically significant, there was an association seen between elevated LV T1 values and RV dysfunction as well (p = 0.08). There were several statistically significant moderate negative correlations including RV T1 to LVEF (r= −0.63, p = 0.01) and RV: IVS T1 to LVEF (r= −0.68, p = 0.006) (Table 2). Indexed RV end systolic volume (RVESVi) was positively correlated with both the RV: Septal T1 ratio (r = 0.64, p = 0.01) and LV: Septal T1 ratio (r = 0.64, p = 0.01) (Fig. 3). Indexed LV end systolic volume (LVESVi) was also positively correlated with RV: Septal T1 ratio (r = 0.63, p = 0.01) and LV: Septal T1 ratio (r = 0.60, p = 0.02). Moderate negative correlations were also seen between LVEF and SIP: Septal T1 ratios (r= −0.54, p = 0.04) and RVEF and IIP T1 (r= −0.59, p = 0.02) (Fig. 4).
Table 2.
Correlation coefficients between native T1 values and T1 ratios
| Correlation coefficient (r) | P-value | |
|---|---|---|
| RVEF - IIP T1 | −0.59 | 0.02 |
| RVEF - IIP: Septal ratio | −0.52 | 0.05 |
| LVEF - RV T1 | −0.63 | 0.01 |
| LVEF - RV: Septal ratio | −0.68 | < 0.01 |
| LVEF - SIP: Septal ratio | −0.54 | 0.04 |
| RVESVi-RV: Septal Ratio | 0.64 | 0.01 |
| RVESVi-LV: Septal Ratio | 0.64 | 0.01 |
| RVEDVi-Septal T1 | 0.57 | 0.03 |
| LVESVi-RV: Septal ratio | 0.63 | 0.01 |
| LVESVi-LV: Septal ratio | 0.60 | 0.02 |
| RV T1-IIP T1 | 0.57 | 0.03 |
RVEF right ventricular ejection fraction, IIP inferior insertion point, LVEF left ventricular ejection fraction, SIP superior insertion point, RVESVi indexed right ventricular end systolic volume, RVEDVi indexed right ventricular end diastolic volume, LVESVi indexed left ventricular end systolic volume
Fig. 3.
Scatter plot demonstrating correlation of elevation of T1 ratios to ventricular ESVi
Fig. 4.
Scatter plot demonstration of correlation of native T1 values and T1 ratios to ventricular function
Six subjects had LGE imaging based on clinical indications. Four subjects had LGE in the IIP with two having coincident SIP LGE. The IIP T1 values of patients with LGE were elevated at 1158 ± 106 ms compared to 1117 ± 96 ms at the IIP for the entire cohort, though extremely limited numbers prevent any significant conclusions. One subject had LGE in the anterior free wall associated with post-surgical scar with LV-PA conduit placement and a single subject had LGE noted in the basal mid-inferior RV wall.
Discussion
This study is one of the first to demonstrate correlations in T1 values to functional and volumetric ventricular data in patients with a systemic right ventricle. Most notably, we find that sub-pulmonary LV T1 values (1122 ± 171 ms) were elevated confirming previously published data by Shehu et al. correlating elevated LV T1 values to diffuse fibrosis of the LV [13]. The LV undergoes atrophic remodeling when relieved of systemic afterload. As such, normal LV myocardium is replaced with fibrotic tissue. The IIP T1 values (1117 ± 96 ms) were also elevated. Spruijt et al. showed that in patients with pre-capillary pulmonary hypertension (PH), interventricular insertion points were significantly elevated as compared to the ventricular free wall T1 values [27]. They posed that the mechanical shear stress of the IVS bowing right-to-left on the ventricular insertion points causing fibrotic changes thus leading to elevated T1 values. In our study population, the systemic afterload on the RV causes the IVS to bow right-to-left and likely has similar shear stress on the ventricular insertion points as seen in PH patients. Systemic afterload significantly increases wall stress of the RV that leads to maladaptive remodeling and ultimately systolic dysfunction. The moderate negative correlation seen in our data between RVEF and IIP T1 value supports this theory. Studies have shown ventricular remodeling in this physiology can also be measured at the matrix level with increased ECV [25, 26]. These studies showed the ECV was markedly increased in the LV as compared to the RV and this correlated with increased T1 values.
Our data also highlights the association of myocardial fibrosis with biventricular systolic dysfunction. There are moderate negative correlations between the RV T1 value and LVEF. There was also a moderate negative correlation between the SIP: Septal T1 ratio to LVEF. It may seem counterintuitive that the T1 values and ratios of the RV and the septum would affect the contralateral ventricle. However, previous studies have shown that because of the shared IVS, there is a contribution of function of one ventricle to the contralateral ventricle due to ventricular interdependence [28].
There is a moderate positive correlation between the LVESVi and the LV: Septal and RV: Septal T1 ratios. As there is increased fibrotic changes in the LV this leads to decreased LV function and dilation. The systemic afterload that the RV faces in this physiology causes bowing of the IVS right to left in systole [29]. This decreases LV output and leads to elevated LVESVi. To further strengthen this evidence, similar moderate correlations were seen in the systemic RV between RVESVi and the LV: Septal and RV: Septal T1 ratios. The RVEDVi had a moderate positive correlation with septal T1 values. As RVESVi is increased with elevated T1 values in several areas, it would be expected that RVEDVi would be increased as well.
Although some LGE data are reported, given the infrequent administration of contrast, no strong conclusions can be drawn. However, there are anecdotal cases demonstrating overlap in LGE and elevated T1 ROIs, specifically the IIP.
Limitations
This was a single center retrospective study with a small patient population, mainly due to the relative rarity of this type of congenital heart disease and its palliation. Despite this, the preliminary data is encouraging and suggests larger scale studies are indicated with a focus on longitudinal follow up to track disease progression. We were unable to compare to validated local normal T1 values given recent adoption of this scanner and mapping protocol, however clinical experience is consistent with published normal ranges. The use of T1 ratios was used as an internal control to compare regions of the same heart and highlight relative differences. The authors recognize that the LV free wall is often very thin in this context, and at times challenging to contour. For this reason, the process was critically reviewed by a second observer with every effort made to isolate the myocardium. Due to the small sample size, our study did not have the power to correlate T1 mapping values or ratios to clinical symptoms or NYHA status. However, this could be a useful metric to associate in larger cohorts.
Conclusion
Fibrosis in the systemic RV as measured by native T1 mapping in the systemic RV is most prominent in the LV lateral wall and septal insertion points. Fibrosis in these areas was associated with decreased biventricular systolic function. Native T1 values can be used as part of a standard non-invasive imaging assessment in this patient population. Routine and longitudinal use of these measures can potentially be used in risk stratification and guide therapy, however further longitudinal study with larger cohorts is needed.
Funding
The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.
Footnotes
Competing interests The authors declare no competing interests.
Ethical approval This research study was conducted retrospectively from data obtained for clinical purposes. We consulted extensively with the IRB of the University of Pittsburgh Medical Center who determined that our study did not need ethical approval. An IRB official waiver of ethical approval was granted from the IRB of the University of Pittsburgh Medical Center.
Consent to participate Informed consent was not needed for this study as this was a retrospective study of clinical images that were already obtained.
Consent for publication No individual person’s data has been presented in any of the figures or tables in this publication.
Data availability
No datasets were generated or analysed during the current study.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
No datasets were generated or analysed during the current study.