Limitations of cardiothoracic ratio derived from chest radiographs to predict real heart size: comparison with magnetic resonance imaging

Chest radiographs (CXR) are routinely used to assess the lungs and mediastinum. Cardiothoracic ratio (CTR) is a simple method to evaluate the heart size on chest radiographs. Despite having been introduced more than 100 years ago [1], it is still commonly reported nowadays, even though new imaging techniques have been developed. This is probably because CTR can be easily measured and simply interpreted on a widely available and inexpensive imaging study. Nevertheless, CTR depends on multiple technical and anatomic factors that can contribute to an inaccurate assessment of the real heart size. CTR is only considered reliable if calculated from a frontal upright postero-anterior (PA) chest radiograph. The supine position and any other antero-posterior (AP) projection overestimate cardiac size due to a magnification effect caused by the heart being closer to the imaging cassette. In addition, there are other cardiac and non-cardiac aspects such as sub-optimal inspiratory effort, patient’s or thoracic cage abnormalities that could influence the value of CTR [2‐4].

CTR is defined as the ratio between the maximal horizontal cardiac diameter and the maximal horizontal inner thoracic cage diameter [2]. A CTR > 0.5 (or > 50%) is considered abnormal. In radiology reports, terms like “cardiomegaly” or “increased heart size” are commonly used to describe an increased CTR. Despite its broad use, some researchers have questioned the real value of this arbitrary cut-off point. For example, in a study with patients undergoing coronary angiography due to angina, a CTR between 42 and 49% was associated with a higher risk of all-cause mortality or major coronary event (death, non-fatal myocardial infarction) compared to patients with CTR < 42% [5].

In modern diagnostic imaging, newer modalities allow to thoroughly examine the three-dimensional structure of the heart, assessing chamber size and function. Some studies have questioned the correlation between CTR and cardiac parameters derived from other imaging techniques with controversial results. In comparisons done within specific cardiac pathologies, there is usually an absence of correlation with CTR or CTR correlates with the size of only one or two cardiac chambers [6, 7]. A systematic review by Loomba et al. showed that CTR is sensitive for identifying an increased left ventricular volume on echocardiography (sensitivity 83.3%) but lacks specificity (45.4%) [8]. Larger CTRs were related to increased mortality risk in adults with congenital heart disease [6]. Apart from chest radiographs, CTR can also be measured using other imaging modalities like CT and MRI. However, Schlett et al. found that CTR derived from CT scout images did not correlate to LV parameters measured from the same CT scan [9].

Cardiac MRI is a modern, high-resolution, ionising radiation-free technique that is now considered the gold standard for cardiac volumetry and function assessment [10‐12]. We hypothesise that the cut off value of CTR = 50% is a poor indicator of cardiac enlargement and should be interpreted with caution. The primary aim of this study was to compare the CTR to indexed cardiac volumetry values. Secondary objectives were: (1) to evaluate the isolated correlation between CTR and individual cardiac chamber measurements, (2) to stratify the results by age and gender using the dedicated normal cardiac MRI values for comparison.

This study aims to determine the reliability of CTR to predict cardiac enlargement by comparing the CTR values to cardiac parameters. Our results have shown a weak but statistically significant correlation between CTR and cardiac MRI defined parameters related to cardiac size. This weak correlation is explained by the substantial overlap of all measured cardiac MRI values in patients with normal and increased CTR. Although patients with CTR > 50% tend to have larger ventricular volumes and atrial areas, many patients with a normal CTR have abnormal cardiac MRI values. Interestingly, CTR correlated significantly with all ventricular and atrial measurements, despite having a broad spectrum of pathologies. In a heterogeneous adult population of our study, the cardiac chamber responsible for an increased CTR is variable, as is the number of enlarged chambers.

Compared to a paediatric population study performed by Grotenhuis et al. [2] (including congenital heart diseases, aortic regurgitation and HCM), our results show that the THVi correlated better with CTR in adults than in children (r = 0.41 vs. r = 0.27). However, correlation with isolated chambers’ enlargement was substantially better in children. In paediatric patients with Tetralogy of Fallot, the RVEDVi and CTR correlated weakly (r = 0.4), and in those with aortic regurgitation, the LVEDVi and CTR showed moderate correlation (r = 0.5). In this regard, a more homogenous sample is a plausible explanation for the stronger correlation between ventricular volumes and CTR, as seen in paediatric patients (i.e. enlargement of the RV is the expected cause of increased CTR in patients with Tetralogy of Fallot, as is dilated LV in patients with aortic regurgitation). On the other hand, Spiewak et al. [7] did not find a correlation between CTR and ventricular volumes in patients with Tetralogy of Fallot but reported a weak but statistically significant correlation with atrial volumes. This weak correlation is maintained in our adult population. Anyhow, the commented heterogeneity of results among studies is in keeping with the poor discriminatory value of CTR regarding true cardiac size, which is likely translatable in routine settings.

Notably, patients with several cardiac pathologies have been included in the present study, thus covering a broad spectrum of cardiac morphologies. Nevertheless, reliance on CTR is based on the fact that even isolated chamber enlargement impacts the whole cardiac silhouette. Typically, LV dilatation causes leftward, downward and backward rotation of the heart in a clockwise direction. However, it can also result in anticlockwise rotation, which is not expressed as increased CTR on chest radiographs [2, 16]. Furthermore, RV does not contribute to the left heart contour unless severely dilated as the sternum limits its expansion. Only if dilated enough, RV may rotate leftwards, push the left ventricle and increase the left heart border [7]. This may help to explain the particularly low correlation found between CTR and RV volumes. As CTR effectively represents the transverse diameter between the RA and LV (which form the right and left heart borders, respectively), it might be expected to reflect more accurately the enlargement of these chambers. However, neither RA area nor LV volume showed stronger correlations with CTR than other parameters.

A large number of cases with normal CTR revealed another interesting aspect of our study. A normal CTR was determined in 62.8% of patients, even though only 8.1% of individuals had normal cardiac MRI scans. Therefore, a CTR < 50% on chest radiographs does not seem to be a reliable indicator to exclude cardiac pathology. Dimopoulos et al. [6] also found that only 56.4% of adult congenital heart disease patients had an increased CTR on chest radiographs. In addition, some authors state that even a normal CTR could be related to poor clinical outcomes [5, 17]. Jun et al. [17] determined that a CTR greater than 42% was an independent predictor of major adverse cardiac events after percutaneous coronary intervention. Of note, in our population, such values were rare, as only 22 individuals out of 309 (7%) had a CTR of ≤ 42%.

ROC curve analysis corroborated the poor discriminatory value of CTR with AUCs only mildly above “chance” when using cardiac MRI values as the gold standard. No single CTR cut-off point was able to classify increased and normal chamber sizes accurately. Low CTR thresholds were associated with many false positives (patients with higher CTR on CXR but normal heart size on cardiac MRI). Larger CTR thresholds failed to identify most patients with abnormal cardiac MRI parameters, thus giving very few true positive results. Yet, CTR showed value when extreme measurements were found. That is to say, the likelihood of having an increased heart size is high when a CTR > 55% is found, as is the likelihood of having a normal heart size with a CTR < 45%.

Although cardiac MRI is considered the gold standard to assess cardiac volumes and function, it is not always accessible or even indicated. Other imaging modalities such as echocardiography and CT are also available for cardiac evaluation. Meta-analysis performed by Loomba et al. showed that CTR was sensitive but not specific to detect left ventricular dilatation determined by echocardiography: after assessing six studies with a total of 466 patients, the authors concluded that CTR had 83.3% sensitivity, 45.4% specificity, 43.5% positive predictive value and 82.7% negative predictive value. However, after one study with a paediatric population was excluded, specificity significantly decreased to 25.2% [8]. On the contrary, CTR in patients with NSTEMI showed lower sensitivity (40%) but higher specificity (91%) in detecting cardiomegaly compared to echocardiography, however in this study, cardiomegaly was described as an enlargement of the right or left ventricle [18]. Furthermore, Chana et al. found CTR to have a limited value in detecting left and/or right ventricular dysfunction (0.7 AUC, 73.9% sensitivity and 47.4% specificity) [19].

Regarding CT, CTR can be derived from the CT itself, using the scout images or axial slices. While this allows overcoming the limitation of a time gap that previous studies encountered when comparing two different imaging modalities, it is important to note that CT images are acquired in the supine position. Schlett et al. used anteroposterior scout images to calculate the CTR and found that CTR did not correlate with CT derived end-diastolic LV volume, mass or size (all p ≥ 0.27). On the other hand, all these mentioned LV parameters showed significant correlation with a simple axial LV area-based measurement, suggesting that on CT, other straightforward measurements may be applied instead of traditional CTR [9]. Regarding CTR as a single parameter, CTRs obtained by CXR and CT correlated (r = 0.802) in a study of cancer patients by Gollub et al. The authors also showed a limited ability of CT-derived CTR to recognise LV hypertrophy determined by echocardiography (AUC was 0.71) [20].

Generally, the complexity of the heart and extracardiac factors, as described in our study, undermines the value of a single cut-off of CTR. Thus, our results support the evidence that the reliability of CTR to predict cardiac size and functional status is limited.

One of the possible limitations of our study is the heterogeneous study population. However, this allowed to assess CTR in a spectrum of pathologies in different categories, likely translatable to broader practice. Secondly, the study was performed in a specialised cardiothoracic centre, meaning there was a low proportion of healthy individuals in the study (8%). Thirdly, our selected maximum interval between chest radiographs and cardiac MRI was one month, although the calculated average time difference was nine days. It is reasonable to assume that a time gap between studies in some cases might have been associated with clinical changes. However, in daily practice, chest radiograph and cardiac MRI are rarely performed on the same day (only 7% in our study sample). Therefore further studies assessing this may give some insight on whether the timeframe could have an influence. Thirdly, it would be interesting to evaluate separate cardiac chamber variations in the heart silhouette and whether this complements CTR to make it a more accurate measure. In this regard, artificial intelligence may play a role in automating and defining cardiac morphology on chest radiograph suggestive of underlying cardiac chamber abnormality. Furthermore, even though cardiac MRI is considered as the gold standard for cardiac volumetry and function, regrettably, the technique, while being increasingly used, is not yet available in every setting and is time-consuming [21]. Hence, CXR cannot be replaced by MRI, but CTR, as an estimate of true cardiac size, should be interpreted with caution and correlated with other available imaging modalities. Finally, CTR itself has limitations due to various cardiac and non-cardiac factors [3, 4]. To address this, we have constrained the impact of this limitation by excluding AP radiographs or patients with pleural or pericardial effusions obscuring the cardiac borders on chest radiographs.

Although CTR has an excellent interobserver agreement, is reproducible and easily measurable, it has little accuracy to distinguish a normal from an increased heart size when used as a single threshold method (i.e. CTR > 50%). Due to the lack of sensitivity and specificity of intermediate CTR values (45–55%), it would be more accurate to report a possibility of cardiac chamber enlargement rather than stating true cardiomegaly.