Introduction
Cardiothoracic ratio (CTR) is used in clinical radiology for the evaluation of cardiomegaly. It is calculated by dividing the maximum cardiac with the maximum thoracic horizontal diameter and a value equal to 0.5 is defined as threshold for cardiomegaly diagnosis [
1]. CTR has been also applied in the postmortem setting [
2‐
4] and a new threshold of 0.57 was suggested for determining cardiomegaly based on postmortem computed tomography (PMCT) [
2]. However, the terminal cardiac dilatative changes lead to CTR overestimation and false-positive diagnosis of cardiomegaly [
3].
According to Michiue et al. [
5], CTR on 367 chest radiographs was larger for cadavers that died because of heart disease/intoxication compared to drowning/asphyxiation and the diaphragm levels were lower in the second group indicating lung hyperinflation [
5]. Cardiac hypertrophy, dilatation, and blood volume overload seem to primarily affect the postmortem CTR [
5]. In another study, Michiue et al. showed lower cardiac dilatation index in mechanical asphyxia than in sudden cardiac deaths [
6]. Sogawa et al. [
7,
8] assessed the heart to both lungs’ volume ratio in different causes of death (
n = 70) and this was higher in sudden cardiac deaths (≈ 0.4) compared to drowning and mechanical asphyxia (both ≈ 0.24) [
8]. In intoxications (≈0.3) the ratio was variable and rather close to that of sudden cardiac deaths indicating a combination of pre-existing cardiac enlargement and acute pulmonary atelectasis [
8].
Cardiac deaths are typically associated with cardiac cavities’ congestion and cardiogenic pulmonary edema at autopsy [
9‐
11]. Intoxications show non-specific findings with generalized congestion of organs and vessels, brain, and pulmonary edema [
9]. On the other hand, all kinds of suffocation (smothering, gagging, choking, chemical asphyxia by air-poison inhalation), mechanical asphyxia (positional asphyxia, traumatic asphyxia), and manual/ligature strangulation can show congestion of the organs, particularly of the right heart, acute pulmonary emphysema, and hemorrhagic edema. In hanging, besides organ congestion, lung hyperinflation may be present or not, depending on what extent the asphyxiation-aspect has taken place. In drowning, lungs are acutely hyperinflated, large, and bulky, almost or completely touching each other in the anterior mediastinal space, so-called emphysema aquosum [
9‐
12]. Hypothermia is histologically associated with pulmonary intra-alveolar edema with interstitial hemorrhages [
10]; however, lung hyperinflation has been recently reported [
13].
This study intended to evaluate the relationship between mediastinum and lungs on PMCT in a large sample with measurements of the mediastinal-thoracic volume ratio, as a more accurate, three-dimensional (3D) version of the one-dimensional CTR, with regard to different causes of death categories, age, gender, BMI, presence of cardiomegaly and lung hyperinflation.
Discussion
Imaging comprises the best tool to examine the intact organs and assess positional relationships in situ [
5]. CTR_VOL, considered a more accurate version of CTR, was assessed on PMCT to evaluate the relationship between postmortem heart and lungs in situ. This is the first attempt based on such a large sample by taking into account several influencing factors. The relatively high
R2 value of the multivariate analysis indicates these factors have described a high percentage of the sample. Mediastinum occupies approximately 20% of the postmortem thoracic cavity in adults with normal BMI, normal-sized heart, and normally inflated lungs.
In a recent study, it was shown CTR on PMCT cannot reliably discriminate cardiomegaly alone and age, gender, and BMI should be taken into account [
4]. Age showed significant effect in both analyses. However, CTR_VOL% increasing 0.1% for every year of age indicates a rather low effect in practice. In contrast, Zeek et al. did not observe any effect of age on heart weight [
14]. Jotterand et al. did not find any association between age and CTR on PMCT in a sample with normal weighted hearts [
3]. This association, however, was substantial for overweighed hearts [
4], while taking into account gender and BMI for the determination of cardiomegaly [
4]. Michiue et al. [
5] found a mild correlation between CTR on postmortem chest X-rays and age.
Gender did not show any effect on CTR_VOL. This agrees with Jotterand et al. [
3] and Michiue et al. [
5], who also did not find any relationship between CTR on PMCT and gender [
3,
5]. Zeek, however, supported that gender has an effect on human heart weight [
14]. Despite males may have heavier hearts because of larger body build, the heart to thorax ratio may remain the same to that of women as males present larger rib cage and lung construction [
24‐
26].
The approximately 0.3% increase of CTR_VOL% for every BMI-unit (β coefficient 0.0025) agrees with Zeek [
14], who stated body length and nourishment affect heart weight [
14] and Jotterand et al. [
3], who found a correlation between CTR on PMCT and BMI for normal weighted hearts with a
β coefficient 0.0022 [
3], which is very close to the one observed in this current study.
Cardiomegaly was associated with higher CTR_VOL compared to normal hearts independently, as well as within all distinct groups. This is interesting indicating that present cardiomegaly cannot be overlaid in situ by any variation of the terminal cardiopulmonary pathophysiology. Cardiomegaly caused a 7% CTR_VOL% in the univariate model and 3% increase adjusted for all co-factors. Previous study, however, showed there is correlation between CTR and heart weight at autopsy only in cases died from heart diseases but not in cases died from asphyxiation and drowning, indicating lung hyperinflation may “mask” cardiomegaly on chest radiographs [
5].
CTR_VOL in overweighed (M = 0.33) and normal hearts (M = 0.25) reflected the differences previously found for CTR (Michiue et al. [
5]: CTR% on postmortem radiographs = 55.6%, Winklhofer et al. [
2]: CTR on PMCT = 0.513 ± 0.07, Okuma et al. [
27]: CTR on PMCT = 0.55 ± 0.08, Jotterand et al. [
3,
4]: CTR on PMCT in normal hearts = 0.47 ± 0.06, in overweighed hearts = 0.53 ± 0.05). CTR_VOL values were similar to the 3D heart to lung ratio measured by Sogawa et al. [
8] (heart/lung volume ratio ≈ 0.2–0.4, depending on cause of death); however, cardiomegaly was not assessed in this previous study. The heart to lung volume ratio was calculated [
8], whereas the ratio of the mediastinal (and not only of the heart) to the whole thoracic volume (and not only the lungs) was calculated in the current study. Despite different measurement methods, 3D-CTR values by Sogawa et al. [
8] were higher for sudden cardiac deaths (0.4) and intoxication (0.3) compared to drowning and mechanical asphyxia (both around 0.24). This is similar to those currently found with cardiac deaths (0.35) and intoxication (0.28) presenting higher CTR_VOL than suffocation-strangulation (0.28), drowning (0.26), and hanging (0.25). Sogawa et al. [
8] described high variability within intoxication, which was also observed for intoxication with wider SD values in the current study.
Similar results demonstrated by Michiue et al. [
5] with CTR on chest X-rays being higher for cardiac diseases/intoxication compared to drowning/asphyxiation. The first are associated with terminal organ congestion and lower aerated lung volumes (≈ 500 ml) and the second with lung hyperinflation and larger aerated lung volumes (≈1500 ml) [
6]. Low CTR_VOL was expected for drowning because diaphragm levels are lower [
5] and lungs appear emphysematous on PMCT compared to non-drowning [
28,
29]. Christe et al. [
28] compared CTR and the anterior distance between lungs on PMCT of 10 drowning compared to 20 non-drowning deaths and did not find any differences. The smaller sample [
28] compared to our study may have led to different conclusions.
Lung expansion was evaluated separately and not only indirectly through the causes of death. It was assumed that terminal pulmonary mechanisms can individually vary and do not only strictly depend on cause of death itself. However, the sign of lungs touching each other anteriorly comprises just an indicator and does not describe hyperinflation in all of its aspects. Thus, cases with severe cardiac congestion or other mediastinal entities that mechanically impeded the lungs to expand till they reach each other anteriorly may have been assessed as without lung expansion in this study, though a hyperinflation aspect has been occurred and this comprises a limitation. Still, this sign seemed to play a crucial role in the positional relationship between lungs and heart. Mediastinum is compressed by the hyperinflated lungs causing approximately 8% CTR_VOL% decrease in the uni- and 6% in the multivariate analysis. Indications about this were described by Michiue et al. [
5], who denoted low CTR in three cases with pulmonary emphysema.
One person conducted the manual segmentation and this is a limitation. However, CTR measurements and volumetric organ measurements have shown high interrater agreements [
2,
3,
6,
30,
31]. Secondly, not all possible causes of death were assessed and hypothermia group was very small so the two hypothermia cases which fulfilled the inclusion criteria had to be excluded from the analysis. Presumably the low incidence of hypothermia deaths and the longer PMIs associated with such cases led to high rates of exclusion during the autopsy reports’ review. Thirdly, not all factors having a possible influence on CTR_VOL were assessed, especially cardiac dilatation [
3,
6]. Fourthly, lung expansion was assessed based on a rather limited single sign. Fifth, this was a single-center study and influence of race could not be assessed. Last, mediastinal volume included paracardial fat, which may have led to CTR_VOL overestimation in cases with prominent paracardial fat deposits.
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