Brief reports

The spectrum of pulmonary abnormalities on computed chest tomographic imaging in patients with advanced heart failure

Signs of pulmonary congestion obtained from cardiac computed tomography angiographic (coronary CTA) images have not previously been related to clinical congestion or outcome and the clinical value is, therefore, unknown. Our objective was to test the hypothesis that signs of pulmonary congestion predict clinical heart failure and adverse outcome in patients with myocardial infarction.

Coronary CTA was performed before invasive treatment in 400 prospectively included patients with non ST segment elevation myocardial infarction in an observational study. Using a previously described chest computed tomography evaluation algorithm, patients were classified as having “no congestion”, “mild to moderate congestion” or “severe congestion”.

Using multivariate analyses, presence of pulmonary congestion on coronary CTA images was associated with age, female gender, left ventricular ejection fraction (LVEF) and left atrial size. The diagnostic accuracy for predicting clinical heart failure, defined as Killip class >1, was: sensitivity: 83%, specificity: 69%, positive predictive value: 25%, and negative predictive value: 97%. The median follow-up time was 50 months and the study end-point of death or hospitalization due to heart failure was reached in 68 (16%) patients. In a Cox proportional hazards model with adjustments for known risk factors and Killip class, the presence of “mild to moderate congestion” and “severe congestion” was independently associated with adverse outcome (Hazard ratio: 2.6 (95% CI:1.3–5.0) and 3.2 (1.3–7.5)).

Signs of pulmonary congestion on coronary CTA images are closely correlated to cardiac dysfunction, predict clinical heart failure, and provide prognostic value independent of LVEF and Killip class.

Left cardiac chambers dilation, interstitial lung changes and pleural effusions are the characteristics of cardiogenic pulmonary oedema on computed tomography (CT) of the chest but mensuration of the left atrial size is not routinely performed. Cardiac chambers normal dimensions are known to be proportional to the patient’s build and anthropomorphic data but adjustment of chambers dimensions to available elements seen on the axial CT images has never been evaluated before.

Our objective was to use data easily available on axial images to directly scale the left atrium. We chose to divide the left atrial diameter by the thoracic vertebral diameter, using the latter as a body-mass indicator. As a preliminary study, we aimed to evaluate the range of values of this left atrio-vertebral ratio (LAVR) by comparing patients suffering from cardiogenic pulmonary oedema with patients free of cardiac disease. We hypothesized that if the difference of values in these two populations of patients was significant enough, this ratio would be relevant and could be used as a quick criterion in different clinical situations.

Two radiologists reviewed CT scans of 32 of patients free of cardiac disease and 40 patients in acute cardiac failure. The maximum diameter of the left atrium at the level of the right inferior pulmonary vein was divided by the vertebral transverse diameter to generate a left atrio-vertebral ratio. Receiver operating characteristic curves identified the threshold associated with pulmonary oedema.

The mean LAVR was 1.85 ± 0.27 in asymptomatic patients and 2.48 ± 0.35 in patients with pulmonary oedema. A LAVR of 2.1 yielded 85% sensitivity and 88% specificity for the diagnosis of cardiogenic pulmonary oedema.

LAVR is a simple new measure directly scaling the left atrial diameter to the anthropomorphic characteristics of the patient. In our series, a ratio above 2.1 is strongly associated with cardiogenic pulmonary oedema indirectly suggesting left atrial dilation. The results were significantly different between the two populations of patients (no heart condition versus cardiogenic pulmonary oedema) suggesting a high potential for clinical application.

The objective of this study was to assess the frequency of mediastinal lymphadenopathy in patients with idiopathic pulmonary arterial hypertension (IPAH) and describe the correlative clinical features.

We conducted a retrospective review of patients with IPAH who underwent right-sided heart catheterization (RHC) and chest CT scan within 3 months of each other. Patients were from a single tertiary institution. CT scans were reviewed for the presence of mediastinal lymphadenopathy (MLAD) with correlating demographic and clinical data, including lymph node size and location, right atrial pressure (RAP), mean pulmonary arterial pressure (mPAP), and the presence of pleural and pericardial effusion.

The study population included 85 patients with a mean age of 48 ± 17.3 years; 70 (82%) were women. Fifteen patients (18%) had MLAD on chest CT scan. The mean short-axis diameter of the largest lymph node in these patients was 13.6 mm (range, 11-20 mm). The enlarged lymph nodes were located predominantly in the lower paratracheal and subcarinal stations. There was no association of MLAD with age, sex, RAP, or mPAP. MLAD was associated with presence of pleural effusion (P < .02) but not pericardial effusion. Mean left ventricular ejection fraction for those with lymphadenopathy was 63% (range, 45%-76%).

MLAD without other identifiable causes is seen in approximately one in five patients with IPAH and is associated with pleural effusion but not mPAP, RAP, or left ventricular function.

Brain natriuretic peptide (BNP) is a useful biomarker for the assessment of cardiogenic pulmonary edema. This study evaluated the relationship between computed tomography (CT) findings and plasma BNP levels in patients with cardiogenic pulmonary edema.

Twenty-nine consecutive outpatients with severe respiratory failure from cardiogenic edema presenting to emergency departments were enrolled. They underwent chest CT and plasma BNP levels were measured in the emergency room. CT findings were independently evaluated by two radiologists who were unaware of the patients’ clinical information.

The plasma BNP levels only correlated with the volume of pleural effusion in each side (right: r_s = 0.519, P = .004; left: r_s = 0.460, P = .012). No significant correlation was observed between the BNP levels and the findings of lung parenchyma or cardiovascular enlargement.

Estimating the pleural effusion volume with CT may be a feasible method as well as measuring the plasma BNP level in the assessment of acute cardiogenic pulmonary edema.

Lead (Pb) exposure during development has been associated with impaired long-term potentiation (LTP). Hypothyroidism happening upon subjects with occupational exposure to Pb is suggestive of an adverse effect of Pb on thyroid homeostasis, leading to the hypothesis that Pb exposure may alter thyroid hormone homeostasis. Hippocampus is one of the targets of Pb exposure, and is sensitive to and dependent on thyroid hormones, leading us to explore whether levothyroxine (L-T₄) administration could alter the thyroid disequilibrium and impairment of LTP in rat hippocampus caused by Pb exposure. Our results show that Pb exposure caused a decrease in triiodothyronine (T₃) and tetraiodothyronine (T₄) levels accompanied by a dramatic decrease of TSH and application of L-T₄ restored these changes to about control levels. Hippocampal and blood Pb concentration were significantly reduced following L-T₄ treatment. L-T₄ treatment rescued the impairment of LTP induced by the Pb exposure. These results suggest that Pb exposure may lead to thyroid dysfunction and induce hypothyroidism and provide a direct electrophysiological proof that L-T₄ relieves chronic Pb exposure-induced impairment of synaptic plasticity.

We evaluated the association between hemodynamic parameters of chronic congestive heart failure (CHF) and mediastinal lymphadenopathy (MLA) in heart transplantation (HT) candidates and the effect of HT on MLA. We also described the results of lymph node (LN) biopsies of MLA in the patients.

Patients who underwent HT evaluation over an 8-year period and had chest CT scans were evaluated retrospectively. Data collected included LN sizes pre-HT and post-HT, echocardiographic measurements, radionuclide-derived ejection fraction, and right-sided heart catheterization hemodynamics. MLA was defined as LNs > 1 cm in smallest dimension.

Of 118 patients, 53 patients had MLA. MLA had weak statistically significant correlations with elevated mean pulmonary artery pressure (MPAP), mitral regurgitation (MR), tricuspid regurgitation (TR), right atrial pressure (RAP), and pulmonary capillary wedge pressure (PCWP). Thirty-six patients with MLA underwent HT, and nine of the 36 had post-HT chest CT scans. All nine patients showed a decrease in LN size post-HT (mean LN diameter pre-HT = 1.16 ± 0.137 cm, post-HT = 0.75 ± 0.32 cm). Seven of 53 patients with MLA underwent biopsies. Four had benign LNs, one had sarcoidosis, and two had lung cancer.

MPAP, MR, TR, RAP, and PCWP had weak statistically significant correlations with MLA. HT led to regression of MLA in patients who underwent CT scans post-HT, implying that MLA is related to CHF. However, we also identified clinically important causes of MLA; therefore, biopsy should be considered if enlarged LNs fail to regress after maximal medical management of CHF.