We have all heard the expression “A picture is worth a thousand words,” and most radiologists try to limit their reports to significantly less than that. Computed tomography (CT) scans contain a plethora of information. Extracting that information may or may not be easy. Certain abnormalities are now relatively easily visualized, identified, and quantified, such as the size and shape of a lung nodule . Others can be easily visualized but not so easily quantified. Emphysema can be relatively easily visualized and qualitatively assessed (eg, minimal, moderate, severe) but are not so easily quantified . However, the advent of density masks has simplified the quantification of emphysema . Still other physiological abnormalities defy easy visual recognition on noncontrast chest CT such as pulmonary hypertension. Pulmonary hypertension is a disease characterized by obstruction of the small pulmonary arteries in association with plexiform lesions, medial hypertrophy, concentric laminar intimal fibrosis, fibrinoid degeneration, and thrombotic lesions . The disease can progress rapidly and is life-threatening.
If the diagnosis of pulmonary hypertension is suspected, a pulmonary artery catheter can be inserted into the patient to measure the pulmonary arterial pressure (PAP) and the pulmonary capillary wedge pressure (PCWP) to make the definitive diagnosis. Although this is routinely done, it is not without risks of increased morbidity and mortality for the patient . In addition, it is frequently useful or necessary to follow the progress of a patient on pulmonary antihypertensive medications, and repeated frequent pulmonary artery catheterization is not optimal. Therefore, a noninvasive technique beyond simply following symptoms would be preferable.
Symptoms from pulmonary hypertension are nonspecific and overlap with those of more common diseases. Dyspnea is the initial symptom in approximately 60% of patients . Less common symptoms included fatigue, chest pain, near-syncope, syncope, peripheral edema, and palpitations . Physical findings usually do not become apparent until right heart failure develops, a late finding . Unfortunately, there are no simple easily visualized radiographic changes that can be quickly identified on a standard chest radiograph or CT scan. There is no “pattern recognition” on a CT scan to detect pulmonary hypertension. Unlike the late Justice Stewart Potter, we do not “know it when [we] see it” because we cannot see it, we only see the subsequent manifestations of the disease such as right heart failure and pulmonary edema, both late findings.
However, there are some simple secondary analytical techniques that have been used on the CT scan to determine the likelihood of pulmonary hypertension, once we suspect or know the diagnosis. One such technique is to manually measure the main pulmonary artery diameter . As the largest vessel in the chest, it is easily identified even without contrast material and simple to measure with electronic calibers. Others have measured several pulmonary vessels to predict pulmonary hypertension with good results . Moving further down the vascular tree, Coste et al. measured the cross-sectional area of smaller vessels, those that can still be visualized on CT, normalized to the lung area . However, this still does not take into account the smallest vessels that are the real “sites of action” of the disease.
Another approach that gets us closer to these “sites of action” is to measure the lung parenchymal density on the CT scan. Given the linear relationship between the amount of blood (water) in the lungs, any change in the vascular volume in the parenchyma may be detectable on CT. Cailes et al. found that patients with pulmonary hypertension had reduced overall lung density and higher global lung density for nondependent zones but not for dependent zones.
Taking this concept one step further, in the current issue of Academic Radiology , Dean et al. described a novel semi-automated quantification method of lung density on chest CTwhich they used as a predictive biomarker of pulmonary venous hypertension. They retrospectively examined noncontrast CT scans from 54 patients without chronic obstructive pulmonary disease scheduled for aortic valve replacement and who had right heart catheterizations. Of the patients, 32 had pulmonary venous hypertension (PCWP ≥ 15 mm Hg) and 33 had pulmonary artery hypertension (PAP ≥ 25 mm Hg). Dean et al. found that the mean lung density was greater in the patients with elevated PCWP compared to the group with normal PCWP. In addition, they found a positive correlation between the mean lung density and the PCWP. Their findings were consistent with the pathophysiology of pulmonary venous congestion associated with pulmonary venous hypertension. However, for the patients with arterial pulmonary hypertension, the results were not so clear. One would have expected the mean lung density to be lower for the patients with pulmonary arterial hypertension compared to those without it. However, they found the opposite; the results were similar to the patients with pulmonary venous hypertension (increased lung density in the group with increased PAP). This raises serious concerns that either the technique may be flawed or there is a confounder or bias in the case-control method they used that is leading to this inconsistent result.
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