Comprehensive MDCT Evaluation of Patients With Pulmonary Hypertension: Diagnosing Underlying Causes With the Updated Dana Point 2008 Classification
Abstract
OBJECTIVE. Pulmonary hypertension is a challenge for imagers and clinicians, with a variety of possible underlying causes, each with its own specific treatment. Although the diagnosis is based on physiologic measurements, ECG-gated MDCT can play a vital role in elucidating underlying cardiac, vascular, and pulmonary causes.
CONCLUSION. A revised system for pulmonary hypertension, the Dana Point classification, can provide a template for review of the myriad causes of this complex condition.
Pulmonary hypertension [1] is a condition that can be easily identified by transthoracic echocardiography [2], but the underlying cause is usually very difficult to find [1, 3, 4]. There is a long list of underlying causes presenting as pulmonary hypertension, and the definitive treatments are also diverse [1, 3, 4]. With extensive publications on clinical observation, clinical trials, and pathogenesis being produced every year, World Symposia on Pulmonary Hypertension were held in 1973, 1998, and 2003, all endorsed by the World Health Organization [1]. The latest (fourth) world expert consensus endorsed by the World Health Organization is the Dana Point 2008 classification [1] (Table 1), which is designed to reflect updated knowledge about pathophysiology and management.
According to current understanding, most of the underlying causes of pulmonary hypertension are of cardiac or pulmonary origin [3, 4]. CT has long been recognized as a reliable tool for pulmonary and vascular diseases [5–8]. Recently, with rapid technical advances in MDCT, the diagnostic role of CT has been extended to cardiac diseases [6, 9–11]. Because of the volume acquisition nature of CT, even though the scan is focused on the heart, a larger FOV reconstruction without ECG signal can be obtained to evaluate the lung condition, which makes MDCT a good one-stop shop for cardiopulmonary evaluation. In clinical practice, ECG-gated MDCT can diagnose or exclude many diseases that echocardiography cannot evaluate, such as coronary artery stenosis, anomalous pulmonary venous return, and some structural heart diseases. An ECG-gated MDCT can replace diagnostic cardiac catheterization and nongated CT, providing a quicker and safer diagnostic algorithm for the patient. Though the concept and technique are feasible, to our knowledge, no educational article in the literature has described the use of ECG-gated MDCT for the evaluation of patients with pulmonary hypertension according to the Dana Point 2008 classification. This article is intended to assist radiologists by providing a thorough overview of MDCT scanning techniques, radiation considerations, and image findings of the underlying causes of pulmonary hypertension.
Techniques
MDCT performed with ECG-gating technique is suggested because left heart disease is the most common cause of pulmonary hypertension [4]. Because valvular function and coronary arteries are the key components of evaluation, scanners with good temporal resolution are recommended. In this article, we will share our protocol using a 256-MDCT scanner (Brilliance iCT, Philips Healthcare). However, use of the widely available 64-MDCT scanners is also feasible if they are operated with proper patient heart rate control.
One hour before the scan, oral propranolol (0–40 mg) is given to the patient by a cardiac radiologist to achieve a heart rate less than 80 beats/min. A 20-gauge IV catheter is inserted into the patient's right antecubital vein, and 100 mL of contrast medium is injected with a flow rate of 3.5 mL/s, followed by 30 mL of saline chaser using the same flow rate. A bolus-tracking technique is used with the region of interest set in the ascending aorta. After the enhancement reaches a threshold of 150 HU, the scan starts after a 15-second delay. Compared with routine cardiac CT, the larger contrast volume, slower injection rate, and longer delay time ensure good opacification of pulmonary vessels, aorta, and all cardiac chambers. The scan parameters are as follows: tube voltage and current adjusted according to the patient's body weight [10], collimation of 128 × 2 × 0.625 mm with smart focal spot technique, rotation time of 0.27 second, and pitch of 0.18, with ECG-gating technique from the carina to the bottom of the heart. The images are reconstructed with slice thickness of 0.67 mm and index of 0.34 mm, from 0% to 90%. Furthermore, a large FOV image set with slice thickness of 1.0 mm and index of 0.6 mm is reconstructed without ECG signal (to increase signal-to-noise ratio) for pulmonary vessel and lung parenchyma evaluation. The average dose-length product of this protocol in our institute is 910.6 ± 200.1 mGy × cm, corresponding to an effective dose of 12.7 ± 2.8 mSv.
For interpretation, a dedicated CT workstation (Extended Brilliance Workspace, Philips Healthcare) is used in our institution to evaluate the coronary arteries [10], cardiac structures [6, 9], valvular motions [9], pulmonary arteries [7, 8], pulmonary veins [7], and lung parenchyma [5, 7], to find any possible underlying causes of pulmonary hypertension.
Diseases by the Updated Dana Point 2008 Classification
In this section, we discuss several underlying causes of pulmonary hypertension, as classified by the Dana Point 2008 classification [1].
Group 1: Pulmonary Arterial Hypertension (PAH)
Group 1 [1] includes PAH associated with underlying disease (Figs. 1A, 1B, 1C, and 1D) and idiopathic PAH (Figs. 2A, 2B, and 2C). To establish the diagnosis of idiopathic PAH, we must clinically and radiographically exclude underlying causes, such as liver disease (Figs. 3A and 3B) or congenital heart disease [6] (Figs. 4A, 4B, 4C, 5A, 5B, and 5C; Figs. S1E, S1F, S3C, and S5D–S11C, supplemental videos, can be viewed from the information box in the upper right corner of this article). ECG-gated MDCT provides structural, functional, and even hemodynamic information [12].
Group 1': Pulmonary Venoocclusive Disease (PVOD) and Pulmonary Capillary Hemangiomatosis (PCH)
PVOD and PCH are both diseases with unknown cause [13]. PVOD is diagnosed pathologically by diffuse occlusion in pulmonary venules and small veins, whereas PCH has a similar pathologic profile in the alveolar capillary bed. Because their presenting symptoms (i.e., dyspnea and fatigue) overlap with those of many other diseases, the diagnosis is usually delayed. Currently, the only definitive treatment is lung or heart-lung transplantation.
Even though PVOD [13] and PCH share many common features (e.g., histology, presentation, and risk factors) with idiopathic PAH [1], they have different treatment responses (e.g., using a potent vasodilator for PAH would cause fatal pulmonary edema in PVOD and PCH [1]) and prognoses. To establish the diagnosis of PVOD (Fig. 6) or PCH, surgical lung biopsy is the reference standard. However, because of the high mortality rate of operation in such patients, noninvasive imaging diagnosis is a clinically acceptable alternative [13]. After recognizing typical vascular changes (e.g., dilated and tortuous pulmonary arteries) of pulmonary hypertension and excluding other potential causes, PVOD is suggested by the numerous thickened interlobular septal lines, whereas PCH shows diffuse small ground-glass-opacity nodules [14].
Group 2: Pulmonary Hypertension Due to Left Heart Disease
Left heart disease is the most common cause of pulmonary hypertension according to Oudiz [4]. Thus, a complete pulmonary hypertension survey should include left heart diseases. Left heart disease could be ischemic (Figs. 7A, 7B, 7C, 7D, 7E, and 7F), valvular (Fig. 8), or structural (Fig. 9). MDCT can provide excellent images and diagnosis [9–11]. The radiologist should review the echocardiographic ejection fraction to avoid β-blocker use in patients with heart failure (at our institution, no β-blocker is used if the ejection fraction is < 25%). Current guidelines do not recommend using PAH medications to treat group 2 patients because the safety and efficacy have not been proved [1]. Standard treatment of left heart disease, such as revascularization or valvuloplasty, is suggested [15–17].
This group of patients best exemplifies why ECG-gating is needed in evaluating pulmonary hypertension. ECG-gating can help in diagnosing or excluding coronary artery disease and in objectively evaluating regional wall motion, myocardial thickness, or even viability. If only nongated MDCT is performed, this group of patients might need routine diagnostic cardiac catheterization and cardiac MRI to provide similar information. However, catheterization is an invasive procedure and cardiac MRI requires longer schedule time and scan time. In comparison, ECG-gated MDCT provides a very fast and noninvasive diagnostic approach.
Group 3: Pulmonary Hypertension Due to Lung Diseases or Hypoxia
In patients with lung diseases, the acoustic window for transthoracic echocardiography is usually limited. MDCT can simultaneously evaluate cardiac, vascular, and lung parenchymal conditions [5–7, 10, 11] to serve as a helpful alternative. In group 3, chronic obstructive pulmonary disease (Fig. 10) and interstitial lung disease (Figs. 11A and 11B) are the most representative diseases. Use of β-blockers in patients with chronic obstructive pulmonary disease can be dangerous and should only be administered with caution, because of the potential bronchoconstriction and acute lung function deterioration. High-temporal-resolution scanners are recommended because they can significantly reduce the use of preprocedural β-blockers. The safety and efficacy of using PAH medications to treat group 3 patients has not been proven [1].
Group 4: Chronic Thromboembolic Pulmonary Hypertension
The powerful diagnostic capability of MDCT for pulmonary embolism has replaced nuclear ventilation-perfusion scan and catheter pulmonary angiography as the first-line imaging modality in clinical practice [7, 8]. In group 4 patients, not only can MDCT accurately diagnose chronic thromboembolic pulmonary hypertension, but it also can serve as a serial follow-up tool (Figs. 12A, 12B, 12C, and 12D) [7, 8]. In regard to treatment, surgical thromboendarterectomy should be considered first. Medications for PAH might be useful but are not yet supported by randomized controlled trial [1].
Group 5: Pulmonary Hypertension With Unclear Multifactorial Mechanisms
Group 5 consists of many diseases with unclear or multifactorial mechanisms, including hematologic (e.g., chronic myeloproliferative disorders), systemic (e.g., sarcoidosis and pulmonary Langerhans cell histiocytosis), and metabolic disorders (e.g., glycogen storage disease). Also, occlusion of the microvasculature by metastatic malignancy could present as pulmonary hypertension (Figs. 13A and 13B).
Conclusion
With the technical advances of MDCT, it has become a reliable diagnostic tool for cardiac, vascular, and pulmonary diseases and is thus very useful in evaluating patients with pulmonary hypertension. Correctly identifying the causes and treating them accordingly will improve the patient's prognosis.
Fig. 1A —35-year-old woman with history of systemic lupus erythematosus who presented with atypical chest pain and pulmonary hypertension (98 mm Hg) on echocardiography. MDCT was performed for cardiopulmonary evaluation. This case shows powerful capability of MDCT to diagnose or exclude many underlying causes.
A, Multiplanar reformation image of coronary arteries shows that all three coronary arteries (circumflex coronary artery [CCA], left anterior descending coronary artery [LAD], and right coronary artery [RCA]) and their branches are patent.
Fig. 1B —35-year-old woman with history of systemic lupus erythematosus who presented with atypical chest pain and pulmonary hypertension (98 mm Hg) on echocardiography. MDCT was performed for cardiopulmonary evaluation. This case shows powerful capability of MDCT to diagnose or exclude many underlying causes.
B, Four-chamber view during end-systole shows dilated right atrium (RA) and right ventricle (RV). Ventricular septum is deviated to left side (arrowhead), which means RV has pressure similar to that of left ventricle (LV) during systole. Peak pulmonary artery pressure measured by catheterization was 93 mm Hg. LA = left atrium. See also Figure S1E, ventricular septal motion in four-chamber view, which can be viewed from the information box in the upper right corner of this article.
Fig. 1C —35-year-old woman with history of systemic lupus erythematosus who presented with atypical chest pain and pulmonary hypertension (98 mm Hg) on echocardiography. MDCT was performed for cardiopulmonary evaluation. This case shows powerful capability of MDCT to diagnose or exclude many underlying causes.
C, Short-axis view during end-systole shows dilated RV with D-shaped LV during end-systole (arrowhead), which means pulmonary artery pressure is similar to that of LV. See also Figure S1F, ventricular septal motion in short-axis view, which can be viewed from the information box in the upper right corner of this article.
Fig. 1D —35-year-old woman with history of systemic lupus erythematosus who presented with atypical chest pain and pulmonary hypertension (98 mm Hg) on echocardiography. MDCT was performed for cardiopulmonary evaluation. This case shows powerful capability of MDCT to diagnose or exclude many underlying causes.
D, Coronal maximum-intensity-projection image of pulmonary vessels shows tortuous lower lobar branch of right pulmonary artery (RPA; arrowheads), indicating chronic pulmonary arterial hypertension. Pulmonary embolism was excluded because of no filling defect. Please note pulmonary veins are straight and not tortuous (arrow), which means pulmonary vein is not under high pressure, and is good indicator to find “source” of pulmonary hypertension. With tortuous pulmonary artery but straight pulmonary vein, source of high pressure is considered to be microvasculature in lung parenchyma. In lung window (not shown), no specific anomaly was found. Using Dana Point 2008 classification, this case is classified as group 1.4.1 (pulmonary arterial hypertension associated with connective tissue diseases), in this case, systemic lupus erythematosus.
Fig. 2A —34-year-old woman with no underlying disease who presented with dyspnea and pulmonary hypertension (94 mm Hg) on echocardiography. Nongated pulmonary CT angiography was performed to exclude pulmonary embolism. This case shows typical findings of idiopathic pulmonary arterial hypertension on MDCT.
A, Axial image shows dilated main pulmonary artery (MPA) as compared with normal-sized ascending aorta (AAO). Right pulmonary artery (RPA) and left pulmonary artery (LPA) are also dilated.
Fig. 2B —34-year-old woman with no underlying disease who presented with dyspnea and pulmonary hypertension (94 mm Hg) on echocardiography. Nongated pulmonary CT angiography was performed to exclude pulmonary embolism. This case shows typical findings of idiopathic pulmonary arterial hypertension on MDCT.
B, Coronal maximum-intensity-projection shows tortuous pulmonary arteries (arrowhead) but straight pulmonary veins (arrow), which means “source” of pulmonary hypertension is microvasculature between pulmonary arteries and pulmonary veins.
Fig. 2C —34-year-old woman with no underlying disease who presented with dyspnea and pulmonary hypertension (94 mm Hg) on echocardiography. Nongated pulmonary CT angiography was performed to exclude pulmonary embolism. This case shows typical findings of idiopathic pulmonary arterial hypertension on MDCT.
C, Four-chamber view shows dilated right atrium (RA) and right ventricle (RV). RV trabeculation is significantly thickened (arrowheads). These long-term compensatory changes indicate chronic pulmonary hypertension. With exclusion of other diagnoses from clinical assessment and imaging, patient was diagnosed as having idiopathic pulmonary arterial hypertension and was treated with sildenafil. Pulmonary arterial pressure (by echocardiography) decreased from 94 to 75 mm Hg after treatment. Case is classified as group 1.1 (idiopathic pulmonary arterial hypertension). LA = left atrium, LV = left ventricle.
Fig. 3A —50-year-old man with hepatitis B and binge drinking history who presented with dyspnea. MDCT was arranged to exclude or diagnose pulmonary embolism. Final diagnosis was portopulmonary hypertension. This case shows that MDCT not only evaluates cardiopulmonary condition but also surveys surrounding organ diseases such as liver cirrhosis and portal hypertension.
A, Axial image shows irregular surface of liver (arrowheads), compatible with liver cirrhosis. Esophageal varices (arrows) also imply portal hypertension of patient.
Fig. 3B —50-year-old man with hepatitis B and binge drinking history who presented with dyspnea. MDCT was arranged to exclude or diagnose pulmonary embolism. Final diagnosis was portopulmonary hypertension. This case shows that MDCT not only evaluates cardiopulmonary condition but also surveys surrounding organ diseases such as liver cirrhosis and portal hypertension.
B, Coronal maximum-intensity-projection image shows tortuous pulmonary artery (arrowhead) but straight pulmonary vein (arrow), indicating chronic pulmonary arterial hypertension. Portopulmonary hypertension was diagnosed after echocardiography revealed systolic pulmonary arterial pressure of 58 mm Hg. This case is classified as group 1.4.3 (pulmonary arterial hypertension associated with portal hypertension). See also Figure S3C, right ventricular hypertrophy and D-shaped left ventricle during systole, also indicating pulmonary hypertension, which can be viewed from the information box in the upper right corner of this article.
Fig. 4A —36-year-old woman who presented with exercise intolerance. Echocardiography showed pulmonary hypertension (103 mm Hg) and suspected sinus venosus type atrial septal defect (ASD), but pulmonary vein connections could not be visualized. MDCT then clearly revealed sinus venosus type ASD with partial anomalous pulmonary venous return. This case shows that echocardiography is limited in evaluating pulmonary venous return.
A, Four-chamber view of MDCT shows right atrium (RA) and right ventricle (RV) dilatation, with interventricular septum (arrowhead) bulging toward left ventricular (LV) side, indicating pulmonary hypertension. LA = left atrium.
Fig. 4B —36-year-old woman who presented with exercise intolerance. Echocardiography showed pulmonary hypertension (103 mm Hg) and suspected sinus venosus type atrial septal defect (ASD), but pulmonary vein connections could not be visualized. MDCT then clearly revealed sinus venosus type ASD with partial anomalous pulmonary venous return. This case shows that echocardiography is limited in evaluating pulmonary venous return.
B, Axial image of MDCT at superior vena cava (SVC) level shows right superior pulmonary vein (RSPV) is entering SVC, rather than LA, indicating partial anomalous pulmonary venous return (arrowhead). Also note larger diameter of main pulmonary artery (MPA) as compared with ascending aorta (AAO), which is another indicator of pulmonary hypertension.
Fig. 4C —36-year-old woman who presented with exercise intolerance. Echocardiography showed pulmonary hypertension (103 mm Hg) and suspected sinus venosus type atrial septal defect (ASD), but pulmonary vein connections could not be visualized. MDCT then clearly revealed sinus venosus type ASD with partial anomalous pulmonary venous return. This case shows that echocardiography is limited in evaluating pulmonary venous return.
C, Axial image of MDCT slightly more caudal than in panel B shows right middle pulmonary vein (RMPV) is entering SVC, indicating partial anomalous pulmonary venous return (arrowhead). Also note sinus venosus type ASD (asterisk) between SVC and LA. This case is classified as group 1.4.4 (pulmonary arterial hypertension associated with congenital heart disease).
Fig. 5A —41-year-old woman who presented with dyspnea, right heart dilatation, and pulmonary hypertension (122 mm Hg) on echocardiography. ECG-gated MDCT was arranged for further evaluation and revealed final diagnosis of atrial septal defect (ASD) with Eisenmenger syndrome. This case shows that MDCT is valuable when echocardiography fails to adequately visualize structures because of poor penetration or poor acoustic window.
A, Axial image shows 18-mm ASD (arrowhead) with significant right-to-left shunt, indicating Eisenmenger syndrome, identified by contrast flow from right atrium (RA) to left atrium (LA). Also note hypertrophied myocardium (arrow) over right ventricular outflow tract (RVOT), indicating chronic pulmonary hypertension. This defect was missed on initial transthoracic echocardiography because of high defect position and overlapping severe tricuspid regurgitation. Follow-up transesophageal echocardiography confirmed defect and shunt direction.
Fig. 5B —41-year-old woman who presented with dyspnea, right heart dilatation, and pulmonary hypertension (122 mm Hg) on echocardiography. ECG-gated MDCT was arranged for further evaluation and revealed final diagnosis of atrial septal defect (ASD) with Eisenmenger syndrome. This case shows that MDCT is valuable when echocardiography fails to adequately visualize structures because of poor penetration or poor acoustic window.
B, Bolus-tracking image analysis graph shows positive gradual pulmonary artery enhancement sign, indicating shunt volume is significant.
Fig. 5C —41-year-old woman who presented with dyspnea, right heart dilatation, and pulmonary hypertension (122 mm Hg) on echocardiography. ECG-gated MDCT was arranged for further evaluation and revealed final diagnosis of atrial septal defect (ASD) with Eisenmenger syndrome. This case shows that MDCT is valuable when echocardiography fails to adequately visualize structures because of poor penetration or poor acoustic window.
C, Axial reconstructed image without ECG signal shows dilated main pulmonary artery (MPA), right pulmonary artery (RPA), and left pulmonary artery (LPA), as compared with normal ascending aorta. Chronic pulmonary hypertension was considered. With Eisenmenger syndrome, surgical or endovascular device correction was not suitable for patient. Patient is now under supportive and palliative medication with stable condition. This case is classified as group 1.4.4 (pulmonary arterial hypertension associated with congenital heart disease). SVC = superior vena cava. See also Figure S5D, to see dilated right ventricle (RV), hypertrophied RV wall, and D-shaped left ventricle during systole, which can be viewed from the information box in the upper right corner of this article.
Fig. 7A —46-year-old man, with coronary artery disease after stent over right coronary artery, who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. MDCT was arranged for survey. This case shows that MDCT is useful in diagnosing most common cause for pulmonary hypertension, which is left heart disease.
A, Coronal maximum-intensity-projection image shows tortuous pulmonary arteries (arrowhead) and pulmonary veins (arrows), indicating “source” of pulmonary hypertension is left heart (downstream of pulmonary veins).
Fig. 7B —46-year-old man, with coronary artery disease after stent over right coronary artery, who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. MDCT was arranged for survey. This case shows that MDCT is useful in diagnosing most common cause for pulmonary hypertension, which is left heart disease.
B, Multiplanar reformation image of right coronary artery shows stent in middle portion. Low density inside stent (arrowhead) represents intrastent restenosis.
Fig. 7C —46-year-old man, with coronary artery disease after stent over right coronary artery, who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. MDCT was arranged for survey. This case shows that MDCT is useful in diagnosing most common cause for pulmonary hypertension, which is left heart disease.
C, Multiplanar reformation image of left coronary arteries shows multiple de novo lesions in left anterior descending (black arrowhead), first diagonal branch (arrow), and circumflex coronary arteries (white arrowheads).
Fig. 7D —46-year-old man, with coronary artery disease after stent over right coronary artery, who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. MDCT was arranged for survey. This case shows that MDCT is useful in diagnosing most common cause for pulmonary hypertension, which is left heart disease.
D, Short-axis view of delayed phase shows myocardial thinning (between arrowheads) and delayed hyperenhancement (arrowheads) over inferolateral wall of left ventricle, compatible with inferolateral wall (circumflex territory) myocardial infarction. Inferolateral wall infarction is usually associated with ischemic mitral regurgitation due to tethering of papillary muscle and chordal tendinae, as in this case. See also Figure S7G, to see inferolateral wall infarction, mitral tethering, and poor coaptation of mitral valve, indicating ischemic mitral regurgitation, which can be viewed from the information box in the upper right corner of this article.
Fig. 7E —46-year-old man, with coronary artery disease after stent over right coronary artery, who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. MDCT was arranged for survey. This case shows that MDCT is useful in diagnosing most common cause for pulmonary hypertension, which is left heart disease.
E, Catheter right coronary arteriography shows intrastent restenosis (arrowhead), as in panel B.
Fig. 7F —46-year-old man, with coronary artery disease after stent over right coronary artery, who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. MDCT was arranged for survey. This case shows that MDCT is useful in diagnosing most common cause for pulmonary hypertension, which is left heart disease.
F, Catheter left coronary arteriography shows critical stenoses over left anterior descending (black arrowhead), first diagonal (arrow), and circumflex coronary arteries (white arrowheads), as in panel C. Three months after revascularization, pulmonary arterial pressure decreased from 75 to 55 mm Hg and symptoms subsided. This case is classified as group 2 (pulmonary hypertension due to left heart disease).
Fig. 11A —75-year-old man presented with dyspnea. Radiograph shows interstitial lung change and echocardiography reveals pulmonary hypertension (75 mm Hg). MDCT was performed for differential diagnosis.
A, Short-axis view in end-systole shows dilated right ventricle (RV) with RV wall thickening (arrow). D-shaped (arrowhead) left ventricle (LV) during end-systole is also noted. Pulmonary hypertension is compatible. See also Figure S11C, to see dilated RV, hypertrophied RV wall, and D-shaped LV during systole, which can be viewed from the information box in the upper right corner of this article.
Fig. 11B —75-year-old man presented with dyspnea. Radiograph shows interstitial lung change and echocardiography reveals pulmonary hypertension (75 mm Hg). MDCT was performed for differential diagnosis.
B, Axial reconstructed image without ECG signal in lung window shows honeycombing (arrows) over bilateral basal lungs. Idiopathic pulmonary fibrosis was diagnosed. This case is classified as group 3.2 (pulmonary hypertension due to interstitial lung disease).
Fig. 12A —42-year-old man who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. d-dimer level was 721 μg/L d-dimer unit (normal, < 324 μg/L). Pulmonary embolism was suspected. Nongated pulmonary CT angiography was performed for evaluation. This case shows that MDCT can be used in diagnosis and also follow-up.
A, Axial image shows eccentric filling defect adhering to vessel wall of both left (arrowhead) and right (arrow) pulmonary arteries. Picture is compatible with chronic pulmonary embolism. MPA = main pulmonary artery.
Fig. 12B —42-year-old man who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. d-dimer level was 721 μg/L d-dimer unit (normal, < 324 μg/L). Pulmonary embolism was suspected. Nongated pulmonary CT angiography was performed for evaluation. This case shows that MDCT can be used in diagnosis and also follow-up.
B, Four-chamber view shows ventricular septum deviated to left side (arrowhead), indicating pulmonary hypertension. Patient then underwent surgical thromboendarterectomy to remove thromboemboli. LA = left atrium, LV = left ventricle, RA = right atrium, RV = right ventricle.
Fig. 12C —42-year-old man who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. d-dimer level was 721 μg/L d-dimer unit (normal, < 324 μg/L). Pulmonary embolism was suspected. Nongated pulmonary CT angiography was performed for evaluation. This case shows that MDCT can be used in diagnosis and also follow-up.
C, Three months later, axial CT image showed recurrent right-side pulmonary thromboembolism (arrow), but left-side pulmonary artery was now patent (arrowhead).
Fig. 12D —42-year-old man who presented with dyspnea and pulmonary hypertension (75 mm Hg) on echocardiography. d-dimer level was 721 μg/L d-dimer unit (normal, < 324 μg/L). Pulmonary embolism was suspected. Nongated pulmonary CT angiography was performed for evaluation. This case shows that MDCT can be used in diagnosis and also follow-up.
D, Three months later, four-chamber view of nongated pulmonary CT angiography showed centrally located ventricular septum (arrowhead). Pulmonary arterial pressure by echocardiography decreased from 75 to 35 mm Hg. This case is classified as group 4 (chronic thromboembolic pulmonary hypertension).
Fig. 13A —38-year-old man who presented with severe dyspnea. Echocardiography revealed pulmonary hypertension (73 mm Hg). Nongated MDCT was performed to exclude pulmonary embolism. Final diagnosis was lung cancer with metastatic tumor emboli.
A, Axial image of nongated MDCT in lung window shows many small faint nodules (arrowheads) over both lungs, especially left side. No pulmonary embolism was found, but 35-mm mass was located over right lower lobe (not shown). Patient underwent left supraclavicular lymphadenopathy, and biopsy revealed metastatic adenocarcinoma of pulmonary origin. Small nodules over both lungs with elevated pulmonary arterial pressure were considered to result from occlusion of microvasculature due to metastatic tumor emboli. Patient then received chemotherapy.
Fig. 13B —38-year-old man who presented with severe dyspnea. Echocardiography revealed pulmonary hypertension (73 mm Hg). Nongated MDCT was performed to exclude pulmonary embolism. Final diagnosis was lung cancer with metastatic tumor emboli.
B, Three months later, follow-up nongated MDCT showed no pulmonary nodules (arrowheads). Dyspnea symptom had subsided. Pulmonary arterial pressure by echocardiography also had decreased from 73 to 32 mm Hg. With image picture and clinical course, diagnosis of metastatic tumor emboli causing pulmonary hypertension was confirmed. This case is classified as group 5.4 (others), in this case, metastatic tumor emboli.
Footnotes
This study was supported in part by Taichung Veterans General Hospital (grants TCVGH-995502C, TCVGH-995503C, TCVGH-995504D, and TCVGH-995505D).
The first two authors contributed equally to the article.
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Fig. S11C—Video shows dilated right ventricle (RV), hypertrophied RV wall, and D-shaped left ventricle during systole.
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Fig. S10B—Video shows dilated right ventricle and D-shaped left ventricle during systole, indicating pulmonary hypertension.
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Fig. S9B—Video shows cor triatriatum in motion.
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Fig. S8B—Video shows mitral valve thickening and mitral stenosis in motion.
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Fig. S7G—Video shows inferolateral wall infarction, mitral tethering, and poor coaptation of mitral valve, indicating ischemic mitral regurgitation.
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Fig. S6B—Video shows dilated right ventricle, hypertrophied right ventricular wall, and D-shaped left ventricle during systole, compatible with pulmonary hypertension.
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Fig. S5D—Video shows dilated right ventricle (RV), hypertrophied RV wall, and D-shaped left ventricle during systole.
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Fig. S3C—Video shows right ventricular hypertrophy and D-shaped left ventricle during systole, also indicating pulmonary hypertension.
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Fig. S1F—Video shows ventricular septal motion in short-axis view.
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Fig. S1E—Video shows ventricular septal motion in four-chamber view.
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© American Roentgen Ray Society.
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Submitted: July 30, 2010
Accepted: February 6, 2011
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