Radiology

Mystery Quiz

July 18, 2009

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 74 year old man complaining of hemoptysis for four days. The patient has a history of hypertension, but had not been followed medically for many years until two weeks earlier when he presented with leg swelling, breathlessness, and atrial flutter. He was admitted, diuresed, begun on antihypertensive medications including hydralazine, aspirin, and anti-coagulated with enoxaparin and warfarin. After discharge, the patient felt well for a few days before the onset of hemoptysis. There was no associated fever, chest pain, arthralgias, headaches, or visual changes. On this admission, the patient did not appear acutely ill. Resting pulse oximetry and vital signs were normal, except for a mildly elevated blood pressure. The chest was clear to auscultation; the lower extremities had mild pitting edema. Labs showed hemoglobin that was decreased nearly 3gm/dL from baseline; INR was 1.5; white blood cell count and serum creatinine were normal; the urinalysis was bland. post_image_1_question   post_image_2_question1                             

 

 

 

 

 

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Class Act: Cardiac CT to Assess Coronary Artery Calcium

May 17, 2009

cacMatthew Nayor

Faculty Peer Reviewed

The patient: a 55 year old male nonsmoker with an HDL of 46, LDL of 120, triglycerides of 70, BP of 135/80 (on meds) and total cholesterol of 180. (Framingham 10-year risk of MI = 12%)

Coronary artery disease is the leading cause of death worldwide. Despite our understanding of how family history, toxic habits, cholesterol, and blood pressure affect the risk of myocardial infarction (MI), there is a clear need to further refine the methods of risk stratification. The Framingham Risk Score (FRS) is an excellent in-office tool that can be used to determine whether a patient is at low (<10%), intermediate (10%-20%), or high (>20%) 10-year risk for future coronary heart disease (CHD) events based on history and basic lab tests. Patients determined to be at low risk by this method rarely suffer cardiac events. On the other hand, high-risk patients are advised to follow the most aggressive pharmacologic and preventive measures available; this approach has greatly reduced the number of adverse outcomes in this population. It is, however, patients identified as intermediate risk by the FRS who now account for the majority of CHD events.

Clearly there is a need to further identify risk factors and screening modalities that can indicate which intermediate-risk patients are at greater risk and might benefit from more aggressive preventive measures. One such possibility is the use of cardiac CT to assess coronary artery calcium (CAC).

Coronary artery calcifications are absent in normal vessels, but are highly correlated with coronary artery disease (CAD). They are therefore pathognomonic for atherosclerosis and can now be reliably detected by CT scanning. When these scans are evaluated, the patient is assigned a score that represents the coronary artery calcification burden. Cardiac CT to identify CAC should not be confused with coronary CT angiography, which is a different modality involving the use of IV contrast and additional radiation. Although the presence of calcification does not necessarily correlate with the degree of stenosis, total atherosclerotic burden has actually been shown to be an excellent determinant of future MI risk. A meta-analysis seeking to discover how well coronary artery calcium scoring predicts clinical events found the risk of major coronary events increased 2.1-fold for scores ranging from 1-100 and 10-fold for scores >400, compared with scores of 0. To evaluate the implications of a negative result, two large studies demonstrated a posttest probability of coronary events to be 0.1% per year if no CAC is detected in asymptomatic individuals.

Despite its apparent power, cardiac CT does have potential risks and limitations. There is a not insignificant financial cost (although it remains relatively cheap) and it obviously involves radiation, although recent technologic improvements have substantially reduced the level of exposure.9 Furthermore, although cardiac CT is highly sensitive for detecting coronary artery calcifications, the specificity (detecting lesions that will actually cause MI) is impossible to gauge and there will surely be some degree of overdiagnosis. The risk to these patients involves the anxiety of a positive test result and the increased possibility of side effects associated with more aggressive medical treatment of cholesterol and blood pressure. Cardiac CT, by nature, also images the surrounding structures, which can lead to incidental findings. In one study, lung nodules were noted in 4.9% of patients. The vast majority of these nodules turned out to be pathologically benign, but “incidentalomas” certainly can cause increased anxiety and lead to further unnecessary diagnostic tests.

So who should be offered cardiac CT? A 2007 AHA/ACCF “Expert Consensus Document on Coronary Artery Calcium Scores” evaluated the available literature and found that a CAC score greater than or equal to 400 in a patient with an intermediate FRS represents a 10-year coronary heart disease risk similar to that of diabetes or peripheral arterial disease and therefore represents a CAD equivalent. These patients could be re-classified as “high-risk” and aggressive prevention could be recommended. The expert consensus concluded that CAC testing was “reasonable” to further risk stratify and guide therapy of these patients. The European Society of Radiology and North American Society for Cardiovascular Imaging went a step further in a joint statement that recommended the use of cardiac CT for risk stratifying intermediate populations. Even more aggressive, the SHAPE task force recommended that all men between 45 and 75 years of age and all women between 55 and 75 years of age (except those identified as “very low risk”) be screened by cardiac CT or carotid intima media thickness and treated accordingly. However, most professional organizations have not yet been so clear in their support. In 2007, the US Preventive Services Task Force assigned calcium screening a level “I” recommendation (for insufficient data).

The mounting evidence suggests that knowledge of CAC can be greatly beneficial in directing the treatment protocols of patients with intermediate FRS’s. Currently, CAC is one in a growing number of possible diagnostic tests (e.g. carotid intima media thickness, C-reactive protein, and biomarker blood tests) that are being evaluated for efficacy in CHD risk stratification of intermediate-risk patients. Although the need is clear, which testing modality will ultimately be found the most beneficial remains to be seen.

Matt Nayor is a fourth year medical student at NYU Medical School

Reviewed by Robert Donnino MD, NYU Division of Cardiology

References:

1. Budoff MJ, Gul KM. Expert review on coronary calcium. Vasc Health Risk Manag. 2008;4(2):315-324.

2. Wexler L, Brundage B, Crouse J, et al. Coronary artery calcification: pathophysiology, epidemiology, imaging methods, and clinical implications: a statement for health professionals from the American Heart Association Writing Group. Circulation. 1996;94(5):1175-1192.

3. Budoff MJ, Diamond GA, Raggi P, et al. Continuous probabilistic prediction of angiographically significant coronary artery disease using electron beam tomography. Circulation. 2002;105(15):1791-1796.

4. Mintz G, Pichard A, Popma J, et al. Determinants and correlates of target lesion calcium in coronary artery disease: a clinical, angiographic and intravascular ultrasound study. J Am Coll Cardiol. 1997;29(2):268-274.

5. Pletcher MJ, Tice JA, Pignone M, Browner WS. Use of the coronary artery calcium score to predict coronary heart disease events: a systematic review and meta-analysis. Arch Intern Med. 2004;164(12):1285-1292.

6. Budoff MJ, Achenbach S, Blumenthal RS, et al. Assessment of coronary artery disease by cardiac computed tomography: a scientific statement from the American Heart Association Committee on Cardiovascular Imaging and Intervention, Council on Cardiovascular Radiology and Intervention, and Committee on Cardiac Imaging, Council on Clinical Cardiology. Circulation. 2006;114(16):1761-1791.

7. Horton KM, Post WS, Bumenthal RS, Fishman EK. Prevalence of significant noncardiac findings on electron-beam computed tomography coronary artery calcium screening examinations. Circulation. 2002;106(5):532-534.

8. Greenland P, Bonow RO, Brundage BH, et al. ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography). Circulation. 2007;115(3):402-426.

9. Oudkerk M, Stillman AE, Halliburton SS, et al. Coronary artery calcium screening: current status and recommendations from the European Society of Cardiac Radiology and North American Society for Cardiovascular Imaging. Eur Radiol. 2008;18(12)2785-2807.

10. Naghavi M, Falk E , Hecht H, et al. The First SHAPE (Screening for Heart Attack Prevention and Education) Guideline. Critical Pathw Cardiology. 2006; 5(4):187-190.

Mystery Quiz- The Answer

May 1, 2009

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is sarcoidosis. The CXR shows diffuse, bilateral infiltration with a predominantly nodular pattern. The pulmonary hila are also prominent. The CT image shows innumerable 2-3mm nodules, many of which have a perilymphatic distribution. The lymphatics, in parallel with the pulmonary vasculature, course through the interstitium. Hence, the perilymphatic nodularity has an interstitial distribution and appears as “studding” along the interstitium which is enhanced by vascular contrast (Image 2, short arrows). Additional nodules, however, have a random distribution (Image 2, arrowhead), while others appear to be centrilobular (Image 2, long arrow). As a granulomatous disease that involves activated CD4 lymphocytes, it is not surprising to find pathological involvement of perilymphatic tissue along with lymph nodes (Image 3, arrows). That said, sarcoidosis may involve any anatomical lung site: airways, interstitium or alveoli.

Perilymphatic nodularity also appears in the fissures and along the pleura where lymphatics are found (not shown). Other lung diseases included in the differential are also characterized by small nodules on chest imaging. Depending on their origin, the nodules have different distributions. Hematogenous spread of disease, such as miliary TB, will appear as interstitial disease because it is perivascular. Interstitial nodules due to miliary TB or metastatic disease, for example, appear to have sharp borders because they are enveloped by the interstitium which gives them a smooth edge on imaging. Nodules that arise from endobronchial spread of disease, such as aspiration or aerogenous spread of infection, often appear in a centrilobular distribution. The centrilobular location is where a bronchiole, filled with material conferring the appearance of a radiographic nodule, enters the lobule. The lobule appears as a polygonal structure (distal interstitium) on CT imaging. Beyond the bronchiole, nodules will manifest with a fuzzy border because they occupy airspace. Such nodules may also appear larger depending on how much neighboring airspace is involved.

Our patient was treated with prednisone to alleviate his cough. His cough improved after a few weeks and repeat imaging showed regression of the pulmonary nodules (Image 4) and mediastinal lymphadenopathy (Image 5). Our case illustrates how patients with sarcoidosis often have imaging that is worse than would be expected from their clinical presentation.

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Mystery Quiz

April 28, 2009

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 42 year old man with a history of non-productive cough for several weeks. Three weeks prior to evaluation by the pulmonary service, the patient presented to the ER with a presumed vasovagal syncopal event that occurred on a subway platform. The patient’s prior medical history included allergic sinusitis and nasal polypectomy. Other than cough, the patient denied constitutional symptoms. The patient was not taking any medications. His social history was negative for smoking, intravenous drug abuse, risk factors for HIV infection, significant occupational exposures and travel. The patient did not own any pets. PPD placed by the pulmonary service was negative. Physical exam revealed a thin man with normal vital signs including normal resting pulse oximetry, clear chest, and otherwise no focal findings.

 

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Mystery Quiz- The Answer

March 10, 2009

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is allergic bronchopulmonary aspergillosis (ABPA). The CXR shows right upper lobe opacities, two of which appear round (Image 3, arrow) and another tubular (Image 3, arrowhead), and a left upper lobe opacity which has the characteristics of subsegmental atelectasis (Image 3, double arrows). The CT scan, performed ten days after the CXR, shows central bronchiectasis of the RUL (Image 4, arrows); tubular branching shadows (Image 6, arrow) as well as ring shadows (Image 5 and 6, arrowhead) all of which represent ectatic airways filled with mucoid material. A left upper lobe ectatic airway with thickening of the bronchial wall is also present (Image 7, arrow). The left upper lobe subsegmental atelectasis seen on the initial CXR was not visible on the CT image, indicating clearing of mucoid impaction.

ABPA is seen in a small percentage of patients with asthma and represents a complex hypersensitivity reaction to aspergillus antigens colonizing the airways. The diagnosis is established when multiple clinical findings are present. These include frequently refractory asthma, eosinophilia, serum IgE reactive to aspergillus antigen, and very elevated total serum IgE levels (>1000 IU). Characteristic imaging shows central bronchiectasis and mucoid impaction (“finger in glove” shadows, Image 6, arrow) that result in subsegmental atelectasis, often in an upper lobe distribution. The atelectasis can appear migratory as one area clears and another becomes impacted. In addition to patients with asthma, ABPA is associated with cystic fibrosis in a small percentage of cases. Treatment consists of high dose glucocorticoids followed by a slow taper. Serum IgE levels decline but typically do not normalize and recurrences of disease are associated with increasing serum IgE levels. There is some evidence that the addition of itraconazole to glucocorticoids may be helpful. The addition of the antifungal agent may decrease the burden of aspergillus colonization and lead to less hypersensitivity. Left untreated, ABPA may progress to irreversible fibrosis.

Our patient was initially treated as an asthma exacerbation due to pneumonia. However, this initial diagnosis gave way to a final diagnosis of ABPA when the serum IgE level returned at 1365 IU (reference range 0-158), serum IgE specific for Aspergillus fumigatus was elevated and the CT imaging showed characteristic findings.

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Mystery Quiz

March 6, 2009

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 42 year old male non-smoker with history of poorly controlled asthma (first diagnosed in 1994, recurrent need for steroid treatments but never intubated), severe seasonal allergies with chronic sinusitis, hepatic steatosis, GERD and gout who presented with complaints of five to ten days of myalgias, productive cough, wheezing and chest tightness. His medications included albuterol, fluticasone and formoteral inhalers, montelukast, colchicine, indomethacin prn, and fexofenadine. Exam was significant for T 97.6, HR 100, BP 120/83, RR 22, O2Sat 95% on RA. The patient was moderately obese, appeared anxious and tachypneic but speaking in full sentences. Heart exam was within normal limits with no JVD. Lung exam with decreased breath sounds and scattered inspiratory and expiratory wheezing throughout. No rales nor rhonchi. Labs were significant for WBC 12.0 with 75% polys, 12.7% lymphs, 8.4% eos; mild transaminitis (ast/alt 48/89—patient’s baseline). Blood cultures pending x 2.

Admission CXR: Images 1 & 2

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X-Ray Visions: What is your radiation risk?

January 29, 2009

xraylogo.jpgCommentary by Michael Hanley MD PGY-3 and James D. Koonce MD PGY-3, Department of Radiology, Medical University of South Carolina

www.X-rayRisk.com – A Free Online Calculator that Estimates an Individual’s Additional Risk of Cancer as a Result of Medical Imaging

An estimated 62 million CT scans are obtained in the United States each year.(1) While debated, a recent study suggests that radiation exposure from medical imaging may be responsible for 1-3% of cancers worldwide.(2) With recent media coverage focusing on the risk of cancer from medical imaging, patients and physicians have become more concerned about the increased use of CT scans and x-rays. Patients are asking their primary care providers and emergency room physicians for information about their personal risk. In 2004, Lee et al concluded that “patients are not given information about the risks, benefits and radiation dose for a CT scan”. Additionally, this study found that both patients and physicians were “unable to provide accurate estimates of CT doses”.(3)

While the need for education in this area has clearly been established, there are no widely available resources that provide information to both patients and health care providers about the increased risk of cancer from medical imaging. X-rayRisk.com is a free educational website that caclulates this risk. The site is specifically designed for both patients and health care providers. One of the site’s main features is a web-based calculator that allows users to track their imaging history and estimate their personal risk. The site also provides basic information about radiation in the form of ‘Frequently Asked Questions’.

There are no published studies that prove the direct causality between medical imaging and cancer, however there is enough data to warrant precaution. Current data on radiation exposure and cancer risk is based on data from survivors of atomic bombs, nuclear accidents and the early use of x-rays. The assumed risk of cancer from medical imaging (primarily CT scans) is based on individuals exposed to atomic bombs and nuclear accidents. The theory that the increased risk of cancer holds true at these lower doses is called the linear no threshold model and is generally accepted in the scientific community.

From the Home Page of X-rayRisk.com, the user can select the ‘Calculate Your Risk’ icon. Next, the user enters his or her gender and age. There is an extensive list of different plain films (x-rays), CT scans, nuclear medicine studies, as well as fluoroscopic and interventional procedures. The user’s radiation dose, age and sex are used to calculate the additional risk of cancer based on that study. After a user builds their complete imaging history, they have the option to print, e-mail or save their report. The user can also log-in (optional) and save their report to revisit and update with subsequent studies.

Exposure data for the website was compiled from the National Academy of Sciences report on the Health Risks From Exposure to Low Levels of Ionizing Radiation in 2006, specifically the Biological Effects of Ionizing Radiation (BEIR) VII Phase 2 Report.(4) Average doses from common imaging studies were used, which were adapted from Mettler et al.(5) If exact dose is known, the user can convert their Dose Length Product (mGy • cm) to Effective Dose (mSv), then calculate additional cancer risk using conversion factors adapted from Huda, et al.(6) The website is also designed to assist in radiation exposure research and clinical record keeping.

Great effort has been made throughout the medical community to ensure patient safety while providing quality diagnostic images. It is important to realize that in a properly performed individual exam, the potential health benefits almost always outweigh the potential risks of radiation exposure. However, patients are expecting their physicians to address these risks. X-rayRisk.com provides accurate information for patients and health care providers to facilitate well-informed discussions about the increased risk of cancer from medical imaging.

References
1. Brenner DJ, Hall EJ. Computed Tomography – An Increasing Source of Radiation Exposure. NEJM 357: 2277-84, 2007. 2. Berrington de Gonzalez A, Darby S. Risk of cancer from diagnostic x-rays: estimates for the UK and 14 other countries. Lancet 363:345-51, 2004.
3. Lee CI, Haims AH, Monico EP, et al. Diagnostic CT Scans: Assessment of Patient, Physician, and Radiologist Awareness of Radiation Dose and Possible Risks. Radiology 231 (2): 393-398, 2004.
4. National Research Council. Health risks from exposure to low levels of ionizing radiation. BEIR VII Phase 2. Washington, DC: National Academies Press, 2006.
5. Mettler FA, Huda W, Yoshizumi TT, Mahesh M: Effective Doses in Radiology and Diagnostic Nuclear Medicine: A Catalog. Radiology 248: 254-263, 2008.
6. Huda W, Ogden KM, Khorasani MR: Converting Dose-Length Product to Effective Dose at CT. Radiology 248:995-1003, 2008.

Cardiac MRI: Assessing Myocardial Viability

December 18, 2008

Commentary by Muhammad Ghumman MD, PGY-3

Faculty Peer Reviewed

Clinical Case:

A 65 year old male with hypertension, iron deficiency anemia, and atrial fibrillation (not anticoagulated due to prior gastrointestinal bleed,) presents with new onset lower extremity edema, dyspnea on exertion, orthopnea, and profound fatigue. Physical exam is significant for jugular venous distention to 17 cm, bilateral basilar crackles on lung exam, 3+ pitting edema in the lower extremities to mid thighs, and guaiac positive brown stool. Labs are significant for hemoglobin of 5.4, normal kidney function, and mildly elevated troponin. Patient denies chest pain and is hemodynamically stable with normal vitals. Electrocardiogram shows new ST depressions in lateral leads. Transthoracic echocardiogram shows new segmental wall motion abnormalities along with a newly reduced ejection fraction of 30%.   Capsule endoscopy shows non-bleeding angioectasias in the jejunum.  The patient is started on medical therapy for congestive heart failure and presumed coronary artery disease (ACE-I, Beta blocker, diuretic) and transfused to hemoglobin goal of 10 with improvement in his symptoms of dyspnea and fatigue. Echocardiogram strongly suggests ischemic cardiomyopathy due to the presence of regional wall motion abnormalities and an assessment of the patient’s coronary anatomy is warranted. However, the medical team and cardiology consult are reluctant to perform cardiac catheterization due to the risk of bleeding in a severely anemic patient who may require coronary artery stenting and subsequent long term anticoagulation. What other modalities are available for assessing this patient’s new cardiomyopathy and coronary anatomy?

Introduction:

Cardiac magnetic resonance imaging (CMR) is a rapidly evolving field which provides high contrast and high resolution 3-dimensional images of the heart, coronary vessels, and the great vessels without subjecting the patient to ionizing radiation. CMR is often considered a “one-stop shop” as it can provide a comprehensive assessment of the heart including myocardial wall motion, cavity size, ventricular ejection fraction, wall thickness, valvular function, infarct area, proximal coronary artery lesions, aortic disease including aneurysm and dissection, pericardial disease, congenital heart defects, and myocardial viability.

Myocardial viability: 

Currently, the most important and common clinical use of CMR is assessing myocardial viability. Dysfunctional myocardium is deemed viable if it can regain function (contractility) after regional blood supply is improved via revascularization. Nonviable myocardium is dead or scar tissue which has permanently lost its function irrespective of its regional blood supply. Viability testing guides clinical practice in patients with left ventricular (LV) dysfunction as revascularization of nonviable myocardium would not improve myocardial contractility, ejection fraction, or mortality and may even increase morbidity and mortality by subjecting the patient to an unnecessary interventional procedure.

CMR is excellent at determining myocardial viability using late gadolinium enhancement (LGE or hyperenhancement). When gadolinium is “taken up” by nonviable or scarred myocardium, it is not washed out as quickly as healthy myocardium due to poor blood flow, and thus images taken > 10 minutes after gadolinium injection will exhibit hyperenhancement or late gadolinium enhancement (regions where gadolinium is retained). The transmural extent of LGE signifies the thickness of nonviable or scar tissue and this correlates well to areas that are less viable and are partially or completely damaged in an irreversible manner. Conversely, absence of LGE corresponds to areas of viable myocardium.(1,2,3 ) A study of 50 patients with ventricular dysfunction undergoing revascularization showed that CMR accurately identified viable myocardium before revascularization. Absence of late gadolinium enhancement correlated well with segments which improved function after revascularization (78% of segments without LGE had improved function). Presence of late gadolinium enhancement correlated accurately with segments which had no improvement after revascularization (less than 2% of segments with LGE had improved function). The probability of improvement in segmental function significantly decreased as the extent of transmural LGE (thickness of scar) increased (see Figure 1).(3 )

Figure 1: Relation between the Transmural Extent of Hyperenhancement before Revascularization and the Likelihood of Increased Contractility after Revascularization.  804 dysfunctional segments were identified by CMR in 50 patients who were scheduled to undergo revascularization. As the transmural extent of late gadolinium enhancement increased, the likelihood of post-revascularization improvement in contractility significantly decreased. (adapted from Kim et al.)(3)

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Figure 2: Cardiac MRI displaying late gadolinium enhancement

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Traditionally, radionuclide myocardial perfusion imaging (using thallium, technetium-sestamibi, or positron emission tomography) and dobutamine echocardiography have been utilized to assess myocardial viability. CMR compares very favorably to these modalities and is even superior in some respects. In a study of 208 patients with suspected coronary artery disease referred for revascularization, dobutamine stress MRI had a 86% sensitivity and 74% specificity in terms of predicting viability when compared to dobutamine stress echocardiography which had a 85% sensitivity and 69% specificity.(4) When compared to positron emission tomography with F- 18 deoxyglucose (FDG-PET), CMR had similar sensitivity and specificity (94% and 84% respectively).(5) In comparison to resting thallium-201 perfusion imaging, CMR performs as well in terms of detecting transmural infarctions but is more accurate in detecting subendocardial infarctions.(6) Several studies have suggested that CMR may be more sensitive in detecting viability in regions of severely dysfunctional myocardium, which are often deemed non-viable by traditional techniques. CMR and conventional modalities are both poor at detecting viability in regions of intermediate residual viability but have similar performance in regions with high and low residual viability.

Clinical case applications:

Cardiac MRI can be used to assess for myocardial viability in our patient and thus guide future therapy (revascularization or optimal medical therapy). Furthermore, CMR can accurately determine ejection fraction and extent of proximal coronary artery atherosclerotic lesions, thus risk stratifying this patient. Left main or triple vessel disease may necessitate a surgical intervention in this patient. However, medical therapy or single vessel PCI may be more appropriate than CABG despite multivessel CAD if there is limited or no viability in multiple infarct areas.

In our patient, cardiac MRI/MRA showed mildly dilated LV with moderately reduced LV ejection fraction, hypokinetic myocardium without scar in LAD territory, hypokinetic myocardium with mild scar in RCA territory, and hypokinetic but viable myocardium in LCX territory. Coronary artery origins were incompletely visualized due to motion but there was patent origin of RCA, LAD, and LCX (L main couldn’t be visualized). Patient was discharged home on medical therapy and planned to return for coronary angiogram and possible revascularization as his coronary anatomy was not completely delineated by the Cardiac MRI.

 

 

REFERENCES

1.         Kim, RJ, Fieno, DS, Parrish, TB, et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 1999; 100:1992.

2.         Fieno, DS, Kim, RJ, Chen, EL, et al. Contrast-enhanced magnetic resonance imaging of myocardium at risk: distinction between reversible and irreversible injury throughout infarct healing. J Am Coll Cardiol 2000; 36:1985.

3.         Kim RJ, Wu E, Rafael A, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 2000; 343:1445-1453.

4.         Nagel, E, Lehmkuhl, HB, Bocksch, W, et al. Noninvasive diagnosis of ischemia-induced wall motion abnormalities with the use of high-dose dobutamine stress MRI: comparison with dobutamine stress echocardiography. Circulation 1999; 99:763.

5.         Kuhl HP, Beek AM, van der Weerdt AP, et al. Myocardial viability in chronic ischemic heart disease: comparison of contrast-enhanced magnetic resonance imaging with (18)F-fluorodeoxyglucose positron emission tomography. J Am Coll Cardiol 2003;41:1341-8.

6.         Bellenger NG, Burgess MI, Ray SG, et al. Comparison of left ventricular ejection fraction and volumes in heart failure by echocardiography, radionuclide ventriculography and cardiovascular magnetic resonance. Are they interchangeable? Eur Heart J 2000;21:1387-96.

Reviewed by Robert Donnino MD, NYU Division of Cardiology:

The case report and discussion provided by Dr. Ghumman highlights some of the important uses of CMR in patients with ischemic cardiomyopathies.  In this case the CMR provided several important pieces of information relevant to this patient’s care. First, by the distribution of myocardial scar (seen as LGE on CMR) we can confirm with high confidence that this patient’s cardiomyopathy is ischemic in etiology.  In addition, the presence of only mild scar (as opposed to transmural or near-transmural scar) indicates that this patient is very likely to have a significant improvement in left ventricular function after revascularization in all three major coronary vessel distributions.  As mentioned, this assessment of viability using CMR has been proven to be very reliable and is being used with increasing frequency in patients undergoing coronary revascularization (particularly in those being considered for bypass surgery). While it was not possible in this patient due to motion artifact, CMR can also provide an assessment of coronary stenosis, particularly of the proximal and larger vessels. Although there is continuing progress, CMR remains somewhat inferior to CT angiography and invasive x-ray angiography for detection of coronary stenosis, particularly of distal arteries and smaller caliber vessels.  Finally, CMR is considered the gold standard for measurements of left ventricular ejection fraction and chamber volume.  This may further assist the clinician in determining therapies such as biventricular pacemakers or cardiac defibrillators, particularly in those patients with technically challenging echocardiograms.

Mystery Quiz- The Answer

November 8, 2008

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is heart failure.  The CXR shows bibasilar opacities with hilar fullness on the right. The CT images are remarkable for bilateral effusions, with dependent opacities that increase in density along the anterior-posterior axis.  The lung appears clear in the anterior zone (Image 5, arrow; Coronal Image 1); ground glass opacification, characterized by parenchymal haziness which does not obscure the underlying pulmonary vessels, is evident in the mid lung (Image 5, double arrows; Coronal Image 2); and consolidation with air bronchograms is evident in the posterior areas (Image 5, arrowhead; Coronal Image 3).  The coronal images show the same increase in density along the anterior-posterior axis (Coronal Images 1-4).  Although the same density gradient of parenchymal fluid may be seen in non-cardiogenic pulmonary edema, the presence of bilateral effusions makes cardiogenic edema much more likely.

 

The mediastinal windows demonstrate adenopathy in precarinal, subcarinal and hilar areas (Image 6A, Image 7B and 7C, respectively).  The fact that enlarged mediastinal and hilar lymph nodes may accompany congestive heart failure was not appreciated until relatively recently (Slanetz PJ et al.  Mediastinal lymphadenopathy and hazy mediastinal fat: new CT findings of congestive heart failure. Am J Roentgenol 1998; 171: 1307-09).   Animal models indicate that enlarged nodes do not result simply from increased flow through interstitial lymphatics.  An additional requirement is that the efferent draining lymphatic vessels empty into a vein that has an elevated pressure (>15cm H2O), as may occur in heart failure, but less likely to occur in cases of non-cardiogenic pulmonary edema. High venous pressures slow lymphatic outflow and contribute to proximal lymph node enlargement.  The few reported biopsies of such nodes show an absence of inflammation, benign sinus histiocytosis, and slight follicular hyperplasia.

 

The CT images six days later show remarkable resolution of the airspace opacification after diuresis, along with a significant decrease in the lymphadenopathy (Images 6 and 7).  We present this case to highlight an underappreciated cause of reversible lymphadenopathy and review the image findings of pulmonary edema, herein due to hypertensive heart disease.

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Mystery Quiz

October 30, 2008

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 61 year old man with a history of diabetes, chronic kidney disease, and poorly controlled hypertension on five medications who was in his usual state of health until three days prior to admission when he noted increasing exertional dyspnea associated with chest pain, abdominal distention, bilateral lower extremity edema (left greater than right).

Exam notable for BP 105/54 (lower than all other prior measurements), HR 74, O2 Saturation 90%. PaO2 57mmHg, bibasilar rales and bilateral lower extremity edema. Labs were significant for BNP 218 (ref range: 0-100), d-dimer 537 (ref range to 230), WBC 11.2 (82% polys), Hgb 9.3 (baseline 10-12), creatinine 4.2 (baseline mid 2), troponin negative x 2. EKG without ischemic changes.

Echocardiogram six months prior to admission notable for hyperdynamic LV, increased EF (70-75%) and mild concentric LV hypertrophy.

Admission CXR:

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Chest CT:

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Mystery Quiz- The Answer

September 27, 2008

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Posted by Vivian Hayashi MD and Robert Smith MD,

Mystery Quiz Section Editors

The answer to last week’s mystery quiz is pneumatocele/pseudocyst likely due to ventilator associated lung injury (VALI) in a patient with ARDS. The patient had

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ARDS on the basis of diffuse infiltrates, hypoxemia with a PaO2/FiO2 <200mmHg, and no strong evidence of LV heart failure. His risk factor for ARDS was pneumonia, evident on his admission CXR with bibasilar infiltrates (R>L); Streptococcus pneumoniae grew on sputum culture. The overall clinical picture is best described as septic shock and multiple organ failure.

VALI may be seen when patients with acute lung injury or ARDS are ventilated with potentially injurious (high) lung volumes or high transpulmonary pressures. These latter conditions will over distend the lung and result in pathologic changes that are indistinguishable from the diffuse alveolar damage seen in cases of ARDS due to the usual causes: pneumonia, trauma, transfusion-related acute lung injury or sepsis. Pneumatoceles and pseudocysts, due to VALI, may be seen on chest imaging as well as in pathological specimens. The concept is that the underlying, initial disease causes heterogeneous lung involvement such that large tidal volumes will be distributed unevenly with regional areas of marked over distension interspersed with poorly aerated areas that are collapsed or congested. Furthermore, over distension and mechanical stress are inflammatory and cause intracellular signaling that results in cytokine synthesis in the lung, followed by spillage from the airspaces into the blood. Remote organ damage then ensues.

A strategy of low tidal volume ventilation was the basis of the ARDSnet trial which showed improved outcomes in patients managed with a tidal volume of 6cc/kg of predicted body weight, and a PEEP level that allows an acceptable PaO2. These historically low tidal volumes are designed to prevent the lung from being over-distended and subject to volutrauma and VALI. Often, the low tidal volume ventilation is associated with hypercapnea which is well tolerated in most cases. The concept includes a corollary, the “open lung,” which is the application of PEEP to prevent the lung from collapsing at end-expiration. PEEP prevents the distal airways and airspaces from undergoing shear stress injury due to cyclic opening and closing.

Our patient was managed with pressure control ventilation, with set inspiratory pressures of 32cm H2O, PEEP of 16 cmH2O, and tidal volume of about 7cc/kg of his predicted weight. The pCO2 level was allowed to remain high (permissive hypercapnia). Despite our good intentions, the patient developed a picture of VALI that was also complicated by rupture of one of the pneumatoceles and a pneumothorax that required drainage with a small bore chest tube (as seen in the soft tissues of the CT scan image). A caveat of protective low tidal volume ventilation is that over or under distension of the lung can occur with “optimal” distending pressures, 30-32cm H2O. If a patient has intraabdominal hypertension, approximately half of the abdominal pressure is transmitted to the pleural space; the transpulmonary pressure (plateau/alveolar pressure – the pleural pressure) may be significantly less than 30-32cm and be associated with under distension of the lung, and consequent atelectasis, shunting and hypoxemia. Conversely, if a patient has emphysematous lungs that are highly compliant and abnormally distensible, a pressure of 30-32cm may be associated with over distension and VALI. We speculated that this scenario was at play in our case.

Mystery Quiz

September 19, 2008

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 76 year old man with history of moderate-to-severe COPD who presented with three days of fever, breathlessness, and productive cough. Past surgical history is significant for vagotomy and partial gastrectomy 16 years earlier and a cholecystectomy 10 months prior to admission. On exam, the patient appeared acutely ill with a blood pressure of 75/45 mmHg, tachycardia, marked hypoxemia and course breath sounds throughout all lung fields. Labs revealed a white count of 2.7 K with 53% bands. The creatinine was elevated to 3.0 mg/dl from a baseline of 1.0 mg/dl. ABG showed pH 7.00, pCO2 61 mmHg, pO2 79 mmHg on 100% O2, and arterial lactate 5.2 mmol/L.

 

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Image 1 – Baseline Chest Radiograph 10 months prior to admission

 

 

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Image 2 – Admission Chest Radiograph

 

 

The patient required pressors for hypotension unresponsive to IV fluids, mechanical ventilation, and broad spectrum antimicrobial therapy.

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Image 3 – Chest Radiograph from HD 1

 

 

Six days later, the chest radiograph revealed:

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Image 4 – Chest Radiograph HD 6

 

 

 


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