Peer Reviewed


A Collection of Cancerous Conditions

Pelvic Chondrosarcoma


Maria Romanova, MD; Sulabha Masih, MD; and Azadeh Lankarani-Fard, MD
VA Greater Los Angeles Healthcare System and David Geffen School of Medicine at UCLA, Los Angeles, California


Consultant. 2018;58(3):104-105. 


A 66-year-old man presented with right hip pain and a 1-day history of an inability to urinate. The patient had noted gradually increasing weakness in his right leg over the past year, which had acutely worsened in the past day. He had had no significant prior illnesses and was not taking any medications.

Physical examination. Physical examination revealed right leg weakness, a nontender firm mass in the right groin, and a distended bladder. Foley catheter placement resulted in the return of 1.5 L of urine.

Diagnostic tests. Laboratory test results were notable for mild normocytic anemia with a hemoglobin level of 12 g/dL. Results of a chemistry panel, including calcium level, were normal. Results of liver function tests were normal, aside from a slightly elevated alkaline phosphatase level of 101 U/L (reference range, 33-94 U/L).

Radiographs revealed the complete destruction of the right pubic ramus (Figure 1). Magnetic resonance imaging of the pelvis showed a mass involving the right acetabulum, ischium, and pubic ramus with mass effect on the pelvic floor organs (Figure 2). Positron emission tomography–computed tomography scans were not suggestive of metastatic disease (Figure 3).


Pelvic Chondrosarcoma

Figure 1: Radiograph of the pelvis showing lytic destruction of the right superior pubic ramus (arrow).

Pelvic Chondrosarcoma

Figure 2: Coronal view, T2-weighted, fat-saturated magnetic resonance imaging scan with contrast showing extension of the right pelvic mass into adjacent structure, with reactive muscle edema and mass effect on the bowel and bladder.

Pelvic Chondrosarcoma

Figure 3: Coronal view computed tomography scan indicating a large mass eroding the right pubic bone, ischium, and acetabulum with extension into the surrounding muscles.


Treatment. The patient underwent right internal hemipelvectomy with removal of the large acetabular and pelvic mass. The right hemipelvis and surrounding muscles and soft tissues were extensively dissected and excised (Figure 4). Pathology examination of the mass revealed that it was a grade 3 chondrosarcoma with dedifferentiated features and clear margins. The patient deferred chemotherapy. Imaging studies 6 months later showed no evidence of disease.


Pelvic Chondrosarcoma

Figure 4: Postoperative radiograph showing resection of the large acetabular and pelvic mass.


Discussion. Urinary retention is a common occurrence and often is attributed to medication use, spinal cord pathology, or prostate disease in men. However, a detailed history and physical examination can suggest other etiologies. In our patient, evaluation of the vague symptom of leg weakness revealed an encroaching chondrosarcoma causing bladder outlet obstruction.

Chondrosarcomas are primary malignant bone tumors with cartilaginous differentiation. They are the second most common primary bone sarcoma after osteosarcoma.1 The tumors are often found in the pelvic region and can arise de novo or from preexisting benign cartilaginous tumors.2

A chondrosarcoma usually manifests as persistent dull skeletal pain or a palpable mass. Radiographically, the tumor appears as a lytic bone lesion with associated soft tissue mass.3 These 2 characteristics on imaging are associated with a limited differential diagnosis. Cancer metastases could appear in this manner, especially with primary malignancies such as kidney cancer, which are predominantly associated with an osteolytic appearance. Although multiple myeloma with an associated plasmacytoma could appear in this manner, our patient’s lack of other lytic lesions and laboratory test results did not support this diagnosis.4 Osteosarcomas could have a similar radiographic appearance but typically affect young children. In older adults, osteosarcomas are often secondary to other disease processes such as Paget disease or prior radiation therapy,5 which are risk factors that were not present in our patient’s case.

The World Health Organization classifies chondrosarcomas as grades 1, 2, or 3 depending on histologic features.6 Dedifferentiated chondrosarcomas are a malignant subtype characterized by the development of a high-grade, noncartilaginous sarcoma in association with a preexisting low-grade cartilaginous tumor. Patients typically present in the fifth or sixth decade of life.7

The grade and subtype are essential in determining treatment and prognosis. Most treatment plans involve primary resection. Low-grade chondrosarcomas are managed with local curettage and surveillance. High-grade and dedifferentiated chondrosarcomas often require wide resection.8 Surgical resection is the main treatment, since chondrosarcomas are notoriously resistant to radiation and chemotherapy.8-10

The estimated 10-year survival rate is 90% to 100% for patients with grade 1 chondrosarcoma, 60% to 75% for grade 2, and 30% to 40% for grade 3.11-13 The prognosis of dedifferentiated chondrosarcomas is lower, with some studies suggesting 20% survival at 2 years despite aggressive therapy.11,14,15



  1. Dorfman HD, Czerniak B. Bone cancers. Cancer. 1995;75(suppl 1):203-210.
  2. Altay M, Bayrakci K, Yildiz Y, Erekul S, Saglik Y. Secondary chondrosarcoma in cartilage bone tumors: report of 32 patients. J Orthop Sci. 2007;12(5):​415-423.
  3. Littrell LA, Wenger DE, Wold LE, et al. Radiographic, CT, and MR imaging features of dedifferentiated chondrosarcomas: a retrospective review of 174 de novo cases. Radiographics. 2004;24(5):1397-1409.
  4. Coleman RE. Metastatic bone disease: clinical features, pathophysiology and treatment strategies. Cancer Treat Rev. 2001;27(3):165-176.
  5. Mirabello L, Troisi RJ, Savage SA. Osteosarcoma incidence and survival rates from 1973 to 2004: data from the Surveillance, Epidemiology, and End Results Program. Cancer. 2009;115(7):1531-1543.
  6. Hogendoorn PCW, Bovee JM, Nielsen GP. Chondrosarcoma (grades I-III), including primary and secondary variants and periosteal chondrosarcoma. In: Fletcher CDM, Bridge JA, Hogendoorn PCW, Mertens F, eds. WHO Classification of Tumours of Soft Tissue and Bone. 4th ed. Lyon, France: IARC; 2013:264. WHO Classification of Tumours; vol 5.
  7. Capanna R, Bertoni F, Bettelli G, et al. Dedifferentiated chondrosarcoma. J Bone Joint Surg Am. 1988;70(1):60-69.
  8. Dickey ID, Rose PS, Fuchs B, et al. Dedifferentiated chondrosarcoma: the role of chemotherapy with updated outcomes. J Bone Joint Surg Am. 2004;​86(11):2412-2418.
  9. Mavrogenis AF, Gambarotti M, Angelini A, et al. Chondrosarcomas revisited. Orthopedics. 2012;35(3):e379-e390.
  10. Moussavi-Harami F, Mollano A, Martin JA, et al. Intrinsic radiation resistance in human chondrosarcoma cells. Biochem Biophys Res Commun. 2006;​346(2):379-385.
  11. Sheth, DS, Yasko AW, Johnson ME, Ayala AG, Murray JA, Romsdahl MM. Chondrosarcoma of the pelvis: prognostic factors for 67 patients treated with definitive surgery. Cancer. 1996;78(4):745-750.
  12. Angelini A, Guerra G, Mavrogenis AF, Pala E, Picci P, Ruggieri P. Clinical outcome of central conventional chondrosarcoma. J Surg Oncol. 2012;​106(8):929-937.
  13. Pring ME, Weber KL, Unni KK, Sim FH. Chondrosarcoma of the pelvis: a review of sixty-four cases. J Bone Joint Surg Am. 2001;83(11):1630-1642.
  14. Yokota K, Sakamoto A, Matsumoto Y, et al. Clinical outcome for patients with dedifferentiated chondrosarcoma. a report of 9 cases at a single institute. J Orthop Surg Res. 2012;7(38). doi:10.1186/1749-799X-7-38
  15. Grimer RJ, Gosheger G, Taminiau A, et al. Dedifferentiated chondrosarcoma: prognostic factors and outcome from a European group. Eur J Cancer. 2007;43(14):2060-2065.

NEXT: Aspergillosis With Acute Myelogenous Leukemia

Aspergillosis With Acute Myelogenous Leukemia


Bridget Louis, PA-S, and Christopher Roman, MMS, PA-C
Butler University, Indianapolis, Indiana


Consultant. 2018;58(3):106-107. 


A 66-year-old man was admitted to a hospital for induction chemotherapy for acute myelogenous leukemia (AML). His chemotherapy regimen consisted of idarubicin and cytarabine. During the resulting period of neutropenia, he developed fever and diarrhea. Stool tests identified Clostridium difficile, and he was treated with a 10-day course of fidaxomicin, which led to resolution of the diarrhea.

Fever returned shortly thereafter, and evaluation of this neutropenic fever revealed a dense pneumonia in the upper and lower lobes of the right lung. Broad-spectrum antibiotic coverage was initiated with piperacillin-tazobactam and vancomycin. Computed tomography (CT) of the chest revealed cavitary lesions in both areas, with a central mass in each cavity (Figures 1 and 2). These findings were highly suspicious for a fungal infection such as aspergillosis, so his antimicrobial therapy was expanded to include anidulafungin and voriconazole. Serum test results were positive for galactomannan, a prominent component of the cell wall of Aspergillus species. All other cultures were negative for pathogens, and antibacterial therapy was discontinued.


Myelogenous Leukemia

Myelogenous Leukemia


Dual antifungal therapy continued for 2 weeks, and follow-up imaging revealed modest improvement in the pulmonary lesions. His clinical status improved during that interval, which coincided with a recovery of his cytopenia. He was discharged in stable condition and was prescribed an additional 2 months of voriconazole with plans for repeated imaging prior to discontinuation of the antifungal therapy. Nevertheless, the patient returned to the hospital 3 weeks later with overwhelming sepsis that was unrelated to his pulmonary aspergillosis, and he died shortly after admission.

Discussion. Aspergillus is a ubiquitous mold found in soil and plant matter.1,2 The most common species to cause infection is Aspergillus fumigatus, followed by A flavus, A terreus, A niger, and A nidulans.1-4 The average person inhales several hundred conidia daily, each of which is approximately 2 µm in diameter, which is small enough to reach the alveoli.1,2,4 Once inhaled, the conidia can germinate and produce hyphae that invade the tissues. Aspergillus can disseminate and cause damage anywhere in the body, but pulmonary aspergillosis is by a wide margin the most common.4 Upon invasion, a fungal ball, or aspergilloma, may form within an existing lung cavity (often the result of previous disease). The aspergilloma is an accumulation of fungal hyphae, mucus, and cellular debris. While Aspergillus is by far the most common, it is not the only fungus capable of forming a fungal ball. For this reason, a fungal ball seen on imaging studies is highly suggestive of aspergillosis but does not conclusively diagnose the infection.1-4

The immune system of healthy persons is generally able to eliminate the fungus before it germinates and causes damage. In immunocompromised hosts, the fungus is able to become invasive and cause major complications. Patients with prolonged neutropenia, with advanced HIV disease, or on a prolonged course of glucocorticoids or other immunosuppressing agents are at high risk for infection. Bone marrow transplant and hematologic malignancy are the 2 most frequent predisposing conditions, with aspergillosis accounting for approximately 7.5% of infections and a major cause of death in patients with neutropenia following induction chemotherapy for AML.1,2

Patients with neutropenia and pulmonary aspergillosis most often present with hemoptysis, fever, and pleuritic chest pain, although they may also have cough, weight loss, and dyspnea, or they may be asymptomatic.1-4 During initial workup of a patient with these symptoms, a chest radiograph may show a cavity and/or a mass,1 but CT is a more sensitive initial study on which an aspergilloma will be visualized as a mass with soft-tissue attenuation formed within a lung cavity. The mass is separated from the preformed cavity by an air space, which is known as the air crescent sign. Pleural thickening is often seen. The air crescent sign is the hallmark finding of aspergillosis.1-4

The most reliable diagnostic confirmation is with histology/cytology and culture testing.5 However, obtaining the necessary samples is invasive, and these patients are often very ill and/or clinically deteriorating. Instead, assays may be used to test for galactomannan or β-glucan, both of which are important fungal cell wall components. According to current guidelines on the treatment of aspergillosis, a positive result from either assay, combined with characteristic CT findings, is sufficient to diagnose probable aspergillosis.6

Empiric therapy is often initiated before formalizing the diagnosis because of the immunocompromised status of most patients. The best outcomes occur with prompt and aggressive treatment with voriconazole plus an echinocandin (eg, anidulafungin). Other treatment options include amphotericin B, itraconazole, posaconazole, or echinocandin monotherapy, although they are generally used only as salvage therapy due to greater toxicities and/or variable success against aspergillosis.6,7 Treatment should continue for 6 to 12 weeks, with a follow-up CT scan obtained within 2 weeks of initiating treatment.5



  1. Al-Alawi A, Ryan CF, Flint JD, Müller NL. Aspergillus-related lung disease. Can Respir J. 2005;12(7):377-387.
  2. Soubani AO, Chandrasekar PH. The clinical spectrum of pulmonary aspergillosis. Chest. 2002;121(6):1988-1999.
  3. Franquet T, Müller NL, Giménez A, Guembe P, de la Torre J, Bagué S. Spectrum of pulmonary aspergillosis: histologic, clinical, and radiologic findings. Radiographics. 2001;21(4):825-837.
  4. Latgé J-P. Aspergillus fumigatus and aspergillosis. Clin Microbiol Rev. 1999;​12(2):310-350.
  5. Patterson TF, Thompson GR III, Denning DW, et al. Practice guidelines for the diagnosis and management of aspergillosis: 2016 update by the Infectious Diseases Society of America. Clin Infect Dis. 2016;63(4):e1-e60.
  6. Walsh TJ, Anaissie EJ, Denning DW, et al. Treatment of aspergillosis: clinical practice guidelines of the Infectious Diseases Society of America. Clin Infect Dis. 2008;46(3):327-360.
  7. Herbrecht R, Denning DW, Patterson TF, et al; Invasive Fungal Infections Group of the European Organisation for Research and Treatment of Cancer and the Global Aspergillus Study Group. Voriconazole versus amphotericin B for primary therapy of invasive aspergillosis. N Engl J Med. 2002;347(6):​408-415.

NEXT: Diffuse Large B-Cell Lymphoma

Diffuse Large B-Cell Lymphoma


Alan Lucerna, DO, and James Espinosa, MD
Jefferson Stratford Hospital, Stratford, New Jersey

Ramneet Wadehra, DO
Jefferson Cherry Hill Hospital, Cherry Hill, New Jersey

Risha Hertz, APNC
Penn Family Medicine Gibbsboro, New Jersey


Consultant. 2018;58(3):107-108. 


A 77-year-old woman presented with progressively enlarging right occipitoparietal scalp masses. She had a several-year history of transient, firm, and nontender occipital scalp masses in the same region. She denied any worsened joint pain, bone pain, or nocturnal worsening of pain over this time. She also reported the presence of chronic left shoulder pain and hand stiffness. There was no history of concurrent bone fracture. The patient denied weight loss, fevers, and night sweats.

History. The patient’s medical history included hypertension. She had undergone cholecystectomy and hysterectomy. She denied smoking and the use of drugs and alcohol. She had no family history of cancers or autoimmune diseases.

Physical examination. Three discrete, soft, nontender, overtly mobile masses were present on the right occipitoparietal scalp. Her vital signs were normal, and she was afebrile. The rest of the physical examination findings were unremarkable.

Diagnostic tests. Laboratory test results showed an alkaline phosphatase level of 85 U/L (reference range, 30-136 U/L). The serum calcium level was 9.3 mg/dL (reference range, 8.8-10.0 mg/dL). A recent radiograph of the skull had demonstrated thickening of the right calvaria, a finding that was suspicious for Paget disease.

Follow-up laboratory tests over a 6-month period revealed persistently normal levels of alkaline phosphatase, and no significant clinical changes occurred over this time. A follow-up radiograph of the skull demonstrated a “moth-eaten” pattern in the right occipitoparietal cortex, again suspicious for Paget disease.

A bone scan revealed increased technetium Tc 99m uptake throughout the right occipitoparietal calvaria. Patchy uptake on the bone scan was noted in the right distal fibula, consistent with Paget disease as opposed to arthritis.

Noncontrast computed tomography (CT) scans of the head showed cortical thickening in the area of several masses, measuring 1.6 × 2 cm, a finding consistent with Paget disease (Figures 1 and 2).


Large B-Cell Lymphoma

Large B-Cell Lymphoma


While the imaging findings suggested Paget disease, there were incongruities among the diagnostic results. A surgical consultation therefore was obtained for biopsy of the scalp lesions. On pathologic examination, the specimen was determined histologically to be early-stage primary diffuse large B-cell lymphoma (DLBCL), a form of non-Hodgkin lymphoma.

Treatment. The patient was referred to an oncologist for further evaluation and treatment. Within 2 months of her biopsy, the patient was started on chemotherapy under the guidance of her oncologist, with plans for radiation therapy after the completion of chemotherapy.

Discussion. Painless soft tissue scalp masses are commonly seen in clinical practice, with the most frequent diagnoses being epidermoid cysts, sebaceous cysts, and benign lipomas.1 Trichilemmal cysts also can present as slowly enlarging soft tissue masses and can be mistaken for a benign lipoma.1

Although the range of possible diagnoses for scalp lesions is quite wide, the incidence in reference to the diagnostic rate and the clinical significance of scalp masses have not been well studied. In one study of 345 patients undergoing operations for scalp masses at a Turkish hospital, approximately 7.8% of patients had clinically significant pathologies (eg, malignancies or needing follow-up).2 Less than 30% of patients received the correct preoperative diagnosis.2 A diagnosis of lymphoma was made in only 2 cases (0.6% of patients).2

The most common presenting sign of lymphoma is a painless scalp mass that enlarges over time,3 a finding similar to that of our patient. Neoplastic etiologies should be considered in the differential diagnosis, even with benign-appearing scalp masses.4

Our patient’s case featured some involvement of the skull noted on CT scans. However, DLBCL can rarely involve the scalp and dura mater without invasion of the skull.5 Jaiswal and colleagues hypothesize that the lymphoma cells of DLBCL might grow through the diploic spaces along the emissary veins and nerves that pass through the dura mater to the leptomeninges, thereby allowing disease progression without direct skull involvement in some cases.4

The potential for metastasis from a distant site also must be kept in mind, since the differential diagnosis of scalp masses covers a very wide variety of cutaneous, dural, and cranial pathologies from a wide spectrum of disease categories.2 Therefore, biopsy should be considered early on—in our patient’s case, a preoperative biopsy led to an unexpected diagnosis with quite clinically significant implications. 



  1. Leung LK. Differential diagnosis of soft scalp lumps. BMJ Case Rep. 2011;​2011:bcr0720114492. doi:10.1136/bcr.07.2011.4492
  2. Türk CÇ, Bacanlı A, Kara NN. Incidence and clinical significance of lesions presenting as a scalp mass in adult patients. Acta Neurochir (Wien). 2015;​157(2):217-223.
  3. Tan LA, Kasliwal MK, Arvanitis LD, Byrne RW. Enlarging scalp mass. J Neurooncol. 2015;122(2):419-420.
  4. Jaiswal M, Gandhi A, Purohit D, Singhvi S, Mittal RS. Primary non-Hodgkin’s lymphoma of the skull with extra and intracranial extension presenting with bulky scalp mass lesion. Asian J Neurosurg. 2016;11(4):444.
  5. Ochiai H, Kawano H, Miyaoka R, Kawano N, Shimao Y, Kawasaki K. Primary diffuse large B-cell lymphomas of the temporoparietal dura mater and scalp without intervening skull bone invasion. Neurol Med Chir (Tokyo). 2010;​50(7):595-598.

NEXT: Hodgkin Lymphoma Radiation Therapy

Coronary Artery Disease Secondary to Hodgkin Lymphoma Radiation Therapy


Luis Alonso Hernandez Mejia, MD
Presence Saint Joseph Hospital, Chicago, Illinois

Andres Carmona, MD; Hashem Azad, DO; Gianina Flocco, MD; Gian Novaro, MD; and Craig Asher, MD
Cleveland Clinic Florida, Weston, Florida


Consultant. 2018;58(3):108-110. 


A 57-year-old man with a history significant for Hodgkin lymphoma (HL), dyslipidemia, and hypertension, who had undergone extensive radiation therapy (RT) to the chest and neck 35 years earlier for lymphoma, presented to the emergency department with a 5-week history of progressively worsening chest tightness and dyspnea. He had been experiencing sudden chest tightness radiating to the arms during exertion that immediately resolved with rest.

Diagnostic tests. An initial electrocardiogram showed sinus rhythm, a heart rate of 104 beats/min, a normal axis, and nonspecific ST-segment changes. The initial troponin T level was 0.497 ng/mL (reference value, < 0.029 ng/mL). He was admitted to the hospital, and his condition was managed as a non–ST-segment elevation myocardial infarction. A transthoracic echocardiogram (TTE) (Figure 1) showed mildly decreased left ventricular function with an ejection fraction of 40%, severe mid-anteroseptal hypokinesis, and basal anteroseptal and mild mid-inferoseptal hypokinesis. Twenty-four hours after admission, his troponin T level had trended up to 0.556 ng/mL.


Hodgkin Lymphoma Radiation Therapy

Figure 1: TTE, parasternal long-axis view, showing an increased systolic dimension consistent with reduced systolic function. The left ventricular ejection fraction was determined to be 40%.


Cardiac catheterization showed left main coronary artery disease with 90% stenosis (Figure 2), diffuse disease in the left circumflex, dominant right coronary artery (RCA) disease with 65% stenosis (Figure 3), and a normal left anterior descending artery (LAD).


Hodgkin Lymphoma Radiation Therapy

Figure 2: Cardiac catheterization image, right anterior oblique caudal view, showing a 90% obstruction in the middle portion of the left main trunk and high-grade ostial left circum ex artery disease.

Hodgkin Lymphoma Radiation Therapy

Figure 3: Cardiac catheterization image, right anterior oblique cranial view; the right coronary artery is dominant, with a 65% lesion in the middle segment.


Treatment. The patient underwent quadruple coronary artery bypass grafting (CABG), during which moderate pericardial adhesions were found. There were no postsurgical complications.

Discussion. For several decades, RT has been used effectively in the treatment of cancer involving the chest and mediastinum. The late effects of radiation generally become evident 3 to 30 years following RT, most frequently appearing in the second or third decade after therapy.1 These patients have an increased risk of coronary artery disease (CAD); congestive heart failure; pericardial, myocardial, and valvular heart disease; conduction disorders, and sudden cardiac death.2,3

Chest RT can result in inflammation of and damage to any of the cardiac structures. Studies have shown that compared with nonirradiated persons, persons who have had chest RT have a 2% increased cumulative risk of cardiac morbidity and death after 5 years and a 23% increased cumulative risk after 20 years.4 CAD has been reported in 5.5% to 12% of patients undergoing therapeutic chest RT,5 usually manifesting 3 to 30 years after radiation exposure.1,5,6

HL is one of the most common cancers in young adults. It has become a highly curable disease, with an overall 5-year survival rate of 85% with modern therapy.7 Late cardiovascular complications after chest RT are the most common cause of treatment-related morbidity after second malignancy in HL survivors.1,8,9

The likelihood of developing CAD secondary to RT depends on the volume of heart irradiated, age at time of RT, preexisting CAD, inadequate or absent shielding, concomitant chemotherapy (anthracyclines), anterior or left chest irradiation, and conventional risk factors (eg, smoking, hypertension, diabetes, hyperlipidemia).8,10 Chest RT can affect all structures of the heart, including the pericardium (pericarditis), myocardium (systolic and diastolic cardiomyopathy), heart valves, coronary arteries and capillaries, and conduction system (complete heart block, sick sinus syndrome, prolonged QTc interval).7,8,11

RT-induced CAD results from intimal proliferation, damage to the intima, and fibrotic and atherosclerotic lesions. Radiation injury causes an increase in capillary wall permeability, the generation of reactive oxygen species, and the activation of an inflammatory cascade that causes disruption of DNA strands. Endothelial dysfunction is believed to be a precipitating factor in the development of cardiac sequelae and that subsequently leads to intimal proliferation with collagen deposition and fibrosis. The histopathologic characteristics of RT-induced CAD lesions tend to differ from those of atherosclerosis. They are more fibrous, with reduced lipid content, and the vessels involved tend to be more friable.3,8,9,12,13

RT-induced CAD may present with differing clinical presentations. Ischemia may be silent, may lead to classic angina symptoms, or may cause sudden cardiac death. The incidence of silent myocardial infarction has been reported to be higher after mediastinal RT than it is in the general population, possibly from damage to nerve endings within the radiation field.6 There is a higher incidence of severe left main artery disease, followed by ostial RCA and LAD disease, correlating with the anatomic location of RT.1,5,8,13 Usually, RT-induced CAD lesions are consistently longer, more proximal, smoother, concentric, and tubular.13

Management of RT-induced CAD is the same as that of non–RT-related CAD.5,12 Treatment is often challenging because of the effects of radiation on other tissues and the risk of revascularization procedures being necessary. Medical therapy and revascularization can be done depending on symptoms, cancer stage, comorbidities, and estimated survival.3,12,13 CABG may be difficult due to mediastinal fibrosis, and the internal thoracic artery may not be available for grafting because of radiation to that vessel.3,11 Percutaneous revascularization generally should be favored over surgical revascularization.14

The European Association of Cardiovascular Imaging and the American Society of Echocardiography have published consensus guidelines for the prevention, diagnosis, and management of cardiovascular disease (CVD) associated with cancer therapy.10 Patients should be carefully screened for CVD risk factors and should undergo a complete clinical examination and echocardiography to identify any cardiac abnormalities prior to receiving RT. During follow-up, a yearly history and physical examination focused on signs and symptoms of heart disease must be done. Brain natriuretic peptide levels, cardiac troponin levels, and the results of blood tests such as fasting serum glucose and lipid profiles also should be reviewed annually. Studies have shown a potential role for posttreatment biomarker screening to identify patients at high-risk of CVD. Annual electrocardiography can help identify or rule out the development of conduction abnormalities.13 In the presence of new-onset cardiopulmonary symptoms or suggestive physical findings, further studies should not be delayed.8,10,13

Asymptomatic patients should have their first TTE 10 years after treatment and continue with surveillance every 5 years. In high-risk patients, it is reasonable to consider noninvasive imaging stress tests to screen for CAD. If the initial stress test results are negative for inducible ischemia, repeated stress testing can be planned every 5 years. In RT-induced CAD, stress echocardiography or stress perfusion imaging is preferred over stress electrocardiography due to their higher specificity. The role of magnetic resonance imaging and computed tomography is not well defined, with no current data about their use as screening tools, except for early detection of porcelain aorta in high-risk patients.8,10,13 Aggressive modification of traditional CVD risk factors such as hypertension, dyslipidemia, and cigarette smoking is essential in patients at risk, since these factors have been shown to potentiate the risks posed by RT. Long-term follow-up with regular screening plays an important role in the management of cancer survivors who have undergone RT.6,14

This case serves as a reminder that RT can cause severe structural damage to the heart that can develop months to years after exposure. With the introduction of new RT techniques, a number of strategies can be used to decrease the incidence of RT-induced cardiovascular complications. Surveillance monitoring is essential, because the timing of medical or surgical intervention can be crucial for optimal patient outcomes. 



  1. Salemi VMC, Dabarian AL, Nastari L, Gama M, Soares Júnior J, Mady C. Treatment of left main coronary artery lesion after late thoracic radiotherapy. Arq Bras Cardiol. 2011;97(3):e53-e55.
  2. Giraud P, Cosset JM. Radiation toxicity to the heart: physiopathology and clinical data [in French]. Bull Cancer. 2004;91(suppl 3):147-153.
  3. Yusuf SW, Sami S, Daher IN. Radiation-induced heart disease: a clinical update. Cardiol Res Pract. 2011;2011:317659.
  4. Galper SL, Yu JB, Mauch PM, et al. Clinically significant cardiac disease in patients with Hodgkin lymphoma treated with mediastinal irradiation. Blood. 2011;117(2):412-418.
  5. Alsara O, Alsarah A, Kalavakunta JK, Laird-Fick H, Abela GS. Isolated left main coronary artery stenosis after thoracic radiation therapy: to operate or not to operate. Case Rep Med. 2013;2013:834164.
  6. Darby SC, Ewertz M, McGale P, et al. Risk of ischemic heart disease in women after radiotherapy for breast cancer. N Engl J Med. 2013;368(11):​987-998.
  7. Groarke JD, Nguyen PL, Nohria A, Ferrari R, Cheng S, Moslehi J. Cardiovascular complications of radiation therapy for thoracic malignancies: the role for non-invasive imaging for detection of cardiovascular disease. Eur Heart J. 2014;35(10):612-623.
  8. Donnellan E, Phelan D, McCarthy CP, Collier P, Desai M, Griffin B. Radiation-induced heart disease: a practical guide to diagnosis and management. Cleve Clin J Med. 2016;83(12):914-922.
  9. Reed GW, Masri A, Griffin BP, Kapadia SR, Ellis SG, Desai MY. Long-term mortality in patients with radiation-associated coronary artery disease treated with percutaneous coronary intervention. Circ Cardiovasc Interv. 2016;9(6):​e003483.
  10. Lancellotti P, Nkomo VT, Badano LP, et al; European Society of Cardiology Working Groups on Nuclear Cardiology and Cardiac Computed Tomography and Cardiovascular Magnetic Resonance; American Society of Nuclear Cardiology, Society for Cardiovascular Magnetic Resonance, and Society of Cardiovascular Computed Tomography. Expert consensus for multi-modality imaging evaluation of cardiovascular complications of radiotherapy in adults: a report from the European Association of Cardiovascular Imaging and the American Society of Echocardiography. J Am Soc Echocardiogr. 2013;26(9):​1013-1032.
  11. Adams MJ, Hardenbergh PH, Constine LS, Lipshultz SE. Radiation-associated cardiovascular disease. Crit Rev Oncol Hematol. 2003;45(1):55-75.
  12. Madan R, Benson R, Sharma DN, Julka PK, Rath GK. Radiation induced heart disease: pathogenesis, management and review literature. J Egypt Natl Canc Inst. 2015;27(4):187-193.
  13. Jaworski C, Mariani JA, Wheeler G, Kaye DM. Cardiac complications of thoracic irradiation. J Am Coll Cardiol. 2013;61(23)2319-2328.
  14. Davis M, Witteles RM. Radiation-induced heart disease: an under-recognized entity? Curr Treat Options Cardiovasc Med. 2014;16(6)317.