Abstract
Background
Nonseminomatous testicular germ cell tumors (TGCTs) rarely metastasize to the heart, posing cardiovascular diagnostic and management challenges.
Case Summary
We present 2 young men (20 and 28 years) with advanced mixed TGCTs. One developed acute ischemic stroke and myocardial infarction, the other a multifocal murmur. Both showed elevated alpha-fetoprotein, beta human chorionic gonadotropin, and pulmonary nodules. Transthoracic echocardiography revealed atrioventricular valves and outflow tract masses.
Discussion
In TGCT, embolic or new cardiovascular findings should prompt urgent transthoracic echocardiography to assess cardiac metastases. Early multimodality imaging can uncover silent disease and guide timely multidisciplinary care. Management focuses on definitive tumor resection and platinum-based chemotherapy.
Take-Home Messages
Cardiac metastases from testicular cancer may first present with neurological or cardiovascular symptoms. Right-sided secondary cardiac tumors may be silent, whereas left-sided involvement may cause embolic events.
Key words: cardiac metastasis, germ cell tumor, testicular cancer, transthoracic echocardiography, stroke
Graphical Abstract
Case 1
A 28-year-old man with a 1-month history of progressive left testicular mass enlargement presented to the emergency department with a sudden-onset severe headache and motor aphasia. On arrival, he was alert and oriented, with preserved strength and sensation but unable to articulate words. Respiratory examination revealed reduced thoracic expansion, slightly dull percussion at both lung bases, and diminished vesicular breath sounds bilaterally. Cardiovascular and abdominal examination were unremarkable. Genitourinary examination revealed an enlarged, firm left hemiscrotum with deformity and asymmetry due to a palpable hard mass, along with a right inguinal reducible swelling, which increased in size with the Valsalva maneuver.
Take-Home Messages
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Cardiac metastases from testicular cancer may first present with neurological or cardiovascular symptoms.
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Right-sided secondary cardiac tumors may be silent, whereas left-sided involvement may cause embolic events.
Laboratory tests showed hemoglobin 15 g/dL, platelets 308 × 103/μL, activated partial thromboplastin time 36 seconds, prothrombin time 15.8 seconds, international normalized ratio 1.2, creatinine 0.73 mg/dL, D-dimer 3,888 ng/mL, lactate dehydrogenase (LDH) 2735 U/L, alpha fetoprotein (AFP) 1,775 ng/mL, and beta human chorionic gonadotropin (β-hCG) 30.86 IU/L.
The electrocardiogram at admission showed a sinus rhythm with no abnormalities. Brain computed tomography (CT) was consistent with a subacute infarct in the M1 segment of the left middle cerebral artery (frontotemporal-insular region) without signs of hemorrhage (Figure 1). Based on these findings, the ischemic stroke was managed with anticoagulation therapy.
Figure 1.
Noncontrast CT Scan of the Brain Showing a Subacute Ischemic Stroke in the Left M1 Segment Middle Cerebral Artery, With No Signs of Hemorrhage
(A) Coronal reconstruction demonstrates hypodensity in the left frontotemporal-insular region with loss of gray-white matter differentiation and left MCA definition (orange arrow). (B) Axial section shows sulcal effacement in the same region and loss of continuity of the left MCA (yellow arrow). (C) Axial section confirms hypodensity extending throughout the left MCA distribution. CT = computed tomography; MCA = middle cerebral artery.
Given the ischemic stroke and markedly elevated tumor markers, transthoracic echocardiography (TTE) was performed to evaluate potential embolic sources (including intracardiac thrombi, tumor extension, or a patent foramen ovale enabling paradoxical embolism). It revealed multiple echogenic masses in the left ventricle and left atrium, adherent to the anterior leaflet of the mitral valve and prolapsing into the left ventricular outflow tract, with preserved left ventricular ejection fraction and no valvular stenosis or regurgitation (Figure 2, Video 1).
Figure 2.
Transthoracic Echocardiography Demonstrating a Large Intracardiac Mass
(A) The parasternal long-axis view shows an irregular, pedunculated echogenic mass attached to the anterior mitral leaflet, projecting into the left ventricular outflow tract (orange arrow). (B) The apical 4-chamber view confirms the heterogeneous mass within the left heart, anchored to the anterior mitral leaflet and extending into the left ventricular cavity (orange arrow). Right-sided chambers are visualized, but no involvement was detected. RA = right atrium; RV = right ventricle.
Chest CT demonstrated multiple bilateral pulmonary nodules distributed over the whole lung parenchyma, the largest measuring 3.3 cm, with bibasilar laminar atelectasis but no pleural effusion or mediastinal lymphadenopathy. Abdominal CT confirmed a left testicular solid mass (8.7 × 10.5 cm) and right inguinal hernia containing adipose tissue, with mild prominence of the left testicular vessels within the spermatic cord, and no retroperitoneal lymphadenopathy.
Left radical orchiectomy was performed uneventfully. Gross pathology showed a 13-cm multilobulated solid mass with necrotic (5%) and hemorrhagic (30%) areas, extending into the epididymis. Histopathology confirmed mixed germ cell tumor: seminoma (50%), embryonal carcinoma (5%), yolk sac tumor (20%) and postpubertal teratoma (25%), with lymphovascular invasion (Figure 3).
Figure 3.
Histopathological Examination of the Resected Testicular Mass, Consistent With a Mixed Germ Cell Testicular Cancer (H&E Stain)
(A) Cystic structures lined by squamous epithelium, compatible with areas of mature teratoma. (B) Sheets of cells with large round nuclei, prominent nucleoli, and clear cytoplasm, characteristic of classical seminoma. (C) Microcystic and myxoid areas with primitive glandular structures, consistent with yolk sac (endodermal sinus) tumor component. H&E = hematoxylin and eosin.
Adjuvant chemotherapy was scheduled. However, before initiation, the patient developed acute myocardial infarction secondary to left coronary artery embolism (Figure 4). Since percutaneous coronary intervention was not available at the time, thrombolysis was established as the next step. Unfortunately, he succumbed to this event before transfer could be arranged.
Figure 4.
Contrast-Enhanced Cardiac CT in a Patient With Suspected Acute Coronary Syndrome
(A and B) Multiplanar reconstructions showing intraluminal filling defect in the proximal left coronary artery (yellow arrows), consistent with acute thrombus and severe luminal narrowing. (C) Right coronary artery with no evidence of thrombus or significant stenosis. CT = computed tomography.
Case 2
A 20-year-old man presented to a tertiary oncology center with an 8-month history of progressively growing, painful left testicular mass. Cardiovascular examination revealed a grade I/VI multifocal murmur.
Biomarker tests showed β-hCG 152 IU/mL, AFP 497.9 ng/mL, and LDH 1,238 U/L. Abdominal CT showed a left testicular mass (8.6 × 7.9 cm) and bulky retroperitoneal lymphadenopathy above and below the renal vessels, the largest measuring 8.1 × 6.3 × 14.4 cm. Chest CT revealed multiple bilateral pulmonary nodules, the largest measuring 2.3 cm in the right lower lobe and 1.7 cm in the left upper lobe.
TTE showed a left ventricular ejection fraction of 56%, left ventricular global longitudinal strain of −21%, E/A ratio of 1.1, E/e′ ratio of 6, tricuspid annular plane systolic excursion of 26 mm, and left atrial volume of 29.5 mL. TTE along with cardiac magnetic resonance (CMR) demonstrated 2 mobile, pedunculated hyperechoic masses on the tricuspid valve, extending into the right heart chambers and right ventricular outflow tract, causing mild pulmonary regurgitation (Figures 5 and 6, Videos 2 to 4).
Figure 5.
CMR Demonstrating a Large Right Heart Intracardiac Mass
(A and B) Axial and coronal views with a heterogeneous mass occupying the right atrium, attached to the tricuspid valve, and extending into the right ventricular outflow tract. (C and D) Sagittal and 4-chamber views confirm the irregular, infiltrative lesion of the right heart chambers with partial obstruction of the right ventricular outflow tract. CMR = cardiac magnetic resonance.
Figure 6.
Three-Dimensional Reconstruction From CMR Showing the Segmented Intracardiac Mass
The intracardiac mass (blue) extended from the right atrium through the tricuspid valve to the right ventricular outflow tract. CMR = cardiac magnetic resonance.
The patient underwent radical left orchiectomy without complications. Histopathology confirmed a mixed germ cell tumor confined to the testis (8.5 × 7.9 cm) with no epididymal, rete testis, or spermatic cord invasion (Figure 7). After completing systemic adjuvant bleomycin-etoposide-cisplatin (BEP) chemotherapy, the patient developed a subclinical decline of left ventricular ejection fraction to 48%, and guideline-directed medical therapy was then initiated with pending follow-up. Owing to the favorable systemic response (approximate 25% reduction of intracardiac mass, with mild reduction in pulmonary nodules), the surgical team scheduled a complete resection of the cardiac tumor with biological tricuspid valve replacement.
Figure 7.
Histopathological Examination of the Resected Testicular Mass, Consistent With a Mixed Germ Cell Testicular Tumor
(A) Choriocarcinoma component with cytotrophoblast and syncytiotrophoblast tissue and hemorrhagic necrosis. (B) Biphasic pattern with endodermal sinus (yolk sac) tumor on the left and mature teratoma with glandular and chondroid elements on the right. (C) Immunohistochemical staining for β-hCG, highlighting the choriocarcinoma component. β-hCG = beta human chorionic gonadotropin.
Discussion
Testicular cancer is the most common solid tumor in men aged 15 to 44 years, with 95% classified as germ cell tumors. Although advances in management have improved prognosis, survival disparities persist, with a 5-year survival rate of 98% in Europe but only 75% to 88% in South America.1 Nonseminomatous types, as in our cases, display more aggressive behavior owing to higher metastatic potential and variable therapeutic response.2
Initial presentation is usually a painless scrotal mass, whereas advanced disease may manifest with systemic symptoms such as fatigue or back pain from retroperitoneal lymphadenopathy. In later stages, lymphovascular invasion enables hematogenous spread to the lungs, liver, brain, and, rarely, the heart.2 Cardiac tumors are mostly secondary, outnumbering primaries by ∼20 to 1, with spread occurring through direct extension, hematogenous dissemination, or lymphatic spread.3 The pericardium is most often affected (leading to effusions or tamponade), while myocardial or intracavitary metastases remain exceptional.4 Clinical manifestations are nonspecific and may include cardiovascular signs (arrhythmias, valvular dysfunction, syncope), systemic symptoms, or embolic events.5 Our patients illustrate this spectrum: case 1 presented with embolic stroke and embolic myocardial infarction from left-sided masses, while case 2 developed only a benign new murmur from right-sided tricuspid involvement despite preserved function. These presentations are indicative of both the aggressiveness of nonseminomatous disease through hematogenous spread and the challenge of early recognition before irreversible complications occur.5
Scrotal ultrasonography is the initial imaging tool for testicular masses, akin to echocardiography for cardiac masses, allowing assessment of chamber dimensions, morphology, and hemodynamic parameters. Transesophageal echocardiography, in particular, enhances detection of valves or atrial growths, providing clear insight into the left heart, offering a better acoustic window, and detection of masses <5 mm.3 CMR excels in tissue characterization, as well as distinguishing between benign and malignant tumors (typically >5 cm, multichamber involvement, effusions, or vascular invasion). CT is critical for assessing the chest, mediastinum, heart, lungs, and local vascular system when metastases are suspected.5,6 In our patients, elevated AFP and β-hCG in the setting of imaging metastatic findings not only raised suspicion for testicular germ cell tumor (TGCT) but also suggested a nonseminomatous subtype. This was later confirmed in orchiectomy pathology, underscoring the complementary role of tumor markers and imaging in establishing both diagnosis and prognosis.
The cornerstone of cardiac metastasis management is treating the primary tumor.5 Radical orchiectomy remains the standard first step, while adjuvant chemotherapy is reserved for advanced stages, with 4 cycles of BEP or etoposide-isofosfamide-cisplatin.2,7 Residual retroperitoneal masses >1 cm after chemotherapy warrant surgical resection, while smaller masses may be monitored.1 Cardiac surgery is generally reserved for hemodynamic compromise or cases with established survival benefits (solitary cardiac metastasis with controlled primary tumor or renal cell carcinoma).5 In our cases, surgical intervention was considered until completion of systemic therapy, consistent with testicular cancer management guidelines.2,5 Case 1 received etoposide-cisplatin but deteriorated before completion, whereas case 2 successfully completed BEP chemotherapy and subsequently is planned for complete resection of the cardiac mass and tricuspid valve replacement.
Although BEP is not considered a cardiotoxic regimen according to current cardio-oncology guidelines,8 preclinical data suggest mechanisms of cisplatin-related myocardial injury, including mitochondrial abnormalities, hypoxic necrosis, and apoptosis.8,9 Isolated reports have also described potential cisplatin-associated left ventricular impairment. For example, Hu et al9 reported a 53-year-old woman who developed reduction in left ventricular ejection fraction from 70% to 48% after 3 weeks of cisplatin therapy, with improvement after treatment discontinuation and initiation of coenzyme Q10 and trimetazidine. Moreover, a CMR study by Beitzen-Heineke et al8 demonstrated that long-term survivors of testicular cancer treated with cisplatin-based regimens exhibited significantly lower left and right ventricular ejection fractions, reduced global longitudinal strain, and decreased T1 values compared with matched controls. While subclinical systolic function reduction after cisplatin-based chemotherapy at long-term follow-up was demonstrated using the gold standard for quantification of cardiac function and volumes (ie, CMR), heterogeneity in chemotherapy regimens limits attribution to any specific agent within the BEP regimen. Moreover, these subclinical alterations may not necessarily progress to clinically overt heart failure.9
Despite the overall favorable prognosis, relapse risk peaks in the first 2 to 3 years.1 Surveillance incorporates physical examination, tumor markers, and imaging, although up to 35% of relapses may occur with negative markers. Both of our patients met International Germ Cell Cancer Collaborative Group criteria for poor prognosis, given nonpulmonary visceral metastases, corresponding to expected 5-year progression-free survival of ∼41% and overall survival of ∼71%.10
Conclusions
Cardiac metastases from TGCTs are exceptionally rare and often clinically silent until advanced stages. Our 2 cases highlight the contrasting presentations of left-sided intracardiac masses causing embolic events and right-sided lesions detected only by a new murmur despite preserved ventricular function. These findings emphasize the importance of maintaining a high index of suspicion for cardiac involvement in patients with advanced nonseminomatous disease and unexplained cardiovascular or embolic symptoms. Echocardiography remains the initial diagnostic tool, while CMR and CT refine characterization and systemic staging.
Management continues to rely on radical orchiectomy and cisplatin-based chemotherapy, with cardiac surgery reserved for select hemodynamic and subtype indications.
Visual Summary.
Case Summary
| Stage | Case 1: Left-Sided Involvement | Case 2: Right-Sided Involvement |
|---|---|---|
| Clinical presentation | 28-year-old man with progressive left testicular and sudden headache with motor aphasia Tumor markers: AFP 1,775 ng/mL, β-hCG 30.9 IU/L, LDH 2,735 U/L |
20-year-old man with progressive left testicular enlargement and new systolic murmur during examination Tumor markers: AFP 497.9 ng/mL, β-hCG 152 IU/L, LDH 1,238 U/L |
| Imaging | TTE: Masses adhered to the anterior mitral leaflet extending into LVOT, preserved LVEF CT: Pulmonary nodules, no retroperitoneal lymphadenopathy |
TTE/CMR: Pedunculated masses on tricuspid valve extending into RVOT, mild pulmonary regurgitation, preserved LVEF CT: Pulmonary nodules and retroperitoneal lymphadenopathy |
| Biopsy | Left mixed germ cell tumor (seminoma, embryonal, yolk sac, and teratoma components) with lymphovascular invasion | Left mixed germ cell tumor (choriocarcinoma and yolk sac) with lymphovascular invasion |
| Treatment | Left radical orchiectomy, planned platinum and chemotherapy | Left radical orchiectomy and planned BEP chemotherapy |
| Outcome | Died from embolic myocardial infarction before chemotherapy was completed | Cardiac mass reduction in 25% with completed BEP chemotherapy, LVEF decreased to 48%. Scheduled for complete intracardiac mass resection with biological tricuspid valve replacement |
AFP = alpha-fetoprotein; β-hCG = beta human chorionic gonadotropin; BEP = bleomycin-etoposide-cisplatin; CMR = cardiac magnetic resonance; CT = computed tomography; LDH = lactate dehydrogenase; LVEF = left ventricular ejection fraction; LVOT = left ventricular outflow tract; RVOT = right ventricular outflow tract; TTE = transthoracic echocardiography.
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
Appendix
For supplemental videos, please see the online version of this paper.
Appendix
Two-Dimensional Transthoracic Echocardiography Demonstrating a Large, Heterogeneous Intracardiac Mass Involving the Left Heart
(A) The parasternal long-axis view shows a pedunculated mass attached to the anterior mitral leaflet, extending on both atrial and ventricular sides and protruding into the left ventricular outflow tract, with adherence to chordae tendineae. (B) The apical 4-chamber view confirms the mass adhered to the anterior mitral leaflet, extending into the left ventricular cavity. (C) The parasternal short-axis view at mitral valve level reveals the irregular, lobulated morphology of the mass occupying the left ventricular chamber. (D) Apical 2-chamber view demonstrates the extent of the mass within the left ventricle.
Two-Dimensional Transthoracic Echocardiography Demonstrating a Large Right-Sided Intracardiac Mass That Prolapses Between the Right Atrium During Systole and Right Ventricle During Diastole
(A) The parasternal long-axis view shows the lobulated echogenic mass on the right ventricle during systole. (B) The parasternal short-axis view at the level of the great vessels shows the mass within the right atrium and apparently tethered to the tricuspid valve apparatus. (C) The apical 4-chamber view confirms displacement of the mass across the tricuspid valve. (D) The modified apical 4-chamber view corroborates the dynamic excursion of the mass into the right chambers.
Three-Dimensional Transthoracic Echocardiography Showing a Large Right-Sided Intracardiac Mass Prolapsing Into the Right Atrium During Systole and Into the Right Ventricle During Diastole
(A) The right 2-chamber view highlights the dynamic displacement of the mass across the tricuspid valve. (B) The parasternal short-axis view at the level of the great arteries with the mass prolapsing into the right atrium and right ventricular outflow tract.
Cardiac Magnetic Resonance Imaging in Cine Mode Showing a Large Right-Sided Intracardiac Mass With Tricuspid Valve Involvement and Extension Into the RVOT
(A and C) Four- and 2-chamber views with a lobulated mass highlighting its insertion into the tricuspid valve apparatus and prolapse through the valve. (B) Parasternal short-axis view during systole with the mass partially occupying the right ventricle. (D and F) Vertical and horizontal long-axis views showing the mass extending into the right ventricular outflow tract. (E) Vertical long-axis view highlighting its insertion into the anterior leaflet of the tricuspid valve.
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Associated Data
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Supplementary Materials
Two-Dimensional Transthoracic Echocardiography Demonstrating a Large, Heterogeneous Intracardiac Mass Involving the Left Heart
(A) The parasternal long-axis view shows a pedunculated mass attached to the anterior mitral leaflet, extending on both atrial and ventricular sides and protruding into the left ventricular outflow tract, with adherence to chordae tendineae. (B) The apical 4-chamber view confirms the mass adhered to the anterior mitral leaflet, extending into the left ventricular cavity. (C) The parasternal short-axis view at mitral valve level reveals the irregular, lobulated morphology of the mass occupying the left ventricular chamber. (D) Apical 2-chamber view demonstrates the extent of the mass within the left ventricle.
Two-Dimensional Transthoracic Echocardiography Demonstrating a Large Right-Sided Intracardiac Mass That Prolapses Between the Right Atrium During Systole and Right Ventricle During Diastole
(A) The parasternal long-axis view shows the lobulated echogenic mass on the right ventricle during systole. (B) The parasternal short-axis view at the level of the great vessels shows the mass within the right atrium and apparently tethered to the tricuspid valve apparatus. (C) The apical 4-chamber view confirms displacement of the mass across the tricuspid valve. (D) The modified apical 4-chamber view corroborates the dynamic excursion of the mass into the right chambers.
Three-Dimensional Transthoracic Echocardiography Showing a Large Right-Sided Intracardiac Mass Prolapsing Into the Right Atrium During Systole and Into the Right Ventricle During Diastole
(A) The right 2-chamber view highlights the dynamic displacement of the mass across the tricuspid valve. (B) The parasternal short-axis view at the level of the great arteries with the mass prolapsing into the right atrium and right ventricular outflow tract.
Cardiac Magnetic Resonance Imaging in Cine Mode Showing a Large Right-Sided Intracardiac Mass With Tricuspid Valve Involvement and Extension Into the RVOT
(A and C) Four- and 2-chamber views with a lobulated mass highlighting its insertion into the tricuspid valve apparatus and prolapse through the valve. (B) Parasternal short-axis view during systole with the mass partially occupying the right ventricle. (D and F) Vertical and horizontal long-axis views showing the mass extending into the right ventricular outflow tract. (E) Vertical long-axis view highlighting its insertion into the anterior leaflet of the tricuspid valve.