Case simulation · Thermo Fisher Scientific

Expert’s Corner

Case · Presentation

Ten kilograms in two months. And her shoes stopped fitting.

The patient is a 50-year-old female with longstanding familial cardiomyopathy who was placed on the transplant waiting list due to severe heart failure. She subsequently underwent orthotopic heart transplantation 6 weeks ago.

Post-transplant, she was initiated on immunosuppression with tacrolimus (target trough levels 8–12 ng/mL), mycophenolate mofetil (MMF), and prednisone. Given her residence in a region endemic for fungal infection, antifungal prophylaxis was also prescribed.

Elevated filling pressures were observed on physical examination, and echocardiographic evaluation indicates early graft dysfunction. Her clinical course raises concerns about potential post-transplant complications.

Risk assessment was refined using the REVEAL Lite-2 score, which incorporates functional class, NT-proBNP, renal function, systolic blood pressure, and heart rate. This simplified score has been validated to predict outcomes, and even a ≥1 point increase is associated with significantly higher mortality and transplant-free survival risk.

She has a history of familial cardiomyopathy, indicating a genetic predisposition to heart disease. She resides in an area that is endemic to fungal infections.

On examination she is conscious and alert, oriented x3, and in no acute distress. Cardiovascular examination reveals jugular venous distension and +1 peripheral edema in the lower extremities, an S4 heart sound is heard, but no murmurs, rubs, or gallops. Pulmonary examination is notable for bibasilar crackles, though no wheezing or stridor is present. Weight today is 78 kg, up from 68 kg two months ago. RR 18 breaths/min, HR 94 bpm, temperature 37.0 °C.

She reports mild fatigue and weight gain due to fluid retention, progressive lower extremity swelling, increased abdominal bloating, occasional lightheadedness when standing, shortness of breath with activity, exercise intolerance, and now sleeps with multiple pillows.

Case · Workup

The biopsy says mild. The molecules disagree.

These are the investigations ordered at today’s visit, with the findings and the reasoning for each.

  • Transplant/immunology

    Today’s results: Today’s results reveal a subtherapeutic tacrolimus level (4 ng/mL), new DSAs detected, and elevated Cell-Free DNA (0.40%). Strongly supporting immunological injury and graft dysfunction.

    Value

  • Endomyocardial Biopsy with Molecular Microscope Diagnostic System (MMDx)

    Today’s results:

    Histopathology: Cell-mediated rejection (ACR): mild (grade 1R)

    AMR: mild (grade pAMR1 (I+)).MMDx Interpretation: Moderate to severe fully-developed ABMR. No TCMR. Moderate parenchymal injury.

    It is appropriate to order an endomyocardial biopsy with MMDX.

    MMDx results demonstrate moderate-to-severe AMR and moderate parenchymal injury, highlighting a discrepancy between traditional histologic findings and molecular phenotyping by MMDx. In this case, MMDx findings correlate better with the patient’s clinical decline (progressive dyspnea, reduced EF, rising BNP, new DSAs), emphasizing its value in identifying clinically meaningful rejection beyond histology alone (Halloran & Madill-Thomsen, 2022; Halloran PF, et al. 2024).

    While the biopsy results suggest a lower level of graft rejection injury, these findings are difficult to reconcile with the patient's clinical course, which includes progressive fatigue, dyspnea, reduced ejection fraction (45%), new DSAs, and evidence of impaired hemodynamics.

    Current ISHLT guidelines recommend integrating biomarkers and molecular diagnostics with biopsy findings to improve the accuracy of rejection assessment and guide management (Velleca A, et al. 2022).

  • Hematology

    Today’s results: Elevated CRP, ESR, slightly prolonged PT, elevated INR, mild anemia, and low hematocrit.

    Value

  • Biochemistry/metabolic panel

    Today’s results: Elevated serum creatinine and BUN, mildly elevated AST and ALT, and borderline elevated bilirubin.

    Value

  • Cardiology

    Today’s results: Mildly elevated troponin and elevated BNP (the prior value of 45 pg/mL, recorded 21 days ago, provides a helpful baseline for comparison).

    Value

  • Imaging

    Today’s results: Echocardiogram.Ejection Fraction: 45%.

    Chamber sizes: Mild left ventricular dilation.

    Valvular function: Mild mitral regurgitation.

    Wall motion: Global hypokinesis.

    Pericardium: No pericardial effusion.

    It is appropriate to order the Echocardiogram.

    Today’s echocardiogram reveals a reduced ejection fraction (from 65% to 45%), mild left ventricular dilation, mild mitral regurgitation, and global hypokinesis, consistent with impaired graft function and ongoing rejection. Decline in ejection fraction and new chamber dilation often occur later in the course of antibody-mediated rejection, reflecting established graft injury. These functional changes correlate with molecular injury signatures on MMDx and rising biomarkers (BNP, troponin, dd-cfDNA) (Halloran PF, et al. 2024).

  • Microbiology/infectious disease

    Today's results: Abnormalities: None were identified in microbiology or infectious disease testing.Blood cultures: No growth after 48 hours (negative).

    Urinalysis: No evidence of infection (normal).

    It is appropriate to order the microbiology/infectious disease panel.

    Today’s results show no evidence of infection, with negative blood cultures and a normal urinalysis. The patient’s presentation and findings are consistent with graft dysfunction and rejection, not an infectious process (Velleca A, et al. 2022).

Considered and not ordered (1)
  • Viral polymerase chain reaction (PCR) panel for cytomegalovirus (CMV) or Epstein-Barr virus (EBV)Not appropriate

    Today's results: Test canceled.

    Ordering the viral PCR panel for CMV or EBV is inappropriate.

    This test is not indicated in this scenario because there are no specific symptoms or findings, such as fever, leukopenia, or systemic signs of infection, to suggest an active viral process (Kobashigawa J, et al. 2023; Velleca A, et al. 2022).

Case · Diagnosis

How severe is the rejection?

The endomyocardial biopsy and the molecular read do not agree on severity.

DecisionHow should the rejection be classified?

Select an answer to continue

  • AMild antibody-mediated rejection (ABMR)Incorrect
  • BModerate to severe antibody-mediated rejection (ABMR)Correct

A · incorrect

This is not the correct diagnosis. The patient’s clinical presentation, diagnostic findings, and molecular diagnostics collectively support a diagnosis of moderate-to-severe antibody-mediated rejection (AMR). While the biopsy shows mild cell-mediated rejection (grade 1R) and mild AMR (grade pAMR1), these findings are at odds with her progressive symptoms of fatigue and dyspnea, reduced ejection fraction (45%), new DSAs, and impaired hemodynamics. MMDx findings of moderate-to-severe ABMR, DSA, elevated BNP, and imaging indicating global hypokinesis and left ventricular dysfunction add to the concern for rejection. These findings suggest a more advanced rejection process than histopathology alone would indicate.

This case underscores the diagnostic uncertainty that arises when histology, biomarkers, and molecular testing diverge, highlighting the need for an integrated, multimodal approach (Velleca A, et al. 2022)Histologic evaluation of rejection in transplant recipients, while widely used, is inherently limited by significant variability and noise in interpretation. Studies have shown low concordance between pathologists, particularly in diagnosing T-cell-mediated rejection (TCMR) in heart transplant patients. Concordance rates for TCMR diagnosis are as low as 28%, reflecting substantial interobserver variability. Low kappa values for TCMR in heart transplants underscore the challenges in achieving reliable and reproducible assessments based on traditional histopathology alone. This variability can lead to discrepancies between reported rejection grades and the patient’s actual clinical condition (Halloran & Madill-Thomsen, 2022).

These limitations affect the clinical utility of endomyocardial biopsy (EMB), even though it remains the gold standard for allograft surveillance. In contrast, MMDx provides an objective, highly reproducible (99%) assessment of biopsy samples, extending knowledge and offering the possibility for increased accuracy in diagnosing and treating patients, rather than competing with histology. By offering molecular phenotyping, MMDx enhances diagnostic confidence and provides additional insights into pathological states, facilitating more precise treatment decisions. In this patient’s case, MMDx findings align more closely with her clinical presentation, imaging, and laboratory abnormalities, suggesting a greater degree of graft injury than indicated by histology alone (Halloran & Madill-Thomsen, 2022). The elevated donor-derived cfDNA (dd-cfDNA 0.40%) provides additional supportive evidence of active graft injury, consistent with molecular AMR, and highlights the complementary role of integrating cfDNA with MMDx (Halloran & Madill-Thomsen, 2022; Halloran & Madill-Thomsen, 2025).

ISHLT 2023 emphasizes integrating histology with molecular diagnostics (MMDx) and cfDNA, particularly in cases where biopsy underestimates clinical severity (Kobashigawa J, et al. 2023).

B · correct

This is the correct diagnosis. The patient’s clinical presentation, diagnostic findings, and molecular diagnostics collectively support a diagnosis of moderate-to-severe rejection. While the biopsy shows mild cell-mediated rejection (grade 1R) and mild AMR (grade pAMR1), these findings are at odds with her progressive symptoms of fatigue and dyspnea, reduced ejection fraction (45%), new DSAs, and impaired hemodynamics. MMDx findings of moderate-to-severe AMR, DSA, elevated BNP, and imaging indicating global hypokinesis and left ventricular dysfunction add to the concern for rejection. These findings propose a more advanced rejection process than is suggested by histopathology alone.

Histologic evaluation of rejection in transplant recipients, while widely used, is inherently limited by significant variability and noise in interpretation. Studies have shown low concordance between pathologists, particularly in the diagnosis of TCMR in heart transplant patients. Concordance rates for TCMR diagnosis are as low as 28%, reflecting substantial interobserver variability. Low kappa values for TCMR in heart transplants underscore the challenges in achieving reliable and reproducible assessments based on traditional histopathology alone. This variability can lead to discrepancies between reported rejection grades and the patient’s actual clinical condition (Halloran & Madill-Thomsen, 2022).

These limitations affect the clinical utility of endomyocardial biopsy (EMB), even though it remains the gold standard for allograft surveillance. In contrast, molecular diagnostics (MMDx) provide an objective, highly reproducible (99%) assessment of biopsy samples, extending knowledge and offering the possibility for increased accuracy in diagnosing and treating patients, rather than competing with histology. By offering molecular phenotyping, MMDx enhances diagnostic confidence and provides additional insights into pathological states, facilitating more precise treatment decisions. In this patient’s case, MMDx findings align more closely with her clinical presentation, imaging, and laboratory abnormalities, suggesting a greater degree of graft injury than indicated by histology alone (Halloran & Madill-Thomsen, 2022). The elevated donor-derived cfDNA (dd-cfDNA 0.40%) provides additional supportive evidence of active graft injury, consistent with molecular AMR, and highlights the complementary role of integrating cfDNA with MMDx (Halloran & Madill-Thomsen, 2022; Halloran & Madill-Thomsen, 2025).

ISHLT 2023 emphasizes integrating histology with molecular diagnostics (MMDx) and cfDNA, particularly in cases where biopsy underestimates clinical severity (Kobashigawa J, et al. 2023).

Review the other options

Case · Treatment

Treat what the molecules found.

Antibody‑mediated rejection is treated by combining agents that act on different parts of the alloimmune response.

Therapies and the immune targets they act on, as given in the case document. A mark means the therapy acts on that target.

TherapyT CellsB CellsPlasma CellsCirculating AntibodyComplement ActivationOther
IVIgXX·XX·
Plasmapheresis···X··
PhotopheresisX····Upregulates regulatory T cells
CorticosteroidsXX····
Cyclophosphamide·X····
MycophenolateXX····
Anti-thymocyte globulinXX····
Rituximab·X····
Bortezomib··X···
Eculizumab····X·
AlemtuzumabXX····
Total lymphoid irradiationXX····
Splenectomy·X····

DecisionWhich treatment approach fits moderate to severe antibody-mediated rejection?

Select an answer to continue

  • AIntravenous immunoglobulin (IVIg) and rituximabPartially correct
  • BTacrolimus 8 mg BID, MMF 1000 mg BID, Prednisone 20 mg QDIncorrect
  • CIVIg and IV methylprednisolonePartially correct
  • DIVIG, IV methylprednisolone, and rituximabPartially correct
  • EAnti-thymocyte globulin (ATG), IVIG, plasmapheresis, and bortezomibCorrect
  • FIVIG, IV methylprednisolone, plasmapheresis, and bortezomibCorrect
  • GIVIG, IV methylprednisolone, plasmapheresis, and rituximabCorrect

A · partially correct

Given the patient’s moderate to severe antibody-mediated rejection (AMR), confirmed by the Molecular Microscope Diagnostic System (MMDx), along with impaired hemodynamics and reduced ejection fraction, treatment is guided by ISHLT classification as pAMR 2 or 3 with elevated DSA. Based on this, initiating IVIg and rituximab is an appropriate therapeutic approach but incomplete as monotherapy in hemodynamically significant AMR (Nguyen VP and Kobashigawa JA, 2020).The core strategies for managing antibody-mediated rejection (AMR) focus on eliminating circulating alloantibodies, inhibiting further alloantibody production, and dampening both T-cell and B-cell activity. No large-scale randomized trials have been conducted to assess AMR therapies specifically in heart transplant patients (Colvin MM, et al. 2015).This table, adapted from the 2015 scientific statement from the American Heart Association (Colvin MM, et al. 2015), summarizes the immune component affected by each therapy.

B · incorrect

While increasing the doses of tacrolimus and MMF may appear reasonable to strengthen immunosuppression, it is inadequate for addressing AMR. This type of rejection is driven by circulating DSAs, which require targeted therapies like IVIg and rituximab for effective management (Velleca A, et al. 2022). Focusing solely on increasing these medications would fail to remove or neutralize these antibodies or suppress B-cell activity, potentially leading to worsening graft dysfunction and rejection.Note:

There is currently no universally accepted standard for managing antibody-mediated rejection (AMR) in heart transplant recipients. Treatment strategies vary across centers and are often guided by individual clinical judgment, severity of graft dysfunction, and institutional protocols. This case reflects commonly used approaches supported by expert opinion and available literature, but acknowledges that multiple valid treatment pathways may exist.

C · partially correct

Given the patient’s moderate to severe antibody-mediated rejection, indicated by the Molecular Microscope Diagnostic System (MMDx), impaired hemodynamics, and decreased ejection fraction, the initiation of IVIg and IV methylprednisolone is appropriate (Nguyen VP and Kobashigawa JA, 2020; Colvin MM, et al. 2015).The core strategies for managing antibody-mediated rejection (AMR) focus on eliminating circulating alloantibodies, inhibiting further alloantibody production, and dampening both T-cell and B-cell activity. Currently, no large-scale randomized trials have been conducted to assess AMR therapies specifically in heart transplant patients (Colvin MM, et al. 2015).This table, adapted from the 2015 scientific statement from the American Heart Association (Colvin MM, et al. 2015), provides a summary of the immune component affected by each therapy.

D · partially correct

This represents a valid option.Given the patient’s moderate to severe antibody-mediated rejection, indicated by the Molecular Microscope Diagnostic System (MMDx), impaired hemodynamics, and decreased ejection fraction, the initiation of IVIg, IV methylprednisolone, and rituximab is appropriate (Nguyen VP and Kobashigawa JA, 2020; Colvin MM, et al. 2015).

The core strategies for managing antibody-mediated rejection (AMR) focus on eliminating circulating alloantibodies, inhibiting further alloantibody production, and dampening both T-cell and B-cell activity. Currently, no large-scale randomized trials have been conducted to assess AMR therapies specifically in heart transplant patients (Colvin MM, et al. 2015).This table, adapted from the 2015 scientific statement from the American Heart Association (Colvin MM, et al. 2015), provides a summary of the immune component affected by each therapy.

E · correct

This represents a valid option.Given the patient’s moderate to severe antibody-mediated rejection, confirmed by the Molecular Microscope Diagnostic System (MMDx), impaired hemodynamics, and decreased ejection fraction, the initiation of ATG, IVIG, plasmapheresis, and bortezomib is appropriate (Nguyen VP and Kobashigawa JA, 2020; Colvin MM, et al. 2015).

The core strategies for managing antibody-mediated rejection (AMR) focus on eliminating circulating alloantibodies, inhibiting further alloantibody production, and dampening both T-cell and B-cell activity. No large-scale randomized trials have been conducted to assess AMR therapies specifically in heart transplant patients (Colvin MM, et al. 2015).This table, adapted from the 2015 scientific statement from the American Heart Association (Colvin MM, et al. 2015), summarizes the immune component affected by each therapy.

F · correct

This represents a valid option.Given the patient’s moderate to severe antibody-mediated rejection, indicated by the Molecular Microscope Diagnostic System (MMDx), impaired hemodynamics, and decreased ejection fraction, the initiation of IVIG, IV methylprednisolone, plasmapheresis, and bortezomib is appropriate (Nguyen VP and Kobashigawa JA, 2020; Colvin MM, et al. 2015).

The core strategies for managing antibody-mediated rejection (AMR) focus on eliminating circulating alloantibodies, inhibiting further alloantibody production, and dampening both T-cell and B-cell activity. Currently, no large-scale randomized trials have been conducted to assess AMR therapies specifically in heart transplant patients (Colvin MM, et al. 2015).This table, adapted from the 2015 scientific statement from the American Heart Association (Colvin MM, et al.2015), provides a summary of the immune component affected by each therapy.

G · correct

This represents a valid option.Given the patient’s moderate to severe antibody-mediated rejection, indicated by the Molecular Microscope Diagnostic System (MMDx), impaired hemodynamics, and decreased ejection fraction, the initiation of IVIG, IV methylprednisolone, and rituximab is appropriate (Nguyen VP and Kobashigawa JA, 2020; Colvin MM, et al. 2015).

The core strategies for managing antibody-mediated rejection (AMR) focus on eliminating circulating alloantibodies, inhibiting further alloantibody production, and dampening both T-cell and B-cell activity. Currently, no large-scale randomized trials have been conducted to assess AMR therapies specifically in heart transplant patients (Colvin MM, et al. 2015).This table, adapted from the 2015 scientific statement from the American Heart Association (Colvin MM, et al. 2015), provides a summary of the immune component affected by each therapy.

Review the other options

Case · Next steps

What follows the treatment.

The orders that follow treatment.

  • 01Medication adherence. This represents a valid option. Non-adherence to medications, as evidenced by the skipped doses of fluconazole, has directly contributed to subtherapeutic tacrolimus levels, increasing the risk of rejection and graft dysfunction. Ensuring strict adherence to the prescribed regimen, including antifungals, is critical to maintaining therapeutic drug levels and preventing further complications (Velleca A, et al. 2022).
  • 02Follow-up EMB Biopsy with MMDx monitoring. It is appropriate to order follow-up testing with MMDx. / MMDx provides molecular insights into rejection severity and evaluation of response to treatment (Halloran & Madill-Thomsen, 2022). Regular follow-up testing ensures timely adjustments to the immunosuppressive regimen and helps prevent further graft injury. ISHLT 2022 guidelines advise routine surveillance with dd-cfDNA or GEP alongside biopsy in the first year post-transplant, and selectively thereafter when clinical or immunologic risk is high (Velleca A, et al. 2022).
  • 03Post-transplant monitoring. It is appropriate to schedule a follow-up appointment for monitoring. / Follow-up appointments are typically scheduled every 7 to 10 days during the initial month post-transplant, every 2 weeks during the second month, monthly throughout the first year, and then every 3 to 6 months for long-term monitoring. A multidisciplinary team should provide follow-up for heart transplant recipients, and the purpose of the follow-up visits is to monitor for rejection and screen for adverse events (Velleca A, et al. 2022).

Case · Takeaways

Histology alone would have undertreated her.

Julia R. is a 50-year-old female who underwent a heart transplant 6 weeks ago for familial cardiomyopathy. Initially, she experienced stable graft function without signs of rejection. However, at this visit, she presents with progressive fatigue, dyspnea, reduced ejection fraction, and evidence of AMR.

The combination of reduced graft function and antibody-mediated injury underscores the value of donor-derived cell-free DNA (dd-cfDNA) as a non-invasive biomarker of graft injury, capable of detecting rejection earlier than histology (Agbor-Enoh S, et al. 2021).

While the biopsy findings indicate mild rejection (grade 1R, pAMR1), MMDx findings suggest a more pronounced antibody-mediated process. This highlights the value of integrating molecular diagnostics alongside traditional histopathology to provide a more comprehensive assessment of graft health. Discordance between histology and molecular diagnostics is common; MMDx rejection categories correlate more strongly with parenchymal injury and survival than conventional grading (Halloran & Madill-Thomsen, 2022; Halloran PF, et al. 2024).Without the Molecular Microscope Diagnostic System (MMDx), this case might have been classified and treated as grade 1 AMR (mild AMR) based on traditional biopsy findings, which reported mild AMR (grade 1) and mild ACR (grade 1). Histopathology’s estimate of rejection severity could have resulted in a more conservative treatment plan, as mild AMR is often managed with adjustments to maintenance immunosuppression rather than more aggressive interventions. However, MMDx suggested a more advanced process of moderate to severe AMR,. This finding led to a shift in management toward high-dose IV corticosteroids, IVIg, and targeted B-cell or plasma cell-directed therapies (such as rituximab or bortezomib) to effectively control the rejection, prevent further alloantibody production, and mitigate progressive graft injury (Halloran PF, et al. 2024; Nguyen VP, et al. 2020; Colvin MM, et al. 2015). By redefining the rejection severity, MMDx prevented therapeutic delay and reduced the risk of undertreatment that could have led to chronic rejection and graft loss (Halloran PF, et al. 2024; Halloran & Madill-Thomsen, 2022).

The case underscores the critical role of molecular diagnostics in accurately identifying the severity of AMR, preventing undertreatment, and guiding more precise and effective therapeutic strategies.Given the impact of missed fluconazole doses on tacrolimus levels and graft function, medication adherence should also be reinforced (Velleca A, et al. 2022). Regular follow-up with histology, MMDx, echocardiography, and laboratory monitoring will ensure a multifaceted and integrated approach to optimizing graft health. ISHLT 2022 guidelines recommend incorporating dd-cfDNA or GEP alongside biopsy in the first year, and selectively thereafter when immunologic risk is high (Velleca A, et al. 2022).

According to ISHLT 2023, this case highlights the evolving standard of care: integrating histology, molecular diagnostics (MMDx), donor-derived cfDNA, imaging, and biomarkers provides the most reliable framework for guiding AMR management and optimizing long-term graft survival (Kobashigawa J, et al. 2023).

Explore more cases at Expert’s Corner

The case · Julia Rhistology, molecules and cell-free DNA

The case 50-year-old, six weeks after heart transplant

  • −6 wkOrthotopic heart transplantation for familial cardiomyopathy. Tacrolimus, MMF and prednisone; antifungal prophylaxis.
  • −2 moWeight 68 kg.
  • TodayFatigue, dyspnoea on exertion, weight 78 kg, jugular venous distension, +1 peripheral oedema, bibasilar crackles, S4.

Key results today

  • MMDxModerate to severeantibody-mediated rejection
  • Endomyocardial biopsyGrade 1R, pAMR1mild by histology
  • Donor-derived cf-DNA0.40%
  • Tacrolimus trough4 ng/mLtarget 8–12 ng/mL
  • Donor-specific antibodies6 detectedMFI 8800 to 12 000
References 10
  1. Agbor-Enoh S, Shah P, Tunc I, et al; GRAfT Investigators. Cell-Free DNA to Detect Heart Allograft Acute Rejection. Circulation. 2021;143(12):1184-1197.
  2. Colvin MM, Cook JL, Chang P, et al. Antibody-mediated rejection in cardiac transplantation: emerging knowledge in diagnosis and management: a scientific statement from the American Heart Association. Circulation. 2015;131(18):1608–39.
  3. Fatly ZA, Betjes MGH, van Gestel J, et al. The burden of gastrointestinal complaints in kidney transplant recipients using tacrolimus with and without mycophenolate mofetil: a randomized controlled study. Front Nephrol. 2022;2:933954.
  4. Halloran PF, Madill-Thomsen KS, Aliabadi-Zuckermann AZ, et al. Redefining the molecular rejection states in 3230 heart transplant biopsies: Relationships to parenchymal injury and graft survival. Am J Transplant. 2024;24(8):1414–26.
  5. Halloran PF, Madill-Thomsen KS. Donor-derived cell-free DNA: A step forward in the quest for Transplant Truth. Transplantation. 2025.
  6. Halloran PF, Madill-Thomsen KS. The Molecular Microscope Diagnostic System: Assessment of rejection and injury in heart transplant biopsies. Transplantation. 2022;107(1):27–44.
  7. Kobashigawa J, Zuckermann A, Zeevi A, et al. The International Society for Heart and Lung Transplantation Guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2023;42(10):1192–134.
  8. Nguyen VP, Kobashigawa JA. Antibody-medicated rejection after heart transplantation: diagnosis and clinical implications. Curr Opin Organ Transplant. 2020;25(3):248–54.
  9. Parkes MD, Aliabadi AZ, Cadeiras M, et al. An integrated molecular diagnostic report for heart transplant biopsies using an ensemble of diagnostic algorithms. J Heart Lung Transplant. 2019;38(6):636–46.
  10. Velleca A, Shullo MA, Dhital K, et al. The International Society for Heart and Lung Transplantation (ISHLT) guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2022;42(5):e1–141.
Age
50 years
Weight
78 kg
Height
172 cm
BMI
26.4