Cardiac magnetic resonance imaging in heart transplant recipients with biopsy-negative graft dysfunction.

AIMS: Graft dysfunction (GD) after heart transplantation (HTx) can develop without evidence of cell- or antibody-mediated rejection. Cardiac magnetic resonance imaging (CMR) has an evolving role in detecting rejection; however, its role in biopsy-negative GD has not been described. This study examines CMR findings, evaluates outcomes based on CMR results, and seeks to identify the possibility of rejection missed through endomyocardial biopsy by using CMR in HTx recipients with biopsy-negative GD. METHODS AND RESULTS: HTx recipients with GD [defined as a decrease in left ventricular ejection fraction (LVEF) by >5% and LVEF < 50%] in the absence of rejection by biopsy or allograft vasculopathy and who underwent CMR were included in the study. The primary outcome was a composite of all-cause mortality, re-transplantation, or persistent LVEF < 50%. Overall, 34 HTx recipients developed biopsy-negative GD and underwent CMR. Left ventricular late gadolinium enhancement (LGE) on CMR was observed in 16 patients with two distinct patterns: diffuse epicardial (n = 13) and patchy (n = 3) patterns. Patients with LGE developed GD later after HTx [4 (1.4-6.8) vs. 0.8 (0.3-1.2) years, P < 0.001], were more often symptomatic (88% vs. 56%, P = 0.06), and had greater haemodynamic derangement (pulmonary capillary wedge pressure: 19 ± 7 vs. 13 ± 3 mmHg, P = 0.002) as compared with those without LGE. No significant difference was observed in the primary composite outcome between patients with LGE and those without LGE (50% vs. 38% of patients with events, P = 0.515). During a median follow-up of 3.8 years, mean LVEF improved similarly in the LGE-negative (37-55%) and LGE-positive groups (32-55%) (P = 0.16). CONCLUSIONS: Biopsy-negative GD occurs with and without LGE when assessed by CMR, indicative of possible rejection/inflammation occurring only in a subset of patients. Irrespective of LGE, LVEF improvement occurs in most GD patients, suggesting that other neurohormonal or immunomodulatory mechanisms may also contribute to GD development.

Successful Treatment of Steroid-Refractory Checkpoint Inhibitor Myocarditis with Globulin Derived-Therapy: A Case Report and Literature Review.

Immune checkpoint inhibitor (ICI) monoclonal antibody drugs are an important interface of immunology and cancer biology with the intended goal to create cancer specific treatments with less systemic toxicity. Recognition of immune-related adverse events is critical and these include significant cardiovascular toxicity and myocarditis. Compared with other immune-related events, ICI associated myocarditis is rare but is associated with high mortality. The majority of cases present early in the course of therapy and patients can rapidly progress to fulminant myocarditis. Initially, the mainstay of treatment in patients with ICI-associated myocarditis is immunosuppressive therapy with glucocorticoids. For those who do not respond to steroids, the optimal treatment is unclear. This review summarizes the potential adjunctive treatment options for patients with steroid-refractory myocarditis by illustrating a case of myocarditis that was treated with Thymoglobulin and immunoglobulin.

Cardiac Transplantation and Consecutive Minimally Invasive Pectus Excavatum Repair.

Pectus excavatum is a common chest wall deformity with inward deviation of sternum and accompanying ribs. The depression can cause symptomatic cardiac compression, although the cardiopulmonary impact remains controversial. We present 2 cases of cardiac transplantation followed by modified minimally invasive pectus excavatum repair due to the hemodynamic consequences of the pectus deformity.

Heart Failure in Adult Congenital Heart Disease: Nonpharmacologic Treatment Strategies.

In early stages, heart failure (HF) in adult congenital heart disease (ACHD) remains an elusive diagnosis. Many ACHD patients seem well-compensated owing to chronic physical and psychological adaptations. HF biomarkers and cardiopulmonary exercise tests are often markedly abnormal, although patients report stable health and good quality of life. Treatment differs from acquired HF. Evidence for effective drug therapy in ACHD-related HF is lacking. Residual ventricular, valvular, and vascular abnormalities contribute to HF pathophysiology, leading to an emphasis on nonpharmacologic treatment strategies. This article reviews emerging perspectives on nonpharmacologic treatment strategies, including catheter-based interventions, surgical correction, and palliative care.

Palliative care and hospice in advanced heart failure.

Advanced heart failure (HF) is a disease process that carries a high burden of symptoms, suffering, and death. Palliative care can complement traditional care to improve symptom amelioration, patient-caregiver communication, emotional support, and medical decision making. Despite a growing body of evidence supporting the integration of palliative care into the overall care of patients with HF and some recent evidence of increased use, palliative therapies remain underused in the treatment of advanced HF. Review of the literature reveals that although barriers to integrating palliative care are not fully understood, difficult prognostication combined with caregiver inexperience with end-of-life issues specific to advanced HF is likely to contribute. In this review, we have outlined the general need for palliative care in advanced HF, detailed how palliative measures can be integrated into the care of those having this disease, and explored end-of-life issues specific to these patients.

Wound healing after trauma may predispose to lung cancer metastasis: review of potential mechanisms.

Inflammatory oncotaxis, the phenomenon in which mechanically injured tissues are predisposed to cancer metastases, has been reported for a number of tumor types, but not previously for histologically proven lung cancer. We review clinical and experimental evidence and mechanisms that may underlie inflammatory oncotaxis, and provide illustrative examples of two patients with squamous cell carcinoma of the lung who developed distant, localized metastatic disease at sites of recent physical trauma. Trauma may predispose to metastasis through two distinct, but not mutually exclusive, mechanisms: (1) physical trauma induces tissue damage and local inflammation, creating a favorable environment that is permissive for seeding of metastatic cells from distant sites; and/or (2) micrometastatic foci are already present at the time of physical injury, and trauma initiates changes in the microenvironment that stimulate the proliferation of the metastatic cells. Further exploration of post-traumatic inflammatory oncotaxis may elucidate fundamental mechanisms of metastasis and could provide novel strategies to prevent cancer metastasis.