Cancer Treatment-Associated Pericardial Disease: Epidemiology, Clinical Presentation, Diagnosis, and Management.

PURPOSE OF REVIEW: Cancer therapeutics have seen tremendous growth in the last decade and have been effective in the treatment of several cancer types. However, with advanced therapies like kinase inhibitors and immunotherapies, there have been unintended consequences of cardiotoxicities. While traditional chemotherapy and radiation-induced cardiotoxicity have been well studied, further research is needed to understand the adverse effects of newer regimens. RECENT FINDINGS: Both immune-mediated and non-immune-medicated cytotoxicity have been noted with targeted therapies such as tyrosine kinase inhibitors and immune checkpoint inhibitors. In this manuscript, we describe the pericardial syndromes associated with cancer therapies and propose management strategies. Pericardial effusion and pericarditis are common presentations in cancer patients and often difficult to diagnose. Concomitant myocarditis may also present with pericardial toxicity, especially with immunotherapies. In addition to proper history and physical, additional testing such as cardiovascular imaging and tissue histology need to be obtained as appropriate. Holding the offending oncology drug, and institution of anti-inflammatory medications, and immunosuppressants such as steroids are indicated. A high index of suspicion, use of standardized definitions, and comprehensive evaluation are needed for early identification, appropriate treatment, and better outcomes for patients with cancer treatment-associated pericardial disease. Further research is needed to understand the pathophysiology and to evaluate how the management of pericardial conditions in these patients differ from traditional management and also evaluate new therapies.

Pericardial diseases in patients with hypothyroidism.

Hypothyroidism is a well-known cause of pericardial effusion (with an incidence of 3%-37%) and can cause cardiac tamponade in severe cases. In this review, we present the current knowledge on the epidemiology of hypothyroid-induced pericardial diseases, the mechanism through which low thyroid hormone levels affect the pericardium, the associated clinical manifestations, diagnostic tests and management options. Hypothyroidism causes pericardial effusion through increased permeability of the epicardial vessels and decreased lymphatic drainage of albumin, resulting in accumulation of fluid in the pericardial space. Interestingly, autoimmunity does not seem to play a major role in the pathophysiology, and a majority of effusions are asymptomatic due to slow fluid accumulation. The diagnosis is generally made when the pericardial disease is associated with an elevated thyroid-stimulating hormone level, and other secondary causes are excluded. Management consists of thyroid replacement therapy, along with pericardial drainage in case of tamponade.In conclusion, hypothyroidism-induced pericardial diseases are underdiagnosed. Initiating treatment early in the disease process and preventing complications relies on early diagnosis through systematic screening per guidelines.

Disparity in spatial distribution of pericardial calcifications in constrictive pericarditis.

Background: Pericardial calcification is seen among patients with constrictive pericarditis (CP). However, the pattern of pericardial calcium distribution and the association with clinical outcomes and imaging data are not well described. Methods: This was a retrospective study from 2007 to 2013 to evaluate the pattern of pericardial calcium distribution by CT in CP using a semiquantitative calcium scoring system to calculate total pericardial calcium burden and distribution. Calcium localisation was allocated to 20 regions named after the corresponding heart structure. Baseline clinical data, imaging data and clinical outcomes were collected and compared between the calcified pericardium and non-calcified pericardium groups. We assessed the effect of pericardial calcium on clinical outcomes and echocardiographic data between the two groups. Results: Of the 123 consecutive patients with CP (93 male; mean age 61±13 years) between 2007 and 2013, 49 had calcified pericardium and 74 had non-calcified pericardium. Distribution of calcium on the left ventricle (LV) basal anterior, mid-anterior and apical segments in addition to right ventricle (RV) apical segment was involved in <30% of the cases with the remaining segments involved in >35% of cases. A potential protective role of RV calcium on regional myocardial mechanics was noted. Conclusion: Preferential distribution of calcium in CP in a partial band-like pattern (from basal anterolateral LV going inferiorly and then encircling the heart to reach the RV outflow tract) with extension into the mitral and tricuspid annuli was noted. Pericardial calcium was not significantly associated to clinical outcomes.