In the cardio-oncology population, drug interactions are of particular importance given the complex pharmacological profile, narrow therapeutic index, and inherent risk of therapies used to manage cardiovascular disease and cancer. Drug interactions may be beneficial or detrimental to the desired therapeutic effect. Clinicians in both cardiology and oncology should be cognizant of these potential drug-drug interactions that may reduce the efficacy or safety of either cardiovascular or cancer therapies. These risks can be mitigated through increased recognition of potential drug-drug interaction, use of alternative medications when possible, and careful monitoring. This scientific statement provides clinicians with an overview of pharmacodynamic and pharmacokinetic drug-drug interactions in patients with cancer exposed to common cardiovascular and cancer medications. 

Cardio-Oncology Drug Interactions: A Scientific Statement From the American Heart Association

Immune checkpoint inhibitor (ICI) induced myocarditis is a rare, severe, and often fatal adverse event. Evidence to guide appropriate immunosuppressive therapy is scarce. We present a case of ICI-induced myocarditis and a review of ICI-induced myocarditis cases to determine the most effective immunosuppressive therapeutic strategy for ICI-induced myocarditis. A systematic search of PubMed was carried out for treatment of ICI-induced myocarditis. Reference lists from identified articles were manually reviewed for additional cases. A total of 87 cases with ICI-induced myocarditis were identified. The majority were melanoma (n = 39), lung cancer (n = 19), renal cell cancer (n = 10), and thymoma cancer patients (n = 4). In 38 (44%) cases, patients received high-dose steroid treatment only. A total of 49 (56%) cases were treated with immunosuppressive agents other than steroid; a total of 13 different immunosuppressive agents were used, including alemtuzumab or abatacept. The median time to onset of symptoms after initiation of ICI was 16 days (range, 1–196 days); cardiotoxic symptoms developed after 2 cycles of ICI (range, 1–13 cycles). A total of 48% of cases were fatal. In cases treated with high-dose steroids only vs. cases treated with other immunosuppressive agents, fatality was 55% and 43% respectively. In 64 out of the 87 cases, tumor control was not described. In patients treated with high-dose steroids only, two patients had stable disease as best tumor response; in patients treated with other immunosuppressive agents, one complete response, one partial response and seven stable disease were noted as best tumor response. Overall, 11 studies were at low risk of bias (12.6%), 38 at moderate risk of bias (43.7%) and 38 at high risk of bias (43.7%). Immune checkpoint inhibitor induced myocarditis is a serious and often fatal adverse event. High-dose prednisolone, alemtuzumab or abatacept are all possible treatments options for ICI-induced myocarditis, whereas infliximab increases the risk of death from cardiovascular causes, and should be avoided. Further research is needed.

/pdf/immune-checkpoint-inhibitor-induced-myocarditis-in-cancer-1tpg63b470.pdf

Immune checkpoint inhibitor-induced myocarditis in cancer patients: a case report and review of reported cases.

Cardiovascular adverse events induced by immune checkpoint inhibitors (ICIs) have gained significant interest over the past decade due to their impact on short- and long-term outcomes. They were initially thought to be rare, but the increasing use of ICIs in the treatment of both advanced and early stages of various malignancies has resulted in a substantial increase in their incidence. Different guidelines have proposed screening measures for ICI-induced myocarditis by incorporating troponin measurements at baseline and during the first few weeks of treatment. However, no specific guidelines have been developed yet regarding the interpretation of an asymptomatic rise in troponins. This state-of-the art review aims to provide an overview of the clinical relevance of elevated troponins during checkpoint inhibition and recommendations on how to manage elevated troponin levels during ICI therapy.

Clinical implications of isolated troponinemia following immune checkpoint inhibitor therapy.

Myocarditis associated with the use of immune checkpoint inhibitors (ICI) is a rare manifestation of their cardiotoxicity, but is characterized by a high mortality rate. A literature search was conducted using PubMed using keywords, which resulted in the selection of 679 scientific works, from which 160 articles that described 244 clinical cases were selected. The median age of the patients was 67 years (IQR, 60–74). The median time from the start of ICI therapy to the development of the first adverse symptoms was 21 days (IQR, 14–38.3). In 37% of cases, myocarditis developed after the first administration of ICI. Cardiac symptoms were present in 47.1% of cases, neuromuscular symptoms in 30.3%, and other symptoms in 12.6%, while myocarditis was asymptomatic in 10.1% of cases. New changes in the electrocardiograms were detected in 85.1% of patients compared to the initial data. A high incidence of complete atrioventricular block (25.4%), right bundle branch block (18.4%), ventricular tachycardia (13%), and sinus tachycardia (12%) were noted. In 97% of the cases, the patients received prednisolone or methylprednisolone therapy. When using ICI, special attention should be paid to the early detection of possible cardiotoxicity by analyzing the condition and function of the myocardium before treatment and its dynamics.

/pdf/immune-checkpoint-inhibitors-related-myocarditis-a-review-of-1vrd8z0g.pdf

Immune Checkpoint Inhibitors-Related Myocarditis: A Review of Reported Clinical Cases

Immune checkpoint inhibitors (ICIs) induce T-cell activation against cancer cells, and due to their anti-tumor function in multiple cancers, ICIs have been considered an important option for oncotherapy. PD-1/PD-L1 inhibitors are now widely used as ICIs for many types of cancers in clinical practices. Myocarditis induced by anti-PD-1/PD-L1 agents is uncommon but shows potentially fatal toxicity. In this review, we attempted to conclude the incidence, characteristics, diagnosis, and treatments, as well as illustrate the potential pathogenesis from the perspectives of T-lymphocyte infiltration, disturbance of regulatory T cells, cytokines, macrophage-mediated inflammatory response, and synergistic effect of PD-1/PD-L1 and CTLA4.

PD-1/PD-L1 Inhibitor-Associated Myocarditis: Epidemiology, Characteristics, Diagnosis, Treatment, and Potential Mechanism

Pulmonary Hypertension (PHT) and Pleural Effusion During Dasatinib Therapy For CML Frequently Lead To Drug Withdrawal

https://minerva-access.unimelb.edu.au/bitstream/handle/11343/231008/Guo et al 2019.pdf

A closer look at immune-mediated myocarditis in the era of combined checkpoint blockade and targeted therapies.

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Pulmonary Hypertension (PHT) and Pleural Effusion During Dasatinib Therapy For CML Frequently Lead To Drug Withdrawal

A closer look at immune-mediated myocarditis in the era of combined checkpoint blockade and targeted therapies.