The Effect of Different Drugs on Heart Disease

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Methodology, Drug and Device Discovery".

Deadline for manuscript submissions: closed (10 April 2021) | Viewed by 6784

Special Issue Editor


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Guest Editor
Division of Cardiology, Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale, 80131 Naples, Italy
Interests: cardiovascular diseases; echocardiography; clinical and translational cardioncology; cardiotoxicity

Special Issue Information

Dear Colleagues,

Improvements in cancer survival in the past few decades have resulted in a large and growing population of long-term cancer survivors, with about half of patients diagnosed with cancer in high-income settings now expected to survive for 10 years or longer. However, significant concerns exist on the potential for increased medium- to long-term risks of cardiovascular diseases after cancer diagnosis, driven by cardiotoxic treatment effects, mechanisms directly related to cancer biology, and shared risk factors. A deeper knowledge of biochemical mechanisms of cardiotoxicity induced by anticancer drugs (chemotherapies, target therapies, and immune checkpoint inhibitors) and the study of new cardioprotective drugs are the main areas of interest in cardio-oncology in recent years.

This Special Issue aims to highlight current preclinical and clinical research activities in the areas of cardio-oncology focused on reducing cardiovascular outcomes in cancer patients.

Dr. Nicola Maurea
Guest Editor

Manuscript Submission Information

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Keywords

  • cancer
  • cancer drugs
  • oncology
  • cardiology
  • cardio-oncology
  • cardiotoxicity

Published Papers (1 paper)

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Research

19 pages, 3661 KiB  
Article
Evidences of CTLA-4 and PD-1 Blocking Agents-Induced Cardiotoxicity in Cellular and Preclinical Models
by Vincenzo Quagliariello, Margherita Passariello, Domenica Rea, Antonio Barbieri, Martina Iovine, Annamaria Bonelli, Antonietta Caronna, Gerardo Botti, Claudia De Lorenzo and Nicola Maurea
J. Pers. Med. 2020, 10(4), 179; https://0-doi-org.brum.beds.ac.uk/10.3390/jpm10040179 - 19 Oct 2020
Cited by 43 | Viewed by 6452
Abstract
Background: Several strategies based on immune checkpoint inhibitors (ICIs) have been developed for cancer therapy, opening to advantages in cancer outcomes. However, several ICI-induced side effects have emerged in these patients, especially a rare but clinically significant cardiotoxicity with high rate of mortality. [...] Read more.
Background: Several strategies based on immune checkpoint inhibitors (ICIs) have been developed for cancer therapy, opening to advantages in cancer outcomes. However, several ICI-induced side effects have emerged in these patients, especially a rare but clinically significant cardiotoxicity with high rate of mortality. We studied the cytotoxic and pro-inflammatory properties of Ipilimumab and Nivolumab, the underlying pathways and cytokine storm involved. Methods: Co-cultures of human cardiomyocytes and lymphocytes were exposed to Ipilimumab or Nivolumab; cell viability and expression of leukotrienes, NLRP3, MyD88, and p65/NF-kB were performed. C57 mice were treated with Ipilimumab (15 mg/kg); analysis of fractional shortening, ejection fraction, radial and longitudinal strain were made before and after treatments through 2D-echocardiography. Expression of NLRP3, MyD88, p65/NF-kB, and 12 cytokines were analyzed in murine myocardium. Results: Nivolumab and Ipilimumab exert effective anticancer, but also significant cardiotoxic effects in co-cultures of lymphocytes and tumor or cardiac cells. Both ICIs increased NLRP3, MyD88, and p65/NF-kB expression compared to untreated cells, however, the most pro-inflammatory and cardiotoxic effects were seen after exposure to Ipilimumab. Mice treated with Ipilimumab showed a significant decrease in fractional shortening and radial strain with respect to untreated mice, coupled with a significant increase in myocardial expression of NLRP3, MyD88, and several interleukins. Conclusions: Nivolumab and Ipilimumab exert cytotoxic effects mediated by the NLRP3/IL-1β and MyD88 pathways, leading to pro-inflammatory cytokine storm in heart tissue. Full article
(This article belongs to the Special Issue The Effect of Different Drugs on Heart Disease)
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