Short Communication - (2022) Volume 6, Issue 6
Received: 01-Nov-2022, Manuscript No. jigc-23-86911;
Editor assigned: 03-Nov-2022, Pre QC No. P-86911;
Reviewed: 15-Nov-2022, QC No. Q-86911;
Revised: 21-Nov-2022, Manuscript No. R-86911;
Published:
28-Nov-2022
, DOI: 10.37421/2684-4591.2022.6.171
Citation: Anderson, Briana. “Specific Symptoms of Acute Cardio Toxicity.” J Interv Gen Cardiol 6 (2022): 171.
Copyright: © 2022 Anderson B. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Due to the cardio toxicity of anticancer drugs, patients receiving treatment for various cancers may experience serious side effects. A few of the factors that influence the severity of this toxicity include the patient's demographics, the molecular site of action, the immediate and cumulative dose, the mode of administration, the presence of any underlying cardiac conditions, and the molecular site of action. Toxicity may also have been affected by previous or current treatment with other antineoplastic drugs. Cardio toxic side effects may manifest immediately following drug administration or may take months or years to manifest after treatment has been administered. In this article, we investigate the likelihood of cardio toxicity in a number of recently approved and frequently used chemotherapy agents. More research will be required to pinpoint the individuals most at risk for cardio toxicity. Additionally, management plans and strategies for reducing cardio toxicity must be established [1].
The treatment of cancer has come a long way in recent years, and many types of cancer's morbidity and mortality have been reduced significantly. Like diabetes and hypertension, early detection, regular monitoring, and coordinated therapeutic decision-making may be used to manage cancer. For cancer survivors, therefore, limiting concurrent conditions is essential. For many cancer survivors, the risk of developing heart disease is actually the same as the risk of developing recurrent cancer. Alternative treatments for cancer patients today include more advanced drug regimens, radiation therapy, and surgical procedures. Several of these treatments, many of which have significant potential adverse cardiac effects, are likely to have a significant impact on patients' outcomes. Recognizing these consequences is therefore essential for effective management. The goal of this review is to highlight the cardiovascular side effects of common cancer treatments [2].
Each chemotherapeutic drug has distinct cardiac effects and the ability to amplify other drugs' adverse effects. Radiation therapy is yet another significant factor in accelerating damage. It is essential to keep in mind that intensively treated cancer patients frequently suffer from severe conditions, and correlations between events are frequently ambiguous. Therefore, in this review, we attempt to summarize the current state of knowledge regarding the cardiovascular side effects of cancer therapy using a review of the literature and the extensive clinical expertise of the Department of Cardiology at The University of Texas M.D. Anderson Cancer Center.
Both preclinical and clinical events may indicate cardiovascular disease. Preclinical toxicity can be detected using biochemical or histopathological techniques. For instance, endomyocardial biopsy specimens may reveal doxorubicin-induced myocardial damage without necessarily raising troponin T or I protein levels. The grading system that the World Health Organization proposed in 1981 to standardize the reporting of medication side effects does not take into account laboratory cardiovascular abnormalities. All significant clinical and laboratory abnormalities are taken into account by the National Cancer Institute's more comprehensive common toxicity criteria [3].
Anthracyclines are the anticancer medications that have the most research behind them and are known to cause cardiotoxicity. The anthracyclines doxorubicin, daunorubicin, and epirubicin, which have received approval from the Food and Drug Administration, are used to treat numerous hematologic and solid cancers. Acute cardiotoxicity is characterized by nonspecific ST-segment and T-wave abnormalities. Contrary to the effects that occur in the early stages, late anthracycline cardiotoxicity progresses over time, is dose-dependent, and, at sufficiently high doses, can result in congestive heart failure (CHF) and left ventricular dysfunction. Direct myocardial damage is thought to be caused by the production of free radicals. Cardiomyopathy occurs significantly more frequently in people who receive doses of doxorubicin greater than 550 mg/ m2. However, more recent studies have shown that similar cardiomyopathy can be caused by smaller doses taken in combination. Early diagnosis and treatment can significantly improve the grim prognosis, despite the fact that it has been hypothesized that the mortality rate among individuals who actually experience late cardiotoxicity is high. Mitoxantrone, a derivative of anthracyclines, has the potential to cause moderate cardiotoxicity in the same way that anthracyclines [4].
The cardiotoxicity of a drug is influenced by a number of factors that are particular to the drug and to each patient. Understanding these factors may reduce the frequency or severity of cardiovascular effects. The dose that is given in each session, the cumulative dose, the delivery schedule, the mode of administration, the combination of drugs that are given, and the order in which these drugs are given are all important aspects of medication that need to be taken into consideration. Patient-related factors also include age, previous cardiovascular disease, radiation therapy, metabolic disorders, and medication hypersensitivity. Knowing the risk factors for circulatory complications caused by chemotherapy can make it easier to focus prevention efforts on reducing cardiotoxicity [5].
High doses of certain chemotherapy drugs only result in cardiotoxicity; CHF and pericarditis with platinum drugs, atrial fibrillation with melphalan, systolic dysfunction with pericarditis with cyclophosphamide, and LV dysfunction with anthracyclines are all examples. At doses of 10 to 18 g/ m2, ifosfamide causes CHF, but only for five days at doses of 1.2 to 2 g/ m2. Busulfan causes tachyarrhythmias, hypertension or hypotension, and LV dysfunction when given intravenously, but not when taken orally. Cardiotoxicity can be reduced by changing the order in which medications are administered. For instance, compared to administering interferon and IL-2 simultaneously for the first two weeks, administering interferon alone caused significantly less cardiovascular damage. The combination of paclitaxel and doxorubicin caused CHF in 20% of cases when there was a gap of 15 to 30 minutes between the two drugs. However, the cardiotoxicity of this combination decreased when there was a gap of 4 to 16 hours.
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Journal of Interventional and General Cardiology received 11 citations as per Google Scholar report
