Drug-Induced Cardiomyopathies

Klimas, Ján

doi:10.5772/29349

Cited by 5 publications

(10 citation statements)

References 197 publications

(218 reference statements)

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“…Negative effects of anthracyclines have influence on many organs and systems, significant alterations are usually connected with gastro-intestinal, hemopoetic and cardiovascular systems. Due to the fact that most oncology patients are geriatric, predispose to pay more attention to myocardium condition (Klimas, 2012;Takemura and Fujiwara, 2007).…”

Section: Introductionmentioning

confidence: 99%

Metabolic Features of Heart Failure with Different Etiology

Arkadievich¹

2017

American Journal of Animal and Veterinary Sciences

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Dilated Cardiomyopathy (DCM) and Chronical Degenerative Valvular Disease (CDVD) are very common in dogs nowadays. However, due to modern level in oncology we can meet chemotherapy-induced cardiomyopathies more often. We have lack of information about pathogenic mechanisms underlying Doxorubicin-induced Cardiomyopathy (DoxCM) and features differentiating it from CDVD and DCM. In this study we investigate several metabolic features of doxorubicin-induced cardiomyopathy, DCM-like phenotype cardiomyopathies and CDVD. We observed some stages of myocardium glucose metabolism in order to estimate life potential of end stage myocardium and respectively survival of patient. The study population consisted of 46 dogs of different age, sex and breed. These dogs were subgrouped due to diagnosis: Healthy dogs without heart failure, DCM, CDVD and DoxCM. Fresh myocardial biopsies taken immediately after euthanasia from left ventricular apex, freezed in liquid nitrogen for ELISA and biochemical study. Differences in metabolic profile found between of CDVD and healthy dogs were not significant. At the same time doxorubicin induced cardiomyopathy and DCM-like phenotype myocardial disease had similar changes. It should be mentioned, DCM patients had previously long history of treatment, but DoxCM group-not. Differences between DoxCM, DCM and CDVD were significant and can be explained by changes what suffering myocardium undergoes. Rapid or slow developing energy depletion leads to myocardiocytes death and heart failure. Doxorubicin-induced cardiomyopathy is far more dangerous due to rapidness of development in observed study. Myocardium, due to lack of time, had no adapting ability for acute energy depletion and massive cell death. This preliminary study shows changes induced by doxorubicin (Dox) in dogs. These findings mostly connected with mitochondrial disturbances, insulin resistance and energy depletion. In this study also shown several features connected with development of CDVD and differences from DCM.

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Section: Introductionmentioning

confidence: 99%

Metabolic Features of Heart Failure with Different Etiology

Arkadievich¹

2017

American Journal of Animal and Veterinary Sciences

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“…The active metabolite of cyclophosphamide is responsible for anticancer activity 24 . However, cardiomyopathy which is likely to be diagnosed within 2 weeks of therapy is reported as a side effect 4 . Cardiotoxicity of cyclophosphamide is due to the effect of toxic metabolite on endothelial cells that causes severe myopericarditis and myocardial necrosis 25 .…”

Section: Cyclophosphamide and Cardiotoxicitymentioning

confidence: 99%

“…Inappropriate use of anabolic steroid is associated with left ventricular hypertrophy 94 . Anabolic steroid when administered, binds with androgenic receptors in the heart and in arteries 4 . Anabolic steroid causes hypertension, dyslipidemia atherosclerosis and impaired contraction-relaxation 95 .…”

Section: Anabolic -Androgenic Steroids and Cardio-toxicitymentioning

confidence: 99%

“…(1) Drugs causing cardiac injury by affecting the performance of cardiac muscles. (2) By altering the ion channels and pump (voltage-gated sodium and potassium ion channel and Na-K ATPase pump) 4 . Exposure to the cardiac-toxic drugs induces prolong cardiac repolarization (QT interval) and causes arrhythmia (Torsades de pointes) 4 .…”

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confidence: 99%

“…(2) By altering the ion channels and pump (voltage-gated sodium and potassium ion channel and Na-K ATPase pump) 4 . Exposure to the cardiac-toxic drugs induces prolong cardiac repolarization (QT interval) and causes arrhythmia (Torsades de pointes) 4 . Since these drugs causes cardiotoxicity as side effect, they can be used as cardiotoxicity inducing agents in preclinical experimental models 6 .…”

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confidence: 99%

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Untitled

2018

IJPSR

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Cardiotoxicity associated with the clinically used drugs is a global concern of safety for healthcare professionals. Various animal models have been used to study the drug-induced cardiotoxicity but the exact molecular involvement of toxicity is not much clear. Despite the recurrent occurrence of toxicities, drugs such as doxorubicin, calcium channel blockers, antiarrhythmics and immunomodulators are regularly used. Anticancer drugs mainly anthracyclines, 5-fluorouracil and cyclophosphamide exert prominent cardiotoxicity. Till date, there is only one drug approved for doxorubicin-related cardiotoxicity i.e. dexrazoxane. Few other drugs are used routinely by clinicians to reduce the severity of toxicity which includes ACE inhibitors, L-carnitine, probucol, CoQ 10 , N-acetylcysteine, Vitamin E and deferoxamine, whereas antidepressants drugs, specifically tricyclic antidepressants are potential candidates for cardiotoxicity. Calcium channel blockers, antiarrhythmic and beta receptor antagonist aggravate cardiac heart failure (CHF) and left ventricular arrhythmia. Interferons, mainly interferon-α is also associated with prominent and dose-dependant toxicity. Some other drugs like zidovudine, chloroquine, cocaine, minoxidil, ketoconazole, prostaglandin E2 and anagrelide are also reported to have cardiotoxic effects. A complication associated with the use of these drugs include hypoxia, coronary ischemia, calcium overload, oxidative stress, contractile dysfunction, left ventricular arrhythmia and cardiomyopathy.

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Oxidative Stress and Cocaine Intoxication as Start Points in the Pathology of Cocaine-Induced Cardiotoxicity. A Systematic Review

Georgieva

Karamalakova

Nikolova

2021

Preprint

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Background: Psychomotor stimulants are the most commonly used prohibited substances after cannabis. Globally, their use reaching epidemiological proportions and is one of the most common causes of death in many countries. In recent years, more research, define drug use as the leading cause of serious cardiovascular pathologies ranging from abnormal heart rhythms to heart attack and sudden cardiac death. The reactive oxygen species generation, toxic metabolites formation and oxidative stress play a significant role in cocaine-induced cardiotoxicity. Main body: In the present review, we discuss various studies related to dopamine neurotransmission and oxidative stress, with a focus on the cardiotoxicity of the cocaine molecule and the cardiovascular complications that occur after cocaine use. Conclusion: Hypothetically, this study can serve as a basis for developing a rapid and effective method for determining oxidative stress levels by monitoring changes in the redox status of patients with cocaine intoxication.

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Drug-Induced Cardiomyopathies

Cited by 5 publications

References 197 publications

Metabolic Features of Heart Failure with Different Etiology

Metabolic Features of Heart Failure with Different Etiology

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Oxidative Stress and Cocaine Intoxication as Start Points in the Pathology of Cocaine-Induced Cardiotoxicity. A Systematic Review

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