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These studies suggest that heart drugs can cause a range of side effects including cardiac toxicity, arrhythmia, and cardiovascular disease, requiring careful monitoring and management.
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Anthracyclines, a class of chemotherapy drugs, are known to cause significant cardiac toxicity. This toxicity is primarily due to oxidative stress and apoptosis, leading to heart damage. Early detection methods include 2D-echocardiography, radionuclide angiography, and newer techniques like tissue Doppler imaging and strain rate echocardiography. Preventive measures such as the use of dexrazoxane have shown effectiveness in reducing dose-related toxicity in both children and adults.
High doses of alkylating agents like cyclophosphamide and ifosfamide can result in reversible heart failure and life-threatening arrhythmias. These drugs are particularly risky for patients with pre-existing cardiovascular conditions.
Antimetabolites such as 5-fluorouracil and capecitabine can induce myocardial ischemia, especially in patients with prior coronary artery disease (CAD). This can significantly impact the prognosis of these patients.
Targeted therapies, including tyrosine kinase inhibitors (TKIs) like trastuzumab, alemtuzumab, and sunitinib, have been associated with heart failure and left ventricular (LV) dysfunction. These side effects can range from asymptomatic to severe, necessitating careful cardiac monitoring during treatment .
Tyrosine kinase inhibitors (TKIs) such as imatinib mesylate, dasatinib, nilotinib, and sunitinib have been linked to cardiac toxicity. This can manifest as electrocardiographic changes, left ventricular ejection fraction decline, congestive heart failure, and acute coronary syndromes. Continuous cardiac monitoring is crucial for patients undergoing treatment with these drugs.
The cardiotoxic effects of TKIs are believed to be due to their impact on cardiac electrophysiology and mitochondrial function. These effects can lead to severe and sometimes irreversible cardiac dysfunction.
Atypical antipsychotic medications, including risperidone and olanzapine, are associated with increased cardiovascular disease risk. These drugs can cause obesity, insulin resistance, dyslipidemia, and hypertension, which collectively elevate the risk of adverse cardiac outcomes. Proteomic studies in mice have shown that these medications alter cardiac mitochondrial function and oxygen consumption, contributing to their cardiotoxic effects.
Tricyclic antidepressants (TCAs) and some antipsychotic agents are linked with prolongation of the QT interval on the electrocardiogram (ECG), which can lead to the arrhythmia torsades de pointes (TdP) and sudden death. This is primarily due to the inhibition of potassium channels encoded by HERG.
Non-aspirin NSAIDs are associated with serious cardiovascular side effects, including hypertension, edema, heart failure, myocardial infarction, and stroke. These risks have led to a general "black box" warning for cardiovascular adverse events associated with NSAIDs.
The side effects of heart drugs span a wide range of cardiovascular complications, from reversible heart failure to life-threatening arrhythmias and myocardial ischemia. Chemotherapy drugs, particularly anthracyclines and alkylating agents, pose significant risks, as do targeted therapies like tyrosine kinase inhibitors. Psychotropic medications and NSAIDs also contribute to cardiovascular morbidity. Careful monitoring and preventive strategies are essential to mitigate these risks and ensure patient safety.
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