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Several groups of drugs slow conduction through the heart, without actually preventing an arrhythmia. These drugs can be used to "rate control" a fast rhythm and make it physically tolerable for the patient. [citation needed] Some arrhythmias promote blood clotting within the heart and increase the risk of embolus and stroke.
Two distinct drug classes in which cardiotoxicity can occur are in anti-cancer and antiarrhythmic drugs. Anti-cancer drug classes that cause cardiotoxicity include anthracyclines, monoclonal antibodies, and antimetabolites. This form generally manifests as a progressive form of heart failure, but can also manifest as an harmful arrhythmia. [2]
The initial classification system had 4 classes, although their definitions different from the modern classification. Those proposed in 1970 were: [2] Drugs with a direct membrane action: the prototype was quinidine, and lignocaine was a key example. Differing from other authors, Vaughan-Williams describe the main action as a slowing of the ...
Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic drugs, as well as drugs for other indications. In other words, it is a tendency of antiarrhythmic drugs to ...
[1] [5] People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) and/or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). [1] [2] Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease. [5] [1]
Most patients with drug-induced QT prolongation are asymptomatic and are diagnosed solely by EKG in association with a history of using medications known to cause QT prolongation. [6] A minority of patients are symptomatic and typically present with one or more signs of arrhythmia, such as lightheadedness, syncope, or palpitations. [6]
Potassium channel blockers exhibit reverse use-dependent prolongation of the action potential duration. Reverse use dependence is the effect where the efficacy of the drug is reduced after repeated use of the tissue. [11] This contrasts with (ordinary) use dependence, where the efficacy of the drug is increased after repeated use of the tissue.
The most common underlying causes are different, depending on the patient's age. Common cardiac causes include coronary artery disease, non-atherosclerotic coronary artery abnormalities, structural heart damage, and inherited arrhythmias. Common non-cardiac causes include respiratory arrest, diabetes, medications, and trauma.
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