Druginduced myocardial damage

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Increases in cardiac troponin have been described in (1) patients treated with certain types of antineoplastic agents, (2) patients presenting to hospitals following alcohol and drug abuse, and (3) patients with therapeutic drug-induced cardiac toxicity. The release of cardiac troponin into the circulation following therapy with antineoplastic agents has been well documented (71-74). Both acute (within hours) and chronic (days to weeks) myocardial toxicity manifested by ischemia, arrhythmias, myocarditis, pericarditis, cardiomyopathy, and/or MI after dosing with the anthracyclines 5-fluorouracil, doxorubicin, and daunorubicin have been associated with minimal and large increases in cTnl. Reports have documented that a medication dose-dependent pattern of myocyte injury is responsible for increases in troponin, even without electrocardiographic or echocardiographic abnormalities. Studies have shown that in patients undergoing high-dose chemotherapy, an increase in cardiac troponin predicts the development of future left ventricular dysfunction (Table 2) (73).

Cumulative Survival

Cumulative Survival

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Follow-up (Days)

Fig. 11. Kaplan-Meier survival curves by baseline cTnT, cTnI, and hsCRP in 399 patients with ESRD. (Reproduced from ref. 106.)

0 120 240 360 480 600 720

Follow-up (Days)

Fig. 11. Kaplan-Meier survival curves by baseline cTnT, cTnI, and hsCRP in 399 patients with ESRD. (Reproduced from ref. 106.)

Several drugs of abuse have been associated with increases in cardiac troponin without evidence of ischemia. These include alcohol when heavily consumed (75), cocaine (76, 77), and amphetamines (7). Small clinical studies and case reports have documented increased cardiac troponin concentrations following CO exposure, theophylline overdose, snake bites, and during treatment with fluvastatin (7,78). Two case reports also documented an apparent propofol-induced cardiac and a skeletal muscle rhabdomyolysis; both cases resulting in fatality (79).

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