Table 1

Potential mechanisms of cardiovascular damage induced by anticancer treatments.

A summary of probable mechanisms of cardiotoxicity induced by a range of
chemotherapeutics and chemoprevention agents*

Effects

Systemic-macroenvironment

Mitochondrial Local-microenvironm

Possible Apoptotic
Examples of cardiovascular DNA ATP protein ROS Endothelial cell
chemotherapeutics damage damage block release generation damage/spasms
Anthracyclines CHF, LVD, acute + + + + −
and myocarditis,
anthraquinolones arrhythmia
Capecitabine, 5- Ischemia, + + + + +
fluorouracil, pericarditis, CHF,
cytarabine cardiogenic shock
Paclitaxel, vinca Sinus bradicardia, + ? ? ? ?
alkaloids ventricular
tachycardia,
atrioventricular
block,
hypotension, CHF,
ischemia
Cyclophosphamide Neurohumoral + ? ? ? +
activation, mitral
regurgitation
Imatinib Arrythmias, CHF, − + + − <>
angioedema, LVD
Sorafenib Hypertension, − − − − <>
arrythmias
Sunitinib Hypertension, − − − − <>
arrythmias

*
*+ = likely; − = unlikely; ? = unknown; < > = probable. ADCC = antibody-dependent cellular

cytotoxicity; CHF = congestive heart failure; COX-2 = cyclooxygenase 2; GI = gastrointestinal tract;

HDL = high-density lipoprotein; LDL = low-density lipoprotein; LVD = left ventricular dysfunction;
ROS = reactive oxygen species; SERMs = selective estrogen receptor modulators. For references, see
text.