J Cardiovasc Pharmacol. 2003 Nov;42(5):680-7
Spindler M, Weilbach F, Beer M, Sandstede J, Kostler H, Strotmann J,
Voelker W, Hahn D, Ertl G, Gold R.
As mitoxantrone is a recently approved immunosuppressant for managing multiple sclerosis, the number of patients treated with this effective but potentially cardiotoxic anthracenedione derivative will increase substantially.
To detect subclinical mitoxantrone-induced cardiotoxicity, sensitive non-invasive diagnostic tools are required.
Assuming that changes in myocardial high-energy phosphate metabolism and alterations in left ventricular (LV) diastolic performance might be early markers of mitoxantrone-induced cardiotoxicity we examined fifteen MS patients treated with mitoxantrone up to 100 mg/m2 compared with 15 matched control MS patients.
31P-magnetic resonance (MR) spectroscopy was employed to measure myocardial high-energy phosphate metabolism, MR imaging for morphometric evaluation of changes in LV geometry.
Indices of diastolic performance were assessed by Doppler echocardiography.
In this exploratory study, phosphocreatine/ATP ratios were comparable between mitoxantrone-treated and control patients (1.48 +/- 0.23 and 1.43 +/- 0.41).
LV mass, LV end-diastolic and systolic volumes, wall motion score, EF and cardiac output did not differ between both groups.
All parameters of diastolic performance (E/A-ratio, isovolumic relaxation time, and E-wave deceleration time) were not different and within normal limits.In conclusion, using advanced diagnostic methodology, including functional, morphometric, and biochemical measurements no cardiotoxic effect of mitoxantrone up to a cumulative dose range of 100 mg/m2 could be detected.