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J Am Coll Cardiol, 2007; 49:2142-2143, doi:10.1016/j.jacc.2007.03.015 (Published online 11 May 2007).
© 2007 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

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Nihat Kalay, MD*, Ibrahim Ozdogru, MD, Ozlem Er, MD and Emrullah Basar, MD

* Department of Cardiology, Sorgun State Hospital, Sorgun Devlet Hastanesi, Kardiyoloji Bolumu, Yozgat, Yozgat, Turkey (Email: nihatkalay{at}hotmail.com).


We thank Drs. Florenzano and Salman for their valuable comments regarding our study (1). Four types of anthracycline cardiotoxicity are described: acute, subacute, chronic, and late onset. Acute complications can be seen in 0.4% to 41% of patients (2). We performed echocardiography after chemotherapy and evaluated both acute and subacute cardiotoxicity. Dilated cardiomyopathy is the most important complication of chemotherapy. It is associated with certain risk factors: dose, administration rate, gender, age, underlying heart diseases, hypertension, irradiation, and the human epidermal growth factor receptor-2.

Mean decrease in left ventricular ejection fraction (LVEF) in our control group was 16.6%. It was demonstrated that gradual decrease in LVEF was 1.9% with every 50-mg anthracycline dose. Decrease in LVEF in our study was concordant with this information. However, both LVEF and cardiomyopathy incidence may change with risk factors. The incidence of subclinical cardiomyopathy is not exactly known. It has been demonstrated that doxorubicin-induced subclinical cardiomyopathy can be 27.6% (3), and the troponin I increase can be 33% of patients after chemotherapy, and this increase is associated with decreased LVEF (4). In another study (5), patients who had received chemotherapy were randomized either to receive or not to receive an angiotensin-converting enzyme inhibitor, and the primary end point was >10% decrease in LVEF. The primary end point was 0% in the treatment group and 43% in control subjects. These results suggest that systolic dysfunction may occur in many patients. Decompensated heart failure was shown in one patient in our groups, but subclinical cardiomyopathy was demonstrated in additional patients.

The main result of our study showed that carvedilol may prevent anthracycline-induced cardiomyopathy. Our study is a preliminary one in this issue. We enrolled cancer patients, so patients with different types of disease at different stages were included in the trial. Although we had a small number of patients, the distribution of disease types and the anthracycline dose used in the patient group were well balanced between the groups. The dose of anthracycline changes with the treatment scheme. Moreover, the number of standard cycles is 6; in some cases additional cycles may be used depending on the scheme employed and the oncologist’s preference. Most of our patients received adriamycin, and the regular dose was 65 to 75 mg/m2, but higher doses were used in some patients. Furthermore, it is known that the cardiotoxicity incidence increases with increased doses of adriamycin and epirubicin above 550 and 900 mg/m2, respectively (6).


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 References
 

  1. Kalay N, Basar E, Ozdogru I, et al. Protective effects of carvedilol against anthracycline-induced cardiomyopathy J Am Coll Cardiol 2006;48:2258-2262.[Abstract/Free Full Text]
  2. Orditura M, Quaglia F, Morgillo F, et al. Pegylated liposomal doxorubicin: pharmacologic and clinical evidence of potent antitumor activity with reduced anthracycline-induced cardiotoxicity Oncol Rep 2004;12:549-556.[ISI][Medline]
  3. Hequet O, Le QH, Moullet I, et al. Subclinical late cardiomyopathy after doxorubicin therapy for lymphoma in adults J Clin Oncol 2004;22:1864-1871.[Abstract/Free Full Text]
  4. Cardinale D, Sandri MT, Martinoni A, et al. Left ventricular dysfunction predicted by early troponin I release after high-dose chemotherapy J Am Coll Cardiol 2000;36:517-522.[Abstract/Free Full Text]
  5. Cardinale D, Colombo A, Sandri MT, et al. Prevention of high-dose chemotherapy-induced cardiotoxicity in high-risk patients by angiotensin-converting enzyme inhibition Circulation 2006;114:2474-2481.[Abstract/Free Full Text]
  6. Takimoto CH. Topoisomerase interactive agentsIn: Devita VT, editor. Cancer Principles & Practice of Oncology. 7th edition. Baltimore, MD: Lippincott, Williams & Wilkins; 2005. pp. 375-390.




This Article
Right arrow Full Text (PDF)
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j.jacc.2007.03.015v1
49/21/2142-a    most recent
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