Pericarditis in a Case of Early Daunorubicin Cardiomyopathy

Harrison, David T.

doi:10.7326/0003-4819-85-3-339

Cited by 33 publications

(8 citation statements)

References 3 publications

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“…Clinicians are familiar with deleterious cardiac effects of anthracyclines and cyclophosphamide [8,9,12]. The myocardium is mainly affected and pericarditis, when observed, usually complicates an underlying myocarditis (Dressler's type reaction).…”

Section: Discussionmentioning

confidence: 99%

Pericarditis induced by high-dose cytosine arabinoside chemotherapy

Hermans

Straetmans

Michaux

et al. 1997

Annals of Hematology

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Pericarditis is a rare side effect of chemotherapy. We report here the case of a patient treated with high-dose cytosine arabinoside (HD ara-c) who developed severe pericarditis. Interruption of HD ara-c and initiation of corticosteroid treatment were effective in resolving the pericardial effusion. This case illustrates this rare but potentially life-threatening cardiac complication of HD ara-c therapy as well as the beneficial effect of corticosteroid treatment.

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Section: Discussionmentioning

confidence: 99%

Pericarditis induced by high-dose cytosine arabinoside chemotherapy

Hermans

Straetmans

Michaux

et al. 1997

Annals of Hematology

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“…Acute doxorubicin cardiotoxicity is associated with relatively low cumulative doses and can occur even after the administration of a single dose (Bristow et al, 1978b). Manifestations of such acute toxicity include the development of acute arrhythmias, a pericarditis-myocarditis syndrome, and left ventricular dysfunction (Harrison and Sanders, 1976). These acute effects are transient, usually asymptomatic, and do not require modification of the dose or schedule of FIGURE 3 -Distribution of patients in relation to total dose of doxorubicin.…”

Section: Discussionmentioning

confidence: 99%

Plasma endothelin‐1 As a marker for doxorubicin cardiotoxicity

Yamashita¹,

Ogawa²,

Shirakusa³

1995

Intl Journal of Cancer

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The use of doxorubicin is often limited by cardiotoxicity that can lead to congestive heart failure (CHF). Although various techniques have been used to predict its cardiotoxicity, none has proven useful. We reported 2 patients in whom the level of plasma endothelin (ET)-1 rose progressively during doxorubicin treatment of breast cancer, and who subsequently developed CHF. Accordingly, we conducted a prospective study of 30 consecutive patients, 23 with breast cancer and 7 with small-cell lung cancer, who were treated with doxorubicin. Serial changes in plasma ET-1 during doxorubicin treatment were measured by a specific radioimmunoassay, and plasma levels of atrial natriuretic peptide (ANP) were determined by a sensitive immunoradiometric assay. M-mode echocardiography was performed serially to monitor the fractional shortening (FS) and the left ventricular ejection fraction (LVEF). The plasma concentrations of ET-1 rose progressively in 5 of the 30 patients during doxorubicin treatment. Two of the 5 patients developed clinically overt CHF after developing cumulative doses of doxorubicin of 500 and 480 mg/m2. Serial measurement of plasma levels of ANP, FS and LVEF showed no abnormalities until the development of CHF. Another 25 patients who had received doxorubicin (cumulative doses ranging from 400 to 660 mg/m2) and had not developed CHF showed no appreciable change in plasma ET-1 or other markers. This prospective study suggests that plasma ET-1 may be useful for predicting the risk of doxorubicin-induced cardiotoxicity.

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“…These effects include acute lifethreatening cardiac arrhythmias, myocarditis-pericarditis syndrome, and myocardial infarction. Vasospasm can oc cur in the first hours of therapy to cause ischemia, infarc tion or sudden death, but this is a very uncommon event [ 1,3], After the first day and within the first month, a rare myocarditis-pericarditis syndrome occurs with cumulative doses of 60-180 mg/m2 [4], The majority of patients who develop significant cardiotoxicity due to anthracycline therapy develop a chronic dilated cardiomyopathy [6,7], Doxorubicin-induced cardiomyopathy usually is man ifested by congestive heart failure (CHF) w'hich is caused Tests for Monitoring Doxorubicin-Induced Cardiomyopathy by a reduction in LV ejection fraction (LVEF). CHF is usually dose-related; CHF rarely occurs at cumulative doxorubicin doses below 450 mg/m2, and has an average incidence of 7% at 550 mg/m2, 15% at 600 mg/m2 and 35% at 700 mg/m2 [6], Low dose CHF probably occurs in patients with underlying risk factors.…”

Section: Introductionmentioning

confidence: 99%

“…Doxorubicin most likely pro duces toxic oxidative metabolites which are not as well metabolized by the heart as they arc by other organs [ 12], Tumoricidal drugs without the cardiotoxic side effects of anthracyclines have not replaced doxorubicin in cur rent cancer therapy protocols. Since myocardial patho genesis is related to the type of anthracycline drug used as well as cumulative dose and dosing schedule, the use of less toxic derivatives, adding cardioprotective agents or reducing the doxorubicin dose, could minimize cardio vascular morbidity and mortality [3][4][5][6][7][8][9][10][11][12][13][14][15], However, these strategies may also limit the efficacy of cancer therapy [13]. Anthracycline morbidity can be reduced by the use of prolonged intravenous infusions of doxorubicin in place of bolus therapy [14]; however, central venous access is needed for prolonged infusional therapy because doxorubicin is a vesicant.…”

Section: Introductionmentioning

confidence: 99%

Review of Tests for Monitoring Doxorubicin-lnduced Cardiomyopathy

Ganz

Sridhar

Ganz³

et al. 1996

Oncology

145

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The objective of this review is to make physicians aware of new radionuclide methods to detect cardiac effects of chemotherapeutic drugs. This knowledge is important because of the limitations of the physical examination and the electrocardiogram for detecting early reversible cardiac damage. Presently left ventricular ejection fraction (LVEF) is routinely used to screen for cardiotoxicity. Since LVEF obtained by radionuclide angiocardiography is more accurate than the LVEF estimated by echocardiography, serial radionuclide LVEF monitoring is most commonly used to monitor cardiotoxicity. Diastolic measurements of left ventricular function (such as peak filling rate) are now being added to routine LVEF measurements to enhance standard radionuclide evaluation. This screening test should be done prior to beginning therapy and at appropriate points based on the baseline study, therapy scheme and the patient’s clinical status. At some centers, exercise LVEF methods are being used to determine if cardiac reserve is adequate for the patient to tolerate additional chemotherapy when cardiac injury may be present. Previously, endomyocardial biopsy was needed to detect and confirm early anthracycline cardiotoxicity. This invasive test may be replaced by a new noninvasive in vivo method using radioactive monoclonal antibodies against cardiac muscle (indium-lll-antimyosin). Because cardiac failure has been associated with adrenergic neuron injury, it has been proposed that radioactive methyliodo-benzylguanine may detect the adrenergic abnormality which may predict future development of congestive heart failure or sudden death months after therapy is discontinued. Advantages and disadvantages of these methods in evaluating cardiotoxicity, and an algorithm to optimally monitor antitumor therapy-induced cardiomyopathy are discussed.

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Pericarditis in a Case of Early Daunorubicin Cardiomyopathy

Cited by 33 publications

References 3 publications

Pericarditis induced by high-dose cytosine arabinoside chemotherapy

Pericarditis induced by high-dose cytosine arabinoside chemotherapy

Plasma endothelin‐1 As a marker for doxorubicin cardiotoxicity

Review of Tests for Monitoring Doxorubicin-lnduced Cardiomyopathy

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