Fatal haemorrhagic myocarditis secondary to cyclophosphamide therapy.

Abstract

Haemorrhagic myocarditis is a rare but important complication of cyclophosphamide therapy. Echocardiographic identification of the disorder can be made. We believe that the ultrasound features of this disorder have not been previously reported.

Fulminant fatal cardiotoxicity following cyclophosphamide therapy

“…Cardiac monitoring including electrocardiography and echocardiography are important in the detection of clinical signs of cardiotoxicity. Diffuse voltage loss as shown by electrocardiogram, increased LV wall thickness and generalized increase in echogenicity by echocardiogram are findings that indicate myocardial hemorrhage [1,6]. Echocardiographic figures of myocardial thickening of the LV wall are also observed in myocarditis of any cause, infiltrative cardiomyopathy, hypertrophic cardiomyopathy, and also in cases of cardiac invasion of malignant lymphoma [1,6,7].…”

The analysis of the parameters of 24‐hr ECG Holter monitoring in patients with blood neoplasms undergoing high‐dose chemotherapy and stem cell transplantation

“…Generally in comment to the influence of chemotherapy on ECG changes there are not many reports in the group of patients undergoing HSCT and especially using 24‐hr Holter monitoring taking the influence of a single agent into consideration. In cases when cyclophosphamide treatment was used in an early period after it there were some changes in standard ECG including low voltage of QRS, QT dispersion and systolic dysfunction of the left ventricle with ejection fraction about 30% as well as dysfunction of the right ventricle, and troponin elevation, however, the changes recovered after 1 month of treatment and only in few patients the diffuse myocardial thickening due to hemorrhagic myopericarditis was present with pericardial effusion leading to tamponade resulting in death (Atalay, Gulmez, & Ozsancak Ugurlu, ; Auner et al., ; Birchall, Lalani, Venner, & Hugh, ; Gottdiener, Appelbaum, Ferrans, Deisseroth, & Ziegler, ; Morandi et al., ; Nakamae, Tsumura, Hino, Hayashi, & Tatsumi, ; Wadia, ). Cardiotoxicity induced by cyclophosphamide is well‐known, with symptoms occurring usually within 1–3 weeks, resolving in some patients without late consequences, with the high mortality rate to 43%, however, no such cases were described in HSCT treatment so this is a novel finding that cyclophosphamide may increase less severe ECG changes at first that should be monitored (Goldberg, Antin, Guinan, & Rappeport, ; Morandi, Ruffini, Benvenuto, Raimondi, & Fosser, ; Slordal & Spigset, ; Yeh et al., ).…”

Acute Systolic Dysfunction within Two Weeks of High‐Dose Chemotherapy Conditioning before Autologous Bone Marrow Transplant: A Case Report

“…2) seen in TTE, reported before with HM. Diagnostic procedures could not be performed because consistently low platelets precluded invasive endomyocardial biopsy 5 . Regarding the low platelet count, basic science data does suggest that HDC may induce an acquired abnormality in platelet secretion and aggregation, which can contribute to the development of hemorrhagic myocarditis after ABMT 6 …”

“…Acute hemorrhagic myocarditis (HM) is another rare, frequently fatal side effect of highdose CY therapy and is reported in some cases. 5 It can also cause an acute decompensation of CHF and usually has a very poor prognosis refractory to standard therapy. Around 85% of analyzed patients in the retrospective analysis done by Lee et al were deceased.…”

“…Diagnostic procedures could not be performed because consistently low platelets precluded invasive endomyocardial biopsy. 5 Regarding the low platelet count, basic science data does suggest that HDC may induce an acquired abnormality in platelet secretion and aggregation, which can contribute to the development of hemorrhagic myocarditis after ABMT. 6 One recent experimental study demonstrated a decrease in the activities of TCA cycle enzymes such as succinate dehydrogenase, malate dehydrogenase, and isocitrate dehydrogenase in CY-treated rats with a simultaneous decrease in the activities of mitochondrial complexes of electron transport chain in the myocardium.…”