Cyclophosphamide is a strong immunosuppressant, commonly used in the treatment of autoimmune diseases such as lupus, interstitial pneumonia and polymyositis. It inhibits cell proliferation, non-specifically kills antigen-sensitive small lymphocytes, prevents them from transforming into immunoblasts, and suppresses humoral and cellular immunity. Common adverse effects include bone marrow suppression, gastrointestinal reactions, hemorrhagic cystitis, hepatic impairment, hair loss and gonadal suppression. Cardiotoxicity can occur at high doses, causing cardiomyopathy and pericarditis, and even fatal congestive heart failure. The mechanism of cardiotoxicity is not known. It has been found that cyclophosphamide and its metabolites can directly damage the vascular endothelium, causing capillary microthrombosis and increased endothelial permeability, resulting in extravasation of blood containing high concentrations of the drug and myocardial cell damage; at the same time, plasma proteins and red blood cells leak into the myocardial interstitium, causing fibrin deposition and focal hemorrhage; and large amounts of protein-rich fluid leak into the pericardial cavity, causing pericardial effusion, leading to refractory congestive heart failure. heart failure. At the same time, cyclophosphamide has anti-diuretic effect and can cause transient water retention, which can promote the development of cardiopulmonary failure. The metabolite acrolein reacts with cytochrome P450 both in vivo and in vitro and denatures it, causing cardiopulmonary toxicity. In patients on cyclophosphamide, autopsy showed severe interstitial edema, increased cardiac weight, wall thickening, ventricular hypertrophy, patchy hemorrhage in the subendocardial and myocardial layers, exudative pericardial effusion, and fibrinous pericarditis. Electron-dense inclusions in the mitochondria, fibrin deposits in the interstitium and myocardial cell cytoplasm, and fibrin deposits in the nucleus of some myocardial cells, which showed a portion of electron-dense chromatin aggregation, replaced by fibers and filaments, with capillary microthrombi, interstitial and myocardial fibers. Fibrin deposition in cardiac myocytes is highly specific and is only seen in acute cardiotoxicity caused by high doses of cyclophosphamide. Cardiotoxicity with cyclophosphamide usually occurs days or weeks after treatment. The diagnosis of cardiotoxicity requires monitoring of cardiac function before, during and after treatment. Clinical manifestations include shortness of breath, dyspnea, chest tightness, chest pain, dysuria, tachycardia, hypotension, odd pulses, jugular venous anger, basilar rales in both lungs, pulmonary or peripheral edema, pericardial effusion, pericardial tamponade, cardiogenic shock, myocardial infarction, and congestive heart failure. The ECG showed transient non-specific low voltage, QRS wave amplitude depression, R wave disappearance, ST segment depression, T wave flattening or inversion and QT interval prolongation. Cardiac ultrasound and cardiac function tests show pericardial effusion, decreased ejection fraction and short-axis shortening rate, increased end-systolic left ventricular internal diameter and end-diastolic volume, increased left ventricular pre-ejection time to ejection time ratio, and decreased left ventricular systolic function, of which left ventricular ejection fraction is a reliable indicator for clinical assessment of basic cardiac function. Chest radiographs may show increased cardiothoracic ratio, increased cardiac shadow and pulmonary stasis. Radionuclide cardiovascular imaging is highly sensitive for myocardial necrosis, but lacks specificity. Electron microscopic observation of endomyocardial and myocardial biopsies is the most accurate and sensitive predictor, but it is not widely used in clinical practice because of its invasive nature. Positron emission tomography, which evaluates myocardial perfusion and metabolic activity, can be used as an adjunctive test to monitor cardiotoxicity. The cardiotoxicity of cyclophosphamide occurs in patients with daily doses greater than 1.55 g/m2 body surface area. It has been reported that the total dose of cyclophosphamide causing cardiac damage after high-dose treatment is above 0.12 g/kg, and at this dose, approximately 20% of patients show ECG changes and 40% show elevated myocardial enzyme profiles, whereas only occasional cases have been reported at conventional doses. In addition, a history of mediastinal radiotherapy or radiotherapy treatment may increase the incidence of cyclophosphamide cardiotoxicity. Patients with a history of cardiotoxic anthracycline antineoplastic agents such as adriamycin, erythromycin, and epiampicin may have an increased incidence of cardiotoxicity with cyclophosphamide. At the same dose, the younger the patient is, the greater the tendency to develop cardiotoxicity, especially in children, and the greater the risk of myocardial injury in women compared to men. In addition, combination chemotherapy, previous history of cardiac disease such as congestive heart failure, electrolyte imbalance (e.g., hypokalemia and hypomagnesemia), and basal ejection fraction less than 50% are risk factors for cardiotoxicity of cyclophosphamide. To prevent cardiotoxicity of cyclophosphamide, it should be avoided in combination with cardiotoxic drugs and used with caution in patients with a history of cardiac disease, radiotherapy and anthracycline chemotherapy. At the same time, monitoring of cardiotoxicity should be strengthened before, during and after treatment, especially in patients with a history of cardiac disease, radiotherapy and anthracycline chemotherapy. Cyclophosphamide treatment should be followed by appropriate hydration, both to reduce the occurrence of hemorrhagic cystitis and to accelerate its excretion rate. Myocardial protective agents such as ATP, coenzyme Q, ginseng pulse injection, antioxidants VE and VC can be added to the treatment as appropriate. In vivo and in vitro, cysteine can prevent cytochrome P450 denaturation, which can be used to prevent cardiotoxicity. Timely correction of water-electrolyte balance disorders is also required. In cases of congestive heart failure due to cyclophosphamide, digoxin, diuretics and angiotensin-converting enzyme inhibitors may be used.