The development of targeted drugs and immune checkpoint inhibitors (ICIs), as well as their implementation into clinical practice has allowed increasing the overall and event-free survival of oncohematological patients. Currently, assessment of the efficacy of a therapeutic strategy in each specific case includes the evaluation of an acceptable tolerability profile. The subject of discussion includes cardiovascular complications induced by target drugs and ICIs. The review mainly presents the issues of cardiovascular toxicity (CVT) in certain groups of oncohematological patients (with chronic lymphocytic leukemia, chronic myeloid leukemia, multiple myeloma). The spectrum of cardiovascular adverse effects associated with targeted and ICI therapy in oncohematological practice is quite wide — coronary artery disease, peripheral arterial disease, myocarditis, heart failure, arrhythmias, hypertension. The high importance of the problem of using targeted and immunosuppressive therapy dictates the need to predict adverse effects. The diagnosis of heart failure (one of CVT manifestations) is based on determining the decreased left ventricular ejection fraction during echocardiography, less often — during cardiac magnetic resonance imaging; global longitudinal myocardial strain is a significant parameter of preclinical heart failure, which is determined using the speckle tracking technique. To determine vascular toxicity, a special attention is paid to the vascular wall structure and microcirculation parameters — capillary density at rest, percentage of capillary recovery and perfused capillaries, stiffness index for large blood vessels, reflection index for small arteries, laboratory markers of inflammation and endothelial dysfunction (C-reactive protein, fibrinogen, homocysteine, endothelin 1, vascular endothelial growth factor). CVT prevention presumes the determination of the risk group, correction of risk factors, and administration of protective therapy to very high and high-risk patients. One of the promising directions for preventing vascular toxicity is the use of sodium-glucose linked transporter-2 inhibitors.