The Assessment of Left Ventricle Function and Subclinical Atherosclerosis in Patients with Acute Myeloid Leukemia

Abstract

Aim To assess the onset of early left ventricular (LV) systolic and diastolic function impairment and the subclinical atherosclerosis following chemotherapy in patients diagnosed with acute myeloid leukemia (AML). Materials and Methods: Thirty patients diagnosed with AML with no cardiac history, having LV ejection fraction (LVEF) >50%, were evaluated at baseline and 6 months after starting four cycles of chemotherapy. We measured LV function, global longitudinal strain and subclinical atherosclerosis markers: intima-media thickness (IMT), arterial stiffness aortic pulse wave velocity (PWVAo) and ankle-brachial index (ABI). Results: LVEF had decreased at 6 months after treatment initialization (p<0.001), the same changes being observed for LV fraction shortening (p<0.001), mitral annular plane systolic excursion and S' wave (p<0.001 and p<0.05). Bilateral IMT and PWVAo significantly increased, 12 out of 30 patients (40%) had LVEF ≤50% after 6 months of chemotherapy, five of them receiving daunorubicin at more than 500 mg/m 2 /injection. Conclusion: LV function is impaired after 6 months of chemotherapy, with early changes of subclinical atherosclerosis becoming evident. Cardiac toxicity represents one of the main side-effects of chemotherapy. One of the most alarming cardiotoxic effects is represented by left ventricular (LV) dysfunction, therefore 1599 This article is freely accessible online.

Early Diagnosis of Cardiotoxicity in Patients Undergoing Chemotherapy for Acute Lymphoblastic Leukemia

“…The S' wave is an indicator of global systolic function, and its reduction indicates LV systolic dysfunction (20). The present results showed a reduction of S' in all the evaluated patients, supporting that the left ventricular systolic function that has suffered modifications, maybe earlier than it was expected; thus, explaining why using several methods of evaluating cardiotoxicity is recommended (21).…”

A penetrating atherosclerotic ulcer rapidly growing into a saccular aortic aneurysm during treatment of leukaemia: a case report

“…Some reports have shown that after anthracycline administration, arterial remodelling parameters (aortic distensibility, intima-media thickness, and pulse wave velocity) are affected early through the following mechanisms: (i) anthracyclines increase the formation of reactive oxygen species and induce oxidative stress, thereby increasing arterial stiffness by causing structural changes within the vascular matrix and interfering with the endothelial regulation of vascular smooth muscle tone; (ii) vascular endothelial damage diminishes nitric oxide synthesis and promotes endothelial cell dysfunction, thereby increasing vascular stiffness; and (iii) anthracyclines promote inflammatory cytokine overexpression, which can cause endothelial injury. 7–9 Therefore, in this case, idarubicin treatment during remission induction therapy may have contributed to SAA progression.…”

Long-term cardiac-specific mortality among 44,292 acute myeloid leukemia patients treated with chemotherapy: a population-based analysis

“…Basic research studies have shown that anthracycline can also cause myocyte necrosis [38,39]. These diverse detrimental effects are associated with polymorphisms of anthracycline metabolism enzymes, which makes tailored safety dosing possible [12,21,40,41]. Although the mechanism of cardiotoxicity in AML has not been clarified, studies in breast cancer patients whose chemotherapy regimens contain anthracycline demonstrated that the impairment of heart cells is mediated by stress protective signaling and reactive oxygen [42,43].…”

“…Previous reports in this field mainly focused on the molecular interactions of heart toxicity, potential biomarkers, and preventive agents or were simply case reports [17][18][19][20][21][22][23]. It is also important to clarify the epidemiology of chemotherapy-related cardiacspecific death in AML patients to find some clues for basic research.…”