Inflammatory, Serological and Vascular Determinants of Cardiovascular Disease in Systemic Lupus Erythematosus Patients

Background and aim: Systemic lupus erythematosus (SLE) is associated with increased risk of cardiovascular disease (CVD). Among many mechanisms, accelerated atherosclerosis, endothelial dysfunction, and hypercoagulability play a main role. Here, we investigate whether inflammatory, serological and clinical markers of SLE determine and correlate with arterial stiffness in SLE patients. Materials and methods: Routine blood samples, inflammatory mediators, specific antibodies, and 24 h proteinuria were measured in 43 SLE patients and 43 age and sex-matched controls using routine laboratory assays. We also assessed arterial stiffness by measuring radial artery applanation tonometry-derived augmentation index (AI), normalized AI (AIx@75), aortic pulse pressure, central systolic, diastolic and peripheral blood pressure. Results: SLE patients showed a significantly greater arterial stiffness vs. controls, as demonstrated by the significantly higher AIx@75 and aortic pulse pressure. Interestingly, regression analysis showed that age, systolic pulse pressure, inflammatory markers (erythrocyte sedimentation rate and C-reactive protein), daily dose of glucocorticoids, and cumulative organ damage positively correlated with arterial stiffness. Conclusions: SLE patients show increased arterial stiffness which correlates with markers of inflammation, that is involved in early alterations in arterial walls. Applanation tonometry can be used to screen SLE patients for subclinical vascular damage to implement prevention strategies for CVD

What is the cardiac impact of chemotherapy and subsequent radiotherapy in lymphoma patients

Anthracyclines are widely used in anticancer protocols, but can induce cardiotoxicity by mechanisms that mainly involve oxidative damage and mitochondrial dysfunction. Radiotherapy can also impair cardiac function by promoting myocardial fibrosis, microvascular damage and decreased density of myocardial capillaries. Hence, we aim at investigating prospectively whether radiotherapy impacts heart function in lymphoma patients who had been already treated with anthracyclines. Twenty-nine consecutive patients with Hodgkin or non-Hodgkin lymphomas underwent echocardiography at baseline (before antineoplastic treatments), and then every two months, until 6 months after treatments completion. Echo evaluation included standard 2D and Speckle Tracking. Twenty-two patients treated with anthracycline-based regimens were eligible. Out of the 22 patients, 8 received chemotherapy only (subgroup 1), while 14 underwent radiotherapy after chemotherapy (subgroup 2). At the end of chemotherapy, ejection fraction was significantly reduced in the whole population. At 6 months after completion of therapies, E/E' increased and Global Longitudinal Strain was compromised in subgroup 2, suggesting additional damage induced by radiotherapy after chemotherapy. On the basis of the data from our small prospective study we can hypothesize that in lymphoma patients anthracyclines can worsen cardiac function, and radiotherapy may have an additional unfavorable myocardial impact