Accelerated Atherosclerosis and Cardiovascular Toxicity Induced by Radiotherapy in Breast Cancer.

The number of patients diagnosed with breast cancer and cardiovascular disease is continuously rising. Treatment options for breast cancer have greatly evolved, but radiotherapy (RT) still has a key role in it. Despite many advances in RT techniques, cardiotoxicity is one of the most important side effects. The new cardio-oncology guidelines recommend a baseline evaluation, risk stratification and follow-up of these patients. Cardiotoxicity induced by RT can be represented by almost all forms of cardiovascular disease, with atherosclerosis being the most frequent. An interdisciplinary team should manage these patients, in order to have maximum therapeutic effect and minimum cardiovascular toxicity. This review will summarize the current incidence, risk factors, mechanisms and follow-up of RT-induced cardiovascular toxicity.

Hyperglycosylated-hCG: Its Role in Trophoblast Invasion and Intrauterine Growth Restriction.

Human chorionic gonadotropin (hCG) is produced by the placenta and its roles have been studied for over a century, being the first known pregnancy-related protein. Although its main role is to stimulate the production of progesterone by corpus luteal cells, hCG does not represent just one biologically active molecule, but a group of at least five variants, produced by different cells and each with different functions. The hyperglycosylated variant of hCG (H-hCG) plays a key role in trophoblast invasion, placental development and fetal growth. During trophoblast invasion, H-hCG promotes extravillous cytotrophoblast cells to infiltrate the decidua, and also to colonize and remodel the spiral arteries in to low resistance, larger-diameter vessels. As fetal growth is heavily reliant on nutrient availability, impaired trophoblast invasion and remodeling of the uterine arteries, leads to a defective perfusion of the placenta and fetal growth restriction. Understanding the function of H-hCG in the evolution of the placenta might unveil new ways to manage and treat fetal growth restriction.

New insights into the potential utility of the left atrial function analysis in heart failure with preserved ejection fraction diagnosis.

AIMS: None of the conventional echocardiographic parameters alone predict increased NTproBNP level and symptoms, making diagnosis of heart failure with preserved ejection fraction (HFpEF) very difficult in some cases, in resting condition. We evaluated LA functions by 2D speckle tracking echocardiography (STE) on top of conventional parameters in HFpEF and preHF patients with diastolic dysfunction (DD), in order to establish the added value of the LA deformation parameters in the diagnosis of HFpEF. METHODS: We prospectively enrolled 125 patients, 88 with HFpEF (68±9 yrs), and 37 asymptomatic with similar risk factors with DD (preHF) (61±8 yrs). We evaluated them by NTproBNP, conventional DD parameters, and STE. Global longitudinal strain (GS) was added. LA reservoir (R), conduit (C), and pump function (CT) were assessed both by volumetric and STE. 2 reservoir strain (S) derived indices were also measured, stiffness (SI) and distensibility index (DI). RESULTS: LA R and CT functions were significantly reduced in HFpEF compared to preHF group (all p<0.001), whereas conduit was similarly in both groups. SI was increased, whereas DI was reduced in HFpEF group (p<0.001). By adding LA strain analysis, from all echocardiographic parameters, SR_CT<-1.66/s and DI<0.57 (AUC = 0.76, p<0.001) demonstrated the highest accuracy to identify HFpEF diagnosis. However, by multivariate logistic regression, the model that best identifies HFpEF included only SR_CT, GS and sPAP (R2 = 0.506, p<0.001). Moreover, SR_CT, DI, and sPAP registered significant correlation with NTproBNP level. CONCLUSIONS: By adding LA functional analysis, we might improve the HFpEF diagnosis accuracy, compared to present guidelines. LA pump function is the only one able to differentiates preHF from HFpEF patients at rest. A value of SR_CT < -1.66/s outperformed conventional parameters from the scoring system, reservoir strain, and LA overload indices in HFpEF diagnosis. We suggest that LA function by STE could be incorporated in the current protocol for HFpEF diagnosis at rest as a major functional criterion, in order to improve diagnostic algorithm, and also in the follow-up of patients with risk factors and DD, as a prognostic marker. Future studies are needed to validate our findings.

COVID-19 presented as acute kidney injury with secondary myocardial damage.

The most common manifestations of the 2019 novel coronavirus disease (COVID-19) include fever, cough, dyspnea. Nevertheless, many atypical forms of presentation might be present, delaying a correct diagnosis. Acute kidney injury (AKI) is one of the important complications of COVID-19, occurring in 0.5-7% of cases and in 2.9-23% of ICU patients. The exact mechanisms by which COVID-19 induces AKI in different clinical settings is still a matter of debate. We present the case of a 53-year old woman, without any prior renal pathology, admitted to a Cardiology Department for atypical thoracic pain and oligo-anuria, without respiratory symptoms, who was diagnosed with SARS-CoV-2 infection. The patient had a significant rise in high-sensitivity cardiac troponin (from 304 ng/L to 889 ng/L in one hour) and mild systolic dysfunction (LVEF 45%), which led to the initial misdiagnosis of an acute myocardial infarction. Blood tests confirmed the diagnosis of acute kidney injury (creatinine 8.8 mg/dL in two different samples). She received hydro-electrolytic rebalancing treatment, with good clinical and biological evolution. To our knowledge this is one of the first reports, that highlights the existence of myocardial injury secondary to acute kidney injury caused by SARS-CoV-2 infection, in a patient without respiratory symptoms.