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Aortic aneurysms represent a very common pathology that can affect any segment of the aorta. These types of aneurysms can be localized on the thoracic segment or on the abdominal portion, with the latter being more frequent. Though there are similarities between thoracic and abdominal aortic aneurysms, these pathologies are distinct entities. In this article, we undertook a review regarding the different mechanisms that can lead to the development of aortic aneurysm, and we tried to identify the different manners of treatment. For a long time, aortic wall aneurysms may evolve in an asymptomatic manner, but this progressive dilatation of the aneurysm can lead to a potentially fatal complication consisting in aortic rupture. Because there are limited therapies that may delay or prevent the development of acute aortic syndromes, surgical management remains the most common manner of treatment. Even though, surgical management has improved much in the last years, thus becoming less invasive and sophisticated, the morbi-mortality linked to these therapies remains increased. The identification of the cellular and molecular networks triggering the formation of aneurysm would permit the discovery of modern therapeutic targets. Molecular and cellular mechanisms are gaining a bigger importance in the complex pathogenesis of aortic aneurysms. Future studies must be developed to compare the findings seen in human tissue and animal models of aortic aneurysm, so that clinically relevant conclusions about the aortic aneurysm formation and the pharmacological possibility of pathogenic pathways blockage can be drawn.

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What started with 41 hospitalized patients identified as having laboratory-confirmed coronavirus disease 2019 (COVID-19) in Wuhan, China, by January 2, 2020, turned into an unprecedented pandemic with more than 113 million confirmed cases and a mortality exceeding 2.5 million deaths worldwide by the beginning of March 2021. Although the course of the disease is uneventful in most cases, there is a percentage of patients who become critically ill and need admission in the intensive care unit for severe respiratory failure. Numerous of these patients undergo invasive mechanical ventilation and have an extremely high mortality rate. For these patients, extracorporeal membrane oxygenation (ECMO) has emerged as a last standing resource. In the present study, the literature was reviewed to evaluate the worldwide data regarding the use of ECMO in the management of critically ill COVID-19 patients. ISI Thomson Web of Science was searched for articles with English language abstracts from inception to March 1, 2021, with 'ECMO in COVID-19' as key words. A total of 214 abstracts were screened (case reports, guidelines, reviews) and the most relevant articles were included in the present review. The use of ECMO in the management of critically ill patients with COVID-19-induced acute respiratory distress syndrome refractory to conventional mechanical invasive ventilation is increasing. By increasing the survival rate from less than 20% to more than 50%, ECMO proved to be a valuable resource in the management of the most challenging critically ill COVID-19 patients.

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Although ischemic heart disease is the major cause of death in diabetic patients, diabetic cardiomyopathy (DCM) is increasingly recognized as a clinically relevant entity. Considering that it comprises a variety of mechanisms and effects on cardiac function, increasing the risk of heart failure and worsening the prognosis of this patient category, DCM represents an important complication of diabetes mellitus, with a silent development in its earlier stages, involving intricate pathophysiological mechanisms, including oxidative stress, defective calcium handling, altered mitochondrial function, remodeling of the extracellular matrix, and consequent deficient cardiomyocyte contractility. While DCM is common in diabetic asymptomatic patients, it is frequently underdiagnosed, due to few diagnostic possibilities in its early stages. Moreover, since a strategy for prevention and treatment in order to improve the prognosis of DCM has not been established, it is important to identify clear pathophysiological landmarks, to pinpoint the available diagnostic possibilities and to spot potential therapeutic targets.

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Aim: To analyze the correlations between inflammation markers and ApoB100 and angiotensin converting enzyme (ACE) gene polymorphism and the severity of coronary artery disease (CAD). Material and Methods: We conducted a study in 58 patients with acute coronary syndromes (ACS) who underwent coronarography at the Iasi "Prof. Dr. George I.M. Georgescu' Institute of Cardiovascular Diseases. the patients included in the studies were selected from those who needed a coronarography for unstable angina or acute myocardial infarction. The data were uploaded and processed using the statistical functions in SPPS 18.0 at a 95% materiality threshold. Results: Elevated inflammation markers were found in all study patients, with small differences in distribution. None of the study patients presented ApoB100 gene mutations. As to ACE polymorphism, a predominance of genotype II in unicoronary patients and ID and DD genotypes in bicoronary and tricoronary patients was found. Conclusions: The results of our study confirm the role of genetic and epigenetic factors in the severity and progression of the coronary disease, leaving room for larger and more comprehensive studies and new research perspectives.

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BACKGROUND/OBJECTIVES: Elevated vasopressin may increase systemic vascular resistance and pulmonary capillary wedge pressure, subsequently decrease stroke volume and cardiac output. Vasopressin receptor antagonists may counteract these effects and improve outcomes in heart failure. We aimed to assess benefits and harms of vasopressin receptor antagonists (VRAs) versus placebo in addition to standard care in adults with heart failure (HF). METHODS: We conducted a systematic review of randomized controlled trials with searches of CENTRAL and MEDLINE to January 2014 and reference lists without language restriction. Meta-analysis using a random-effects model was done for all-cause and cardiovascular mortality, hospitalization for heart failure, changes in clinical assessment of HF, serum sodium concentration (Na), kidney function and treatment-specific side effects. RESULTS: We identified 13 trials and 5,525 participants. In 10 trials, participants received standard therapy for HF. In low-quality evidence, VRAs in patients with HF had no effect on all-cause mortality risk ratios (RR 0.98; CI 0.88-1.08), cardiovascular mortality (RR 1.03; CI 0.91-1.16) or change in creatinine mean difference (MD -0.01; CI -0.10 to 0.09 mg/dL), but reduced body weight by 0.8 kg from baseline (MD -0.83; CI -1.10 to -0.55 kg) and increased Na (MD 2.61; 95 % CI 1.88-3.35 mmol/L). Compared with placebo, VRAs increased the risk of adverse events by 14 % (RR 1.14; CI 1.04-1.26). Studies were generally limited to short-term follow-up with limited data available on patient important outcomes. CONCLUSIONS: Vasopressin receptors antagonists may reduce body weight and increase Na but do not improve all-cause mortality, cardiovascular mortality or kidney function. In addition, acceptability of long-term treatment side effects and hospitalization appears problematic.

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UNLABELLED: The aim of our study was to investigate whether the disorder of coagulation and fibrinolysis factors are mechanisms that contribute to the prothrombotic state in patients with polycythemia vera (PV) syndrome with or without cardiovascular disease (CVD), in order to identify the patients having high risk for thrombotic events. MATERIAL AND METHODS: The study comprises 20 patients divided in 2 groups: 10 patients with PV syndrome (PV) and 10 patients with PV and cardiovascular diseases associated (PV+CVD). The patients were tested by determining three factors of coagulation profile: protein S, free fraction (PS), antithrombin III (AT III) and Protein C (PC). RESULTS: The level of the three parameters were found significantly modified in the both groups (p < 0.05); comparing the results between the two groups of patients, in the second group (PV+CVD) the level of the parameters were significantly lower than in the first group (PV). CONCLUSIONS: In PV syndrome the risk for thrombosis is also due to the changes in coagulation factors. Patients with associated cardiovascular disease, present a more severe risk for trombothic events, so regarding the disorder of coagulation factors, this represent a major mechanism implicated in the etiology of thrombosis in these categories of patients.

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