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Modern antineoplastic therapy improves survival and quality of life in cancer patients, but its indisputable benefits are accompanied by multiple and major side effects, such as cardiovascular ones. Endothelial dysfunction, arterial spasm, intravascular thrombosis, and accelerated atherosclerosis affect the coronary arteries, leading to acute and chronic coronary syndromes that negatively interfere with the oncologic treatment. The cardiac toxicity of antineoplastic agents may be mitigated by using adequate prophylactic measures. In the absence of dedicated guidelines, our work provides the most comprehensive, systematized, structured, and up-to-date analyses of the available literature focusing on measures aiming to protect the coronary arteries from the toxicity of cancer therapy. Our work facilitates the implementation of these measures in daily practice. The ultimate goal is to offer clinicians the necessary data for a personalized therapeutic approach for cancer patients receiving evidence-based oncology treatments with potential cardiovascular toxicity.

Thrombophilia, also called hypercoagulability or prothrombotic condition, usually reflects a certain imbalance that occurs either in the coagulation cascade or in the anticoagulation/fibrinolytic system. A similar imbalance may be induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Thrombotic complications are associated with multiorgan failure and increased mortality. In this context, activation of coagulation and thrombocytopenia appeared as prognostic markers in COVID-19. Our work provides a structured and updated analysis of inherited thrombophilia and its involvement in COVID-19, emphasizing the importance of diagnosing and initiating thromboprophylaxis. Since the state of hypercoagulation is directly correlated with COVID-19, we consider that studies on the genetic profiles of proteins involved in thrombophilia in patients who have had COVID-19 and thrombotic events are of great importance, both in treating and in preventing deaths due to COVID-19.

Thrombophilia is a condition of hypercoagulability, which is defined as an abnormality of blood clotting, disturbing the balance between procoagulants and anticoagulants in favor of the former, thus increasing the risk of thrombosis. It can be classified into different categories, such as genetic/administered; primary/secondary; permanent/transient; low risk/high risk. Venous thromboembolism is the main and most common complication of a hypercoagulable condition, with an enormous impact on any national health system. The pathophysiological mechanisms involved are at various stages of research, some of which are far from being fully elucidated. Treatment of thrombophilia differs—while most conditions do not require anticoagulation as primary prophylaxis, secondary prophylaxis may require transient or permanent anticoagulation. Treatment options include parenteral unfractionated heparin, low molecular weight heparin (LMWH), fondaparinux or orally administered vitamin K antagonists, and direct oral anticoagulants (DOAC), such as rivaroxaban, apixaban, dabigatran, with increasing indications as data accumulate from recent and ongoing studies and trials.

Venous thromboembolism (VTE) is a major healthcare problem due to its high incidence, significant mortality rate from pulmonary embolism, high recurrence rate and morbidity from long-term complications. After a first episode of VTE all patients must receive anticoagulant treatment for 3 months. Further anticoagulation is recommended in patients without transient risk factors for VTE or patients with active cancer, if they are not at a high risk for bleeding. The VTE-BLEED risk score was created with the purpose of enabling a better stratification of the bleeding risk during stable anticoagulation after a first VTE. Currently, it is the most validated risk score in VTE settings (selected and non-selected cohorts). It has a good prediction power for major bleeding events in patients receiving any of the currently available classes of oral anticoagulants, and it can identify patients at risk of intracranial and fatal bleeding events. The aim of our review was to highlight the strengths of the VTE-BLEED risk score, to acknowledge its weak points and to properly position its use in current medical practice.

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.

The non-valvular AF, beyond the guidelines, include 2 types of patients. We aimed to analyze the clinical and biological profile of patients with non-valvular atrial fibrillation (AF)andhemodynamicsignificantvalvular heart disease. We includedretrospectively 513 patients admitted in our hospitalwithnon-valvular AF, and we divided into:study group(333 patients; 64.9%) andcontrole group(180 patients; 35.1%) hemodynamic significant valvular heart disease. From the studied group 5.5% of patients associated all four valvular heart disease, 26.7% ofpatients associated mitral, aortic and tricuspid regurgitation and 71.9%of patients associated two valvular heart disease: 32.7% with mitral and aortic, 31.4% with mitral and tricuspid, 4.5% with tricuspid and pulmonary, and3.3% withtricuspid and aortic. Dyslipidemia (higher cholesterol and trygliceride levels) was present in 14.5% of patients, statistic significantly more frequently in patients from the control group (11.4% vs 18.3%, P= 0.033). Dyslipidemia showed a significantly higher estimated risk for AF (RR=1.25; IC95%: 0.99-1.56), as well as diabetes mellitus (RR=1.36; IC95%: 1.12-1.64)and coronary heart disease (RR=3.70; IC95%: 1.83-7.46). Therefore patients with non-valvular AF and hemodynamic significant valvular heart disease, beyond the curent guidelines, could has a completely different profile and prognosis.

Diabetes mellitus is one of the costliest chronic pathology worldwide with a continuous rising incidence. Diabetes mellitus is linked to frequent cardiovascular events. It is associated with vascular events, especially when the glycated hemoglobin has elevated values. Diabetic patients seem to develop abnormalities of the haemostatic process, such as alterations of the thrombocytic function, modifications of the coagulation and of the fibrinolysis that lead to a thrombophillic status. The acquired thrombophilia present in diabetic patients may be due to the non-enzymatic glycosilation of clotting inhibitors such as antithrombine. Antithrombin III has both an anticoagulant and an antiinflammatory effect. The anticoagulant effect appears after acting upon endothelial heparan sulfate or on the molecule of heparine, thus leading to an inhibition of thrombin. A decrease in antithrombin III levels may lead to a diminished neutralisation of thrombin and a lower activity of proteins C and S, thus inducing procoagulant consequences and increasing the susceptibility for thrombotic events. Our research tried to establish whether the levels of antithrombin III in type 2 diabetic patiens are modified, thus creating a predisposition for thrombotic events. Therefore we conducted an observational study on a sample composed of 60 patients having a diagnostic of type 2 diabetes associated with coronary artery disease, controlled with diet or with oral antidiabetics and we evaluated the levels of antithrombin III in function of the metabolic, inflammatory and coronarographic parameters. Our research showed that even though all patients were characterized by the diabetic dyslipidemia, there was no statistic relationship between antithrombin III and the lipidic fractions. As a result we cannot say that the adverse cardiac events seen in type 2 diabetic patients are influenced by the levels of antithrombin III, as a marker of an increased clotting activity.

Atherosclerosis is the main cause of myocardial infarction. This process involves a complex interplay between metabolic pathways governing lipid deposition, inflammatory and immune responses to oxidized lipids, and endothelial dysfunction. Myocardial infarction appears when these processes culminate with a thrombotic event. Markers of inflammation, such as C-reactive protein (CRP), myeloperoxidase (MPO) and leukocyte levels are strong predictors of cardiovascular death, myocardial infarction, and stroke. This process involves a complex interplay between metabolic pathways governing lipid deposition, inflammatory and immune responses to oxidized lipids, and endothelial dysfunction. Myocardial infarction appears when these processes culminate with a thrombotic event. Markers of inflammation, such as C-reactive protein (CRP), myeloperoxidase (MPO) and leukocyte levels are strong predictors of cardiovascular death, myocardial infarction, and stroke. This review will summarize the molecular and cellular links between inflammation and thrombosis in the context of myocardial infarction, which support the concept of a thrombo inflammatory state leading to the vessel obstruction and to the subsequent myocardial necrosis.

Hemophilia is a hereditary coagulopathy caused by factor VIII (hemophilia type A) or by coagulation factor IX (hemophilia type B) dysfunction, characterized by an increased bleeding predisposition, which is either spontaneous or secondary to minimal trauma. Currently, hemophilia may also be considered an 'orthopedic' condition, due to the fact that it affects the musculoskeletal system of most hemophilic patients. In recent years, constant prophylaxis using coagulation factors has led to a significant improvement in the hemophilic patient's quality of life, by reducing both life-threatening hemorrhagic phenomena, as well as the occurrence of chronic complications. Nevertheless, progressive joint bleeding remains unavoidable in this category of patients, and the onset of chronic arthropathy with secondary motor deficiency remains the main complication with an invalidating character. In such cases, orthopedic management is imperative; osteoarticular complications being managed most often with the help of conservative or surgical techniques. The purpose of this review is to provide an overview of modern orthopedic practices which are useful in the management of hemophilic patients suffering from osteoarticular disorders.

Haemophilia is an inherited disease that requires a different approach in order to evaluate, monitor and treat patients. Despite the great advances in therapeutic agents that have emerged, reports on the impact of monitoring outcomes on treatment decisions are rarely presented. Haemophilia A and haemophilia B are inherited bleeding disorders caused by deficiencies in blood clotting factor proteins. A systematic review was performed to identify literature reports on the current practices in haemophilic patients undergoing orthopedic surgery. The best therapy for haemophilic patients consists in performing primary prophylaxis to prevent joint bleeding and other complications. Besides the primary prophylaxis, thromboprophylaxis is used to prevent venous thrombosis in patients with hemophilia who undergo surgical orthopedic procedures. Further research is needed to better manage the pharmacologic approaches in haemophilic patients undergoing orthopedic surgery. Although patients with haemophilia present low risk for thromboembolic complications, such events have been reported in surgical procedures. The recommendations in patients with haemophilia are considerably variable in the current guidelines and clinical practice. The best therapy for haemophilic patients consists in performing primary prophylaxis to prevent joint bleeding and other complications.

Coronary artery disease (CAD) is the first cause of morbidity and mortality worldwide. An important goal is to diagnose patients in early stages, in order to reduce acute cardiovascular events. The angiotensin-converting enzyme (ACE) is an important element for the cardiovascular system, through its actions on hydro-salin balance and vascular tone. ACE polymorphism consists of insertions (I)/deletions (D) and there are 3 genotypes: II, ID, DD. It is speculated that the DD genotype may be a genetic basis for severe CAD, while the II genotype may have a protective effect on the coronary arteries. The present study included 154 patients with acute coronary syndroms admitted to the Institute for Cardiovascular Disease 'George I.M. Georgescu', Iasi. The patients underwent coronary angiography in order to assess the severity of the lesions and the ACE genotypes were determined for each patient. The genotypes were correlated with the severity of the vessel-disease and the exposure to classic risk factors. It was concluded that the D-allele is associated with a greater risk for acute coronary events and severe coronary stenosis, especially when risk genotype and risk phenotype interact.

Diabetes is one of the most important cardiovascular risk factors. Hyperglycemia leads to several metabolic alterations, thus creating conditions for a poor cardiovascular outcome. Our study phocussed on the prevalence of glucidic metabolism alterations in the acute coronary disease, as well as the association between hyperglycemia, diabetes and severe coronary lesions. We performed a study on 58 patients with acute coronary artery disease, divided in two groups, unstable angina and acute myocardial infarction and we evaluated the severity of the disease based on the angiographical results: no vessel disease (no significant lesions), one-vessel disease (one arterial stenosis/occlusion), two-vessel disease (two stenotic coronary arteries) and three-vessel disease (lesions of all three coronary arteries). Blood samples were collected in heparinated tubes and rapidly transferred to the laboratory for analysis, using automated glucose analyzers, in order to prevent errors due to glycolysis. More than half of the patients were diabetic and glycemic values were significantly higher in patients with myocardial infarction (126.67 vs 163.64 mg/dL). The prevalence of diabetes was significantly higher among the three vessel disease patients, both with unstable angina (38.9%; p=0.037) and with myocardial infarction (35.1%; p=0.345). In conclusion, diabetes and hyperglycemia create the setting for acute coronary disease, especially with lesions of all the three coronary arteries.

Atrial septal defects represent an abnormal communication between the left and the right atria. Some patients may experience dyspnoea, fatigue, others may suffer directly from complications, like arrhythimias, paradoxal embolisation, resulting in stroke, but some remain asymptomatic until adulthood. When possible, the gold standard treatment is percutaneous closure with nitinol messh occluder. We are presenting the case of a 50-year-old patient with an acute anterior myocardial infarction, whose echocardiography showed akinesia of the left ventricular apex and anterior wall, as well as a surprise element, not connected to the myocardial infarction, a 22 mm atrial defect, with a shunt ratio higher than 1.5. Our first concern was the cardiovascular emergency. The coronarography revealed a critical stenosis of the proximal left anterior descendent and we introduced a stent. In a second phase,we evaluated the atrial septal defect. Since it had indication for percutaneous closure, we decided to use an Amplatzer occluder. The intervention was a success, with no residual shunt. The patient�s follow up was good, with no cardiovascular events. Most of time, cardiovascular diseases are not isolated, but come together, related or not to one another. An adequate management implies treating the cardiovascular emergency first and solving the associated lesions in a second phase.

Atherosclerosis and platelet activity are two important chain factors linked together in the onset and the severity of coronary artery disease. Our study included 60 diabetic patients with ischemic heart disease, all having underwent coronary angiography. In this substudy from a larger epigenetical and genetical study, we phocused on the interrelationship between vessel disease and primary hemostasis. The haematological parameters included were platelet count (PLT), the platelet distribution width (PDW), the mean platelet volume (MPV) and the platelet larger cell ratio (P-LCR). ). The severity of the coronary disease was defined by the number of stenotic/occluded coronary arteries. We demonstrated a positive corelation with the duration of diabetes (p=0.032), as 34% of the patients with a long duration of the diabetes had a higher number of platelets. The mean platelet volume was slightly elevated in diabetic females over 65 years old, compared to younger diabetic men, though not statistically significant (p=0.101). Although the investigated parameters were mostly in the normal range, the fact that for some cathegories of patients they were orientated towards the upper limit, raises some questions for the next studies. Future adjustments of lot number and selection criteria for the following studies are needed. Using the MPV as a prediction test for cardiovascular complications is still a controversial subject, since the scientifical background contains both positive and negative studies on this matter.

Hemophilia is a genetic or acquired disease that leads to spontaneous and recurrent bleedings, which affect the joints and muscles, thus determining chronic damage to the cartilage which will lead to joint disease and hemophilic arthropathy. Even though hemophilic patients were initially thought to have a low incidence of atherothrombotic complications, it is now clear that atherothrombotic events occur. The administration of plasmatic factor VIII has better clinical results in type A hemophilic patients than the transfusion with plasma. We analyzed five patients with hemophilia type A, aged between 35 and 62 years. Two of them had a severe form of hemophilia with factor VIII less than 1%, while the other three had a moderate form with factor VIII ranging between 1 and 5%. The five patients underwent total knee repair interventions and received substitution treatment with clotting factors but also prophylactic anticoagulant treatment. The postsurgical evolution of these patients was favorable, with similar hemostatic profile as the non-hemophilic patients. Moroctocog alfa is an efficient substitutive treatment that manages to normalize the hemostatic profile of patients. Therefore, it is recommended to provide prophylactic antithrombotic therapy after the orthopedic interventions.