Thoracic aortic pseudoaneurysm: Inside its pathophysiology.

OBJECTIVES: Our aim was to investigate pathophysiology of pseudoaneurysm of the thoracic aorta, an acute or chronic pathology, respectively, secondary to blunt thoracic trauma and aortitis, or complicating a deep penetrating aortic ulcer, intraparietal hematoma, aortic aneurysm, and even aortic graft, often with atherosclerosis as a common background. METHODS: Given the relative rarity of this disease, an "inductive" retrospective method made it possible to retrieve clinical, radiological, and histopathological elements, which were mutually compared and validated through a "deductive" process of reinterpretation. RESULTS: We have identified three main structural constituents of this disease: a cavity, a single blood entry port, communicating with the aortic lumen, and a pseudocapsule. It is often caused by a chronic degenerative pathology of the intima and medial layers of the aorta, typically involving elastic fibers and smooth muscle cells, with possible intermediate stages of deep aortic ulcer or intraparietal hematoma. Otherwise, the acute onset may be secondary to acute aortitis or aortic injury. CONCLUSIONS: Today, thanks to the current angiographic tools represented by 3-D high resolution multidetector CT and MRI angiography, the diagnosis of thoracic aortic pseudoaneurysm is easier, as well as its surgical indications.

Labile plasma iron and echocardiographic parameters are associated with cardiac events in ß-thalassemic patients.

BACKGROUND AND AIM: Notwithstanding the improvement in therapies, patients affected by thalassemia major (TM) and intermedia (TI) are still at high risk of cardiac complications. This study aimed at evaluating the incidence and predictive factors for developing cardiac events in adult ß-TM and TI patients. POPULATION AND METHODS: Data on diagnosis and clinical history were collected retrospectively; prospective data on new-onset cardiac failure and arrhythmias, echocardiographic parameters, biochemical variables including non-transferrin-bound iron (NTBI) and labile plasma iron (LPI), magnetic resonance imaging (MRI) T2* measurement of hepatic and cardiac iron deposits, and iron chelation therapy were recorded during a 6-year follow-up. RESULTS: Thirty-seven patients, 29 TM and 8 TI, were included. At baseline, 8 TM patients and 1 TI patient had previously experienced a cardiac event (mainly heart failure). All patients were on chelation therapy and only 3 TM patients had mild-to-severe cardiac siderosis. During follow-up, 11 patients (29.7%) experienced a new cardiac event. The occurrence of cardiac events was correlated to high LPI levels (OR 12.0, 95% CI 1.56-92.3, p .017), low mean pre-transfusion haemoglobin (OR 0.21, 95% C.I. 0.051-0.761, p .21) and echocardiographic parameters suggestive of myocardial hypertrophy. Multivariate analysis disclosed high LPI and left ventricle mass index (LVMI) as independent variables significantly associated with cardiac events. Cardiac iron deposits measured by MRI T2* failed to predict cardiac events. CONCLUSION: LPI, Hb levels and echocardiographic parameters assessing cardiac remodelling are associated with cardiac events in adult TM and TI patients. LPI might represent both a prognostic marker and a potential target for novel treatment strategies. Further studies are warranted to confirm our findings on larger populations.

Effects of sildenafil on right ventricle remodelling in Portopulmonary hypertension.

Portopulmonary hypertension (PoPH) is a clinical condition associated with end-stage liver disease, described by the coexistence of pulmonary arterial hypertension (PAH) and portal hypertension. In PoPH patients, there is a right ventricle (RV) remodeling to compensate for the increased resistance in the lung circulation. There are no studies on the effects of the PAH-targeted pharmacological treatment on the RV dimension and function. The present study summarizes our experience in patients with PoPH treated with sildenafil in a period of 6 years (from 2013 to 2019). We enrolled 64 consecutive patients identified as PoPH, all treated with sildenafil (57.6% in monotherapy; in the other cases in association with macitentan; in 19.0% with initial combination therapy). A hemodynamic invasive cardiopulmonary study was performed at baseline and after 6 months of sildenafil treatment. In our population we showed a significative improvement in RV performance, with a significant increase in RV stroke volume (+33%), RV ejection fraction (+31%) and RV stroke work index (+17.5%). We registered the reduction of the RV cavity dimension over time in all patients treated with sildenafil (RV end diastolic diameter decreased by 15% after 6 months of follow-up). Regarding diastolic function, we highlighted a very significant reduction in RV end-diastolic pressure (-50% concerning baseline). Sildenafil was effective both when used as monotherapy and in combination with macitentan. In conclusion, Sildenafil had a positive impact on RV systolic and diastolic function in patients with PoPH and was able to conditionate the reverse remodeling of the RV.

Acute hemodynamic effects of intravenous adenosine in patients with associated pulmonary arterial hypertension: Comparison with intravenous epoprostenol.

Exogenous intravenous (IV) adenosine and epoprostenol are effective vasodilator agents, causing a substantial reduction in pulmonary vascular resistance in patients affected by idiopathic pulmonary arteriolar hypertension (PAH). Their action, in patients with PAH associated with other pathological conditions, is not well defined. In the present paper the authors retrospectively analyzed the acute hemodynamic effects of intravenous adenosine and epoprostenol in 30 consecutive patients (mean age: 58 ± 15 years; 21 females, and 9 males) affected by PAH associated with other pathological conditions, as determined by changes from baseline in systemic and pulmonary hemodynamic parameters. Acute IV administration of adenosine decreased pulmonary vascular resistance index (PVRI) by 3 Wood U/m2 (- 20%) compared to baseline (p = 0.02). We noted a slight, not significant, decrease in mean pulmonary artery pressure (mPAP) of 4 mmHg. Cardiac index (CI) increased by 0.5 L/min/m2 (15% increase respect to baseline; p = 0.03). The heart rate and mean systemic blood pressure (BP) did not change significantly. Acute IV administration of epoprostenol decreased PVRI by 6 mmHg (- 40%) respect to baseline (p < 0.0001). CI increased by 1.4 L/min/m2 (p < 0.0001); while mPAP decreased by 5 mmHg (nearly 10%) (p = 0.04). This decrease of mPAP was accompanied by a mean BP decrease of 11 mmHg compared to baseline (p = 0.003). Our results indicates that, in patients with PAH associated with other pathological conditions, adenosine is predominantly a positive inotropic agent; and epoprostenol a potent vasodilator of both pulmonary and systemic vessels, and a strong positive inotropic agent.

Inflammation, atherosclerosis and hypertension: the impact of depression and stress on their complex relationship.

This future perspective analyzes the complex relationship between inflammation and atherosclerosis and arterial hypertension. The involvement of inflammation in atherosclerosis has led to research therapies that target inflammation to prevent or treat cardiovascular disease. This aspect has recently been included in the treatment management of residual cardiovascular risk. The recent pandemic has exacerbated cardiovascular risk both through an increase in unhealthy lifestyle behaviors and through the reduction of cardiovascular screening. What actions to take? Primary prevention campaigns for healthy subjects with specific attention to young people.

What is this article talking about? This article talks about how inflammation, atherosclerosis (a condition where arteries get narrow), and high blood pressure are connected. It looks deeply into how these things work together and can lead to heart problems. What is the point of the study? Learning about how inflammation is linked to atherosclerosis has made scientists study new ways to treat or prevent heart diseases. This is now a part of how we think about treating the risk of heart problems. How can we check the risk of heart problems in women? To make the risk of heart problems less, it's really important to start looking at and dealing with things that might cause these problems early on. Pregnancy is a good time to start doing this for young women. What changed because of the pandemic? The pandemic made it harder to prevent heart problems, and it made people more stressed. Women, especially, faced more challenges during and after the pandemic in terms of society and money.

The Impact of Stress and Social Determinants on Diet in Cardiovascular Prevention in Young Women.

The prevention of cardiovascular diseases is a fundamental pillar for reducing morbidity and mortality caused by non-communicable diseases. Social determinants, such as socioeconomic status, education, neighborhood, physical environment, employment, social support networks, and access to health care, play a crucial role in influencing health outcomes and health inequities within populations. Social determinants and stress in women are interconnected factors that can significantly impact women's health and well-being. Pregnancy is a good time to engage young women and introduce them to beneficial behaviors, such as adopting essential life skills, especially diet, and learning stress management techniques. Stress influences diet, and women are more likely to engage in unhealthy eating behaviors such as emotional eating or coping with stress with food. Strong action is needed to improve women's lifestyle starting at a young age considering that this lays the foundation for a lower cardiovascular risk in adults and the elderly. The objective of this review is to examine cardiovascular primary prevention in young healthy women, focusing particularly on unresolved issues and the influence of social determinants, as well as the correlation with stressors and their influence on diet.

Maternal-fetal dyad beyond the phenomenology of pregnancy: from primordial cardiovascular prevention on out, do not miss this boat!

Pregnancy represents a stress test for every woman's cardiovascular (CV) system, and a pre-existing maternal unfavorable cardio-metabolic phenotype can uncover both adverse pregnancy outcomes and the subsequent development of cardiovascular disease (CVD) risk factors during and after pregnancy. Moreover, the maternal cardiac and extracardiac environment can affect offspring's cardiovascular health through a complex mechanism called developmental programming, in which fetal growth can be influenced by maternal conditions. This interaction continues later in life, as adverse developmental programming, along with lifestyle risk factors and genetic predisposition, can exacerbate and accelerate the development of CV risk factors and CVD in childhood and adolescence. The aim of this narrative review is to summarize the latest evidences regarding maternal-fetal dyad and its role on primordial, primary and secondary CV prevention.

Long COVID: A New Challenge for Prevention of Obesity in Women.

The long COVID affects individuals that do not recover for several weeks or months following the onset of symptoms of COVID-19. Obesity could play a role in the long COVID syndrome. During the pandemic, various factors contributed greatly to aggravating obesity in women leading to a pro-inflammatory and prothrombotic status. The present commentary explores the relationship between long COVID and obesity in women.

Changes in coffee and caffeine intake during the pandemic in women smokers and non-smokers: a future challenge for cardiovascular prevention.

BACKGROUND: The recent pandemic has led to major lifestyle changes, especially in women, changes that will impact cardiovascular risk. The aim of the present observational study was to evaluate changes occurred during pandemic in coffee and caffeine intake in a group of adult women and compare changes in smoking versus non-smoking women. METHODS: A web questionnaire was sent through a online survey platform to a group of unselected adult women. The consumption of coffee and caffeine were investigated in 2 groups of women by comparing smokers and non-smokers. RESULTS: A total of 435 adult women (256 non-smokers and 179 smokers) answer to all questions. Smokers increase the number of cigarette/days (mean + 3.4 cig/day). Coffee intake was significantly increase in smokers compared to non-smokers (3.1+1.0 versus 1.5+0.6 cups/day p<0.01). In smokers, self-perception of increase stress was related to increased coffee intake (r = 0.84; p <0.001), increased sugar- rich foods (r=0.81; p<0.001), increased chocolate rich snacks (r=0.72; p<0.01), increased sitting time (r=0.79; p<0.01). CONCLUSIONS: These preliminary data must suggest to undertake social campaigns aimed at encouraging a return to a healthy lifestyle that certainly includes a healthy diet but also the suspension of smoking. These observational results need further evaluation with prospective studies in order to quantify the effects of pandemic-induced changes in lifestyle on cardiovascular risk in women.

Effects of Ivabradine on Right Ventricular Systolic Function in Patients With Chronic Obstructive Pulmonary Disease and Cor Pulmonale.

Cor pulmonale is a clinical syndrome associated with pulmonary hypertension, frequently complicated by congestive heart failure, commonly caused by chronic obstructive pulmonary disease (COPD). Most patients with cor pulmonale have tachycardia. However, heart rate (HR) reduction represents a primary treatment goal to improve the survival and quality of life in these patients. Ivabradine can selectively slow HR at rest and during exercise. In this prospective study, we tested the hemodynamic effects, invasively determined using right-sided cardiac catheterization, of reducing HR with ivabradine. We selected 18 patients (13 men [72.2%], mean age 67 ± 10 years) with COPD and cor pulmonale, presenting with sinus tachycardia. All patients performed clinical evaluation, electrocardiogram, spirometry, echocardiogram, 6-minute walking distance, and right-sided cardiac catheterization within 1 month of enrollment. All tests were repeated after 6 months of ivabradine treatment (median assumed dose 11.9 mg/die). We noticed a significant decrease of HR (from 98 ± 7 to 77 ± 8 beats/min, p = 0.0001), with a concomitant reduction of the congestion index (from 25.9 ± 5.1 to 19.4 ± 5.7 mm Hg, p = 0.001), and the consequent improvement of the right ventricular systolic performance (right ventricular stroke volume augmented from 56.7 ± 7.9 to 75.2 ± 8.6 ml/beat, p = 0.0001). This allows an improvement in clinical status and exercise tolerance (Borg scale score decreased from 5.2 ± 1.4 to 4.1 ± 1.3, p = 0.01 and the 6-minute walking distance increased to 252 ± 65 to 377 ± 59 m, p = 0.001). In conclusion, HR reduction significantly improves hemodynamic and clinical status of patients with tachycardia affected by COPD and cor pulmonale.

Risk Factors and Cellular Differences in Heart Failure: The Key Role of Sex Hormones.

Patients with heart failure are conventionally stratified into phenotypic groups based on their ejection fraction. The aim of this stratification is to improve disease management with a more targeted therapeutic approach. A further subdivision based on patient gender is justified. It is recognized that women are underrepresented in randomized controlled clinical trials, resulting in limited clinical and molecular differentiation between males and females. However, many observational studies show that the onset, development, and clinical course of the disease may substantially differ between the two sexes. According to the emerging concept of precision medicine, investigators should further explore the mechanisms responsible for the onset of heart failure due to sex differences. Indeed, the synergistic or opposing effects of sex hormones on the cardiovascular system and underlying heart failure mechanisms have not yet been clarified. Sex hormones, risk factors impact, and cardiovascular adaptations may be relevant for a better understanding of the intrinsic pathophysiological mechanisms in the two sexes. Despite the differences, treatment for HF is similar across the whole population, regardless of sex and gender. In our review, we describe the main differences in terms of cardiovascular dysfunction, risk factors, and cellular signaling modifications related to the hormonal pattern.